Oxford Anesthesia 2022
Oxford Anesthesia 2022
Oxford Anesthesia 2022
Anaesthesia
FIFTH EDITION
Rachel Freedman
Consultant Anaesthetist, Imperial College Healthcare NHS
Trust, London, UK
Lara Herbert
Consultant Anaesthetist, Royal Cornwall Hospitals NHS
Trust, UK
Aidan O’Donnell
Consultant Anaesthetist, Waikato District Health Board,
Hamilton, NZ
Nicola Ross
Consultant Anaesthetist, Royal Devon and Exeter NHS
Foundation Trust, UK
Keith G Allman
Consultant Anaesthetist, Royal Devon and Exeter NHS
Foundation Trust, UK
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1
Great Clarendon Street, Oxford, OX2 6DP,
United Kingdom
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© Oxford University Press 2022; Chapter 15 © Tim Cook, Julius Cranshaw,
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Second edition 2006
Third edition 2011
Fourth edition 2016
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vii
Contents
Contributors ix
Abbreviations xiv
Index 1217
xvi
xiv
Abbreviations
2D two-dimensional APL adjustable pressure-limiting
3D three-dimensional APTT activated partial
5-HT serotonin thromboplastin time
(5-hydroxytryptamine) AR aortic regurgitation
AAA abdominal aortic aneurysm ARB angiotensin receptor blocker
AADR anaesthetic adverse drug ARDS acute respiratory distress
reaction syndrome
AAGA accidental awareness during AS aortic stenosis
general anaesthesia ASA American Society of
ABC airway, breathing, circulation Anesthesiologists
ABG arterial blood gas ASD atrial septal defect
AC alternating current ASIS anterior superior iliac spine
ACC American College of AST aspartate transaminase
Cardiology AT anaerobic threshold
ACE angiotensin-converting enzyme ATLS® Advanced Trauma Life
ACF antecubital fossa Support®
ACT activated clotting time AV atrioventricular
ACTH adrenocorticotrophic A–V arteriovenous
hormone AVM arteriovenous malformation
ADH antidiuretic hormone AVR aortic valve replacement
ADHD attention-deficit hyperactivity AVSD atrioventricular septal defect
disorder
BCIS bone cement implantation
ADP adenosine diphosphate syndrome
AEC airway exchange catheter bd bis diem (twice daily)
AED automated external BiPAP bilevel positive airway pressure
defibrillator
BIS bispectral index
AF atrial fibrillation
BLS basic life support
AFE amniotic fluid embolism
BMI body mass index
AFOI awake fibreoptic intubation
BMS bare-metal stent
AHI apnoea–hypopnoea index
BNF British National Formulary
AIC Aintree intubation catheter
BNFc British National Formulary for
AIDS acquired immune deficiency Children
syndrome
BNP brain natriuretic peptide
AKI acute kidney injury
BP blood pressure
ALF acute liver failure
bpm beats per minute
ALI acute lung injury
BURP backward, upward, and
ALP alkaline phosphatase rightward pressure
ALS advanced life support Ca2+ calcium ion
ALT alanine aminotransferase CABG coronary artery bypass grafting
a.m. ante meridiem (before noon) CAD coronary artery disease
AMI acute myocardial infarction CBF cerebral blood flow
AoA Association of Anaesthetists CC creatinine clearance
AP anteroposterior CCF congestive cardiac failure
APAGBI Association of Paediatric CEA carotid endarterectomy
Anaesthetists of Great Britain
and Ireland CF cystic fibrosis
Abbreviations xv
• Technology and engineering have facilitated big gains in patient safety, e.g.
pin-indexing of cylinders, mandatory SpO2 and capnography, advanced
intubating devices and ultrasound for vessel and nerve visualisation.
• Use of guidelines, protocols and good practice standards, e.g. National
Institute for Health and Care Excellence (NICE), Royal College
of Anaesthetists (RCoA) and Association of Anaesthetists (AoA)
guidance. In the UK, the RCoA is leading the way with programmes
for excellence, such as Anaesthesia Clinical Services Accreditation
(ACSA), where participating anaesthesia departments measure their
performance against a robust set of standards.
• Outcome measures may be immediate (complication rate),
medium term (length of stay, 30d mortality) or long term (quality
of life improvements and functional improvement over 1y, National
Emergency Laparotomy Audit (NELA)3). We improve what we measure
and what we measure must be important to the patient.
• Quality improvement, audit and research: a growing trend is where data
from small quality improvement projects conducted by local hospital
teams are pooled at a national level, thereby giving the data greater
validity. The National Audit Projects (NAPs) and the Sprint National
Anaesthesia Projects (SNAPs) have generated information on large
numbers of patients, giving evidence-based insight into deficits in care
and incidence of problems.4,5 The Healthcare Quality Improvement
Partnership is a huge resource of strategies for examining and instituting
best practice.
• Morbidity and mortality reviews are important, both locally and
nationally (e.g. National Confidential Enquiry into Perioperative Deaths
and the maternal morbidity and mortality reviews). They examine
themes that lead to harm and aid delivery of better care through
education, training and constant review.6,7
• There is increasing evidence that simulation-based team training
to improve technical and non-technical skills improves both team
performance and patient outcomes.8
• Coordinated, safe care requires high-quality handovers. There is
growing evidence that these can make a significant difference, not only
to patient morbidity, but also to mortality.
• Checklists have been shown to decrease human error, improve patient
safety and teamwork and increase the quality of care, e.g. the World
Health Organization (WHO) checklist and checklists for handovers,
procedures and emergency situations.9
• Patient education (e.g. joint schools) and assessment (e.g.
preassessment clinics) allow amelioration of risk through optimisation
and planning (for detail, see % pp. 49–52).
The WHO checklist
The WHO Second Global Patient Safety Challenge addressed surgical and
anaesthesia safety and looked at the evidence base behind surgical com-
plications. The result was a comprehensive clinical review and a 19-point
WHO Surgical Safety Checklist (Fig. 1.1) intended to focus on key parts of
the surgical journey.10
Looking after the patient
Fig. 1.1 World Health Organization Surgical Safety Checklist. Reproduced with permission from the World Health Organization. M http://
whqlibdoc.who.int/publications/2009/9789241598590_eng_Checklist.pdf © World Health Organization 2009.
5
6
Drug safety
Anaesthetists are at high risk of making drug errors due to the frequency
and rapidity of drug administration. Prospective data suggest errors may
occur in 1 in every 133 anaesthetics.15,16
• H Any drug can be harmful if given in the wrong quantity, wrong
dilution or by the wrong route.
• The appearance of ampoules changes with alarming frequency as
hospitals reduce costs by sourcing the cheapest formulation. Do not
rely on pattern recognition. Pay particular attention to ampoules of
drugs that look alike or sound alike.
• Avoid distractions. Do not talk to someone else or allow other
distractions while drawing up drugs. Drug error is more likely when
fatigued, busy or distracted or when multiple anaesthetists work
together.
• Do not assume that the drug in the ampoule is the same as the drug
labelled on the outside of the box.
• Many drugs are available in different concentrations in the same hospital
(e.g. propofol, ketamine, heparin, insulin, atropine). Before drawing up
any drug, always check the generic name, concentration, volume and
expiry date on the ampoule, preferably with a second person.
• Label syringes immediately after drawing up a drug; do not put a syringe
containing a drug down until it is labelled.
• Consider a second person to check drugs prone to errors (potassium,
insulin, heparin, inotropes).
• If you have never given the drug before, or not by that route, check
with someone who has.
• Always check controlled drugs. Sign for what you have given and what is
discarded.
• Dilution of medications for paediatric patients is very anaesthetist-
dependent (e.g. suxamethonium 50mg/mL or 10mg/mL, fentanyl
50 micrograms/mL or 10 micrograms/mL). Confirm with your team which
dilutions are being used and write these on the syringes clearly. It is easy
to make a mistake by a factor of 10 if you are in a rush. Work out doses
before the patient arrives and if in doubt, check with a second person.
8
Level Description
1 Meta-analysis of RCTs (with homogeneity) or individual RCT
with narrow confidence interval
2 Low-quality RCT or cohort studies
3 Case-control study
4 Case series (and poor-quality cohort and case-control studies)
5 Expert opinion or based on basic science research
p-values
A null hypothesis states that there is no relationship between the two
variables being studied and any discrepancy in results is due to chance, ra-
ther than being a significant finding. Levels of statistical significance are de-
scribed by the p-value. The smaller the p-value, the stronger the evidence
that the null hypothesis should be rejected. A p-value of 0.05 is taken as
12
Fig. 1.2 Example forest plot showing four trials comparing paravertebral block with
epidural analgesia to reduce pulmonary complications. See text for details. Source:
data from Davies RG, Myles PS, Graham JM (2006). A comparison of the analgesic efficacy and
side-effects of paravertebral vs epidural blockade for thoracotomy—a systematic review and meta-
analysis of randomized trials. Br J Anaes, 96, 418–426.
If you feel well during pregnancy, you should be able to do most things
normally, but you should not put yourself at risk or carry on working if you
are fatigued or unwell. Departments and training programme directors will
be grateful for early notification to allow them the maximum time to cover
your maternity leave.
Personal protective equipment (PPE)
Employers have a duty to protect you from avoidable risks in the workplace.
H Keep yourself safe, first and foremost.
• Before undertaking any procedure, you should assess the likelihood
of exposure to potentially harmful agents and wear appropriate PPE.
There will be local policies to guide you. Examples of PPE include:
gloves (sterile and non-sterile), aprons, masks of varying protection (e.g.
fluid-resistant, respirator, aerosol-resistant), laser goggles, lead shields,
aprons and radiation badges.
• PPE is only as good as the person putting it on. Make sure it is
appropriate for the task, fits you, you know how to don and doff it
correctly and you know how to dispose of it safely.
Blood and bodily fluid exposure
Exposure to blood and bodily fluids is a daily hazard for the anaesthetist.
Develop safe practice from the very beginning of your career to minimise
your likelihood of inoculation injury. It is hard to change your habits later
in your career.
Prevention
Ensure your vaccinations are up-to-date; always wear PPE as per local pol-
icies, and dispose of sharps correctly.
Exposure
Broken skin or mucous membranes can be contaminated with blood or
bodily fluid. Apply protective dressings to broken skin.
First aid
Remove the contaminant. If the skin is contaminated, wash with soap
and water. If the skin is breached, encourage bleeding if possible. Irrigate
contaminated mucous membranes with copious volumes of 0.9% sodium
chloride; then dry and cover if possible. Remove contact lenses if eyes are
contaminated. If in doubt about the seriousness of the injury, attend the ED.
Report
Report to your supervisor and fill out a Reporting of Injuries, Diseases
and Dangerous Occurrences Regulations (RIDDOR) form or your local
equivalent.
Risk assessment
Should not be done by the recipient (contaminated person). The type of
incident, infective state of the donor (usually the patient), lifestyle risks and
vulnerability of the recipient are all important. A hollow needle that breaks
the skin carries the greatest risk of transmission (1:3 hepatitis B, 1:30 hepa-
titis C, 1:300 human immunodeficiency virus (HIV)).
18
Occupational health
(Out of hours, notify the ED.) Post-exposure prophylaxis may be required
(hepatitis B and HIV), and baseline bloods should be taken from the re-
cipient. A third party needs to obtain informed consent from the donor
before blood can be sent for testing.
Follow-up
This can be very stressful. Follow-up with occupational health is important.
The recipient may be temporarily suspended from carrying out exposure-
prone procedures until transmission is confirmed as negative.
Manual handling
Look after yourself by using the correct equipment and technique and at-
tending any training offered. Do not compromise your safety or that of
your team or the patient for the sake of rapidity. It is usual for the anaes-
thetist to take charge of movement of the patient in theatre; use clear com-
mands to protect both the patient and staff from injury.
• The anaesthetist is responsible for protecting unconscious patients from
harm when they are being moved. Pay attention to connected drips,
wires, airway tubing, catheter bags, surgical drains and other potential
hazards to avoid problems that can cause accidental injury to patients
or staff.
• If you are carrying an injury, contact occupational health for advice
before musculoskeletal injuries are exacerbated.
Anaesthetising colleagues and their relatives
During your career, you may be asked to anaesthetise a colleague, a friend
or their relative. The initial flattery of being approached is invariably re-
placed quickly by anxiety. It may be something you are expert in or do rou-
tinely, but the added stress of knowing the patient can be a potential hazard.
You may feel pressurised into doing something you would not normally do
at personal request or be less thorough with your consent, having assumed
understanding. Only agree if you feel happy to do so and if you have any
concerns, politely decline or ask for senior help. If you are faced with this
situation in an emergency, be aware of potential pitfalls; remain vigilant for
differences from your normal practice, and ask for senior help if needed.
Dealing with a complaint/coroner’s inquest
Unfortunately, many of us will have to deal with a complaint, an investiga-
tion or a coroner’s inquest regarding aspects of our care during our careers.
This is an upsetting and stressful time and should not be faced alone. Seek
advice from colleagues, mentors and friends, along with your medical de-
fence organisation and your hospital’s legal team if needed.
• Sometimes the complaint occurs in your presence, but more often, it
is via written communication to a third party. Coroner’s inquests and
investigations may take many months or years to come to a conclusion,
during which time you may or may not be aware of the process.
• If you have any concerns about an event in which you have been
involved, or think there is a possibility further investigation may occur, it
is worthwhile contacting your medical defence organisation. Most have
a 24h helpline and the advice, support and reassurance they offer is very
helpful.
Looking after yourself 19
References
1 The International Surgical Outcomes Study Group (2016). Global patient outcomes after elective
surgery: prospective cohort study in 27 low-, middle-and high-income countries. Br J Anaesth,
117, 601–9. doi:10.1093/bja/aew316.
2 Reason J (1990). Human Error, 1st edn. Cambridge: Cambridge University Press.
3 National Emergency Laparotomy Audit. M https://www.nela.org.uk/
4 National Audit Projects. M https://www.nationalauditprojects.org.uk/
5 Health Services Research Centre. SNAP-2 (EpiCCs). M https://www.nationalauditprojects.org.
uk/SNAP-2-EpiCCS
6 National Confidential Enquiry into Patient Outcome and Death (NCEPOD).
M https://www.ncepod.org.uk/
7 National Perinatal Epidemiology Unit. MBRRACE-UK: Mothers and Babies: Reducing Risk through
Audits and Confidential Enquiries across the UK. M https://www.npeu.ox.ac.uk/mbrrace-uk/
reports
8 Higham H, Baxendale B (2017). To err is human: use of simulation training to enhance training and
patient safety in anaesthesia. Br J Anaesth, 119, i106–14. doi:10.1093/bja/aex302
20
9 Saxena S, Krombach JW, Nahrwold DA, et al. (2020). Anaesthesia-specific checklists: a system-
atic review of impact. Anaesth Crit Care Pain Med, 39, 65–73.
10 World Health Organization (2009). WHO guidelines for safe surgery 2009. Safe surgery saves lives.
M http://whqlibdoc.who.int/publications/2009/9789241598552_eng.pdf
11 Haynes AB, Thomas WG, Berry WR, et al. (2009). A surgical safety checklist to reduce morbidity
and mortality in a global population. N Engl J Med, 360, 491–9.
12 General Medical Council (2013). Good medical practice. M https://www.gmc-uk.org/ethical-
guidance/ethical-guidance-for-doctors/good-medical-practice
13 Utting JE (1987). Pitfalls in anaesthetic practice. Br J Anaesth, 59, 888–90.
14 The Association of Anaesthetists (2015). Standards of monitoring during anaesthesia
and recovery. M https://anaesthetists.org/Home/Resources-publications/Guidelines/
Standards-of-monitoring-during-anaesthesia-and-recovery
15 Glavin RJ (2010). Drug errors: consequences, mechanisms, and avoidance. Br J Anaesth,
105, 76–82.
16 Jensen LS, Merry AF, Webster CS, Weller J, Larsson L (2004). Evidence-based strategies for
preventing drug administration errors during anaesthesia. Anaesthesia, 59, 493–504.
17 Civility Saves Lives. M https://www.civilitysaveslives.com/
18 Royal College of Anaesthetists. Revalidation for anaesthetists. M https://www.rcoa.ac.uk/
training-careers/working-anaesthesia/revalidation-anaesthetists
19 McClelland L, Holland J, Lomas JP, et al. (2017). A national survey of the effects of fatigue on
trainees in anaesthesia in the UK. Anaesthesia, 72, 1069–77. M https://onlinelibrary.wiley.com/
doi/full/10.1111/anae.13965
20 McClelland L, Plunkett E, McCrossan R, et al. (2019). A national survey of out-of-hours working
and fatigue in consultants in anaesthesia and paediatric intensive care in the UK and Ireland.
Anaesthesia, 74, 1509–23. M https://onlinelibrary.wiley.com/doi/full/10.1111/anae.14819
21 View-Kim Wong A, Olusanya O (2017). Burnout and resilience in anaesthesia and intensive
care medicine. BJA Educ, 17, 334–40. M https://academic.oup.com/bjaed/article/17/10/334/
3865410
22 Association of Anaesthetists (2014). Occupational health and the anaesthetist. M https://anaes-
thetists.org/Portals/0/PDFs/Guidelines%20PDFs/Guideline_occupational_health_anaesthe-
tists_2014_final.pdf?ver=2018-07-11-163755-740&ver=2018-07-11-163755-740
Chapter 2 21
Preoperative
considerations
Tom Blincoe, Ian Densham and David Kotwinski
Better perioperative care 22
Preoperative assessment 23
Preoperative history 24
Preoperative examination 27
Preoperative investigations 28
Consultation models 31
Functional assessment 32
Risk assessment 36
Outcomes 39
Shared decision-making 40
Consent 41
Planning postoperative care 43
Enhanced recovery after surgery 44
2
Before surgery
Functional assessment
Risk prediction
Shared decision-making
During surgery
Standardised care pathways
Best practice evidence-based standards
Preoperative assessment
All patients should be assessed prior to anaesthesia. There are two main
parts to a preoperative assessment.
For planned surgery:
• A nurse-led, protocol-driven triage process may be the only assessment
for fit patients prior to surgery, or this may be followed by a face-to-
face consultation with a preoperative specialist nurse.
• Less fit patients undergoing major surgery require a comprehensive
preoperative assessment. This should be performed by an anaesthetist
or a perioperative physician who will engage in a meaningful, shared
decision-making process.
• The second part occurs on the day of surgery. It involves a brief
systemic enquiry for new or progressive symptoms, a check of fasting
status, medications, allergies and a relevant examination.
• It is also an opportunity to discuss the planned anaesthetic technique, to
establish rapport and to alleviate concerns.
For emergency or urgent surgery in the patient with an unplanned admission:
• The two parts described above merge into a more focused risk
assessment.
Objectives of preoperative assessment
• Take a full history.
• Perform an examination.
• Establish optimal management of concomitant disease.
• Establish functional status/exercise capacity.
• Establish and discuss risk.
• Establish and discuss possible anaesthetic plans.
• Discuss concerns and expectations.
• Build rapport.
• Discuss immediate perioperative measures.
• Provide written information for further consideration.
• Document the process.
• Prevent cancellation on the day of surgery.
Further reading
There are robust guidelines for the delivery of preoperative assessment
services and recommendations for the management of comorbidities, avail-
able from the AoA, RCoA, NICE and The Preoperative Association.4,5,6,7
24
Preoperative history
Preoperative history taking in the preoperative assessment clinic should be
comprehensive and cover the following areas.
Anaesthetic history
• Previous adverse events related to anaesthesia
• Airway difficulties (review of old charts)
• Anaphylaxis
• Postoperative nausea and vomiting (PONV)
• Difficult vascular access
• Unplanned critical care admission
• Family history of anaesthetic problems
• Malignant hyperthermia (MH) and suxamethonium apnoea.
Surgical history
• Indication for current procedure
• Patient’s attitude towards condition
• Duration and progression of symptoms
• Effect of symptoms on the patient’s life
• Trial of conservative measures/alternative options
• Previous surgical procedures:
• May increase complexity/duration of proposed procedure
• May have implications for regional anaesthesia/analgesia
• Will inform risk–benefit discussion.
Medical history
A systemic enquiry is necessary to identify symptoms where further treat-
ment or investigation may be required. Key areas of concern are:
Respiratory
(For detail, see % p. 164.)
• Asthma, chronic obstructive pulmonary disease (COPD), obstructive
sleep apnoea (OSA)
• Admissions and management of respiratory diseases
• Comparison of current and previous lung function tests.
Cardiovascular
(For detail, see % Chapter 5.)
• Ischaemic heart disease (IHD), hypertension, pulmonary hypertension,
myocardial dysfunction, valvular disease, arrhythmias
• Anaemia, previous transfusions and attitudes towards transfusion.
Endocrine
(For detail, see % Chapter 9.)
• Diabetes.
Preoperative history 25
Neurology
(For detail, see % Considerations for the older patient, pp. 89–94;
% Chapter 12; % Chapter 41.)
• Acute or chronic pain
• Frailty and cognitive impairment
• Previous cerebrovascular event (CVE)/transient ischaemic attack (TIA)
and residual deficit.
Gastrointestinal
• Gastro-oesophogeal reflux disease (see % p. 58)
• Nutritional status (see % p. 50; % p. 82).
Renal
(For detail, see % Chapter 7.)
• Level of impairment/cause.
Musculoskeletal
• Considerations for positioning
• Considerations for regional anaesthesia.
Social history
• Occupation or retired occupation
• Family members, relationships and local support
• Accommodation arrangements
• Level of independence and ability with activities of daily living
• Alcohol consumption/misuse
• Smoking
• Recreational/illicit drug use.
Drug history and allergy status
• Record a full list of current medications and details of significant
historical use, e.g. recent steroids, disease-modifying antirheumatic
drugs (DMARDs) and chemotherapy.
• Careful perioperative management of certain medications, such as
anticoagulants and diabetic medications, is required (see % pp. 269–75;
% pp. 216–21).
• It is essential that instructions regarding medications are clear.
• Most medications can and should be continued until the morning of
surgery.
• Be attentive for drugs that interact with anaesthetics (Table 2.1).
26
Preoperative examination
The completeness of the physical examination as part of a preoperative
assessment will depend on the patient and the procedure. The following
aspects of physical examination, however, are usually relevant.
General appearance
• Body habitus
• Vital signs
• Fluid status
• Nutritional status
• Mobility/aids.
Airway assessment
(For detail, see % pp. 363–7.)
• Mouth opening/Mallampati score
• Jaw protrusion
• Dentition
• Neck range of movement
• Facial hair.
Respiratory
(For detail, see % p. 164.)
• Presence of dyspnoea and/or cyanosis
• Medical interventions (oxygen (O2), nebulisers, chest drain)
• Clarity of lung fields
• Scarring/previous surgery.
Cardiovascular
(For detail, see % Chapter 5.)
• Arterial pulses and rhythm
• Vascular access options
• Heart sounds
• Peripheral oedema
• Presence of cardiac implantable electronic devices.
Neurological
(For detail, see % Chapter 12.)
• Any pre-existing deficit.
Musculoskeletal
• Range of movements relevant to positioning (e.g. shoulder joints for
proning)
• Examination of potential regional block sites.
28
Preoperative investigations
• Preoperative investigations should be conducted according to individual
patient circumstances.
• National guidelines exist8 and should be taken into account to prevent
unnecessary tests and target those in whom investigations will inform
discussion of risk and support shared decision-making.
• Standardised referral pathways (with specific fitness for referral criteria)
between 1° and 2° care should minimise duplication of investigations.
• NICE guidelines8 make recommendations for investigations based on
the grade of surgery and American Society of Anesthesiologists (ASA)
score (Table 2.2). They also recommend the following:
• Pregnancy testing in all women with childbearing potential
• HbA1c testing only if diabetic and no test within last 3mo
• No other tests should be offered routinely. These include chest X-ray
(CXR), urine dipsticks, resting echocardiography and tests for sickle
cell disease or trait.
Specialist investigations
• Some specialist investigations and functional assessment (see %
pp. 32–5) may be performed at preoperative assessment clinic. Some
require referral.
• Detail on these investigations is provided in the relevant specialty
chapters. A brief overview is provided here.
Preoperative investigations 29
Cardiac investigations
(See % Chapter 5, in particular pp. 104–5.)
Valvular disease
• Patients with clinically suspected valvular disease (> moderate stenosis
or regurgitation) should undergo preoperative echocardiography if
there is:
• No prior echocardiogram within 1y
• A significant change in clinical status or physical examination since the
last examination.
Assessment of left ventricular function
• d left ventricular (LV) systolic function is associated with perioperative
complications, particularly postoperative heart failure.
• The association is greatest in patients with high predicted perioperative
mortality.
• In non-cardiac surgery, consider echocardiography in patients who:
• Have unexplained dyspnoea
• Have known heart failure and worsening dyspnoea, or who have not
had assessment of their LV function within 1y
• Are potential candidates for solid organ transplant.
• Patients with significant LV impairment should be referred for specialist
cardiology opinion and optimisation of cardiac function if urgency of
surgery allows.
Cardiac stress testing
• Echocardiography at rest will not detect stress-inducible ischaemia.9
• Exercise ECG or pharmacological stress testing has a high negative
predictive value for postoperative myocardial infarction (MI) or
cardiac death.
• Local variation will exist as to the type of stress testing preferred.
• If cardiopulmonary exercise testing (CPET) is available (and the patient
is able to exercise), then this should be considered, as it gives an
assessment of functional capacity and cardiorespiratory fitness. (For
CPET, see % pp. 33–5.)
Cardiac implantable electronic device testing
• The function of cardiac implantable electronic devices should be
checked prior to surgery if this has not been done routinely within
12mo for permanent pacemakers or 6mo for implantable cardioverter–
defibrillators (ICDs).10
Respiratory investigations
(See % p. 164.)
Spirometry
• Spirometry has not been shown to be predictive of postoperative
outcomes.
• Preoperative spirometry can be used to:
• Aid in the diagnosis of unexplained dyspnoea
• Monitor lung function in those with known chronic lung disease
• Assess lung function in patients with neuromuscular disorders
• Predict postoperative lung function in those undergoing lung resection
surgery.
30
Lung ultrasound
• Particularly useful in the context of urgent and emergency surgery. Its
uses include:
• Exclusion of pneumothorax
• Assessment of lung parenchyma
• Diagnosis of pleural effusion.
Consultation models
Consultation models provide a structure for complex interactions that
occur between patients and doctors. They may also enable more effective
communication to take place. Many consultation models exist. One that is
frequently applied to preoperative consultation is the Calgary–Cambridge
model.12 This consists of the following elements.
Initiating the session
• Preparation
• Establishing initial rapport
• Identifying the reason(s) for the consultation.
Gathering information to explore the case fully
• Biomedical perspective (symptoms, signs, clinical investigations)
• Patient’s perspective
• Background information.
Building the relationship
• Using appropriate non-verbal behaviour
• Developing rapport
• Involving the patient.
Providing structure to the consultation
• Making the consultation organisation overt (summarising at the end of
a specific line of enquiry and progressing from one section to another,
using signposting and transitional statements)
• Attending to flow (structuring the consultation in a logical sequence and
attending to timing).
Explanation and planning
• Providing the correct amount and type of information
• Aiding accurate recall and understanding
• Achieving a shared understanding and incorporate the patient’s
perspective
• Planning with shared decision-making.
Closing the session
• Ensuring appropriate point of closure
• Forward planning.
While these elements tend to be sequential, ‘building the relationship’ and
‘providing structure’ continue throughout the consultation.
32
Functional assessment
• Evaluation of functional capacity is integral to preoperative risk
assessment; a fundamental prerequisite for safe perioperative care.
• Objective functional capacity assessments are required to support
preoperative risk stratification. Unfortunately, functional assessment
tools suffer from a paucity of evidence and a lack of unified definition
regarding the outcomes that are of most importance to patients (see %
p. 39).
• Subjective assessments have been shown to be less accurate at
identifying those with poor cardiopulmonary fitness or predicting
postoperative complications.13
• There are physical and non-physical functional assessment tests.
Tests of functional capacity
6-minute walk test (6MWT)
• Formal conduct of the 6MWT has been defined by the American
Thoracic Society.14 It involves the patient walking as many laps as
possible in 6min of a flat, indoor 30m course.
• It has the advantage of being simple and cheap.
• Recent evidence suggests weak correlation between the 6MWT and
CPET, and moderate correlation between the 6MWT and Duke Activity
Status Index (DASI) scores.15
Exercise ECG and pharmacological stress testing
(See % pp. 104–5.)
• For the detection of myocardial ischaemia and identification of those
in whom percutaneous coronary intervention (PCI) or coronary artery
bypass grafting (CABG) are indicated prior to major surgery.
• Exercise ECG also provides an indication of functional capacity.
• Those with pre-existing ECG abnormalities may undergo
pharmacological stress testing or a myocardial perfusion scan.
Perioperative cardiac biomarker screening16
• There is likely a significant amount of undiagnosed/asymptomatic
perioperative myocardial ischaemia contributing to 30d mortality.
• Cardiac biomarker screening represents a promising alternative to,
or in conjunction with, other risk stratification methods to predict
postoperative cardiovascular morbidity and mortality.
• Tests consist of preoperative natriuretic peptides (brain natriuretic
peptide (BNP), N-terminal proBNP (NT-proBNP)) and early
postoperative troponins.
• Postoperative troponin surveillance may help identify high-risk patients,
particularly those urgent and emergency surgical patients lacking
detailed preoperative investigation.
• Relatively simple, well-established medical risk reduction strategies
(including antiplatelets, statins, β-blockade and direct oral
anticoagulants) exist for those identified with abnormal results at high
risk of morbidity and mortality.
• Cardiac biomarker testing is less expensive and resource-intensive than
cardiac imaging, with promising predictive value for both cardiac and
non-cardiac morbidity and mortality.
• More evidence is required prior to widespread implementation.
Functional assessment 33
Test conduct
There are four stages to an exercise test:
• Rest (3min):
• To record resting baseline data.
• Unloaded cycling (3min):
• For the patient to become accustomed to a cadence of 60/min.
• Ramp exercise (8–12min):
• Cycling continues until failure to maintain cadence of 60/min.
• A Borg score (rating of perceived exertion) should be recorded.
• Recovery (5min):
• Cycling continues unloaded for a short period.
• Monitor the patient until variables return to near baseline values.
Risk assessment
• Surgical and anaesthetic intervention decisions are made by balancing
the benefits against the risks.
• The actual risks and benefits of any given intervention are unique to
individuals, the procedure, the type of anaesthesia and an individual’s
perception of what is risky and what a good outcome is.
• Meaningful outcomes for individual patients should be central to any
discussion on risk and the context will guide specific risk disclosure.
• Risk assessment, shared decision-making (% p. 40) and informed
consent (% p. 41) are closely related, but distinct entities and should be
treated as such.
Estimating risk
• Reliably informing patients about risk remains a challenge.19
• Accurate and early risk stratification to identify high-risk patients
supports the introduction of targeted measures to reduce modifiable
risk via prehabilitation and optimisation, robust intraoperative
management plans and appropriate postoperative support.
• It is essential for minimising adverse outcomes and relies on high-quality
data at individual, institutional and national levels.
• It empowers patients and informs shared decision-making, facilitates
communication and underpins the legal consent process.
• There are a variety of tools for risk assessment. They vary widely in
their ease of use, accuracy and what cohort or risk they refer to.
• The process of risk assessment has been shown to positively influence
patients’ care, regardless of level of risk.20
Risk can be estimated using
• Biomarkers (see % p. 32; % p. 104)
• Functional assessment (see % pp. 32–5)
• Risk assessment tools:
• Scoring systems such as ASA, Lee’s Revised Cardiac Risk Index
and the Assess Respiratory Risk in Surgical Patients in Catalonia
(ARISCAT) risk index
• Prediction models such as Surgical Outcome Risk Tool (SORT),
Portsmouth-Physiological and Operative Severity Score for the
enUmeration of Mortality and morbidity (P-POSSUM), the National
Emergency Laparotomy Audit (NELA) risk prediction tool and
the American College of Surgeons National Surgical Quality
Improvement Programme (ACS NSQIP).
• Improving risk estimation tools, so that they predict outcomes that are
important to patients, remains a key challenge.
• Being able to predict outcomes that are meaningful to patients will
facilitate more informed decision-making prior to surgery.
Risk assessment 37
Discussing risk
• Disclosure of risk has changed (following Montgomery vs Lanarkshire
Health Board21) from the practice of medical professionals informing the
patient of what they consider to be appropriate, to what a reasonable
patient would want to know.
• This reflects the legal and moral shift away from paternalism towards
autonomy and self-determination with respect to decision-making about
health.
• Clinicians need to explore what patients consider to be relevant:
• It may not be appropriate to detail very serious, very rare
complications to a young, fit patient having a minor procedure, but
this should not be assumed.
• The focus of discussion for an elderly, comorbid patient listed for
major complex surgery would likely focus on survival benefit and
complications that may lead to loss of independence or a decline in
functional status. This, however, cannot be assumed.
• Ideally, comprehensive written information ± direction to online
resources should be provided and documented.
• The entire risk conversation is subject to bias and interpretation.
• Clinicians should seek to minimise such influences and support patients
in their decision-making by providing them with information which is
tailored to their individual needs.
• Factors that may alter the perception of a given risk include:
• Exposure bias: under-or over-publicity
• Regional bias: geographical variation
• Severity: anxiety and fixation on serious complications, or serious
events perceived as higher risk, despite rarity
• Vulnerability: denial, ‘it won’t happen to me’
• Controllability: more accepting of risk, more understanding of
complications
• Certainty: knowledge and understanding of events
• Familiarity: experience of prior interventions
• Presentation: spin on absolute vs relative risks, positive vs negative
presentation of numbers, e.g. ‘90% survival’ rather than ‘10%
mortality’.
• Words, pictures or numbers can be used to communicate risk.
• Evidence suggests considerable variation in the numerical translation of
verbal probability expressions such as ‘negligible’, ‘low’, ‘moderate’ and
‘high’ risk.22
• Patient leaflets and clear information, including an infographic of
anaesthetic risks and probability phrases, are available on the RCoA
website.23 (See Table 2.4 for summary.)
38
Shivering >1 in 10
Temporary memory loss (mainly in over 60s) >1 in 10
Sickness >1 in 10
Thirst >1 in 10
Sore throat >1 in 10
Bruising >1 in 10
Common: between 1 in 10 and 1 in 100
Equivalent to one person in a street
Outcomes
• Audit, quality improvement and research can be used to review and
analyse patient outcome data to improve patient care.
• Routinely collecting patient outcome data and using these to guide
local practice is increasingly widespread in UK centres. For example,
Patient Reported Outcome Measures (PROMs) following hip and knee
replacement surgery have been collected since 2009.
• Measurement of outcome after surgery is essential. Well-defined
outcome measures enable comparison between interventions, individual
practitioners and institutions, and enhance risk stratification.
• Outcome measures can be considered as either clinical outcomes or
patient-reported outcomes.
• Clinical outcomes include mortality and morbidity; 30d and 1y mortality
are routinely and relatively easily collected.
• Morbidity has a much higher prevalence than mortality in the general
surgical population and can be assessed using various tools such as
the Postoperative Morbidity Survey (POMS)24 or the Clavien-Dindo
classification.25
• Recent emphasis has focused on the use of patient-reported outcomes
as the more traditional and crude measures, such as 30d mortality,
unsurprisingly fail to adequately determine the impact of interventions
on patients’ lives.
• There is a need for more meaningful measures that occur more
frequently such as short-term complications and longer-term mortality.
• More common outcomes also yield more statistically meaningful
comparisons.26
• The Perioperative Quality Improvement Programme (PQIP)27 was
established in 2016 and aims to look at perioperative care of patients
undergoing major non-cardiac surgery. It measures complication rates,
failure to rescue and patient-reported outcomes. Participating hospitals
are provided with a live dashboard of their results, along with quarterly
and annual reports.
• The Standardised Endpoints in Perioperative Medicine (StEP) initiative
aims to define measures used in future studies to enable comparison
between studies and consolidate the evidence base.28
40
Shared decision-making
• The context in which clinical decisions are made is wide-ranging.
• Patients vary considerably in their attitudes towards their health, their
ability to make informed decisions and their understanding of options
and possible outcomes of those options.
• The legal and moral landscape in which health care decisions are made
is also changing (see % Risk assessment, pp. 36–8).
• If possible, establish patients’ values and preferences, as these should
determine the significance of various risks.29
• Shared decision-making is the process in which clinicians and patients
work together to select tests, treatments, management or support
packages using both clinical evidence and the patient’s informed
preferences.30
Essential components of shared decision-making include:
• Reliable, balanced, evidence-based information that outlines options,
outcomes and uncertainties
• Decision support counselling with a clinician to clarify options and
preferences
• Recording, communicating and implementing patient preferences
• Shared decision-making recognises two forms of expertise, as shown in
Box 2.2.30
Decision aids
• Most clinical decisions are not straightforward, with multiple options
and outcomes as possibilities. Just as clinicians are supported by clinical
guidelines, patients also require decision aids.
• Decision aids are tools that not only provide information on options,
but also help patients to decide which option to choose.
• Examples of decision aids include the following, with guidelines for
assessing the quality of any given resource: patient information sheets,
computer programs, smart phone or social media applications,
interactive websites and filmed patient/clinician interviews.31
• The use of decision aids has been shown to result in: greater knowledge
and understanding, more accurate risk perception, greater comfort
with decisions, less regret with complications, better adherence to
treatment, no increase in anxiety and fewer patients choosing major
surgery.32
Consent 41
Consent
• The legal stance on consent is changing, and professionals need to keep
abreast of evolving legal developments in the jurisdiction in which they
practise.
• The key principles of biomedical ethics, autonomy and self-
determination require clinicians to obtain consent prior to medical
intervention.
• Health professionals who carry out procedures without valid consent
are liable to legal action and investigation by professional bodies.33
Guidance on the process of consent34,35
• Information should be:
• Provided as early as possible
• Written or online for future reference
• Tailored to the individual.
• Discussion should:
• Include risks, benefits and alternatives
• Include opportunity for questions
• Be fully documented.
• Exceptions to the requirement for providing information:
• Patients consistently express desire not to know
• Informing the patient would pose a serious threat
• Emergency treatment in the patient’s best interests.
• In the UK, separate written consent is not required for anaesthesia
for another procedure, although it is recommended for independent
procedures.
• Consent is an ongoing process and should be obtained by either the
individual performing the procedure or a suitable delegate. It may
require repeated discussion and/or confirmation, with documentation
at every stage.
• Patients can qualify consent by refusing aspects of treatment.35
Capacity
• Valid consent requires that the patient has capacity.
• To have capacity for consent, the patient must understand and recall
the information provided, weigh up the risks and benefits, consider the
consequences of not having the procedure and communicate a decision
without coercion.
• It is the responsibility of the clinician obtaining the consent to establish
whether or not an individual has capacity.
• Capacity is not absolute. It is time-and decision-specific, and is subject
to change.
• The Mental Capacity Act (MCA) 200536 sets out the action required
by law when a patient over the age of 16y lacks capacity. The main
principles of the MCA 2005 are that an individual must:
• Be assumed to have capacity unless proven otherwise
• Be given all practicable help to make a decision before being treated
as lacking capacity
• Not be treated as lacking capacity merely because they make an
unwise decision.
42
Level Description
0 Patients whose needs can be met through normal ward care in an
acute hospital
1 Patients at risk of their condition deteriorating, or those recently
relocated from higher levels of care whose needs can be met on an
acute ward, with additional advice and support from the critical care
team
2 Patients requiring more detailed observation or intervention, including
support for a single failing organ system or postoperative care and
those ‘stepping down’ from higher levels of care
3 Patients requiring advanced respiratory support alone or basic
respiratory support, together with support of at least two organ
systems. This level includes all complex patients requiring support for
multiorgan failure
4
Ongoing care
• The surgical team is responsible for patients not requiring higher-level
care once they leave the recovery area.
• An anaesthetist must be available to review and provide advice for
patients with any problems/complications potentially related to
anaesthesia and related procedures.
Enhanced postoperative care
• Centres in the UK are now setting up enhanced care areas that provide
care between levels 1 and 2 (sometimes called ‘level 1.5 units’) for
those higher-risk patients who do not require admission to a high
dependency unit (HDU) but need a level of support higher than that
offered on a ward.
• Enhanced care is a relatively new and evolving concept, with the aim of
providing a higher level of observation, monitoring and interventions
than on the general ward.
• Enhanced advice and support from the critical care team should be
more easily accessible.
• Patients are under the combined care of the anaesthetic and
surgical teams.
Enhanced recovery after surgery 45
References
1 Centre for Perioperative Care. M https://cpoc.org.uk
2 Fowler AJ, Abbott TEF, Prowle J, et al. (2019). Age of patients undergoing surgery. Br J Surg, 106,
1012–18.
3 Royal College of Anaesthetists (2015). Perioperative medicine: the pathway to better surgical
care. M https://www.rcoa.ac.uk/sites/default/files/documents/2019-08/Perioperative%20
Medicine%20-%20The%20Pathway%20to%20Better%20Care.pdf
4 Association of Anaesthetists (2010). Pre-operative assessment and patient preparation –the role
of the anaesthetist. M https://anaesthetists.org/Home/Resources-publications/Guidelines/
Pre-operative-assessment-and-patient-preparation-the-role-of-the-anaesthetist-2
5 Royal College of Anaesthetists (2017). Risk explained. M https://www.rcoa.ac.uk/patient-
information/patient-information-resources/anaesthesia-risk/risk-explained?mini=2017-12
6 National Institute for Health and Care Excellence. Improving health and social care through
evidence-based guidance. M https://www.nice.org.uk/
7 The Preoperative Association. M https://www.pre-op.org/
8 National Institute for Health and Care Excellence (2016). Routine preoperative tests for elective
surgery. M https://www.nice.org.uk/guidance/ng45
9 Sicari R, Nihoyannopoulos P, Evangelista A, et al. (2009). Stress Echocardiography Expert
Consensus Statement—Executive Summary: European Association of Echocardiography (EAE)
(a registered branch of the ESC). Eur Heart J, 30, 278–89.
10 Bryant HC, Roberts PR, Diprose P (2016). Perioperative management of patients with cardiac
implantable electronic devices. BJA Educ, 16, 388–96.
11 Kruisselbrink R, Gharapetian A, Chaparro LE, et al. (2019). Diagnostic accuracy of point-of-care
gastric ultrasound. Anesth Analg, 128, 89–95.
12 Kurtz SM, Silverman JD (1996). The Calgary–Cambridge Referenced Observation Guides: an aid
to defining the curriculum and organizing the teaching in communication training programmes.
Med Educ, 30, 83–9.
13 Wijeysundera DN, Pearse RM, Shulman MA, et al. (2018). Assessment of functional capacity be-
fore major non-cardiac surgery: an international, prospective cohort study. Lancet, 391, 2631–40.
14 American Thoracic Society (2002). ATS statement: guidelines for the six-minute walk test. M
https://www.thoracic.org/statements/resources/pfet/sixminute.pdf
15 Shulman MA, Cuthbertson BH, Wijeysundera DN, et al. (2019). Using the 6-minute walk test to
predict disability-free survival after major surgery. Br J Anaesth, 122, 111–19.
16 Ruzycki SM, Prystajecky M, Driedger MR, et al. (2020). Peri- operative cardiac biomarker
screening: a narrative review. Anaesthesia, 75, e165–73. doi:10.1111/anae.14920
17 Levett DZH, Jack S, Swart M, et al. (2018). Perioperative cardiopulmonary exercise testing
(CPET): consensus clinical guidelines on indications, organization, conduct, and physiological in-
terpretation. Br J Anaesth, 120, 484–500.
18 Hlatky MA, Boineau RE, Higginbotham MB, et al. (1989). A brief selfadministered questionnaire
to determine functional capacity (the Duke Activity Status Index). Am J Cardiol, 64, 651–4.
19 Royal College of Anaesthetists (2019). Perioperative Quality Improvement Programme (PQIP) Annual
report 2018–19. M https://pqip.org.uk/pages/ar2019
20 National Emergency Laparotomy Audit (2019). The Fifth Patient Report of the National Emergency
Laparotomy Audit. M https://www.nela.org.uk/reports
21 UK Supreme Court (UKSC) (2015). Montgomery (Appellant) v Lanarkshire Health Board
(Respondent) (Scotland) UKSC 11. M https://www.supremecourt.uk/cases/uksc-2013-0136.
html
22 Wiles MD, Duffy A, Neill K (2020). The numerical translation of verbal probability expressions
by patients and clinicians in the context of peri-operative risk communication. Anaesthesia, 75,
e39–45.
23 Royal College of Anaesthetists. Patient information resources: risk explained. M https://www.rcoa.
ac.uk/patient-information/patient-information-resources/anaesthesia-risk/risk-explained
24 Grocott MP, Browne JP, Van der Meulenm J, et al. (2007). The Postoperative Morbidity Survey
was validated and used to describe morbidity after major surgery. J Clin Epidemiol, 60, 919–28.
25 Dindo D, Demartines N, Clavien PA (2004). Classification of surgical complications: a new pro-
posal with evaluation in a cohort of 6336 patients and results of a survey. Ann Surg, 240, 205–13.
26 Myles PS, Boney O, Botti M, et al. (2018). Systematic review and consensus definitions for the
Standardised Endpoints in Perioperative Medicine (StEP) initiative: patient comfort. Br J Anaesth,
120, 705–11.
27 Perioperative Quality Improvement Programme. M https://pqip.org.uk/content/home
46
28 Moonesinghe SR, Jackson AI, Boney O, et al. (2019). Systematic review and consensus definitions
for the Standardised Endpoints in Perioperative Medicine initiative: patient-centred outcomes. Br
J Anaesth, 123, 664–70.
29 Sturgess J, Clapp JT, Fleisher LA (2019). Shared decision-making in perioperative medicine: a
narrative review. Anaesthesia, 74, 13–19.
30 The King’s Fund (2011). Making shared decision-making a reality: no decision about me, without me.
M https://www.kingsfund.org.uk/publications/making-shared-decision-making-reality
31 Elwyn G, O’Connor AM, Bennett C, et al. (2009). Assessing the quality of decision support tech-
nologies using the International Patient Decision Aid Standards instrument (IPDASi). PLoS One, 4,
e4705. M https://doi.org/10.1371/journal.pone.0004705
32 O’Connor AM, Stacey D, Entwistle V, et al. (2017). Decision aids for people facing health treat-
ment or screening decisions. Cochrane Database Syst Rev, 4, CD001431.
33 Department of Health (2009). Reference guide to consent for examination or treatment, 2nd edn.
M http://webarchive.nationalarchives.gov.uk/20130107105354/http://dh.gov.uk/prod_
consum_dh/groups/dh_digitalassets/documents/digitalasset/dh_103653.pdf
34 General Medical Council (2008). Dcisions making and consent. M https://www.gmc-uk.org/
ethical-guidance/ethical-guidance-for-doctors/consent
35 Yentis SM, Hartle AJ, Barker IR, et al. (2017). AAGBI: consent for anaesthesia 2017. Anaesthesia,
72, 93–105.
36 Mental Capacity Act 2005 (2005). Chapter 9: Lasting powers of attorney. M http://www.legisla-
tion.gov.uk/ukpga/2005/9/contents
37 ERAS® Society. M https://erassociety.org/guidelines/list-of-guidelines/
Chapter 3 47
Preoptimisation
Tom Blincoe, David Kotwinski, and Ian Densham
Preoptimisation 48
Prehabilitation 49
Patient blood management, anaemia and iron deficiency 53
Fasting 57
Venous thromboembolism prophylaxis 59
Antibiotic prophylaxis 62
Perioperative medications 64
Herbal medicines and anaesthesia 65
Premedicants 66
48
48 Chapter 3 Preoptimisation
Preoptimisation
The role of the preoperative team has evolved over the past decade and
the focus is now not only on assessment, but also on patient optimisation.
This is where a collaborative approach is taken to get patients as fit for sur-
gery as possible in the time frame available.
Preoptimisation includes both lifestyle and medical optimisation of
comorbidity. The preoperative team works together with hospital special-
ists and GPs to identify and minimise risk factors for postoperative compli-
cations. With the facts, patients are then empowered to be fully involved in
shared decision-making.
Patients’ attitudes towards surgery are likely to shift in the future. Far
from being passive participants on the ‘conveyor belt’ to surgery, patients
are being encouraged to motivate and engage in physical and psychological
training, so as to ‘get fit’ for their operations, an approach analogous to how
an athlete would prepare for a marathon.
Prehabilitation 49
Prehabilitation
Habilitation is derived from the Latin ‘habilitare’, meaning ‘to make suitable’
or ‘to enable’. Prehabilitation is the practice of enhancing a patient’s func-
tional capacity before surgery, with the aim of improving postoperative out-
comes (Fig. 3.1).1 This may include lifestyle and nutritional advice, structured
physical exercise and psychosocial support.
Physical exercise
Physical inactivity is one of the leading risk factors for death worldwide
(WHO, 2018). In 2015/16, 26% of UK adults were classified as inactive
(<30min of physical activity per week).
• There is extensive evidence that exercise prolongs life and reduces CVS
disease in a dose-related fashion.
• A sedentary lifestyle is associated with twice the risk of premature
death, compared to physically active people.2
• Patients should be encouraged to undertake a minimum of 150min of
moderate exercise or 90min of vigorous exercise per week.
• Social prescribers can signpost patients to local physical activity
initiatives. GPs may be able to prescribe free or subsidised gym
memberships.
• Well-designed studies have demonstrated that preoperative exercise
can improve exercise capacity.
• There is limited evidence to suggest preoperative exercise programmes
reduce length of stay and postoperative pain and improve physical
function following major surgery.3
• Large multicentre RCTs are under way, aiming to demonstrate a
reduction in morbidity and mortality.
• Exercise programmes need to be tailored to individual patients,
according to baseline fitness levels and the time frame available.
Psychological support
There may be a role for preoperative psychological support in those at risk
of developing persistent and difficult-to-control postoperative pain.
50 Chapter 3 Preoptimisation
Nutrition
(See % p. 82 for the malnourished patient.)
Patients who are at high risk of being undernourished should have formal
dietetic referral prior to surgery (Fig. 3.2).
• Consider delaying their surgery to allow time for improvement in
nutritional state.
• All patients having major surgery should have minimal fasting times and/
or complex carbohydrate loading (including non-insulin-dependent
diabetic patients).4
Behavioural change
Making Every Contact Count (MECC) is a behavioural change consensus
statement published by NHS Health Education England in 2016. It recog-
nises that telling people what to do is not the most effective way to change
behaviour.
• Staff across health, local authority and voluntary sectors have thousands
of contacts with individuals every day.
• MECC describes using these opportunities to raise awareness,
encourage change and signpost to supporting agencies using an ‘Ask,
Advise, Assist’ structure to promote health and healthy lifestyles.5
Alcohol
Alcohol is the most consumed recreational drug in Great Britain; 57% of
adults drink alcohol regularly and nearly 10% drink on ≥5d per week.6
• Established liver cirrhosis presents a significant risk for perioperative
morbidity and mortality, but even moderate consumption of alcohol is
associated with i rates of postoperative infection.
• Abstinence from alcohol for 6–8w preoperatively has been
demonstrated to significantly reduce morbidity.7
• Using screening tools, such as the Fast Alcohol Screening Test and the
Alcohol Use Disorders Identification Test, can identify those at risk of
alcohol dependence/withdrawal and allow referral to specialist services
for detoxification programmes.
Smoking
(See % p. 173.)
In the UK, 14.4% of adults smoke regularly (2018).8
• Smoking is strongly associated with higher rates of significant
postoperative complications (relative risk 1.3–2.5).9
• Smoking cessation should occur at least 4w prior to surgery to produce
a significant reduction in risk. The longer the period of abstinence, the
greater the risk reduction.
• A meta-analysis of preoperative smoking cessation concluded that intense
behavioural interventions significantly reduced postoperative complications
and long-term abstinence, compared to brief interventions.10
Prehabilitation 51
52 Chapter 3 Preoptimisation
Obesity
(See % p. 70.)
UK obesity prevalence i from 15% in 1993 to 27% in 2015. In the UK, it
is the 2nd leading risk factor for developing cancer.
• Patients with BMI >40 and obesity-related comorbidities are particularly
at risk of postoperative complications. For example, obesity doubles
the risk of joint infection after hip and knee arthroplasty.11
• Preoperative weight loss not only reduces perioperative risk,12 but may
also reduce the need for surgery.
PATIENT BLOOD MANAGEMENT, ANAEMIA & IRON DEFICIENCY 53
54 Chapter 3 Preoptimisation
Iron physiology
• About 65% of iron is stored in Hb within red blood cells (RBCs) ±
15–20% is stored in macrophages, myoglobin, tissue enzymes and
cytochromes, and ± 15–20% within the liver, spleen and marrow as
haemosiderin and ferritin.
• Circulating (ferric) iron is primarily transported on transferrin, with
typically ± 30% of the binding sites being saturated.
• Systemic iron homeostasis is primarily regulated by the hepatically
produced peptide hormone hepcidin, which inhibits the movement of
iron into the circulation. In addition to high systemic iron levels, hepcidin
levels increase in response to infection, inflammation and malignancy.
• Iron used for the synthesis of new RBCs is mainly from macrophage-
recycled senescent RBCs.
• Normally, daily iron losses are balanced by gastrointestinal (GI)
absorption.
Aetiology
The causes can be broadly classified into causes of absolute and functional
iron deficiency:
• Absolute iron deficiency is caused by i iron requirements, limited
supply (insufficient intake or d absorption) and chronic blood loss.
• Functional iron deficiency is caused by i hepcidin concentrations, which
may be either genetic or caused by a chronic inflammatory state.
Investigating iron deficiency
• The hallmark blood test for iron deficiency is serum ferritin (sF).
Normal sF levels are >100 micrograms/L, with sF of <15 micrograms/L
considered pathognomonic of iron deficiency.
• Transferrin saturation (Tsat) values of >20% are required for normal
erythropoiesis.
• The main problem with sF is that it is an acute phase reactant, so iron
deficiency can exist with normal sF levels.
• In the presence of inflammation and/or Tsat <20%, an sF level <100
micrograms/L is indicative of iron deficiency.16
• GPs should be informed of any new diagnosis of iron deficiency
anaemia made by the preassessment service, so that the cause can be
fully investigated.
• Fig. 3.3 shows an example algorithm for the diagnosis of iron deficiency
anaemia.
Treatment of iron deficiency anaemia
• The aim of preoperative iron treatment is replenishing iron stores
(sF >100 micrograms/L) and achieving Hb ≥130g/dL, irrespective of
gender.
• Despite the focus on patients with a high transfusion risk, it is
considered good practice to treat all surgical patients with iron
deficiency anaemia.
• Patients with iron deficiency (without anaemia) undergoing high-
transfusion risk surgery should also be considered for supplementation.
• Treatment options are either oral (PO) or intravenous (IV) iron
preparations.
Patient blood management, anaemia and iron deficiency 55
Laboratory workup
Hb <130g/L
Iron investigations2
Other
Normal
anaemias
Abnormal
Fig. 3.3 Algorithm for management of patients with iron deficiency anaemia. CRP,
C-reactive protein (mg/L); sF, serum ferritin (micrograms/L); Tsat, transferrin
saturation (%).
Notes:
1
Transfusion risk >10% or estimated blood loss >500mL. Includes CABG, cardiac valve proced-
ures, colorectal resection, cystectomy, nephrectomy, 1° and revision hip or knee replacement, open
carotid artery procedures and other open aortic/iliac vascular operations.
2
International consensus suggests iron investigations include sF, Tsat and CRP (or equivalent inflam-
matory marker). However, some centres use reticulocyte Hb content.
Reproduced from Klein AA, et al. (2016). International consensus statement on the peri-operative
management of anaemia and iron deficiency. Anaesthesia, 72, 233–47, with permission from John
Wiley & Sons Ltd. © 2016 The Authors.
56
56 Chapter 3 Preoptimisation
Oral iron
• If >6w until surgery, then consider a trial of PO iron (40–60mg daily
or 80–100mg alternate days) and check Hb at 4w before surgery. If an
inadequate response or intolerant (gastric upset), then switch to an IV
treatment strategy.
• Effective in many but requires time and education to work.
IV iron
• If <4–6w to surgery, give IV iron.
• Highly efficacious, with symptom relief achieved at d3 and an Hb
response at d5 (maximal at 2–3w).18
• Even giving 1d preoperatively has been shown to aid postoperative
recovery.19
• Side effects: irreversible skin discoloration with extravasation (use an
infusion pump), fishbone reaction—a self-limiting reaction with flushing,
chest tightness and myalgia, and without hypotension, wheezing, stridor
or oedema (pause infusion for 15min), hypersensitivity <1/25 000 (less
frequent with newer preparations).
• Expert haematology and pharmacist advice should be sought when
developing local policies and considering which preparations to use.
• Whilst it is recommended practice, and considered safe and effective,
to treat patients with iron deficiency preoperatively, it is important
to acknowledge the recently published PREVENTT trial. This was a
UK-based randomised controlled trial of 487 patients that concluded
that preoperative IV iron was no better than placebo in reducing the
need for blood transfusion or improving 30-day mortality in anaemic
patients undergoing major abdominal surgery.20
Postoperative iron deficiency anaemia
• All patients who had major surgery with preoperative anaemia or
moderate to severe blood loss should be screened for iron deficiency
anaemia postoperatively for a minimum of 3d.
• Early high-dose IV iron is recommended as 1st-line therapy.
• High blood loss requiring blood transfusion may also require
postoperative supplementary IV iron.
Further reading
Muñoz M, Acheson AG, Bisbe E, et al. (2018). An international consensus statement on the man-
agement of postoperative anaemia after major surgical procedures. Anaesthesia, 11, 1418–31.
doi:10.1111/anae.14358
Fasting 57
Fasting
Preoperative fasting is defined as the restriction of fluid or food intake prior
to general anaesthesia (GA) or sedation.
Prolonged periods of fasting are unnecessary and have been associated
with deleterious effects, including distress, confusion, dehydration, CVS in-
stability, electrolyte disturbance, PONV, hypoglycaemia, insulin resistance,
worse outcomes and morbidity.
Preoperative fasting
The aim of preoperative fasting, by reducing the volume and nature of gas-
tric content, is to mitigate the risk of peri-procedural pulmonary aspiration.
• Patients should receive fasting guidance, including information on the
underlying rationale, during the anaesthetic preassessment.21
• Fasting times should be minimised, with specific consideration given to
the management of routine medication.
• ASA guidance (Table 3.1) is consistent with well-established practice.21
• The ongoing administration of clear fluids should be addressed
continuously over the course of an operating list. A 2h fast for clear
fluids can translate into significantly longer periods in reality.
• In 2018, an international consensus statement was issued, advising a
reduced fasting period for clear fluids to 1h (with a maximum volume of
3mL/kg) for children, in the absence of contraindications, undergoing
elective procedures22 (see % pp. 915–16). There is mounting pressure
for adult guidelines to adopt this reduced time frame.
• Examples of clear fluids include water, non-particulate juice, black tea or
coffee and carbohydrate nutritional drinks, but not alcohol.
• The ASA considers carbonated beverages to be clear fluids, but this is
not universally accepted—local guidelines should be followed.
• Non-human milk is considered solid, as when mixed with gastric juices,
it congeals. Small amounts (<20%) of milk in tea and coffee divide
opinion23—local guidelines should be followed.
• Normal gastric emptying of solids is slower and more variable than that
of fluids. Light meals (e.g. toast) have faster gastric emptying times than
foods with a high-fat or meat content.
• Patients should not have their surgery delayed for chewing gum, sucking
a boiled sweet or smoking a cigarette immediately before coming to
theatre.23
• A vital, if obvious, practical point is to ensure that chewing gum is
removed before anaesthesia to prevent it from being aspirated.
Table 3.1 Summary of 2017 ASA guidance for adult preoperative fasting periods
58 Chapter 3 Preoptimisation
60 Chapter 3 Preoptimisation
More than one VTE risk should prompt thromboprophylaxis. The risk of bleeding should
be balanced against the risk of VTE when deciding whether to offer pharmacological
thromboprophylaxis to surgical and trauma patients.4
*
For oestrogen-containing contraceptive and HRT, see % p. 64.
Source: data from Risk assessment for venous thromboembolism (VTE), Department of Health,
M https://webarchive.nationalarchives.gov.uk/20130123195034/http://www.dh.gov.uk/en/
Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_088215
62 Chapter 3 Preoptimisation
Antibiotic prophylaxis
• Antibiotic prophylaxis is administered to patients as part of a care
bundle to mitigate the risk of surgical site (wound) infection.33
• Other anaesthetic components of this bundle include maintaining
patient homeostasis such as normothermia, adequate oxygenation,
tissue perfusion and targeted glycaemic control.
Surgical antibiotic prophylaxis34
• Antibiotic prophylaxis is recommended before:
• Clean surgery involving prosthesis or implants
• Clean-contaminated surgery
• Contaminated surgery.
• It is not recommended for clean, non-prosthetic, uncomplicated
surgery.
• A patient’s antibiotic allergy and meticillin-resistant Staphylococcus aureus
(MRSA) status should be identified during preoperative assessment, and
prophylactic antibiotic choices tailored accordingly.
• Best practice is to inform patients preoperatively if they will need
antibiotic prophylaxis. They should also be informed postoperatively if
they received antibiotics during the operation.
• A course of antibiotic treatment should be given to patients having
surgery on dirty or infected wounds or to those with proven or
suspected systemic sepsis.
Timing of prophylactic antibiotics
• The WHO recommends that antibiotic prophylaxis is given within
60min of surgical incision.
• One exception is with infected patients where it is planned to take
surgical samples prior to administering antibiotics.
• It is recommended that prophylactic antibiotics are administered on
starting anaesthesia; however, earlier prophylaxis may be needed for
procedures requiring a tourniquet.34
• Antibiotics with long infusion durations should be commenced, so that
the infusion is complete before whichever is the earlier of knife to
skin or tourniquet inflation (e.g. vancomycin and fluoroquinolones are
infused over 60–120min).
• Repeat antibiotic doses should be administered for procedures >2–4h
(typically where the duration >2 half-lives of the antibiotic) or with
associated significant blood loss (>1.5L).33,35
• It is important to note that certain patient factors, such as extensive
burns or renal failure, may impact on the half-life of the antibiotic.
• Decisions on the choice of antibiotics and redosing should follow local
guidelines or the advice of a microbiologist.
Decolonisation
• For procedures where S. aureus is a likely cause of surgical site infection,
consider preoperative decolonisation, e.g. with a course of nasal
mupirocin and chlorhexidine body wash.
• Screening for both MRSA and meticillin-sensitive S. aureus can help
guide decision-making for decolonisation and subsequent prophylactic
antibiotic choice.
Antibiotic prophylaxis 63
General recommendations
• Antibiotics indicated for surgical procedures should be given as normal.
• For ‘infected surgery’ in patients at risk of IE, appropriate antibiotic
prophylaxis should be administered.
• In patients at high risk of IE, the decision to provide prophylactic
antibiotics for dental treatment should be made by treating clinicians
after discussion with the patient.
• Administration of antibiotics is not risk-free, and local protocols should
be followed.
64
64 Chapter 3 Preoptimisation
Perioperative medications
Prescribed, over-the-counter, herbal and recreational medications need
to be carefully considered at the time of the preoperative assessment.
Individualised plans that take into account patient and surgical factors (and
based on local guidelines) should be made and clearly communicated (in
written form) to the patient and teams involved in their perioperative care.
Some specific considerations include:
• Anticoagulants and antiplatelet therapies (see % pp. 269–79)
• Diabetic medications (see % pp. 216–21)
• Antipsychotics (see % p. 334)
• Renin–angiotensin system antagonists (see % Chapter 5, in particular
% p. 107, p. 113 and p. 116)
• β-blockers (see % Chapter 5, in particular % p. 107, p. 113 and p. 116)
• Antiepileptics (see % pp. 300–2) and anti-Parkinson’s medications
(see % pp. 292–5).
Statins
• Statins should be continued due to their effects on improved endothelial
function, enhanced stability of atherosclerotic plaques and reduced
vascular inflammation, causing a decrease in perioperative cardiac
events.38
Oestrogen therapy
• NICE guidance39 recommends that women consider stopping oestrogen
therapy (contraception or HRT) 4w before elective surgery due to the
theoretical i risk of VTE.
• There is, however, no consensus on the perioperative advice to give
patients due to insufficient evidence for i perioperative VTE risk and
the risks of unwanted pregnancy, or the recurrence of troublesome
menopausal symptoms. These should be considered in a patient’s
decision-making process.
• Patients should be advised on a case-by-case basis. If contraception is
stopped, advice must be given about alternative contraceptive measures
and discussions documented.
Herbal medicines and anaesthesia 65
Further reading
Skinner CM, Rangasami J (2002). Preoperative use of herbal medicines: a patient survey. Br J Anaesth,
89, 792–5.
6
66 Chapter 3 Preoptimisation
Premedicants
• Premedicants are given before the induction of anaesthesia.
• The aims of premedication are to improve patient comfort and reduce
perioperative risk.
• Changes in anaesthetics agents and short postoperative stays have led
to the decline in premedicant prescription.
• Commonly used premedicants are outlined below. (See % p. 917 for
paediatric premedicants.)
Analgesics
• Paracetamol. Can be considered in all patients unless contraindicated.
Single dosing >1g for higher body weight patients is safe if max 4g/day.
PO dose 1–2g.
• NSAIDs. Commonly prescribed (avoid in patients with a history of
gastric ulceration and renal impairment, and caution in older patients).
Suggested PO doses: ibuprofen 400mg, diclofenac 50–100mg.
• Topical LAs (e.g. prilocaine, EMLA®), often used in paediatrics (see
% p. 916).
Anxiolytics
(See % p. 419 for sedation.)
• Benzodiazepines. Most commonly used anxiolytics. Longer-acting agents
may delay recovery. Effects range from mild anxiolysis to deep sedation,
depending on dose. Temazepam PO 10–20mg, lorazepam PO 1–2mg.
• Opioids. Strong analgesic agents that produce sedation more than
anxiolysis. Less commonly used as premedicants. PO/intramuscular
(IM) dose of morphine10–20mg.
• Ketamine. Produces rapid sedation and analgesia. Particularly
useful in reduced/non-compliant patients. Co-administration with
benzodiazepines may reduce hallucinations. Suggested doses: PO 5–
7mg/kg, IM 2–5mg/kg, IV 0.5–1mg/kg.
Antacids and prophylaxis of aspiration pneumonitis
• Sodium citrate (PO 30mL of 0.3M solution). Often given prior to GA
for Caesarean section (CS), increases pH but does not decrease volume
of gastric contents.
• Proton pump inhibitors decrease volume and increase pH of gastric
contents. Also used to decrease gastric irritant effects of NSAIDs.
Omeprazole PO 20–40mg.
• Histamine (H2) receptor antagonists decrease gastric acid secretion.
Ranitidine can be given IV or PO (IV 50mg, diluted in 20mL of 0.9%
sodium chloride, given over 2min; PO 150mg).
• Metoclopramide increases gastric emptying and decreases gastric
volume, and also has antiemetic effects. Given as 10mg PO/IV.
Antisialagogues
• Anticholinergic. Glycopyrronium bromide often used prior to awake
tracheal intubation. Dose: IV 200–400 micrograms.
Premedicants 67
References
1 Ditmyer MM, Topp R, Pifer M (2002). Prehabilitation in preparation for orthopaedic surgery.
Orthop Nurs, 21, 43–51.
2 Moholdt T, Moe B, Nilsen TIL (2019). Patterns of physical activity over 22 years and mor-
tality: the HUNT Study, Norway. Eur Heart J, 40, 627. M https://doi.org/10.1093/eurheartj/
ehz747.0235
3 Santa Mina D, Clarke H, Ritvo P, et al. (2014). Effect of total body prehabilitation on postoperative
outcomes: a systematic review and meta-analysis. Physiotherapy, 100, 196–207.
4 British Association for Parenteral and Enteral Nutrition (BAPEN) (2012). Perioperative nutrition—
decision tree. M https://www.bapen.org.uk/pdfs/decision-trees/perioperative-nutrition.pdf
5 NHS Health Education England. Making Every Contact Count. M https://www.
makingeverycontactcount.co.uk/
6 Office for National Statistics (2017). Statistical bulletin: adult drinking habits in Great Britain:
2017. M https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/
drugusealcoholandsmoking/bulletins/opinionsandlifestylesurveyadultdrinkinghabitsingreatbrit
ain/2017
7 Tonnesen H, Kehlet H (1999). Preoperative alcoholism and postoperative morbidity. Br J Surg,
86, 869–74. M https://doi.org/10.1046/j.1365-2168.1999.01181.x
8 National Statistics (2019). Statistics on Smoking, England 2019. M https://www.gov.uk/govern-
ment/statistics/statistics-on-smoking-england-2019
9 Grønkjær M, Eliasen M, Skov-Ettrup LS, et al. (2014). Preoperative smoking status and
postoperative complications: a systematic review and meta-analysis. Ann Surg, 259, 52–71. M
https://doi.org/10.1097/SLA.0b013e3182911913
10 Thomsen T, Villebro N, Møller AM (2010). Interventions for preoperative smoking cessation
(review). Cochrane Database Syst Rev, 7, CD002294. doi:10.1002/14651858.CD002294.pub3.
M http://www.ncsct.co.uk/usr/pub/interventions-for-preoperative.pdf
11 Kerkhoffs GMMJ, Servien E, Dunn W, et al. (2012). The influence of obesity on the complication
rate and outcome of total knee arthroplasty: a meta-analysis and systematic literature review. J
Bone Joint Surg Am, 5, 1839–44. doi:10.2106/JBJS.K.00820.
12 Anderin C, Gustafsson UO, Heijbel N, et al. (2015). Weight loss before bariatric surgery and
postoperative complications: data from the Scandinavian Obesity Registry (SOReg). Ann Surg,
261, 909–13. doi:10.1097/SLA.0000000000000839
13 Leahy MF, Hofmann A, Towler S, et al. (2017). Improved outcomes and reduced costs associated
with a health-system-wide patient blood management program: a retrospective observational
study in four major adult tertiary-care hospitals. Transfusion, 57, 1347–58.
14 Muñoz M, Laso-Morales MJ, Gómez-Ramírez, S, et al. (2017). Pre-operative haemoglobin levels
and iron status in a large multicentre cohort of patients undergoing major elective surgery.
Anaesthesia, 72, 826–34. doi:10.1111/anae.13840
15 Musallam KM, Tamim HM, Richards T, et al. (2011). Preoperative anaemia and postoperative
outcomes in non-cardiac surgery: a retrospective cohort study. Lancet, 378, 1396–407.
16 Muñoz M, Acheson AG, Auerbach M, et al. (2017). International consensus statement on the
peri-operative management of anaemia and iron deficiency. Anaesthesia, 72, 233–47.
17 Vos T, Allen C, Arora M, et al. (2015). Global, regional, and national incidence, prevalence,
and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic ana-
lysis for the Global Burden of Disease Study 2015. Lancet, 388, 1545–602. doi:10.1016/
S0140-6736(16)31678-6
18 Goodnough LT, Skikne B, Brugnara C (2000). Erythropoietin, iron, and erythropoiesis. Blood, 96,
823–33.
19 Johansson PI, Rasmussen AS, Thomsen LL (2015). Intravenous iron isomaltoside 1000
(Monofer®) reduces postoperative anaemia in preoperatively non-anaemic patients undergoing
elective or subacute coronary artery bypass graft, valve replacement or a combination thereof:
a randomized double-blind placebo-controlled clinical trial (the PROTECT trial). Vox Sang, 109,
257–66.
20 Richards T, Baikady RR, Clevenger B, et al. (2020). Preoperative intravenous iron to treat an-
aemia before major abdominal surgery (PREVENTT): a randomised, double-blind controlled
trial. Lancet, 6376, 1–9. doi:10.1016/S0140-6736(20)31539-7
21 American Society of Anaesthesiologists (ASA) (2017). Practice guidelines for preoperative fasting
and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to
healthy patients undergoing elective procedures. M https://anesthesiology.pubs.asahq.org/article.
aspx?articleid=2596245
22 Thomas M, Morrison C, Newton R, et al. (2018). Consensus statement on clear fluids fasting for
elective paediatric anaesthesia. Paediatr Anaesth, 28, 411–14.
68
68 Chapter 3 Preoptimisation
23 Smith I, Kranke P, Murat I, et al. (2011). Perioperative fasting in adults and children guidelines from
the European Society of Anaesthesiology. Eur J Anaesthesiol, 28, 556–69.
24 Song I-K, Kim H-J, Lee J-H, et al. (2016). Ultrasound assessment of gastric volume in children
after drinking carbohydrate-containing fluids. Br J Anaesth, 116, 513–17.
25 Gagey A-C, de Queiroz Siqueira M, Monard C, et al. (2018). The effect of pre-operative gas-
tric ultrasound examination on the choice of general anaesthetic induction technique for non-
elective paediatric surgery. A prospective cohort study. Anaesthesia, 73, 304–12.
26 Anderson DR, Morgano GP, Bennett C, et al. (2019). American Society of Hematology 2019
guidelines for management of venous thromboembolism: prevention of venous thrombo-
embolism in surgical hospitalized patients. Blood Adv, 3, 3898–944. M https://doi.org/10.1182/
bloodadvances.2019000975
27 Nicolaides AN, Fareed J, Kakkar AK, et al. (2006). Prevention and treatment of venous thrombo-
embolism. International Consensus Statement (guidelines according to scientific evidence). Int
Angiol, 25, 101–61. M https://venousdisease.com/site/wp-content/uploads/2013/08/
venous-thromboembolism-international-consensus-guidelines.pdf
28 Department of Health (2010). Venous thromboembolism (VTE) risk assessment. M https://
webarchive.nationalarchives.gov.uk/ 2 0130123195034/ h ttp:// w ww.dh.gov.uk/ e n/
Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_088215
29 National Institute for Health and Care Excellence (2018). Venous thromboembolism in over 16s:
reducing the risk of hospital acquired deep vein thrombosis or pulmonary embolism. M https://www.
nice.org.uk/guidance/ng89/
30 Venous Resource Center. Are you at risk for DVT? M https://venousdisease.com/caprini-dvt-risk-
assessment/
31 Afshari A, Ageno W, Ahmed A, et al. (2018). European guidelines on periopera-
tive venous thromboembolism prophylaxis. Eur J Anaesthesiol, 35, 77– 83. doi:10.1097/
EJA.0000000000000729. M https://journals.lww.com/ejanaesthesiology/fulltext/2018/
02000/european guidelines on perioperative_venous.2.aspx
32 Morgan J, Checketts M, Arana A, et al. (2018). Prevention of perioperative venous
thromboemolism in paediatric patients: guidelines from the Association of Anaesthetists of
Great Britain and Ireland (APAGBI). Paediatr Anaesth, 28, 382–91. M https://www.apagbi.org.
uk/sites/default/files/inline-files/APA%20Thromboprophylaxis%20guidelines%20final.pdf
33 Global Alliance for Infections in Surgery (2019). Principles of antibiotic prophylaxis in surgery. M
https://infectionsinsurgery.files.wordpress.com/2019/02/prophylaxis-principles-1-1.pdf
34 National Institute for Health and Care Excellence (2019). Surgical site infections: prevention and
treatment. M https://www.nice.org.uk/guidance/ng125/chapter/Recommendations
35 Health Improvement Scotland and Scottish Antimicrobial Prescribing Group (SAPG) (2018).
Recommendations for re-dosing antibiotics for surgical prophylaxis. M https://www.sapg.scot/
media/3880/good-practice-recommendations-for-re-dosing-surgical-prophylaxis-final.pdf
36 National Institute for Health and Care Excellence (2008). Prophylaxis against infective endocar-
ditis. M https://www.nice.org.uk/guidance/CG64/chapter/Recommendations#adults-and-
children-with-structural-cardiac-defects-at-risk-of-developing-infective-endocarditis
37 Tulunay Kaya C, Erol C (2018). How to achieve infective endocarditis prophylaxis. e-Journal of
Cardiology Practice, 16, no. 33. M https://www.escardio.org/Journals/E-Journal-of-Cardiology-
Practice/Volume-16/vol16no33
38 Schouten O, Boersma E, Hoeks SE, et al.; Dutch Echocardiographic Cardiac Risk Evaluation
Applying Stress Echocardiography Study Group (2009). Fluvastatin and perioperative events in
patients undergoing vascular surgery. N Engl J Med, 361, 980–9.
39 National Institute for Health and Care Excellence (2018, updated August 2019). Venous thrombo-
embolism in over 16s: reducing the risk of hospital acquired deep vein thrombosis or pulmonary em-
bolism. M https://www.nice.org.uk/guidance/ng89/
40 Ang-Lee MK, Moss J, Yuan CS (2001). Herbal medicines and perioperative care. JAMA, 286,
208–16.
41 Haller CA, Benowitz NL (2000). Adverse cardiovascular and central nervous system events as-
sociated with dietary supplements containing ephedra alkaloids. N Engl J Med, 343, 1833–8.
42 Wong A, Townley S (2011). Herbal medicines and anaesthesia. Contin Educ Anaesth Crit Care Pain,
11, 14–17.
43 Bebbington A, Kulkarni R, Roberts P (2005). Ginkgo biloba: persistent bleeding after total hip
arthroplasty caused by herbal self-medication. J Arthroplasty, 20, 125–6.
44 Ernst E (2002). St John’s wort supplements endanger the success of organ transplantation. Arch
Surg, 137, 316–19.
45 Patel S, Robinson R, Burk M (2002). Hypertensive crisis associated with St John’s wort. Am J Med,
112, 507–8.
Chapter 4 69
At-risk populations
Nicholas Kennedy and Katherine Reeve
Obesity introduction 70
Common comorbidities in obesity 71
Obstructive sleep apnoea 73
Airway considerations in obesity 76
Practicalities with obese patients 77
Pharmacology in obese patients 80
Thromboprophylaxis in obesity 81
Elizabeth Fontaine
The malnourished patient 82
Cachexia related to chronic illness or malignancy 83
Anorexia nervosa 86
Short gut (bowel) syndrome 88
Stuart White
Considerations for the older patient 89
Anaesthesia for older patients 92
When not to operate on older people 94
Obesity introduction
The prevalence of obesity is increasing worldwide and so the number of
obese surgical patients increases. Recent UK government statistics, pub-
lished in 2019, suggest that the majority of adults are either overweight
or obese (64%).1 Obesity prevalence i steeply between 1993 and around
2000, with a slower rate of increase after that. In 2017, the proportion of
adults who were obese in the UK was 29%. Obesity is more common in
women (30%) than in men (27%). Morbid obesity has also i, with <1% in
1993, to nearly 4% in 2017.1 The rise in obesity applies not only to adults,
but also to children. Globally, the obesity rate in the United States (US) is
the highest at 40%; however, countries such as Japan and Korea have rates
lower than 10%.2
Anaesthesia and surgery may entail considerable risk for obese patients.
Obesity is a multisystem disorder, particularly involving the respiratory
system and CVS; therefore, a multidisciplinary approach is required.
Definitions
Obesity is defined by the BMI. BMI is defined as weight (in kg) divided by the
height (in m squared) (Table 4.1).
Perioperative consideration
Preoperative assessment
• OSA is undiagnosed in 80% of patients. Preoperative evaluation should
include a review of previous medical records, a history from the patient
and/or family and a physical examination. In a recent Canadian study, in
267 preassessed patients with moderate to severe OSA, 92% and 60%
were not diagnosed by their surgeons and anaesthetists, respectively.9
• Check for airway difficulty with previous anaesthetics, hypertension and
other CVS problems. Use a screening tool such as STOP-Bang.
• OHS is the extreme end of OSA. These patients are morbidly obese,
have significant daytime somnolence and breathlessness and are
particularly sensitive to anaesthesia and opioids. It is important to
identify them preoperatively.
• Note any current treatment and compliance such as with CPAP.
• Day surgery may be reasonable, depending on OSA severity,
comorbidities, analgesic requirements and nature of the proposed
surgery.
• In patients with a new diagnosis of OSA treated with CPAP, it is
advisable to delay surgery for 1–3mo. However, consideration for the
urgency of surgery and patient preference should be given.
Investigations
• In known OSA, perform FBC (polycythaemia), SpO2 and ECG (right
heart strain). If the ECG shows right heart strain, echocardiography is
indicated to exclude RV hypertrophy.
• If hypoxic on air, consider performing an arterial blood gas (ABG).
Obstructive sleep apnoea 75
Conduct of anaesthesia
• Avoid night sedation and sedative premedication.
• Anticipate that mask ventilation and intubation may be difficult, and
prepare for this.
• A local or regional anaesthetic technique is preferred where suitable.
Use short-acting anaesthetic/analgesic agents where possible.
• GA preceded by preoxygenation, with tracheal intubation and
mechanical ventilation, is preferred to sedation or GA with spontaneous
ventilation (SV).
• Give NSAIDs and paracetamol.
• At the end of the procedure, ensure NMB is fully reversed and
extubate fully awake in the sitting position.
Postoperative care
• Nurse the patient sitting up whenever possible.
• High-risk patients may require admission to HDU/intensive care
unit (ICU).
• Administer supplementary O2, and ensure continuous SpO2 monitoring
on the ward.
• Unless contraindicated, CPAP should be administered continuously to
patients who were using it preoperatively.
• Aim to maintain the O2 saturation that the patient had preoperatively,
titrating O2 to the minimum required.
• Minimise opioid analgesics. If used, consider postoperative location,
level of staff training and need for i monitoring.
76
Thromboprophylaxis in obesity
(See also % p. 59; % p. 72.)
Obesity and surgery are known risk factors for VTE, but there is limited
information about the independent effects of obesity on the incidence of
postoperative VTE. The Million Women Study14 concluded that VTE risk
increases with increasing BMI and the associated excess risk is much greater
following surgery than without surgery. In the UK, NICE has offered guid-
ance on VTE prophylaxis in its publication Venous thromboembolism in over
16s: reducing the risk of hospital-acquired deep vein thrombosis or pulmonary
embolism, last updated in August 2019.15
Start mechanical VTE prophylaxis on admission. Choose any one of:
• Antiembolism stockings (thigh or knee length)
• Intermittent pneumatic compression devices (thigh or knee length).
Continue mechanical VTE prophylaxis until the patient no longer has signifi-
cantly reduced mobility.
Add pharmacological VTE prophylaxis for patients who have a low risk
for major bleeding, taking into account individual patient factors and ac-
cording to clinical judgement.
This should continue until the patient no longer has significantly reduced
mobility (minimum 7d). Some bariatric surgical centres in the UK use ex-
tended prophylaxis for up to 3w and others use a higher dosage. There
has been no guidance on the duration or dosing for the obese. Therefore,
local guidelines must be consulted when considering VTE prophylaxis in
this group.
82
Anaesthetic approach18
Preoperative
• Nutritional assessment:
• History: disease, infections, surgery, recent weight loss, caloric intake,
relevant drugs
• Examination: appearance, hydration status, CVS examination, BMI
• Investigation: bloods (FBC, urea and electrolytes (U&E), liver function
tests (LFTs), calcium (Ca2+), phosphate, magnesium (Mg2+), glucose,
transferrin, albumin), urine (protein and ketones), ECG, echo if
appropriate
• Tools: Nutritional Risk Assessment Scale, Subjective Global
Assessment.5 Practically, these can be time-consuming.
• Nutritional optimisation where possible, especially in leucopenia
or hypoalbuminaemia. In severe malnutrition (Box 4.3), 7–14d of
preoperative parenteral nutrition is advisable, especially if gut function
is unlikely to return to normal postoperatively.16,20 Only consider a delay
to surgery if severe malnutrition is present.16
• Evidence suggests that preoperative carbohydrate drinks preserve
insulin sensitivity postoperatively and reduce length of stay. Limit
perioperative fasting where possible (induces metabolic stress and
impairs mitochondrial function and insulin sensitivity)16.
• Correct electrolytes, including phosphate. Hydrate the patient.
• Monitor and maintain blood glucose.
• Prokinetic and antacid recommended. Consider NGT.
Intraoperative
• Monitoring:
• Have a low threshold for invasive cardiac monitoring (susceptibility to
cardiac arrhythmia or collapse).
• Consider continuous central temperature monitoring.
• Consider calibrated neuromuscular monitoring to minimise muscle
relaxant dose and monitor for prolonged effect.
• Venous access may be challenging. Central access may be required for
monitoring and nutritional support postoperatively.
• Induction may cause CVS collapse if underfilled.
• Rapid sequence induction (RSI) recommended. Treat as having a full
stomach.
• Protect pressure areas and exposed nerves (reduced muscle mass and
soft tissue).
• Bony fragility; take care when moving/positioning.
• Avoid hypothermia with warm fluids, forced air warming blanket, heat
and moisture exchanger (HME).
• Avoid hyperventilation—can lower potassium (K+) further.
Pharmacology
• Pay attention to patient weight, lean and total body mass, albumin and
volume of distribution. Adjust doses appropriately.
• Muscle bulk may be reduced (reduce water-soluble drug doses).
• Consider regional techniques to spare opioids and other drugs
metabolised by the liver.
Cachexia related to chronic illness or malignancy 85
Postoperative
• Extubation may be difficult (respiratory weakness and impaired upper
airway reflexes).
• Postoperative nutritional support: encourage early enteral feeding.
• Correct pH and electrolytes. Limit excessive fluids and opioids.
Prokinetics are recommended.
• Have a low threshold for ICU if available.
• Refeeding syndrome is a risk (see also % p. 87).
• Parenteral nutrition is reserved for those who cannot meet their
calorific needs within 7–10d postoperatively (GI dysfunction, ileus,
bowel discontinuation).
86
Anorexia nervosa
Chronic, severe, multisystem disorder with the highest morbidity and mor-
tality rate of any psychiatric disorder (up to 20%). BMI <17.5kg/m2 is a
diagnostic criterion. Severe cases have BMI <13kg/m2.20
Complications
• Metabolic/GI: hypoglycaemia, liver injury, delayed gastric emptying.
Excessive loss of sodium (Na+), K+, chloride and hydrogen ions
(H+) from the stomach, hypochloraemic metabolic alkalosis and
hypokalaemia. Severe hypokalaemia is uncommon. Correct with
caution preoperatively. Hypocalcaemia may accompany hypokalaemia.
• Musculoskeletal: osteopenia, osteoporosis, i risk of fractures and
hypothermia.
• Respiratory: loss of lung elasticity, higher airway pressures.
• Haematological: pancytopenia (anaemia and immunodeficiency).
• CVS: sinus bradycardia, d LV forces, orthostatic hypotension, mitral
prolapse, prolonged corrected QT interval, i vagal tone, pericardial
effusion, congestive heart failure, arrhythmia (very sensitive to
catecholamines or neostigmine). Cardiac arrest can occur 2° to
corrected QT interval prolongation or cardiac arrhythmia.
• Renal: d GFR, proteinuria.
• Immunological: 1° cause of death is severe sepsis (especially very low
BMI). 3 Granulocyte stimulating factor can be used.
• Endocrine: amenorrhoea, impaired thyroid function and glycaemic
control. May mimic panhypopituitarism.
Anaesthetic approach
Preoperative
• Full nutritional assessment (see also % p. 84), including psychiatric
assessment.
• Correct hypoglycaemia (cautiously and gradually; beware rebound
hyperinsulinaemia and profound hypoglycaemia).
• Acute refeeding can be risky. There is evidence that delaying surgery
to achieve BMI >14.5kg/m2 improves hypoglycaemia and leucopenia,
which decreases mortality.20
• Correct other electrolytes, especially K+ and phosphate. Replace Ca2+
and vitamin D.
Intraoperative
• Short, minimally invasive operations are better due to cardiac risk.
• RSI recommended. Fasting does not guarantee an empty stomach.
• Reduce doses of NMBAs. Prolonged recovery 2° to hypokalaemia and
hypocalcaemia. Monitor neuromuscular block. Consider sugammadex
over neostigmine to reduce risk of cardiac arrhythmia.
• Carefully consider drug doses. Take into account patient weight,
hypoalbuminaemia (reduced protein binding) and renal and liver
function (reduced metabolism and excretion).
• Carefully maintain body temperature with forced air warming devices
and warmed infusions.
• Beware of positioning due to risk of pressure necrosis and nerve palsies.
• Do not overfill. Can lead to pulmonary oedema and cardiac failure.
Anorexia nervosa 87
Postoperative
• Beware refeeding syndrome (hypophosphataemia, hypokalaemia,
hypomagnesaemia and hypoglycaemia in response to feeding after a
period of starvation) and use an appropriate refeeding regime with
nutritional support, cardiac monitoring, and electrolyte monitoring and
supplementation.
• As per the NICE-SUGAR study, avoid ‘intensive’ glucose control.20
• Be wary of postoperative infection, with rigorous attention to the
surgical site infection bundle and care of vascular access.
8
Renal
• Renal mass and the number of glomeruli fall progressively (by 30%
in the 8th decade), resulting in reduced GFR. CC falls comparably,
although serum creatinine may not rise because of d production from
reduced muscle mass (see % p. 192).
• Tubular function deteriorates, leading to reduced renin–aldosterone
response, antidiuretic hormone (ADH) sensitivity and concentrating
ability. As a result, all renal homeostatic functions deteriorate,
rendering elderly patients more susceptible to both fluid overload and
hypovolaemia. Hypo-and hypernatraemia are also more likely.
• Reduced clearance of renally excreted drugs necessitates dose
adjustment. Particular care must be taken with potentially nephrotoxic
drugs such as aminoglycosides.
Hepatic
• Hepatic mass and blood flow fall by up to 40% by the 9th decade.
Although cellular function is relatively well preserved in healthy patients,
the reduction in size reduces clearance and prolongs the effect of drugs
that are metabolized and excreted by the liver. These include opioids,
propofol, benzodiazepines and NMBAs.
Central nervous system
• Brain size and neuronal mass decrease. The average brain weight falls
by 18% between the ages of 30 and 80y. Mild cognitive impairment
may progress to dementia, which affects 10% of patients over 65y of
age, and 20% of those over 80y. It is important to distinguish between
dementia and reversible confusional states due to hypoxia, sepsis, pain,
metabolic derangement and depression. The hospital environment can
precipitate anxiety and confusion.
• The elderly have fewer requirements for opioids and sedatives and
are more susceptible to opioid-induced depressed consciousness and
respiration. This is likely to be due to both pharmacodynamic and
pharmacokinetic effects. Pain threshold may be i.
• Postoperative delirium (POD) and postoperative neurocognitive
disorder (POND, formerly postoperative cognitive dysfunction
(POCD)) are common in the elderly, occurring in >10% of patients.
Disturbances of cerebral perfusion and cellular oxygenation are likely
to be contributory factors. Potentially reversible risk factors for POD
include severe pain, infection, malnutrition, electrolyte imbalance,
dehydration, environmental disturbances and substance withdrawal
(alcohol, medication).
• POND describes significant perioperative decline in mental status or
awareness, occurring up to 30d (delayed neurocognitive recovery)
or 12mo (POND) after surgery, and which may persist beyond that.
It is associated with i mortality, impaired quality of life and loss of
employment.
• POND is more common after major surgery, cardiac surgery
and emergency surgery. Multifactorial causes are likely, related to
inflammatory reactions, altered hormonal homeostasis and/or direct
anaesthetic agent toxicity. Focused anaesthesia interventions (treatment
of hypoxaemia and hypotension), guided by the depth of anaesthesia
and cerebral saturation monitoring, may ameliorate these.
Considerations for the older patient 91
Endocrine
• Glucose loading is increasingly poorly tolerated in elderly patients. The
incidence of DM rises to 25% in patients >80y.
Haematology and the immune system
• Hypercoagulability and DVT are more common with advancing age.
• Anaemia is more common, and the response of the marrow to anaemia
is impaired.
• Immune responses are reduced in the elderly, putting them at i risk of
infection. This is due to reduced bone marrow and splenic mass with
loss of the thymus.
Thermoregulation
• Thermoregulation is impaired, increasing the risk of hypothermia.
• Postoperative shivering increases skeletal muscle O2 consumption, while
vasoconstriction increases myocardial work and O2 demand.
Pharmacology
• TBW is reduced, while fat percentage is i. The volume of distribution
of water-soluble drugs is reduced, reducing dose requirements, while
that of lipid-soluble drugs is i, which may prolong clearance.
• The initial volume of distribution falls because of reduced CO. This
reduces the dose requirement and is particularly relevant for induction
agents. Arm–brain circulation time is prolonged, increasing the time
taken for induction agents to take effect.
• Reduced plasma albumin concentration decreases the dose requirement of
drugs such as benzodiazepines and opioids, which are bound to albumin.
• The minimum alveolar concentration (MAC) of inhaled agents
decreases steadily with age (6% reduction per decade) and is reduced
by around 40% by the age of 80y (see % pp. 411–12). This may be
related to a reduction in neuronal mass. Reductions in blood/gas
partition coefficient and CO in the elderly result in shorter onset time.
• The risk of GI bleeding due to NSAIDs is i. These agents may also
contribute to the development of AKI in the presence of impaired renal
perfusion. ACE inhibitors exacerbate this risk. Fluid retention due to
NSAIDs may precipitate heart failure in susceptible patients.
92
Nutrition
• Nutritional status is frequently poor in older people, under-recognised
by clinicians and compounded by a lack of appetite resulting from
surgery, pain and nausea.
• Perioperative complications and length of hospital stay may be reduced
by nutritional supplementation prior to major surgery.
Perioperative management
• The type of anaesthesia appears less important than the care with
which it is given with regard to the patient’s physiological condition.
However, regional anaesthesia may reduce bleeding, risk of DVT,
respiratory infection and cognitive dysfunction (particularly if given
without/with minimal sedation). MAC should be age-adjusted or, if
using TIVA, infusions should be target-controlled (TCI).
• Careful monitoring is necessary to detect hypotension during
GA induction and shortly after spinal anaesthesia administration.
Consideration should be given to invasive BP and depth of anaesthesia
monitoring. Prolonged arm–brain circulation time delays the onset of IV
induction agents; flush the drugs with 0.9% sodium chloride and remain
patient to avoid an inadvertent overdose.
• Temperature should be measured, and hypothermia prevented using
fluid warmers, active body-warming devices and elevation of ambient
temperature.
• Prolonged surgery and periods of hypotension increase the risk of
pressure sores. Care should be taken to reduce pressure with soft
padding. During long procedures, it is advisable to relieve pressure and
massage vulnerable areas intermittently.
Postoperative management
• High dependency facilities should be considered if this is likely to reduce
morbidity or mortality significantly, or if an identifiable organ support is
required.
• Fluid balance, vital signs, serum electrolytes and haematology must
be carefully monitored and treated appropriately. Patients with CVS
disease may need to have their Hb kept >90–100g/L.
• Reversible factors should be sought if the patient exhibits delirium
(pain, hypoxaemia, distended bladder, myocardial/cerebral ischaemia,
electrolyte disorder, drugs).
• Pain is common but undertreated in elderly surgical patients, particularly
if cognitively impaired. Regular paracetamol prescription and regional
analgesia should always be considered and are preferable to opioids and
NSAIDs.
• Anaesthetists should facilitate postoperative patient remobilisation and
‘re-enablement’ through age-appropriate anaesthesia, fluid therapy,
thermoregulation, analgesia and good communication.
94
Postoperative
• As for induction, emergence from anaesthesia should involve minimal
physical or sensory stimulation. Early presence of carers/family in
recovery is often invaluable.
• IV cannulae and selected monitoring should be removed as soon as it is
safe to do so, to reduce patient distress.
• Communication difficulties frequently impede pain assessment.
• Always consider pain (while excluding hypoxia) as a source of i
agitation. Behavioural serial pain scoring systems are often beneficial.
• ASD patients may experience explosive behavioural ‘meltdowns’.
Triggers include disorientation, sensory or communication issues, feeling
out of control and anxiety. Be aware of each individual’s warning signs
and minimise stimulation on waking.
• Modify discharge criteria (e.g. eating/drinking) to allow patients to
return to their own routine and environment as soon as possible.
• Discharge documentation, instructions and prescriptions should be
completed in advance to facilitate a potentially abrupt discharge.
Autistic spectrum disorder 99
Further reading
Lyall K, Croen L, Daniels J, et al. (2017). The changing epidemiology of autism spectrum disorders.
Annu Rev Public Health, 38, 81–102.
Short J, Calder A (2013). Anaesthesia for children with special needs, including autistic spectrum
disorder. Contin Educ Anaesth Crit Care Pain, 13, 107–12.
References
1 Health and Social Care Information Centre, Lifestyles Statistics (2014). Statistics on
obesity, physical activity and diet: England, 2014. Data quality statement. M https://
digital.nhs.uk/data-and-information/publications/statistical/health-survey-for-england/
health-survey-for-england-2014
2 Organisation for Economic Co-operation and Development (OECD) (2017). Obesity update.
M https://www.oecd.org/health/obesity-update.htm
3 Chapman DG, Irvin CG, Kaminsky DA, Dixon AE (2020). Weight loss reduces airway closure
during bronchoconstriction in obese asthmatics. Am J Resp Crit Care Med, 187, A3791.
4 Lindsay RS, Howard BV (2004). Cardiovascular risk associated with the metabolic syndrome.
Curr Diab Rep, 4, 63–8.
5 Arabi YM, Dara SI, Tamim HM, et al.; Cooperative Antimicrobial Therapy of Septic Shock
(CATSS) Database Research Group (2013). Clinical characteristics, sepsis interventions and out-
comes in the obese patients with septic shock: an international multicenter cohort study. Crit
Care, 17, R72.
6 Habbu A, Lakkis NM, Dokainish H (2006). The obesity paradox: fact or fiction? Am J Cardiol,
98, 944–8.
7 Eichinger S, Hron G, Bialonczyk C, et al. (2008). Overweight, obesity, and the risk of recurrent
venous thromboembolism. Arch Intern Med, 168, 1678.
8 Hall A (2015). Sleep physiology and the perioperative care of patients with sleep disorders.
Contin Educ Anaesth Crit Care Pain, 4, 167–72.
9 Singh M, Liao P, Kobah S, et al. (2013). Proportion of surgical patents with undiagnosed ob-
structive sleep apnoea. Br J Anaesth, 110, 629–36.
10 Cook T, Woodall N, Frerk C (2011). Major complications of airway management in the United
Kingdom: results of the 4th National Audit Project of the Royal College of Anaesthetists and the
Difficult Airway Society. M http://www.rcoa.ac.uk/nap4
11 Nightingale CE, Margarson MP, Shearer E, et al. (2015). Perioperative management of the obese
surgical patient. Anaesthesia, 70, 859–76.
12 Ingrande J, Lemmens HMJ (2010). Dose adjustment of anaesthetics in the morbidly obese. Br J
Anaesth, 105, i16–23.
13 Taha SK, El-Khatib MF, Baraka AS, et al. (2010). Effect of suxamethonium vs rocuronium on onset
of oxygen desaturation during apnoea following rapid sequence induction. Anaesthesia, 65, 358–61.
14 Parkin L, Sweetland S, Balkwill A, et al.; Million Women Study Collaborators (2012). Body mass
index, surgery, and risk of venous thromboembolism in middle-aged women: a cohort study.
Circulation, 125, 1897–904.
15 National Institute for Health and Care Excellence (2018, updated August 2019). Venous
thromboembolism in over 16s: reducing the risk of hospital-acquired deep vein thrombosis or
pulmonary embolism. NICE guideline [NG89]. M https://www.nice.org.uk/guidance/ng89
16 Ali Abdelhamid Y, Chapman MJ, Deane AM (2016). Peri- operative nutrition. Anaesthesia,
71(Suppl 1), 9–18.
17 NHS (2017). Health A–Z: Malnutrition. M http://www.nhs.uk/conditions/malnutrition/causes/
18 Edwards S (2016). Anaesthetising the malnourished patient. Update Anaesth, 31, 31–7.
19 Morley JE, Thomas DR, Wilson MG (2006). Cachexia: pathophysiology and clinical review. Am J
Clin Nutr, 83, 735–43.
20 Hirose K, Hirose M, Tanaka K, Kawahito S, Tamaki T, Oshita S (2014). Perioperative manage-
ment of severe anorexia nervosa. Br J Anaesth, 112, 246–54.
21 Lomax S, Klucniks A, Griffiths J (2011). Anaesthesia for intestinal transplant. Contin Educ Anaesth
Crit Care Pain, 11, 1–4.
22 Szczygiel B, Jonkers-Schuitema CF, Naber T (2010). Basics in clinical nutrition: nutritional support
in extensive gut resections (short bowel). e-SPEN, the European e-Journal of Clinical Nutrition and
Metabolism, 5, e63–8. M https://clinicalnutritionespen.com/article/S1751-4991(09)00052-3/pdf
23 World Health Organization (2018). International classification of diseases for mortality and mor-
bidity statistics, 11th revision. M https://icd.who.int/browse11/l-m/en
01
Chapter 5 101
Cardiovascular disease
Sonja Payne
Ischaemic heart disease 102
Perioperative acute myocardial ischaemia and infarction 109
Heart failure 111
Hypertension 116
Valvular heart disease 118
Aortic stenosis 120
Aortic regurgitation 122
Mitral stenosis 124
Mitral regurgitation 126
Pericardial disease 128
Cardiomyopathy 129
Patients with a transplanted heart 132
James Ip
Congenital heart disease and non-cardiac surgery 134
Specific congenital heart disease lesions 136
Adults with congenital heart disease 138
Guillermo Martinez
Pulmonary hypertension 139
Sonja Payne
Perioperative arrhythmias 145
Narrow complex arrhythmias 147
Broad complex arrhythmias 152
Disturbances of conduction (heart block) 154
Pacemakers and defibrillators 160
See also
% Cardiac disease and pregnancy pp. 891–2
% Severe bradycardia pp. 1060–1061
% Atrial fibrillation pp. 149–51
% Narrow complex tachycardia pp. 1062–1064
% Broad complex tachycardia p. 1062
021
Functional capacity
Cardiopulmonary fitness is commonly used to estimate perioperative risk.
The physiological response to major surgery increases O2 demand by up to
40%, requiring a subsequent increase in O2 delivery. The ability to exercise
is an indicator of CVS reserve. It is expressed in metabolic equivalents of
task (METs) (Box 5.1). One MET is the resting O2 consumption of a 40y-old
70kg ♂ (3.5mL/kg/min). Patients who cannot sustain 4 METs of physical
activity frequently have adverse outcomes following high-risk surgery (see
also % p. 35).
METs are most commonly assessed subjectively, based on patient his-
tory, which may result in substantial misclassification of risk. More objective
measures, such as the Duke Activity Status Index (a self-reported question-
naire about usual physical activities) or CPET, have been shown to improve
identification of patients at risk of perioperative MACE and death.2
Surgical factors are also important in determining perioperative risk
(Table 5.2).3
Perioperative testing
Evaluation of patients with IHD depends on the planned surgery, facilities
and time available. Special investigations are discussed below. Precise re-
commendations remain controversial, but careful history, examination and
practical application of preoperative screening tests are important. Little
advantage is gained from complex examinations which will not alter man-
agement. The positive predictive value of most tests is low. In high-risk
patients, alternative surgical procedures or medical management may need
to be considered, with input from anaesthetists, cardiologists, surgeons and
the patient.
Special investigations
12-lead electrocardiogram
A preoperative ECG should be performed on patients over 65y undergoing
intermediate-risk surgery and anyone with risk factors for IHD. Patients
with IHD may have a normal or non-specific resting ECG.
Cardiac biomarkers
• Preoperative measurement of BNP and cardiac troponins in the
perioperative period predicts myocardial injury after non-cardiac
surgery (MINS) in patients undergoing non-cardiac surgery.
• Biomarker assessment may complement risk prediction in patients at
high risk of MACE.3,4
• Daily troponin measurements and postoperative ECGs for 48–72h
after non-cardiac surgery in patients at high risk of MACE may be
recommended to detect perioperative MINS, facilitating monitoring and
medical management.
Ischaemic heart disease 105
Assessment of LV function
• Echocardiography is the most widely available test for diagnosis and
serial assessment of patients with dyspnoea or known LV dysfunction.
• Cardiac MRI provides reliable assessment of LV function, as well as
coronary artery evaluation.
Coronary CT angiography
A non- invasive alternative to coronary angiography. Calculates the
Coronary Artery Calcium Score which estimates risk of IHD and need for
invasive coronary angiography, but overestimates the risk of MACE, so is
not recommended for routine cardiac risk estimation.
Exercise ECG
A functional test in patients with known coronary artery disease (CAD).
Detects myocardial ischaemia through changes in ST-segment morphology.
Interpretation is difficult if there are pre-existing ST-segment abnormalities
and if the patient fails to achieve target HR. High prevalence of false posi-
tives and negatives, so no longer used for CAD diagnosis. Of limited use for
risk prediction for postoperative MACE.
CPET
(See also % pp. 33–5.)
CPET is an integrative assessment of cardiovascular, respiratory and mus-
culoskeletal systems. It provides an objective assessment of functional cap-
acity. It takes 30min to perform but requires expensive equipment. It has a
low positive predictive value but may be used to guide perioperative SDM
in high-risk patients.
Pharmacological stress testing
Moderate/large areas of reversible ischaemia are associated with i risk of
MACE. Pharmacological stress tests provide a dynamic assessment of myo-
cardial perfusion. A normal study has a high negative predictive value. High-
risk patients should be tested if testing will change management. Patients
who have large areas of reversible ischaemia should be considered for cor-
onary angiography.
• Myocardial perfusion imaging (thallium scintigraphy) uses a coronary
vasodilator (dipyridamole or adenosine) and a radioisotope,
thallium-201, that rapidly accumulates within perfused myocardium.
Comparisons are made between resting and stress images. Changes
in uptake reflect reversible ischaemia, while fixed defects represent
irreversible infarcted/scarred myocardium.
• Dobutamine stress echocardiography uses an increasing dose of
dobutamine (max 40 micrograms/kg/min), with simultaneous two-
dimensional (2D) precordial echocardiography. New or worsening
regional wall motion abnormality (RWMA) is an indicator of impaired
perfusion.
• Stress cardiac MRI can incorporate dobutamine and vasodilator stress
testing principles to assess for RWMA and myocardial perfusion
abnormalities, helping predict the risk of future MACE.
061
About 75% of perioperative MIs are type 2,6 and the other 25% are
type 1. Reduction of the risk of MACE requires a multimodal approach,
dependent on time available and patient engagement, but involves lifestyle
changes as well as pharmacological therapy.
• Medical therapy should be continued perioperatively to protect against
ischaemic stress. If GI absorption is impaired or the patient is kept nil by
mouth, drugs should be given IV if possible.
• Aspirin alone has not been shown to reduce MACE or 30d mortality in
patients undergoing non-cardiac surgery.3
• Long-term β-blockade should be continued perioperatively due to the
cardioprotective effects (decrease myocardial O2 demand).
• Initiation of β-blockade within 24h prior to surgery is not
recommended.4
• There is limited evidence to suggest that high-risk patients who
demonstrate inducible ischaemia on preoperative stress testing may
benefit from carefully titrated β-blockade (to a HR of 60–80bpm)
started at least 1w prior to surgery. Low-dose bisoprolol is commonly
used. Dose titration is challenging.
• Nitrates should be continued perioperatively, IV or transdermally,
if necessary. There is no evidence that prophylactic administration
decreases the risk of perioperative cardiac complications.
• Calcium channel blockers should be continued preoperatively and
resumed as soon as possible postoperatively. Verapamil has been
shown to confer a small measure of cardiac protection in small RCTs
but must be avoided in LV impairment.
• ACE inhibitors and angiotensin II receptor blockers (ARBs) improve
survival following MI and in patients with LV dysfunction. They do not
protect against perioperative MACE. ACE inhibitors and ARBs have
been shown to increase the risk of intraoperative hypotension, but
not MACE. Other studies have shown clinically important hypotension
to be independently associated with an i risk of death, MI and CVE,
but the highest risk comes from hypotension 24h after surgery. It
has been suggested4 that withholding ACE inhibitors and ARBs 24h
before surgery and recommencing them 2d after surgery may be
appropriate, but the quality of evidence is currently low and these
drugs are very important in the management of these patients. Others
suggest stopping them only if used to treat hypertension.3 In those with
severe LV dysfunction, it may be prudent to continue ACE inhibitors
throughout the perioperative period. Cardiology advice may be needed.
• Perioperative statin administration has been shown to improve both
short-term and long-term cardiac outcome following non-cardiac and
coronary bypass surgery.3,4 Statins enhance plaque stability, making
plaque rupture less likely.
081
Anaesthetic considerations
The main goal is to maintain O2 demand and supply matching.
• Consider 5-lead ECG monitoring.
• Invasive cardiovascular monitoring (arterial line ± central venous
pressure ± CO monitoring) should be considered for high-/
intermediate-risk patients.
• Point-of-care ultrasound can provide real-time assessment of
cardiovascular and respiratory function.
• Avoid hypotension, hypertension and tachycardia to minimise
myocardial demand and supply mismatching. Anticipate phases of
sympathetic stimulation (e.g. intubation, emergence) and consider using
a short-acting β-blocker to attenuate this.
• Pain causes sympathetic stimulation: provide effective pain control.
• Central neuraxial and regional blocks can be very effective, but not
always possible in the context of DAPT.
• Liberal transfusion triggers (Hb 90–100g/L) reduce the risk of MACE.7
• Consider admission to HDU postoperatively for close monitoring.
PERIOPERATIVE ACUTE MYOCARDIAL ISCHAEMIA & INFARCTION 109
Heart failure
Heart failure is the commonest cause of admission to hospital in those
aged >65y. Incidence rises with increasing age, with a 5y mortality of 750%.
Pertinent to the anaesthetist, indices estimating perioperative MACE and
mortality include heart failure as an independent prognostic variable, with
unstable or decompensated heart failure bestowing a greater burden of risk.
Heart failure is a clinical syndrome characterised by typical symptoms
(breathlessness, ankle swelling and fatigue) with or without signs (raised
jugular venous pressure (JVP), pulmonary crackles and peripheral oedema),
caused by structural and/or functional cardiac abnormality, resulting in a
reduced CO and/or raised intracardiac pressures at rest or during stress.8
LV systolic and diastolic dysfunction can be asymptomatic precursors
of heart failure.8 Terminology has been based on left ventricular ejection
fraction (LVEF), but symptoms may not fit with the degree of reduction in
LVEF. Current terminology used to describe heart failure is as follows: heart
failure with reduced ejection fraction (HFrEF), heart failure with preserved
ejection fraction (HFpEF) and heart failure with mid-range ejection fraction
(HFmrEF) (is treated as per HFpEF) (Table 5.4).
Heart failure can be graded by severity of symptoms ± exercise intoler-
ance or structural disease by the New York Heart Association (NYHA)
functional classification (Table 5.5) or the American College of Cardiology/
American Heart Association stages of heart failure (Table 5.6).
Other classification systems used to describe heart failure include:
• Chronicity: acute, subacute and chronic
• Symptoms: stable and unstable (deterioration from stable symptoms is
referred to as decompensation)
• Affected side(s): left-and/or right-sided ventricular failure
• Diastolic and/or systolic dysfunction.
Management8, 13
Aims to delay progression of symptoms, optimise symptom management
and functional capacity and reduce mortality. Modifying risk factors (e.g.
hypertension, glycaemic control) may delay disease progression.
Medical treatment of HFrEF
The evidence for best management is clearest for HFrEF.
• ACE inhibitors reduce morbidity and mortality. Beneficial effects include
reduction in pre-/afterload and neurohormonal antagonism of the
renin–angiotensin–aldosterone system. Titrate to maximum tolerated
dose. ARBs are recommended in patients intolerant of ACE inihibitors.
• The combination of neprilysin inhibitor with ARB (sacubitril/valsartan)
reduces cardiovascular mortality by 20% and all-cause mortality by 16%. The
neprilysin inhibitor increases the bioavailability of natriuretic peptides. This
leads to ventricular unloading and vasodilatory effects. This combination may
be used instead of ACE inhibitor or ARB in refractory cases.
• β-blockers (carvedilol, bisoprolol) reduce HR and myocardial O2
demand. β-blockers should be continued throughout the perioperative
period. Use with caution in new-onset or decompensated heart failure.
• Mineralocorticoid receptor antagonists, e.g. spironolactone, reduce
mortality in symptomatic patients already treated with ACE inhibitors.
Use with caution in patients with impaired renal function. Other
diuretics may be added for symptom control.
• Inotropes: digoxin may be used to control AF with rapid ventricular rate
in symptomatic heart failure or in patients in SR with severe heart failure.
• Anticoagulation: if in AF or at risk of VTE.
• Calcium channel blockers are not safe for use in HFrEF.
Device treatment
• ICDs may be indicated for high-risk symptomatic patients or after unstable
ventricular arrhythmias. They reduce the risk of sudden cardiac death.
• Cardiac resynchronisation therapy (CRT) for those with prolonged QRS
duration. Biventricular pacing wires are placed. This aims to improve
symptoms and reduce mortality in select patients.
Medical treatment of HFpEF and HFmrEF
No specific treatments have demonstrated a reduction in morbidity or
mortality in these groups.14
• Diuretics are used as the mainstay of symptom management. They
probably reduce morbidity and mortality.
• Spironolactone reduces heart failure hospitalisations.
• β-blockers and ACE inhibitors may be used for BP control.
• Manage AF in accordance with established clinical guidelines.
Right-sided heart failure15
RV dysfunction is an independent predictor of MACE after non-cardiac
surgery. Right heart failure can be broadly divided into three categories,
depending on its causation:
• 2° to pulmonary hypertension
• 2° to pericardial disease
• 2° to ventricular or valvular pathology.
Pulmonary hypertension is most commonly caused by LV failure, but other
causes include chronic lung disease, OSA and PE.
Table 5.7 lists the causes of RV failure.
14
Hypertension
About 25% of the adult UK population has hypertension, defined as sys-
tolic blood pressure (BP) >140mmHg and diastolic BP >90mmHg (stage
1 hypertension). Triggers for consideration for treatment in 1° care are
≥160/ 100mmHg or average ambulatory BP ≥150/ 95mmHg (stage 2
hypertension).16 The link between elevated arterial pressure and CVS dis-
ease is well established, with the greatest risk associated with the highest
arterial pressures.
Evidence that moderate hypertension is associated with i perioperative
risk is limited, although CVS lability may be i. In adults undergoing non-
cardiac surgery, maintaining systolic arterial pressure >100mmHg and mean
arterial pressure (MAP) >60–70mmHg may reduce the risk of periopera-
tive myocardial injury, AKI and death. The degree of injury is dependent on
the severity and duration of hypotension. The association of hypertension
with end-organ damage (IHD, heart failure, renal failure) contributes to the
likelihood of perioperative CVS complications.
Perioperative management17
Ambulatory NIBP measurement is the optimal method to establish baseline
values. Preoperative readings are unlikely to be an accurate representation
of long-term BP control.
• 1° (essential) hypertension accounts for 95% of all cases, but consider
the possibility of 2° hypertension (e.g. renal parenchymal disease,
thyroid dysfunction, hyperaldosteronism, phaeochromocytoma). 2°
hypertension is more likely with early-onset or malignant/accelerated
hypertension and has specific anaesthetic implications.
• Do not defer surgery on the basis of a single BP reading on admission
to hospital. Refer to ambulatory BP reading or contact GP for a more
accurate baseline record.
• Preoperative BP targets are unclear for those on antihypertensives, but
both preoperative hypotension and hypertension are associated with an
increase in perioperative risk.
• There is insufficient evidence to support the introduction of
hypertensive medical management in the immediate preoperative
period to reduce perioperative risk.
• There is currently no upper limit of MAP that necessitates medical
management. Current evidence is contradictory, but expert opinion
recommends postponement of elective surgery in patients with arterial
pressure exceeding 180mmHg systolic and/or 110mmHg diastolic.
• The presence of end-organ dysfunction (including coronary or
cerebrovascular disease, impairment of renal function, signs of LVH and
heart failure) increases perioperative risk. These conditions may require
further investigation and/or treatment, in addition to the control of
elevated arterial BP.
• Withhold ACE inhibitor/ARB 24h prior to surgery to reduce the risk of
intraoperative cardiovascular instability (use caution in heart failure).
• Continue β-blockers, calcium channel blockers and thiazide diuretics in
the perioperative period.
Hypertension 117
Prosthetic valves
• Bioprosthetic (tissue) valves do not require long-term anticoagulation
due to low risk of thrombosis and thromboembolism.
• Mechanical valves require lifelong anticoagulation with warfarin (target
INR 2–3.5, depending on type of valve).
• Direct oral anticoagulants are not currently recommended for
mechanical prosthetic valves.19
• Aspirin is recommended, in addition to warfarin, if low risk of bleeding.
• Anticoagulation may need to be withheld, depending on the type of
surgery (warfarin usually stopped for 5d preoperatively).
• Bridging with LMWH (or UFH if renal failure) may be required.
• Requirement for bridging therapy is dependent on risk of
thromboembolism (e.g. mechanical mitral valve, older mechanical AV,
history of thromboembolism, presence of AF).
• Newer-generation bileaflet mechanical AV has <4% per annum risk
of thromboembolism, so bridging is not required in the absence of
additional patient-specific risks for thromboembolism.
• Consult local policies on bridging regimes.20
201
Aortic stenosis
AS is the commonest valvulopathy in Europe and North America. The
prevalence increases exponentially with age and 2% of the general popu-
lation have a congenital bicuspid valve, a risk factor for AS. The annual
mortality rate in patients with symptomatic severe AS is 25%.21 The risk of
perioperative MACE is high due to anaesthetic and surgical stresses.
AS is commonly due to AV calcification. Degenerative AV sclerosis is an
antecedent to clinically significant AS. Progressive valve narrowing increases
afterload, leading to concentric LVH and reduced diastolic compliance.
Elevated filling pressures and SR are required to fill the non-compliant LV.
Normal LVEDP may reflect hypovolaemia.
Atrial contractions contribute up to 40% to the left ventricular end-
diastolic volume (LVEDV) in AS (normally only 20–30%). Arrhythmias will
reduce CO. There is a high risk of myocardial ischaemia due to O2 supply–
demand mismatch. Increasing LV mass increases O2 demand. Resultant
increases in systolic wall tension and intraventricular cavity pressure com-
press subendocardial vessels during systole, making the subendocardium
vulnerable to ischaemia.
Even with normal coronary vessels, 30% of patients with AS experience
angina. Tachycardia (stress, pain) further increases O2 demand and shortens
diastole, increasing compromise of coronary perfusion and increasing is-
chaemia. Diastolic BP is crucial to maintain coronary perfusion.
History and examination
Symptoms do not correlate well with the severity of stenosis, but exertional
angina, dyspnoea and pre-/syncope may be present. On examination, there
may be a slow-rising pulse with narrow pulse pressure. An ejection systolic
murmur is typically maximal at the 2nd intercostal space, right sternal edge,
and radiates to the neck.
Investigations
• ECG: LVH and strain (with 2° ST–T wave abnormalities).
• CXR: post-stenotic dilation of the aorta, calcified aortic annulus and
signs of LV heart failure.
• Echocardiography: assesses AS severity (Table 5.8) and LV function.
• Cardiac catheterisation allows measurement of AV gradient.
Perioperative management1,3,21
Risk
• Guidelines prioritise the presence and progression of symptoms in
decision-making for elective non-cardiac surgery.
• Irrespective of symptoms, a large meta-analysis demonstrated higher
rates of MACE, but not mortality, in patients with AS undergoing non-
cardiac surgery. Patients with AS and CAD probably represent a higher-
risk population.
• With appropriate haemodynamic monitoring, it is reasonable
for asymptomatic patients with severe AS to undergo elective,
intermediate-risk non-cardiac surgery.
• Symptomatic patients with severe AS may be considered for valvular
intervention prior to elective surgery.
Haemodynamic goals
• Low-normal HR
• Maintain SR
• Adequate preload
• Maintain systemic vascular resistance (SVR) and avoid hypotension.
Perioperative
• Patients with severe AS have a fixed CO. They cannot compensate for
a reduced SVR, resulting in hypotension, myocardial ischaemia and a
downward spiral of reduced contractility.
• Balance myocardial O2 supply–demand by maintaining afterload and
avoiding tachycardia (‘slow and tight’).
• An arterial line is extremely useful—place prior to induction.
• Titrate drugs carefully and treat hypotension promptly and aggressively.
Insertion of a CVC allows reliable administration of vasoconstrictor
therapy. Intraoperative TOE may be useful.
• Arrhythmias must be treated promptly, or haemodynamic collapse may
ensue. Consider the role of DCCV.
• Effective analgesia avoids catecholamine-induced tachycardia and
hypertension. Central neuraxial blocks (CNBs) must be used with
caution due to significant reduction in afterload. Regional blocks can be
used alone or in conjunction with GA.
• Have a low threshold for admission to ICU/HDU for observation and
possible need for vasopressors.
21
Aortic regurgitation
Aortic regurgitant lesions are better tolerated than stenotic lesions.
Asymptomatic patients with normal LVEF have a favourable prognosis.
Pathophysiology
Aortic regurgitation (AR) results from diseases involving the aortic leaflets
themselves, or aortic root/annulus incompetence.
• Aortic leaflet: degenerative disease, IE, rheumatic heart disease,
connective tissue disease, bicuspid valve
• Aortic root/annulus: Marfan’s syndrome, connective tissue disease,
aortic dissection.
Acute AR (e.g. endocarditis or acute type A aortic dissection)
With a large regurgitant volume, the LV becomes overwhelmed acutely. LV
diastolic pressure rises, approaching aortic diastolic pressure. Untreated,
mitral regurgitation (MR) follows, leading to pulmonary oedema and circu-
latory failure. Treatment is emergency valve surgery.
Chronic AR
The return of blood back to the ventricle during diastole contributes to
preload. i LVEDV produces a compensatory increase in force of contrac-
tion and stroke volume. Aortic systolic pressure rises, but aortic diastolic
pressure is reduced due to regurgitation.
• Eccentric LVH followed by LV dilation prevents significant increases in
LV filling pressures despite large regurgitant volume. Progressive LV
dilation increases wall stress. Initially, LVEF is maintained, followed by
dilation. LV dysfunction may be masked by raised preload.
• Decompensation can be caused by further increase in LV wall stress,
leading to d diastolic compliance and LV systolic dysfunction. Heart
failure symptoms ensue.
History, examination and investigations
Most of the symptoms are 2° to heart failure in decompensated AR, but
patients may experience palpitations or angina due to reduced coronary
perfusion pressure in the setting of i LV wall stress.
• On examination, a collapsing (‘waterhammer’) pulse illustrates a wide
pulse pressure resulting in: visible neck pulsation (Corrigan’s sign),
head nodding (de Musset’s sign) or visible capillary pulsations in the
nail beds (Quincke’s sign). A diastolic murmur may be heard at the 2nd
intercostal space, right sternal edge.
• CXR: cardiomegaly, boot-shaped heart.
• ECG: non-specific LVH.
• Echocardiogram provides quantitative analysis of the aortic leaflets and
aortic root. Doppler studies allow estimation of regurgitant severity. LV
size and function are assessed.
Aortic regurgitation 123
Perioperative risk1
• AR increases cardiac risk during non-cardiac surgery, especially if LV
function is reduced.
• In asymptomatic patients with severe AR, elective intermediate-risk
non-cardiac surgery is reasonable with appropriate perioperative
haemodynamic monitoring.
• Patients with poor functional capacity should be considered for valve
replacement surgery prior to elective surgery.
Haemodynamic goals
• High-normal HR (790bpm)
• Adequate preload
• Low SVR
• Maintain SR
• Maintain contractility.
The selected anaesthetic technique aims to promote forward systemic flow.
Maintaining a faster HR reduces diastolic regurgitation time. A reduction in
SVR to the low-normal range decreases afterload while maintaining cor-
onary perfusion pressure (‘full, fast and forward’).
• Spinal and epidural anaesthesia is well tolerated.
• Intra-arterial pressure monitoring is useful for major surgery and/or
high-risk symptomatic patients. Non-invasive CO monitoring is
inaccurate. TOE, if available, may guide optimisation of LV function.
• Treat perioperative supraventricular tachycardia (SVT)/AF promptly
with synchronised DCCV (see % p. 149), particularly if associated with
hypotension. Persistent bradycardia may need to be treated with β-
agonist or anticholinergic agents.
241
Mitral stenosis
Rheumatic fever is the commonest cause. A minority have isolated stenosis;
the majority have mixed mitral valve disease (stenosis and regurgitation).
• Mitral valve stenosis (MS) causes underfilling of the LV and increasing
pressure and volume upstream of the valve (Table 5.9). The LV
functions normally but is small and poorly filled.
• Pulmonary vascular pressures are initially maintained by left atrial
dilation. As disease progresses, the pulmonary artery pressure
(PAP) increases. Reactive pulmonary vasoconstriction contributes to
development of pulmonary hypertension.
• Adaptive RV hypertrophy fails to compensate for volume and pressure
overload, leading to progressive RV dilation and failure.
• The pressure gradient across the narrow mitral orifice increases with
the square of the CO. Rapid HRs, especially with AF, decrease the
diastolic filling time and markedly decrease the CO.
• Chronic left atrial dilation greatly increases the risk of AF.
• Intracardiac thrombus, either in the left atrium or left atrial appendage,
may develop due to low-velocity blood flow. If present, anticoagulation
is required.
• Critical MS is a fixed, low CO state.
History
Patients complain of dyspnoea, haemoptysis and recurrent bronchitis.
Fatigue and palpitations are common.
Examination
• Mitral facies: malar flush on cheeks
• Peripheral cyanosis
• Signs of right heart failure
• Tapping apex beat. Loud 1st heart sound, opening snap (if in SR) and
low-pitched diastolic murmur heard best at the apex (with the bell of
the stethoscope).
Mitral stenosis 125
Investigations
• ECG: P mitrale (left atrial enlargement) if SR. AF common
• CXR: valve calcification. Large left atrium (lateral film). Double shadow
behind the heart on posterior-to-anterior (PA) film. Splaying of the
carina. Kerley B lines indicating pulmonary congestion
• Echocardiogram measures the gradient and valve area (Table 5.9).
Allows assessments of RV function. Assesses for presence of
intracardiac thrombus.
Perioperative risk1
Patients with MS who meet standard criteria should undergo valvular
intervention prior to elective surgery (open or percutaneous mitral
commissurotomy).
• In asymptomatic patients with severe MS, elective intermediate-risk
non-cardiac surgery is reasonable with appropriate perioperative
hsemodynamic monitoring.
Haemodynamic goals
• Low-normal HR 50–70bpm
• Maintain SR. Cardiovert if AF occurs perioperatively
• Adequate preload
• High-normal SVR
• Avoid hypercapnia, acidosis and hypoxia, which may exacerbate
pulmonary hypertension.
Anaesthetic goals aim to maintain the delicate balance of adequate LV filling,
while minimising decompensation of chronically i pulmonary pressures.
• Tachycardia should be avoided, as i HR reduces time for LV filling.
Short-acting β-blockers may be used for HR control.
• Maintain an adequate afterload. However, fluid overload may precipitate
acute pulmonary oedema. Measurement of CVP and pulmonary
capillary occlusion pressure and TOE, if available, will guide intravascular
volume management and ventricular function.
• Inotropic support may be required to optimise RV function.
• Spinal and epidural anaesthesia may be hazardous.
261
Mitral regurgitation
Mitral regurgitant lesions are better tolerated than stenotic lesions.
Asymptomatic patients with normal LVEF have a favourable prognosis. MR
results from leaflet, chordal or papillary muscle abnormalities or as a conse-
quence of LV dysfunction (functional MR).
• Leaflet: complication of endocarditis, rheumatic disease or mitral valve
prolapse, myxomatous degeneration
• Chordal: chordae rupture after AMI or after bacterial endocarditis
• Papillary muscle: ischaemic posterior papillary muscle dysfunction
• LV failure leads to dilation of mitral valve annulus.
The left atrium is subjected to volume and pressure overload—adaptive
dilation occurs gradually. As much as 50% of the LV volume flows into the
dilated left atrium before the aortic valve opens. LVEF is i and over time,
LV dysfunction may occur. The degree of regurgitation is determined by
the afterload, size of the regurgitant orifice and HR. A moderately i HR
(>90bpm) decreases the time for regurgitation in systole and decreases the
time for diastolic filling, reducing LV overload. Chronic MR will lead to pul-
monary vascular congestion, followed by pulmonary hypertension and right
heart failure.
History, examination and investigations
• Fatigue, dyspnoea, palpitations, symptoms of right heart failure. Acutely,
MR may present with flash pulmonary oedema
• Displaced and forceful apex due to LVH, soft S1, apical pansystolic
murmur radiating to the axilla and loud S3
• ECG: left atrial enlargement. AF is common
• CXR: left atrial and LV enlargement. Mitral annular calcification
• Echocardiogram gives quantitative estimate of regurgitant fraction,
including measuring the vena contracta (narrowest cross-sectional area
of a fluid jet) which corresponds to the regurgitant orifice area and MR
severity. Assess ventricular function. TOE particularly useful as the left
atrium is adjacent to the oesophagus.
Mitral valve prolapse
• Common (incidental finding in 5% of population)
• Usually asymptomatic, but may be associated with atypical chest pain,
palpitations, syncope and emboli
• Mid-systolic click and late diastolic murmur
• Echocardiogram shows enlarged redundant mitral valve leaflets
prolapsing into the left atrium during mid-to late systole, causing
arrhythmias and regurgitation
• Antiarrhythmics must be continued perioperatively.
Perioperative risk1
MR increases cardiac risk during non-cardiac surgery, especially if LV func-
tion is reduced.
• In asymptomatic patients with severe MR, elective intermediate-risk
non-cardiac surgery is reasonable with appropriate perioperative
haemodynamic monitoring.
• Patients with poor functional capacity should be considered for valve
repair/replacement surgery prior to elective surgery.
Mitral regurgitation 127
Haemodynamic goals
• High-normal HR (790bpm).
• Adequate preload.
• Low SVR.
• Low PVR.
• Maintain SR.
Anaesthetic goals aim to promote forward systemic flow. Maintaining a
faster HR reduces systolic regurgitation time. Bradycardia will increase LV
diastolic filling, leading to LV distension.
• A reduction in SVR to the low-normal range decreases afterload while
maintaining coronary perfusion pressure. Spinal and epidural anaesthesia
is well tolerated.
• Intra-arterial pressure monitoring is useful for major surgery and/or
high-risk symptomatic patients.
• Preload can be difficult to estimate; for major non-cardiac surgery, a
pulmonary artery (PA) catheter and/or TOE, if available, may be useful
to guide intravascular volume management.
• In advanced disease, pulmonary hypertension is common. Avoid factors
that increase the PAP (hypoxia, hypercapnia, high inspiratory pressures,
acidosis).
• Inotropic support may be required to optimise ventricular function.
281
Pericardial disease
Acute pericarditis
• Inflammatory disease of the pericardium.
• May be idiopathic, infective, non-infective (e.g. post-cardiac surgery)
or autoimmune. Usually presents with chest pain. The diagnosis is
supported by widespread saddle-shaped ST-elevation on ECG.
• Frequently occurs with myocarditis, which may increase the likelihood
of arrhythmia and sudden death.
• Elective surgery should be postponed for at least 6w.
Constrictive pericarditis
• Chronic inflammation of the pericardium causes thickening and reduced
compliance.
• Common causes include post-infective and autoimmune diseases (e.g.
systemic lupus erythematosus (SLE). The only effective treatment is
pericardiectomy which may be dramatically effective.
• Pulsus paradoxus (exaggerated fall in systolic BP with inspiration) may
be seen due to the thickened pericardium preserving intrapericardial
pressure. The normal maximum fall is 10mmHg.
• Systolic function of the myocardium is well maintained, but diastolic
function is severely impaired. When exercise tolerance is reduced, GA
carries a significant risk.
• Bradycardia and reduced cardiac filling are poorly tolerated.
• Elevations in intrathoracic pressure, such as during intermittent positive
pressure ventilation (IPPV), can result in profound hypotension.
• If anaesthesia is unavoidable, and regional block is not possible, then a
spontaneously breathing technique is preferable to IPPV. Preload should
be maintained, and tachycardia avoided.
Pericardial effusion
• Excessive fluid accumulation within the pericardial space.
• Effusion may be transudate, exudate, haemorrhagic or purulent,
depending on the aetiology.
• Progressive accumulation may lead to compression of cardiac chambers
and tamponade.
• Non-specific symptoms include dyspnoea, orthopnoea, chest pain and
tachycardia.
• Clinical signs of tamponade include Beck’s triad: raised JVP, hypotension
and muffled heart sounds.
• Echocardiography is a useful diagnostic tool.
• Urgent pericardiocentesis or a pericardial window may be required.
• Elective surgery should be postponed for at least 6w.
Cardiomyopathy 129
Cardiomyopathy
‘A heterogenous group diseases of the myocardium associated with mech-
anical and/or electrical dysfunction which usually exhibit inappropriate ven-
tricular hypertrophy or dilation.22
Cardiomyopathies are either confined to the heart (1°) (Table 5.10) or
a manifestation of a systemic disease (2°), e.g. amyloidosis, haemochroma-
tosis, sarcoidosis or thyroid disease.22 Regardless of the aetiology, there is a
potential final common pathway of myocardial injury, leading to ventricular
dysfunction and clinical heart failure. Often, no disease-specific treatment is
available. Management focuses on heart failure therapy.
There is little evidence on perioperative risk evaluation in patients
with non- ischaemic cardiomyopathy undergoing non- cardiac surgery.1,23
Markers of disease severity include poor functional capacity and reduced
LVEF. Other factors associated with poor prognosis include resting tachy-
cardia, low BP, interventricular conduction abnormalities and LV diastolic
dysfunction.
Stress-induced cardiomyopathy
• Also known as Takotsubo and apical ballooning syndrome.
• Reversible cardiomyopathy characterised by transient systolic
dysfunction indistinguishable from AMI, but in the absence of CAD.
• Responsible for 72% of all acute coronary syndrome events.
• Differing mechanisms have been suggested, but possibly due to
catecholamine release.
• Commonly precipitated by sudden, emotionally (occasionally
physiologically) stressful events.
• Commonest in women aged 58–75y (90%).
• RWMAs are beyond single vascular territory.
• Patients are often critically ill acutely: congestive cardiac failure
(CCF), arrhythmias, cardiogenic shock, left ventricular outflow tract
obstruction.
• Mortality is in the region of 1%.
• Symptoms resolve quickly; about 10% may reoccur.
• Treatment is supportive.
301
Restrictive cardiomyopathy
• Rare condition. The commonest cause is myocardial infiltration by
amyloid.
• Characterised by stiff ventricles that impair ventricular filling. Right heart
failure is often prominent. Echo shows diastolic dysfunction.
• Anaesthesia is potentially associated with high risk.
• Peripheral vasodilation, myocardial depression and reduced venous
return may cause catastrophic cardiovascular decompensation and may
precipitate cardiac arrest.
• Venous return may be further compromised by positive pressure
ventilation. Wherever possible, maintain spontaneous respiration.
• Ketamine may be useful, as it increases myocardial contractility and
peripheral resistance.
• Fluids should be given to maintain elevated right heart pressures.
Haemodynamic goals
• Maintain SR
• Adequate volume loading
• High-normal SVR
• Avoid myocardial depression.
Dilated cardiomyopathy
This manifests as cardiac failure with impaired systolic function and dilation
of both ventricles, predominantly the LV. Functional mitral and tricuspid
incompetence occurs commonly, due to dilation of the valve annulus,
exacerbating heart failure.
• The commonest problems are heart failure, arrhythmias and embolic
phenomena.
• Heart failure is treated according to established guidelines (see %
pp. 111–15). Medical management includes ACE inhibitors, β-
blockers and mineralocorticoid antagonists. Patients are frequently
anticoagulated. Synchronised biventricular pacing may be used. Some
patients may require an ICD for prevention of sudden cardiac death
(see % pp. 830–1 and p. 161).
• Peripheral nerve blocks (PNBs) minimise sympathetic activation. CNB
reduces afterload. Associated hypotension must be avoided.
• Invasive monitoring with arterial and central venous catheters should be
used. Intraoperative TOE, where available, will guide fluid management
and ventricular support.
• Inotropic support may be provided with a variety of β-agonists and
inodilators.
Haemodynamic goals
• Maintain SR. Avoid tachycardia.
• Adequate volume preload.
• Normal SVR. Avoid increases in afterload.
• Avoid myocardial depression; inotropic support is frequently required
with dobutamine or PDE inhibitors.
Cardiomyopathy 131
Tetralogy of Fallot
• Pulmonary stenosis, VSD, overriding aorta and RV hypertrophy.
• May be prone to cyanotic episodes (‘tet spells’) due to intermittent RV
infundibular spasm causing i right-to-left shunting. If this occurs under
anaesthesia, treatment includes: 100% O2, IV fluid, adequate analgesia/
anaesthesia to reduce circulating catecholamines and increasing SVR
(e.g. by bringing the knees towards the chest and/or IV vasopressors).
• Before full repair, may be treated medically with β-blockers or surgically
via a modified Blalock–Taussig shunt—a Gore-Tex® tube interposed
between the subclavian and pulmonary arteries.
• Full repair of ToF is usually undertaken in the first 6mo of life.
Transposition of the great arteries
• Accounts for 7–8% of CHD, in which the aorta arises from the RV and
the PA from the LV; a VSD occurs in 730%.
• In order to be compatible with life, there must be a source of mixing
(i.e. PDA, ASD or VSD) to allow oxygenated pulmonary venous blood
to reach the systemic circulation.
• Preoperative management usually consists of a prostaglandin infusion ±
balloon atrial septostomy if mixing is inadequate.
• Repair is usually with an arterial switch procedure in the first 2w of life.
Hypoplastic left heart syndrome and the Fontan circulation
• Hypoplastic left heart syndrome accounts for around 2% of CHD and
carries a significant mortality risk, with 770% surviving to 5y.
• Patients with hypoplastic left heart syndrome undergo a 3-stage repair,
usually involving a neonatal Norwood operation, followed by a Glenn
shunt at 3–6mo, and finally a completion Fontan procedure (also called
a total cavopulmonary connection) at 3–5y.
• After total cavopulmonary connection, all superior vena cava (SVC)
and IVC blood flows directly into the PA, bypassing the right heart.
Pulmonary blood flow is thus passively dependent on systemic venous
pressure.
• The aim is to volume-offload the RV, while providing acceptable arterial
saturations (75–85%); however, the Fontan circulation inevitably leads
to high venous pressures, liver congestion, protein-losing enteropathy
and pleural and pericardial effusions.
• Hypovolaemia can lead to hypoxia and CVS collapse. IPPV results in
a fall in CO, and high ventilatory pressures result in poor pulmonary
perfusion.
• These children are particularly vulnerable and should be managed in a
specialist centre, whenever possible.
381
Pulmonary hypertension
Pulmonary hypertension describes a situation of elevated pressure in the
pulmonary circulation. Pulmonary hypertension has many aetiologies and
can complicate most cardiovascular and respiratory conditions (Table 5.11).
Although the aetiology may be different, the sequelae of endothelial dys-
function, vasoconstriction and vascular remodelling are common.25
Normal mean pulmonary artery pressure (mPAP) is 14mmHg. Pulmonary
hypertension is defined as a mPAP ≥25mmHg measured by right heart cath-
eterisation at rest.
• Mild mPAP 25–40mmHg
• Moderate mPAP 41–55mmHg
• Severe mPAP >55mmHg.
Pulmonary artery hypertension (PAH) is distinct from the other classes of
pulmonary hypertension and is defined as pre-capillary pulmonary hyper-
tension with PA occlusion pressure ≤15mmHg and PVR >3 Wood units,
in the absence of other causes of pre-capillary pulmonary hypertension.
PAH accounts for 45% of pulmonary hypertension, with chronic thrombo-
embolic pulmonary hypertension being the second commonest (19%), fol-
lowed by left heart disease. Pulmonary hypertension is classified into groups
of similar pathophysiological mechanisms, clinical presentation and haemo-
dynamic characteristics (Table 5.11).26
Class
1 Pulmonary hypertension with no symptoms or limitation to ordinary
physical activity
2 Pulmonary hypertension with mild symptoms and slight limitation during
ordinary activity
3 Pulmonary hypertension with marked limitation of physical activity.
Comfortable at rest
4 Pulmonary hypertension with signs of right heart failure, possibly even at
rest. Inability to carry out any activity without symptoms
Treatment Notes
Non-specific treatment Anticoagulation (idiopathic
PAH only)
Diuretics for decompensated right
heart failure
O2 reduces PVR, but no evidence
for long-term O2 therapy
Calcium channel blockers <10% of patients benefit
Synthetic prostacyclin analogues Epoprostenol shown to improve
(epoprostenol, iloprost, treprostinil) survival in idiopathic PAH
Treprostinil and inhaled iloprost
shown to improve symptoms and
reduce clinical events
Endothelin receptor antagonists Macitentan reduces progression of PAH
and death. Ambrisentan and bosentan
improve symptoms ± progression
PDE-5 inhibitors Sildenafil and tadalafil improve exercise
capacity and symptoms
Guanylate cyclase stimulation Riociguat beneficial in PAH
Transplantation Heart–lung and double-lung
transplantation improves survival in
idiopathic PAH
421
Anaesthesia
(See % pp. 524–5 for cardiac surgery and pulmonary hypertension.)
Evidence is lacking, but postoperative mortality after non-cardiac surgery
ranges from 4–20% depending on the series. Although RV contractility can
be normal in mild disease, systolic dysfunction is common and progresses
with worsening class of pulmonary hypertension. Systemic BP is usually low
(disease-and treatment-related). Table 5.14 lists some of the factors that
are used to assess the 1y mortality risk.27 Consider referring any patient in
the intermediate-or high-risk categories to a specialist pulmonary hyper-
tension centre for their surgery.
Risk factors associated with increased perioperative mortality and morbidity25
• NYHA class ≥2
• 6MWT <300m
• PVR >400dyn.s.cm–5
• Elevated right atrial pressure (>14 mmHg)
• Low cardiac index in right heart catheterisation (<2.4L/m2)
• History of: CAD, PE, chronic kidney disease (CKD) and RV
hypertrophy with severe systolic dysfunction
• Emergency surgery
• Intermediate-/high-risk surgery
• Duration of surgery >3h
• Intraoperative vasopressor requirement.
Perioperative management25
H Maintain RV and pulmonary circulation coupling, and prevent a pul-
monary hypertension crisis.
• Many anaesthetic drugs affect RV contractility and PVR (Table 5.15).
• Basic haemodynamic goals:
• Maintain systolic BP at baseline if possible, or at least a minimum
systolic pressure of 90mmHg and 40mmHg above systolic PAP.
• MAP ≥65mmHg and 20mmHg above mPAP.
• Lowest right atrial pressure to maintain MAP >65mmHg.
• Give supplementary O2 (O2 is a pulmonary vasodilator); avoid hypoxic
pulmonary vasoconstriction.
• Avoid hypothermia (causes pulmonary vasoconstriction and V/Q
mismatch).
• Invasive arterial monitoring to aid rapid response to changes in BP and
allow for intermittent sampling.
• Intraoperative TOE or PA catheter should be considered in all patients
with severe pulmonary hypertension or evidence of right heart failure.
• Obtund sympathetic response to laryngoscopy to avoid increase in
PVR and atrial tachyarrhythmias, which can lead to right heart failure
and death. For rhythm control, amiodarone is the drug of choice; use
digoxin if rhythm control not possible. β-blockade is poorly tolerated.
Medication Effect
Isoflurane, desflurane, Marked, dose-dependent reduction in RV
sevoflurane contractility
Increase in PVR (not sevoflurane)
Propofol Reduces RV contractility, RV ejection fraction and
cardiac index
Thiopental Reduced RV contractility and SVR
Ketamine Increases PVR (adults only)
Vasopressors: noradrenaline, Improve perfusion of right coronary artery, reduce
vasopressin PVR/SVR ratio, enhance RV contractility and
marginally improve CO
Inotropes: adrenaline, Increase RV contractility
dobutamine, levosimendan
Inodilators: PDE-3 inhibitors Reduce PVR and improve PVR/SVR ratio.
(e.g. milrinone) Reduction in SVR can compromise coronary artery
blood flow
IV vasodilator: sildenafil Can be given PO and IV, so could be an option for
patients already on oral therapy
Inhaled pulmonary Nitric oxide, epoprostenol, prostacyclin, iloprost
vasodilators and treprostinil have all been used perioperatively,
but in small numbers
41
Perioperative arrhythmias
(See also % Chapter 39.)
Perioperative cardiac arrhythmias are common and may result in signifi-
cant morbidity and mortality. In the setting of pre-existing arrhythmia, rate
and rhythm control should be optimised prior to surgery, as perioperative
stressors can lead to marked deterioration.
Preoperative recognition of potential risk factors and triggers may allow
prevention and/or rapid management of arrhythmia.
When providing IV drug treatment for arrhythmia management, ensure a
defibrillator is readily available in case of rhythm deterioration.
Risk factors for new-onset perioperative arrhythmia or deterioration of
pre-existing arrhythmia may be classified according to patient factors and
context-specific triggers (Table 5.16).
Fig. 5.1 This patient has WPW syndrome as they have delta waves (slurred QRS
upstrokes) in beats 1 and 4 on this rhythm strip. The delta wave both broadens the
ventricular complex and shortens the PR interval. If a patient with WPW has AF,
avoid AV node blockers such as diltiazem, verapamil and digoxin—but flecainide
may be used. Reproduced with permission of Oxford Publishing Limited through PLSclear from
Wilkinson I et al. Oxford Handbook of Clinical Medicine. © Oxford University Press 2017.
Narrow complex arrhythmias 149
Atrial flutter
Often caused by a re-entry circuit at the tricuspid valve. Associated with
cardiac disease. Atrial depolarisation is 7300bpm. However, ventricular rate
is determined by AV conduction, resulting in an AV block. The commonest
AV ratio is 2:1. Higher degrees of AV block can occur, usually due to drugs
which lower ventricular conduction.
Associated risk of thromboembolism similar to AF.
Acute management entails:
• Synchronised DCCV if adverse features are present or new onset under
anaesthesia. Requires sedation or GA, but lower energy (70–120J) may
suffice.29 Nearly 100% conversion.
• If haemodynamically stable: vagal manoeuvres, carotid sinus massage or
Valsalva manoeuvre may terminate re-entry SVT and may be helpful in
differentiating SVT from atrial flutter and fast AF. Adenosine blocks AV
nodal conduction and is especially useful for terminating re-entry SVT.
Give 6mg IV rapidly, followed by a large 0.9% sodium chloride flush into
a large proximal vein (e.g. antecubital). Record ECG during the injection.
If rate slows, look for atrial activity to aid diagnosis. If no effect, give
12mg IV bolus. The effects of adenosine last only 10–15s. It should be
used with caution in asthma due to risk of bronchospasm.
• Acute rate and rhythm control: β-blockers (rate) or amiodarone
(rhythm), as per treatment for AF below. Digoxin should be avoided
as it facilitates conduction through the AV accessory pathway in WPW
syndrome and may worsen tachycardia.
Irregular supraventricular tachycardia
Atrial fibrillation
• The most commonly sustained arrhythmia after surgery. Associated
with increase in length of stay, incidence of postoperative CVE and
in-hospital mortality.30 Table 5.17 illustrates strategies to prevent
perioperative AF.31
• Disordered generation of atrial electrical impulses leads to
uncoordinated atrial activity that is conducted intermittently and
irregularly to the ventricles via the AV node (Fig. 5.2).
• Atrial contraction contributes up to 30% of ventricular filling. The
onset of AF, particularly in the setting of rapid ventricular rate, causes a
reduction in ventricular filling and CO.
• Thrombi may form within the atria, due in part to blood stasis, and
embolise systemically. Annual risk of thromboembolic events and need
for anticoagulation may be estimated with prognostic models (i.e.
CHA2DS2-VASc).
• ECG demonstrates: irregularly irregular rhythm without P waves,
narrow QRS (<120ms) unless conduction abnormality (e.g. pre-
existing bundle branch block), variable ventricular rate and absence of
isoelectric baseline. Aberrancy, or functional conduction delay, refers to
the broadening of the QRS as the rate gets faster.
Management of acute atrial fibrillation
• Goal: restore CO and ensure adequate oxygenation.
• Determine presence of adverse features: shock, syncope, myocardial
ischaemia and heart failure.31
501
Fig. 5.2 (a) AF: note the irregular spacing of QRS complexes and lack of P waves.
(b) AF with a rapid ventricular response (sometimes referred to as ‘fast AF’). No
pattern to QRS complex spacing, and rate >100bpm. (c) Atrial flutter with 2:1 block
(two P waves for every one QRS complex). The P waves have the classic ‘sawtooth’
appearance. Alternate P waves are merged with the QRS complex. Reproduced with
permission of Oxford Publishing Limited through PLSclear from Wilkinson I et al. Oxford Handbook
of Clinical Medicine. © Oxford University Press 2017.
521
Fig. 5.3 Bigeminy—a normal QRS is followed by a ventricular ectopic beat (*), then
a compensatory pause; this pattern then repeats. The ectopic beats have the same
morphology as each other, so probably all share an origin. Reproduced with permission
of Oxford Publishing Limited through PLSclear from Wilkinson I et al. Oxford Handbook of Clinical
Medicine. © Oxford University Press 2017.
Ventricular tachycardia
This is a serious, potentially life-threatening arrhythmia. The QRS is always
wide. P waves may be seen if there is AV dissociation (Fig. 5.4). May be
monomorphic (a single ventricular focus with uniform QRS complexes) or
polymorphic (multiple ventricular foci with an irregular QRS morphology).
Perioperative triggers include:
• Myocardial ischaemia, hypoxia and hypotension
• Fluid overload
• Electrolyte imbalance (low K+, Mg2+, etc.)
• Injection of adrenaline or other catecholamines
• Drugs which prolong the QT interval (e.g. amiodarone, ondansetron,
haloperidol).
Fig. 5.4 VT with a rate of 235/min. Reproduced with permission of Oxford Publishing
Limited through PLSclear from Wilkinson I et al. Oxford Handbook of Clinical Medicine. © Oxford
University Press 2017.
Management29,34
• Confirm the presence of CO (central pulse, arterial line waveform,
capnography).
• If no evidence of CO, commence cardiopulmonary resuscitation (CPR)
and advanced cardiovascular life support with immediate defibrillation.
Broad complex arrhythmias 153
Fig. 5.6 VF. Reproduced with permission of Oxford Publishing Limited through PLSclear from
Wilkinson I et al. Oxford Handbook of Clinical Medicine. © Oxford University Press 2017.
541
Trifascicular block
Sometimes used to indicate the presence of a prolonged P–R interval to-
gether with bifascicular block.
P P P P
P P P P
P P P P P
P P P P P P P
Fig. 5.7 Rhythm strips of heart blocks. Reproduced with permission of Oxford Publishing
Limited through PLSclear from Wilkinson I et al. Oxford Handbook of Clinical Medicine. © Oxford
University Press 2017.
561
Preoperative management
• First-degree heart block in the absence of symptoms is common. It
needs no specific investigation or treatment.
• Second-or 3rd-degree heart block may need pacemaker insertion.
If surgery is urgent, this may be achieved quickly by inserting a
temporary transvenous wire prior to definitive insertion.
• Bundle branch, bifascicular or trifascicular block (bifascicular with
1st-degree block) will rarely progress to complete heart block during
anaesthesia, and so it is not common practice to insert a pacing wire,
unless there have been episodes of syncope.
Indications for preoperative pacing
• Symptomatic 1st-degree heart block
• Symptomatic 2nd-degree (Mobitz type I) heart block
• Second-degree (Mobitz type II) heart block
• Third-degree heart block
• Symptomatic bifascicular block or symptomatic 1st-degree heart
block plus bifascicular block (trifascicular block)
• Symptomatic sinus node disease.
158
Chapter 5
Cardiovascular disease
Fig. 5.9 Left bundle branch block: wide QRS with a W pattern in V1 (slight notching in upstroke of S wave—clearer in V3) and the M pattern in V6.
WiLLiaM = LBBB. Reproduced with permission of Oxford Publishing Limited through PLSclear from Wilkinson I et al. Oxford Handbook of Clinical Medicine. © Oxford
University Press 2017.
Fig. 5.10 ECG showing bifascicular block. There is a wide QRS complex with an RSR pattern in V1 and a deep, slurred S wave in V6 (=
RBBB). The QRS in lead 1 is positive and lead aVF negative (= left anterior hemiblock). There is also second-degree AV nodal block (Mobitz
type I or Wenckebach). Observing the rhythm strip from the 1st P wave, there is a gradually prolonging PR interval and the P wave that
follows the 6th QRS complex is blocked. Reproduced with permission of Oxford Publishing Limited through PLSclear from Wilkinson I et al. Oxford
Disturbances of conduction (heart block)
Implantable cardioverter–defibrillators
ICDs should be deactivated prior to surgery where diathermy might be
used (the ICD will detect the signal as VF and deliver a shock). A magnet
placed over the ICD inhibits their function. The patient should be moni-
tored throughout surgery, and then the device reactivated postoperatively.
While deactivated, an external defibrillator should be immediately available,
with pads applied pre-emptively.
Further reading
Andropoulos DB, Stayer SA, Mossad EB, Miller-Hance WC, eds. (2015). Anesthesia for Congenital
Heart Disease. Hoboken, NJ: Wiley-Blackwell.
Nasr VG, Dinardo JA (2017). The Pediatric Cardiac Anesthesia Handbook. Hoboken, NJ:
Wiley-Blackwell.
Thorne S, Bowater S (2017). Adult Congenital Heart Disease. Oxford: Oxford University Press.
References
1 Fleisher LA, Fleischmann KE, Auerbach AD, et al. (2014). ACC/AHA guideline on perioperative
cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report
of the American College of Cardiology/American Heart Association Task Force on practice
guidelines. J Am Coll Cardiol, 64, e77–137.
2 Wijeysundera DN, Pearse RM, Shulman MA, et al. (2018). Assessment of functional capacity be-
fore major non-cardiac surgery: an international, prospective cohort study. Lancet, 391, 2631–40.
3 Kristensen SD, Knuuti J, Saraste A, et al. (2014). ESC/ESA guidelines on non-cardiac surgery;
cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: car-
diovascular assessment and management of the European Society of Cardiology (ESC) and the
European Society of Anaesthesiology (ESA). Eur Heart J, 35, 2383–431.
4 Duceppe E, Parlow J, MacDonald P, et al. (2017). Canadian Cardiovascular Society guidelines on
perioperative cardiac risk assessment and management for patients who undergo noncardiac
surgery. Can J Cardiol, 33, 17–32.
5 Mehta SR, Bainey KR, Cantor WJ, et al. (2018). CCS/CAIC Focused update of the guidelines for
the use of antiplatelet therapy. Can J Cardiol, 34, 214–33.
6 Helwani MA, Amin A, Lavigne P, et al. (2018). Etiology of acute coronary syndrome after non-
cardiac surgery. Anesthesiology, 128, 1084–91.
7. Cortes-Puch I, Wiley BM, Sun J, et al. (2018). Risks of restrictive red blood cell transfusion strat-
egies in patients with cardiovascular disease: a meta-analysis. Transfus Med, 28, 335–45.
8 Devereaux PJ, Biccard BM, Sigamani A, et al. (2017). Association of postoperative high-
sensitivity troponin levels with myocardial injury and 30-day mortality among patients undergoing
noncardiac surgery. JAMA, 317, 1642–51.
9 Thygesen K, Alpert JS, Jaffe AS, et al. (2018). Fourth universal definition of myocardial infarction.
J Am Coll Cardiol, 72, 2231–64.
10 Devereaux PJ, Szczekilk W (2019). Myocardial injury after non-cardiac surgery: diagnosis and
management. Eur Heart J, ehz301
11 Devereaux PJ, Duceppe E, Guyatt G, et al. (2018). Dabigatran in patients with myocardial injury
after non-cardiac surgery (MANAGE): an international, randomised, placebo-controlled trial.
Lancet, 391, 2325–34.
12 Buse GL, Manns B, Lamy A, et al. (2018). Troponin T monitoring to detect myocardial injury after
noncardiac surgery: a cost-consequence analysis. Can J Surg, 61, 185–94.
13 Ponikowski P, Voors AA, Anker SD, et al. (2016). ESC guidelines for the diagnosis and treatment
of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and
chronic heart failure of the European Society of Cardiology (ESC). Eur Heart J, 37, 2129–200.
14 Yancy CW, Jessup M, Bozkurt B, et al. (2017). ACC/AHA/HFSA focused update of the 2013
ACCF/AHA guideline for the management of heart failure: a report of the American College of
Cardiolgy/American Heart Association Task Force on Clinical Practice Guidelines and the Heart
Failure Society of America. Circulation, 136, e137–61.
15 Konstam MA, Kiernan MS, Bernstein D, et al. (2018). Evaluation and management of right-sided
heart failure: a scientific statement from the American Heart Association. Circulation, 137,
e578–622.
16 National Institute for Health and Care Excellence (2019). Hypertension overview. M http://path-
ways.nice.org.uk/pathways/hypertension
621
17 Sessler DI, Bloomstone JA, Aronson S, et al. (2019). Perioperative Quality Initiative concensus
statement on preoperative blood pressure, risk and outcomes for elective surgery. Br J Anaesth,
122, 563–74.
18 McEvoy MD, Gupta R, Koepke EJ, et al. Perioperative Quality Initiative concensus statement on
postoperative blood pressure, risk and outcomes for elective surgery. Br J Anaesth, 122, 75–86.
19 Nishimura RA, Otto CM, Bonow RO, et al. (2017). AHA/ACC Focused update of the 2014
AHA/ACC Guideline for the management of patients with valvular heart disease. Circulation,
135, 1159–95.
20 Douketis JD, Johnson JA, Turpie AG (2004). Low- molecular weight heparin as bridging
anticoagulation during interruption of warfarin. Assessment of a standardized perioprocedural
anticoagulation regime. Arch Intern Med, 164, 1319–26.
21 Kwok CS, Bagur R, Rashid M, et al. (2017). Aortic stenosis and non-cardiac surgery: a systematic
review and meta-analysis. Int J Cardiol, 240, 145–53.
22 Maron BJ, Towbin JA, Thiene G, et al. (2006). Contemporary definitions and classification of
cardiomyopathies. Circulation, 113, 1807–16.
23 Wu AH (2007). Management of patients with non-ischemic cardiomyopathy. Heart, 93, 403–8.
24 Subramaniam K, Sakai T (2017). Anesthesia and Perioperative Care for Organ Transplantation. New
York, NY: Springer Science+Business Media.
25 Pilkington SA, Taboada D, Martinez G (2015). Pulmonary hypertension and its management in
patients undergoing non-cardiac surgery. Anaesthesia, 70, 56–70.
26 Simmonneau G, Montani D, Celermajer DS, et al. (2019). Haemodynamic definitions and up-
dated clinical classification of pulmonary hypertension. Eur Respir J, 53, 1801913.
27 Galie N, Humbert M, Vachiery JL, et al. 2015 ESC/ERS Guidelines for the diagnosis and treat-
ment of pulmonary hypertension. Eur Respir J, 46, 903–75.
28 Farina S, Correale M, Bruno N, et al. (2017). The role of cardiopulmonary exercise tests in pul-
monary arterial hypertension. Eur Respir Rev, 27, 170134.
29 Pitcher D, Nolan J (2015). Guidelines: peri-arrest arrhythmia. Resuscitation Council UK. M http://
www.resus.org.uk/resuscitation-guidelines/peri-arrest-arrhythmias
30 Kalra R, Parcha V, Patel N, et al. (2020). Implications of atrial fibrillation among patients with ath-
erosclerotic cardiovascular disease undergoing noncardiac surgery. Am J Cardiol, 125, 1836–44.
31 Karamchandani K, Khanna AK, Bose S, et al. (2020). Atrial fibrillation: current evidence and man-
agement strategies during the perioperative period. Anesth Analg, 130, 2–13.
32 January CT, Samuel Wann L, Calkins H (2019). AHA/ACC/HRS focused update of the 2014
AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the
American College of Cardiology/American Heart Association Task Force on Clinical Practice
Guidelines and the Heart Rhythm Society. Circulation, 140, e125–51.
33 Kirchhof P, Benussi S, Kotecha D, et al. (2016). ESC Guidelines for the management of atrial fib-
rillation developed in collaboration with EACTS. Eur Heart J, 37, 2893–962.
34 Kristensen SD, KKnuuti J, Saraste A, et al. (2014). ESC/ESA guidelines on non-cardiac surgery;
cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: car-
diovascular assessment and management of the European Society of Cardiology (ESC) and the
European Society of Anaesthesiology (ESA). Eur Heart J, 35, 2383–431.
Chapter 6 163
Respiratory disease
Sarah Jarvis
Assessment of respiratory function 164
Effects of surgery and anaesthesia on respiratory function 167
Predicting postoperative pulmonary complications 168
Strategies to reduce postoperative pulmonary
complications 170
Postoperative admission to HDU/ICU 172
Smoking and respiratory tract infections 173
Asthma 174
Chronic obstructive pulmonary disease 178
Bronchiectasis 181
Cystic fibrosis 182
Restrictive pulmonary disease 184
Sleep-related breathing disorders 186
Sarcoidosis 187
Anaesthesia after lung transplantation 188
641
Predictor Score
Age 60–69y 4
Age ≥70y 6
COPD 6
Partially or fully dependent functional status 7
Blood urea nitrogen >30mg/dL 8
Albumin <3g/dL 9
Neck surgery 11
Neuro, upper GI, peripheral vascular surgery 14
Thoracic surgery 21
Abdominal aortic surgery 27
Emergency surgery 11
Reproduced from Arozullah A et al., Multifactorial risk index for predicting postoperative re-
spiratory failure in men after major noncardiac surgery, Annals of Surgery, 232(2), 242–53, with
permission from Wolters Kluwer Health, Inc. © 2001.
Predictor Score
Age 51–80 3
Age >80 16
Preoperative SpO2 91–95% 8
Preoperative SpO2 ≤90% 24
Respiratory infection within 1mo 17
Preoperative Hb ≤100g/L 11
Upper abdominal incision 15
Intrathoracic incision 24
Surgery 2–3h 16
Surgery ≥3h 23
Emergency 8
Reproduced from Canet J et al., Prediction of Postoperative Pulmonary Complications in a
Population-based Surgical Cohort, Anesthesiology,113(6), 1338–50, with permission from Wolters
Kluwer Health, Inc. © 2010. M https://pubs.asahq.org/anesthesiology/article/113/6/1338/9603/
Prediction-of-Postoperative-Pulmonary.
701
Predictable Unpredictable
Borderline or established failure of Unexpected perioperative complications
gas exchange preoperatively (e.g. fluid overload, haemorrhage)
Intercurrent respiratory infection Inadequate or ineffective regional
(with urgent surgery) analgesia with deterioration in respiratory
function
Chest disease productive of Unexpectedly prolonged procedure
large amounts of secretions (e.g.
bronchiectasis)
Major abdominal or thoracic surgery Acidosis
Major surgery not amenable to Hypothermia
regional analgesia and necessitating
systemic opioids
Long duration of surgery Depressed conscious level/slow recovery
from anaesthetic/poor cough
Smoking and respiratory tract infections 173
Asthma
Asthma16,17,18 is a disorder of variable severity, which causes symptoms re-
sulting from airway obstruction, inflammation and hyper-responsiveness.
• Symptoms are most frequently a combination of shortness of breath,
wheeze, cough and sputum production.
• Bronchial wall inflammation is a fundamental component and results in
mucus hypersecretion, epithelial damage and an i tendency for airways
to constrict.
• It is differentiated from COPD by the presence of childhood symptoms,
diurnal variation, specific trigger factors (especially allergic), absence of
smoking history and response to previous treatments.
General considerations
• Most well-controlled asthmatic patients tolerate anaesthesia and surgery
well. The incidence of perioperative bronchospasm and laryngospasm
in routine surgery is <2%, especially if routine medication is continued.
• The frequency of complications is i in patients >50y and in those with
active disease.
• Poorly controlled asthmatic patients are at risk of perioperative
problems (bronchospasm, sputum retention, atelectasis, infection,
respiratory failure).
• Avoid anaesthetising patients with suboptimally controlled asthma for
elective surgery.17
Preoperative assessment
• The severity of asthma is frequently underestimated, especially if it is
long-standing.
• Key indicators of severe disease include a history of frequent
exacerbations, hospital visits and, most importantly, prior tracheal
intubation and mechanical ventilation to manage a severe attack.
• Document any allergies/drug sensitivities, especially the effect of
aspirin/NSAIDs. The prevalence of aspirin-induced asthma (measured
by oral provocation) is 21% in adult and 5% in paediatric asthma
patients. Much lower rates are quoted if verbal history is used to assess
prevalence (3% and 2%, respectively).
• Ask about trigger factors and recent respiratory tract infections. Viral
infections are potent triggers of asthma, so postpone elective surgery if
symptoms suggest URTI.
• The type, dose, frequency and degree of benefit of therapy provide
important clues about the severity and control of the disease.
• Examination is often unremarkable but should focus on detecting signs
of acute bronchospasm, active lung infection (which should defer
surgery), chronic lung disease and right heart failure.
• Advise patients to stop smoking at least 8w prior to surgery.
• Patients with mild asthma (peak flow >80% of predicted and minimal
symptoms) rarely require extra treatment prior to surgery. Consider
adding a short-acting β2-agonist just prior to surgery.18
• Moderately controlled patients should add inhaled corticosteroids to
their β2-agonists 1w prior to surgery.
Asthma 175
Investigations
(For preoperative respiratory investigations, see Table 6.2.)
• Serial home measurements of PEFR are more informative than a single
reading. Measure the response to bronchodilators, and look for ‘early
morning dip’ (suggesting suboptimal control).
• Spirometry helps to detect the chronic residual effects of acute asthma
and to stratify the severity of the disease.
• Results of peak flow and spirometry are compared with predicted
values based on age, sex and height.
• Blood gases are only necessary in assessing patients with severe asthma,
particularly prior to major surgery.
761
• ECG may show right atrial or RV hypertrophy, acute strain, right axis
deviation and right bundle branch block, although these are often
associated with acute asthma attacks and are reversible.19
• CXRs reveal flattened diaphragms if the lungs are hyperinflated. Useful
to evaluate for pulmonary congestion, oedema or infiltrates.
Conduct of anaesthesia
• The overriding goal is to avoid bronchospasm.
• Consider premedicating the patient with nebulised salbutamol 2.5mg
and an anticholinergic agent, such as glycopyrronium or atropine, to dry
out secretions and suppress upper airway vagal responses.
• Consider the need for an arterial line intraoperatively in high-risk cases
to facilitate ABG measurement.
• No definitive evidence shows that one method is superior to another.
• When asthma is poorly controlled, regional techniques are ideal for
peripheral surgery. Spinal anaesthesia or plexus/nerve blocks are
generally safe, provided the patient is able to lie flat comfortably.
• Where GA is necessary, use short-acting anaesthetic agents. Short-
acting opioid analgesics (e.g. alfentanil, remifentanil) are appropriate for
procedures with minimal postoperative pain or when a reliable regional
block is present (Table 6.8).
• Intubation may provoke bronchospasm. Consider potent opioid cover
(alfentanil). LA to the cords may help. Only instrument the airway when
the patient is in a deep plane of anaesthesia. The use of an SGA may
be preferable to tracheal intubation in asthmatic patients; however, the
benefits of these must be weighed up against the risks of an unsecured
airway.
• Ventilatory strategies, such as limiting peak inspiratory pressures and VT
and decreasing the inspiratory: expiratory (I:E) ratio, assist in avoiding
air trapping and auto-PEEP.
• Caution with/avoid desflurane and histamine-releasing drugs such as
morphine, atracurium and mivacurium.
• Inspired gases should be humidified to avoid airway irritation.
• Stimulating manoeuvres, such as airway suctioning, should be avoided or
only performed while the patient is deeply anaesthetised.
• Caution with acetylcholinesterase inhibitors in asthmatics due to
their muscarinic side effects such as bronchospasm. Consider using
rocuronium as this can be reversed with sugammadex if required.
• Prophylactic use of antiemetic agents or antacids should be considered
to avoid aspiration, which can trigger severe bronchospasm.
Preoperative assessment
• Ask about smoking, dyspnoea, cough and sputum production.
• Establish the exercise tolerance, asking specifically about hills and
stairs. A simple exercise test such as stair climbing is safe and simple to
perform and correlates well with more formal exercise testing.
• Enquire as to the frequency of exacerbations, timings of the most
recent course of antibiotics or steroids, hospital admissions and
previous requirements for invasive and non-invasive ventilation.
• Poor nutritional status (albumin <30g/L) is a strong predictor of
postoperative pulmonary complications.
• d breath sounds, prolonged expiration and wheeze are predictive of
postoperative pulmonary complications.
• If possible, postpone surgery and commence appropriate treatment if
symptoms and signs of an active respiratory infection are found.22
Investigations
• Preoperative spirometry is useful both to assess severity of disease and
to evaluate whether the patient is at their best baseline. Identification of
severe airflow obstruction is important in patients who are candidates
for upper abdominal or thoracic surgical procedures.
• Check ABGs in patients with moderate to severe COPD. Useful to
determine postoperative respiratory parameters.
• ECG may reveal right heart disease (RV hypertrophy or strain) or
concomitant IHD. Consider echocardiography.
• CXR is not mandatory. It should be considered if there is clinical
evidence of current infection or recent deterioration in symptoms.
Preoperative optimisation
(For generic information on preoptimisation, see % Chapter 3.)
• Every effort should be made to assist patients in stopping smoking.
• All patients with symptomatic COPD should receive daily inhaled
ipratropium or tiotropium.23
• Inhaled β-agonists should be used, as needed, for symptoms and
wheezing in the perioperative period.
• Continue patients’ usual inhaled medication perioperatively.
• Patients with COPD, persistent wheeze and functional limitations,
despite bronchodilators, should be treated with perioperative
glucocorticoids. Ideally, these patients should be reviewed by a
respiratory physician preoperatively.
• If patients have severe COPD, postoperative respiratory failure is
likely after abdominal or thoracic surgery. Plan for elective HDU/ICU
admission.
• Preoperative chest physiotherapy may reduce the incidence of
intraoperative bronchial plugging or pneumonitis.
• Pulmonary prehabilitation in the form of patient education, exercise
training and behavioural interventions may be useful.24
• Consider the need for preoperative nutritional supplementation.
801
Conduct of anaesthesia
• GA, and in particular tracheal intubation and IPPV, is associated
with adverse outcomes. Such patients are prone to bronchospasm,
laryngospasm, CVS instability, barotrauma, hypoxaemia and i rates of
postoperative pulmonary complications.
• Consider avoiding GA by using a regional anaesthetic technique. This
may be limited by some patients’ inability to lie flat.
• Consider using an arterial line for both beat-to-beat BP and repeated
blood gas analysis.
• Where GA cannot be avoided, preoxygenate attentively.
• Avoid intubation where possible. Some patients, however, are
unsuitable for a spontaneously breathing technique (particularly those
who are obese and breathless and require long operations). Patients
with heavy sputum production may benefit from endotracheal toilet.
• If using IPPV, consider using PEEP and allowing more time for exhalation
by decreasing the RR or the I:E ratio (typically 1:3–1:5). These
approaches may help to reduce air trapping and the development
of auto-PEEP, both of which can cause an increase in intrathoracic
pressure, leading to CVS instability, pulmonary barotrauma, hypercapnia
and acidosis.
• Ensure the NMBA is fully reversed and the patient is warm and well
oxygenated and has a PaCO2 close to their normal preoperative values
prior to extubation.
• Extubate in the sitting position.
• Bronchodilator treatment may be helpful peri-extubation.
• Extubation of the high-risk patient directly onto non-invasive ventilation
may reduce the work of breathing and air trapping.
Postoperative care
• Those patients with severe disease or significant comorbidities should
be managed in a high dependency setting capable of regular ABG
measurements and the provision of non-invasive ventilation.
• Hypoventilation as a result of residual anaesthesia or opioids should be
avoided, as this may lead to hypercapnia and hypoxia.
• Encourage early mobilisation.
• Use of 0.9% sodium chloride nebulisation, suctioning and physiotherapy
are useful to prevent atelectasis and to encourage sputum production.
• Continue with nebulised salbutamol (2.5mg four times daily (qds)) and
ipratropium (500 micrograms qds) until fully mobile. Change back to
inhalers at least 24h before discharge.
• Effective analgesia is a significant determinant of postoperative
pulmonary function. Epidural anaesthesia is an attractive option, as it
reduces the risk of respiratory failure because of excessive sedation
from opioids. It should therefore be considered if appropriate.23
Bronchiectasis 181
Bronchiectasis
Bronchiectasis has similar features to COPD. The diagnosis is usually estab-
lished clinically on the basis of a chronic daily cough with thick, mucopurulent
sputum production, and radiographically by the presence of bronchial wall
thickening, dilation of the bronchi and bronchioles on chest CT scans.
• Acquired disorder characterised by permanent abnormal dilation and
destruction of the bronchial and bronchiolar walls.
• Multiple aetiologies can lead to the pathophysiological processes that
cause bronchiectasis, including airway obstruction (e.g. foreign body
aspiration), defective host defences, cystic fibrosis (CF), rheumatic
diseases, dyskinetic cilia, smoking, pulmonary infections and allergic
bronchopulmonary aspergillosis.
General considerations
• Patients with bronchiectasis need to be optimised before undergoing
any major surgery which will inhibit coughing and impair respiratory
function.
• Once established, bacterial infections can be difficult or impossible to
eradicate. Pseudomonas aeruginosa is a common pathogen that may be
chronic and associated with intermittent exacerbations of respiratory
symptoms.
• The mainstay of treatment for bronchiectasis is regular physiotherapy,
frequent courses of appropriate antibiotics and treatment of any
asthmatic symptoms.
Preoperative assessment
• Consultation with the patient’s chest physician is essential.
• Send a sputum sample for culture. A course of IV antibiotics and
physiotherapy for 3–10d immediately prior to surgery may be
necessary. Use current or most recent sputum cultures, with advice
from the microbiologist/local protocols, to guide appropriate
prescribing. If in doubt, assume P. aeruginosa infection.
• Maximise bronchodilation by converting to nebulised bronchodilators
and increase the dose of prednisolone by 5–10mg/24h if on long-term
oral steroids.
Investigations and conduct of anaesthesia
• As per COPD (see % pp. 179–80). Also send a sputum sample for
culture.
Postoperative care
• Arrange regular physiotherapy (three times daily (tds)) and nightly if
severely affected.
• Continue appropriate IV antibiotics for at least 3d postoperatively or
until discharged.
• Maintain adequate nutrition, especially if any malabsorption.
• Refer to the respiratory physician early if there is any deterioration in
respiratory symptoms.
821
Cystic fibrosis
CF25,26,27 is a multisystem, autosomal recessive disease and is the commonest
lethal genetic disease in Caucasians.
• Caused by mutations in a single gene, the CF transmembrane regulator
(CFTR) gene on chromosome 7.
• The CFTR is a chloride channel found at the apical border of epithelial
cells which line most exocrine glands in the body. All mutations causing
CF affect chloride conductance through this channel, resulting in loss of
chloride transport and disturbance of the Na+/chloride balance needed
to maintain a normal thin mucus layer.
• In CF, the mucus is viscid and less well cleared by the cilia.
• Clinical manifestations include progressive lung disease (frequent
LRTIs, chronic hypoxaemia and cor pulmonale), nasal problems
(chronic sinusitis and nasal polyps), hepatobiliary system disease due to
obstruction of bile ductules (focal biliary cirrhosis, portal hypertension,
multinodular biliary cirrhosis), meconium ileus, recurrent abdominal
pain, pancreatic exocrine insufficiency and CF-related diabetes, infertility
and osteoporosis.
General considerations
• Patients with severe disease are best managed in a major centre with
multidisciplinary input.25
• Neonates may present for surgical treatment of meconium ileus.
• Common elective surgical procedures for CF patients include nasal
polypectomy, enteral feeding or vascular access device placement.
• Almost all patients with CF have symptoms of bronchiectasis.
• The postoperative complication rate in CF is only 10% (mostly
pulmonary), but half of these operations are for minor ear, nose and
throat (ENT) procedures.
• Day case surgery is uncommon in CF patients; however, it is possible if
disease is stable and there is good baseline function.
Preoperative assessment
• Gain a history of therapy, medications and exacerbations.
• Exclude or treat active chest infection.
• Ascertain the patient’s functional ability.
• Note details of the non-respiratory components.
• Always inform the patient’s physician of a surgical admission.
Investigations
• Perform FBC, U&E, coagulation study, LFTs and blood glucose.
• Respiratory tests include CXR, baseline ABG analysis and spirometry.
Spirometry generally shows an obstructive pattern, with d FEV1 and
FEV1/FVC ratio.
• In advanced disease, an ECG and echocardiogram are useful to
diagnose cor pulmonale.
• A 6MWT or CPET forms part of the prelung transplant workup in
many centres. The results of this may be available when patients
present for non-transplant surgery.
Cystic fibrosis 183
Conduct of anaesthesia
• Consider placing an arterial line to facilitate frequent ABG analysis.
• Consider using CO monitoring in patients with cor pulmonale who
present for major surgery.
• For short/non-abdominal/non-thoracic procedures, an SGA with a
spontaneously breathing patient may minimise the adverse effects of
GA on respiratory mechanics.
• An ETT allows bronchial toilet and improved ventilatory control.
• Avoid nasal intubation, where possible, due to the high incidence of
nasal polyposis.
• Keep airway pressures as low as possible when using positive pressure
ventilation. Monitor for pneumothorax.
• Use humidified gases.
• Short-acting drugs should be used, wherever possible, to facilitate rapid
emergence.
• Patients are often cachectic, so careful positioning and padding are
important.
• Consider a regional anaesthetic technique, where appropriate, to avoid
airway manipulation and to optimise postoperative analgesia.
Postoperative care
• Aim to minimise the risk of development of a postoperative respiratory
tract infection.
• Aim to extubate early.
• Ensure NMB is fully reversed.
• For patients who use home non-invasive ventilation, ensure that the
patient’s own equipment is available immediately postoperatively.
• Chest physiotherapy should be resumed as early as possible.
• It is appropriate for patients with advanced disease to be monitored in a
high dependency setting.
• For patients with FEV1 <1L, PaO2 <9.3kPa or PaCO2 >6.6kPa, consider
a period of postoperative ventilation.
• 80% of CF patients have pancreatic malabsorption. Maintaining
adequate nutrition after surgery is essential, as is the advice of an
experienced dietitian.
841
Preoperative assessment
• Should focus on determining the degree of respiratory impairment and
establishing the extent of involvement of other organs.
• A history of exertional dyspnoea (or at rest) should be evaluated
further with ABGs and PFTs.
• Discuss seriously affected patients with a respiratory physician.
• Many patients are stable and only slowly deteriorate over some years.
These patients may tolerate surgery relatively well.
Investigations
• ABGs often remain normal until late. Reduced PaO2 reflects significant
disease, and CO2 retention is a late sign, implying impending ventilatory
failure.
• Obtain spirometry (lung volumes are d) and gas transfer if these have
not been done within the previous 8w. A VC of <15mL/kg is indicative
of severe dysfunction.
• Echocardiogram to look for evidence of right heart failure.
• CPET may aid perioperative risk stratification for patients undergoing
high-risk intra-abdominal surgery.28
• CXR changes will be according to the underlying condition.
Conduct of anaesthesia
• As for other pathologies, consider regional techniques.
• Minimise positive pressure ventilation and airway instrumentation. Spinal
disease may preclude subarachnoid or epidural blocks.
• If IPPV is necessary, minimise peak airway pressures using pressure-
controlled ventilation with a high rate and low VT.
• Check need for additional steroid cover for those patients on regular
steroid therapy (see % pp. 230–1).
• Maintain a high index of suspicion for pneumothorax.
Postoperative care
• Consider postoperative ICU/HDU admission following major
surgery. May be suitable for elective training in non-invasive ventilation
techniques preoperatively.
• The work of respiration is optimised by slow deep breaths and is easier
in the sitting position. Extubate sitting upright.
• Give supplemental O2, and maintain SpO2 >92%.
• Good physiotherapy and analgesia are vital to achieve sputum clearance.
With severe disease, minor respiratory complications may precipitate
respiratory failure.
• Mobilise early.
• Treat respiratory infection vigorously.
• Ensure steroid cover continues in appropriate formulation.
861
Sarcoidosis
Multisystem disease of unknown aetiology characterised by the formation
of non-caseating granulomata, which occur in any body tissue and heal with
fibrosis.
• Affects all ages, with highest prevalence at 20–40y
• More common in black individuals in the US.
General considerations
• Pulmonary changes occur in 50% of cases. Pleural, peribronchial and
alveolar granulomata are replaced by fibrosis. Hilar lymphadenopathy
may cause bronchial obstruction and distal atelectasis. Infiltration of the
bronchial mucosa may cause stenosis. Mucosal infiltration of the nose,
nasopharynx, tonsils, palate or larynx can occur.
• Cardiac effects (in 20%). RV failure 2° to lung disease. Myocardial
and valvular granulomata are rare. Conduction abnormalities, VT and
sudden death have been reported.
• Can also involve skin and cause uveitis/iritis and hypercalcaemia.
Preoperative assessment
• Pulmonary and cardiac features are most important.
• May have extensive pathology, but only minor symptoms.
• Note steroid treatment or other immunosuppressive drugs.
Investigations
• Preoperative PFTs may reveal a restrictive defect. TLCO (DLCO) may
be d. ABGs will determine the level of hypoxaemia.
• ECG may show RV hypertrophy or arrhythmias.
• Check serum Ca2+ for hypercalcaemia (treat with systemic steroids).
Conduct of anaesthesia
• If respiratory function is impaired, consider avoidance of GA and the
use of LA/regional anaesthesia.
• Consider regional analgesia for abdominal surgery if significant
respiratory disease.
• Give appropriate steroid cover if needed.
Postoperative care
• Nurse the patient sitting upright.
• Good postoperative analgesia.
• Chest physiotherapy/breathing exercises.
81
Conduct of anaesthesia
• The interaction of immunosuppressive drugs (ciclosporin, steroids,
azathioprine) with anaesthetic drugs is more theoretical than clinical.
• Stress doses of steroids will be required in most cases.
• Attention to aseptic techniques is important, as immunosuppression
occurs with most chemotherapeutic drugs.
• There is no evidence to suggest that placing CVCs on the side opposite
the transplanted lung is safer.
• Monitor neuromuscular function and avoid high doses of opioid in
order to achieve early extubation.
• To minimise the risk of damage to the tracheal/bronchial anastomosis,
intubation should leave the tube just through the cords and the cuff
carefully inflated and checked intraoperatively. Place double-lumen
tubes under direct vision using a flexible optical bronchoscope (FOB).
• The basic goal in ventilation is ensuring adequate oxygenation and
ventilation while minimising peak airway pressures and O2.
• A mask or SGA is not contraindicated, although there is a risk of silent
aspiration in patients with no carinal cough reflex.
• Strict attention to fluid balance is required.
• Aim for early return of pulmonary function and extubation.
Postoperative care
• Postoperative admission to ICU is only indicated when anaesthesia is
complicated by inadequate recovery of respiratory function, the surgical
condition or the presence of rejection or infection.
• Chest physiotherapy, postural drainage and incentive spirometry in the
postoperative period may be beneficial.
Further reading
Elsharkawy H, Lewis B, Farag E (2008). Anesthetic challenges in patients after lung transplantation.
Internet J Anesthesiol, 20, N1.
References
1 Lawrence VA, Dhanda R, Hilsenbeck SG, et al. (1996). Risk of pulmonary complications after
elective abdominal surgery. Chest, 110, 744–50.
2 Brooks-Brunn JA (1997). Predictors of postoperative pulmonary complications following abdom-
inal surgery. Chest, 111, 564–71.
3 Chung F, Yegneswaran B, Liao P, et al. (2008). STOP questionnaire: a tool to screen patients for
obstructive sleep apnea. Anesthesiology, 108, 812–21.
4 Canet J, Gallart L, Gomar C, et al. (2010). Prediction of postoperative pulmonary complications
in a population-based surgical cohort. Anesthesiology, 113, 1338–50.
5 Qaseem A, Snow V, Fitterman N, et al. (2006). Risk assessment for and strategies to reduce peri-
operative pulmonary complications for patients undergoing noncardiothoracic surgery: a guide-
line from the American College of Physicians. Ann Intern Med, 144, 575.
6 Guazzi M, Arena R, Halle M, et al. (2018). 2016 focused update: clinical recommendations for
cardiopulmonary exercise testing data assessment in specific patient populations. Eur Heart J, 39,
1144–61.
7 Smetana GW, Lawrence VA, Cornell JE; American College of Physicians (2006). Preoperative
pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American
College of Physicians. Ann Intern Med, 144, 581–95.
8 Memtsoudis S, Liu SS, Ma Y, et al. (2011). Perioperative pulmonary outcomes in patients with
sleep apnea after noncardiac surgery. Anesth Analg, 112, 113–21.
9 Price LC, Montani D, Jaïs X, et al. (2010). Noncardiothoracic nonobstetric surgery in mild-to-
moderate pulmonary hypertension. Eur Respir J, 35, 1294–302.
901
10 Murphy GS, Szokol JW, Marymont JH, et al. (2008). Residual neuromuscular blockade and critical
respiratory events in the postanesthesia care unit. Anesth Analg, 107, 130–7.
11 Arozullah AM, Daley J, Henderson WG, et al. (2000). Multifactorial risk index for predicting
postoperative respiratory failure in men after major noncardiac surgery. The National Veterans
Administration Surgical Quality Improvement Program. Ann Surg, 232, 242–53.
12 Celli BR (1993). Perioperative respiratory care of the patient undergoing upper abdominal sur-
gery. Clin Chest Med, 14, 253–61.
13 Futier E, Constantin J-M, Paugam-Burtz C, et al. (2013). A trial of intraoperative low-tidal-volume
ventilation in abdominal surgery. N Engl J Med, 369, 428–37.
14 Fennelly ME, Hall GM (1990). Anaesthesia and upper airway respiratory tract infections—a non-
existent hazard? Br J Anaesth, 64, 535–6.
15 Levy L, Pandit UA, Randel GI, et al. (1992). Upper respiratory tract infections and general anaes-
thesia in children. Anaesthesia, 47, 678–82.
16 Woods BD, Sladen RN (2009). Perioperative considerations for the patient with asthma and
bronchospasm. Br J Anaesth, 103 (suppl 1), i57–65.
17 Applegate R, Lauer R, Lenart J, et al. (2013). The perioperative management of asthma. J Allergy
Ther, S11, 007.
18 National Institute for Health and Care Excellence (2017, updated 2020). Asthma: diagnosis,
monitoring and chronic asthma management (NICE quality standard NG80). M
https:// w ww.nice.org.uk/ g uidance/ n g80/ r esources/ a sthma- d iagnosis- m onitoring-
and-chronic-asthma-management-pdf-1837687975621
19 Siegler D (1977). Reversible electrocardiographic changes in severe acute asthma. Thorax,
32, 328.
20 National Institute for Health and Care Excellence (2018, updated 2019). Chronic obstructive
pulmonary disease in over 16s: diagnosis and management (NICE quality standard NG115). M
https://www.nice.org.uk/guidance/ng115/resources/chronic-obstructive-pulmonary-disease-
in-over-16s-diagnosis-and-management-pdf-66141600098245
21 Global Initiative for Chronic Obstructive Lung Disease (2018). Global strategy for the diag-
nosis, management, and prevention of chronic obstructive pulmonary disease (2019 Report). M
https://goldcopd.org/wp-content/uploads/2018/11/GOLD-2019-v1.7-FINAL-14Nov2018-
WMS.pdf
22 Lumb A, Biercamp C (2014). Chronic obstructive pulmonary disease and anaesthesia. Contin
Educ Anaesth Crit Care Pain, 14, 1–5.
23 American Thoracic Society (2005). COPD guidelines for health professionals. M http://www.
thoracic.org/go/copd
24 Lumb AB (2019). Pre-operative respiratory optimisation: an expert review. Anaesthesia, 74
(Suppl 1), 43.
25 Della Rocca G (2002). Anaesthesia in patients with cystic fibrosis. Curr Opin Anesthesiol, 15,
95–101.
26 Huffmyer JL, Littlewood KE, Nemergut EC (2009). Perioperative management of the adult with
cystic fibrosis. Anesth Analg, 109, 1949–61.
27 Fitzgerald M, Ryan D (2011). Cystic fibrosis and anaesthesia. Contin Educ Anaesth Crit Care Pain,
11, 204–9.
28 Moran J, Wilson F, Guinan E, et al. (2016). Role of cardiopulmonary exercise testing as a risk-
assessment method in patients undergoing intra-abdominal surgery: a systematic review. Br J
Anaesth, 116, 177.
29 Sateia MJ (2014). International Classification of Sleep Disorders—third edition: highlights and
modifications. Chest, 146, 1387–94.
30 Haddow GR (1997). Anaesthesia for patients after lung transplantation. Can J Anaesth, 44,
182–97.
Chapter 7 191
191
Renal disease
Quentin Milner
Glomerular filtration rate and creatinine clearance 192
Chronic kidney disease 193
Anaesthetic drugs in CKD 196
Acute kidney injury 198
921
Classification of CKD
CKD is classified based on the GFR and the level of proteinuria. Patients
are classified as G1–G5 based on the eGFR, and A1–A3 based on the
albumin:creatinine ratio. The higher the stage (G1–G5) (Table 7.1) and the
greater the amount of protein present in the urine (A1–A3), the more ‘se-
vere’ the CKD.1
Preoperative
• Determine the underlying cause, previous surgery, including
transplantation, and drug therapy.
• These patients are high risk, particularly diabetics with CKD G3–G5.
• Check for hypertension, DM and anaemia. IHD is common and often
silent, especially in diabetics. Incidence of calcific valvular heart disease
and LV failure is i. Autonomic neuropathy is common. Pericardial
effusions are rare if dialysis is effective.
• Check the type of dialysis: peritoneal or haemodialysis? Do they have a
central line or fistula?
• Determine the residual urine output per day.
• Examine for fluid overload (dependent oedema, basal crepitations,
dialysis record, dry and wet weights) or hypovolaemia (postural
hypotension, low JVP, thirst, skin turgor, oliguria).
941
• Anaesthesia for A–V fistula formation: ask the surgeon where the fistula
is to be formed. Local infiltration works well for brachiobasilic fistulae.
An axillary/supraclavicular brachial plexus block is recommended for
a brachiocephalic fistula, and evidence shows a better fistula outcome.
Patients may need extra LA in the axilla and mild sedation. Avoid
hypotension to prevent fistula thrombosis. The fistula may be used for
dialysis after 3–4w. Synthetic grafts can be used immediately but do not
last as long.
• Peritoneal dialysis uses the large surface area of the peritoneum to
exchange fluid and metabolites via temporary (hard) or permanent
Tenckhoff (soft) catheters in the lower abdomen. It is inefficient
but can run continuously. Catheter placement or removal usually
requires a mini-laparotomy but can be done under LA ± sedation if
necessary. Dialysis fluid should be drained before anaesthesia to prevent
respiratory function compromise. Patients can usually omit 24–48h of
postoperative dialysis, but a period of haemodialysis may be needed if
undergoing bowel surgery.
• Most antibiotics are excreted by the kidney. It is common to use a
normal loading dose, with reduced and/or delayed maintenance doses.
If in doubt, check in the British National Formulary (BNF) or with a
microbiologist.
Considerations
• Preoperative rehydration is essential, and any fluid deficit should be
corrected before surgery. Invasive monitoring may be needed.
• Remember that an adequate BP is needed for renal perfusion and
this is relative to the patient’s baseline. A MAP under 80mmHg for
≥10min has been linked to i risk of AKI,4 but this may be inadequate in
hypertensives. Inotropes may be required.
Acute kidney injury 199
Further reading
National Institute for Health and Care Excellence (2013). Acute kidney injury: prevention, detection and
management. NICE guideline [NG148]. M https://www.nice.org.uk/guidance/ng148
References
1 Kidney Disease Improving Global Outcomes (2012). KDIGO 2012 clinical practice guideline for
evaluation and management of chronic kidney disease, Kidney Int, 3, 1–150. M https://kdigo.org/
wp-content/uploads/2017/02/KDIGO_2012_CKD_GL.pdf
2 McLean DJ, Shaw AD (2018). Intravenous fluids: effects on renal outcomes. Br J Anaesth, 120,
397–402.
3 de Souza CM, Tardelli MA, Tedesco H, et al. (2015). Efficacy and safety of sugammadex in the
reversal of deep neuromuscular blockade induced by rocuronium in patients with end stage renal
disease. Eur J Anaesthesiol, 32, 681–6.
4 Wesselink EM, Kappen TH, Torn HM, et al. (2018). Intraoperative hypotension and the risk of
postoperative adverse outcomes: a systematic review. Br J Anaesth, 121, 706–21.
Chapter 8 201
Hepatic disease
Ashleigh Williams and John Christie
Liver disease 202
Anaesthetic management of patients with liver disease 205
Drug metabolism and liver disease 211
Postoperative liver dysfunction or jaundice 212
20
Liver disease
Liver disease can be classified as chronic liver disease (CLD) and acute liver
failure (ALF). ALF can be subclassified into hyperacute, subacute, and acute.
Common causes of ALF and CLD are listed in Table 8.1.
Chronic liver disease
• CLD is defined as impairment of liver synthetic and metabolic function
present for >26w.
• Chronic inflammation leads to fibrosis and cirrhosis (nodular
regeneration and disruption of liver architecture), leading to portal
hypertension.
• Cirrhosis can be compensated (function preserved) or decompensated
(presence of ascites, encephalopathy or oesophageal varices).
• Once there is evidence of decompensation, survival is around 5y, so
assessment for transplantation should be considered.
• Portal hypertension in CLD leads to engorgement of the anastomoses
between portal and systemic circulations, leading to varices at the
gastro-oesophageal junction, haemorrhoids and dilated abdominal
wall veins (caput medusae). Patients with varices are at risk of acute
bleeding, which is associated with a high mortality rate.
• Impaired hepatic synthetic function leads to low albumin and plasma
proteins. This contributes to oedema/ascites and has implications for
drug protein-binding.
• Ascites: liver fibrosis leads to portal hypertension and, in combination
with salt/water retention 2° to hyperaldosteronism, splanchnic
vasodilation and low serum albumin, fluid accumulates in the peritoneal
cavity. More commonly seen in CLD. Spironolactone long term may
exacerbate electrolyte disturbances and renal dysfunction.
Acute liver failure
• ALF is a process involving rapidly progressing liver necrosis and an
inflammatory response with physiological derangement similar to sepsis.
• Patients develop the triad of hepatocellular dysfunction (jaundice),
coagulopathy and encephalopathy, without prior known liver disease.
• ALF can be classified by time interval from onset of jaundice to
encephalopathy (Table 8.2).
• Hyperacute ALF is typical of paracetamol overdose, although jaundice
is often absent (coagulopathy and deranged LFTs used as surrogate for
onset time).
• The precipitating cause ultimately results in liver necrosis and an
inflammatory response with physiological derangement similar to sepsis.
Absence of hepatic encephalopathy, defined as acute liver injury, has a
better prognosis.
• For specific ALF management and referral criteria, see % p. 210.
Liver disease 203
Hepatopulmonary syndrome
Occurs when intrapulmonary vascular dilations contribute to hypoxia in
liver disease, possibly 2° to i production or d clearance of vasodilators
such as nitrous oxide (N2O). Intrapulmonary shunting further contributes
to V/Q mismatch, i A–a gradient and low PaO2. The only definitive treat-
ment is liver transplantation.
Pulmonary hypertension
A serious complication present in 0.25–4% of all patients with cirrhosis. It
is thought to occur due to local pulmonary production of vasoconstrictors
that occurs while systemically vasodilation predominates.
Encephalopathy
Toxic metabolites build up (particularly ammonia, due to deranged amino
acid metabolism), leading to progressive encephalopathy (Box 8.1). Give
regular lactulose to prevent constipation. Encephalopathy in CLD her-
alds decompensation and a precipitating cause should be sought. Reduced
Glasgow coma scale (GCS) and loss of airway reflexes may cause respira-
tory failure. Patients with grade III/IV encephalopathy need intubation to
protect their airway and ventilation permits manipulation of ICP.
Nutrition
CLD is associated with a poor nutritional state and predisposes to i inci-
dence of postoperative complications. Preoperative nutrition may help to
reduce this in major elective surgical procedures.
Other
The presence of varices in patients with known liver disease must be es-
tablished, as this is a contraindication for the use of oesophageal Doppler
probes/TOE and oesophageal temperature probes.
208
Perioperative considerations
Premedication
PPIs or H2 antagonists should be used preoperatively. RSI will further re-
duce the risks of gastric aspiration. Sedative medication may precipitate or
worsen encephalopathy.
Monitoring
Standard monitoring should be used, with consideration given to invasive
arterial and CVP monitoring. CVP monitoring is controversial but allows
for centrally administered vasopressors and venous access. Perioperative
haemodynamic instability can worsen hepatic function; MAP should be
maintained within 10–20% of preoperative levels. Hepatic blood flow and
O2 delivery should be maintained; CO monitoring may be useful, although
transthoracic echocardiography or oesophageal Doppler may be contra-
indicated in varices.
Drug effects
Even in severe liver disease, the problem is usually one of exaggerated ef-
fects on the CNS, rather than poor liver metabolism. Hepatic blood flow is
altered by anaesthetic drugs (e.g. α- and β-agonists/antagonists), positive
pressure ventilation, PEEP and surgical technique. In most cases, anaesthesia
reduces hepatic blood flow. (See % Drug metabolism and liver disease,
p. 211.) Desflurane best preserves hepatic blood flow, is least metabolised
and has a quicker emergence time, but sevoflurane and isoflurane are also
acceptable volatiles to use.
Regional techniques
Can be useful adjuncts, but neuraxial techniques are contraindicated in the
presence of coagulopathy. Most LAs are metabolised by the liver.
Cardiovascular
Low SVR and arterial pressure, i HR and volume expansion 2° to an acti-
vated renin–angiotensin system seen in both ALF and CLD. Vasopressors
may be required; maintain MAP >75mmHg. Portosystemic, pulmonary and
cutaneous shunting (spider angiomata) contributes to a hyperdynamic, high
CO state, often i by up to 50%. Alcohol excess is associated with car-
diomyopathy; cirrhosis is associated with a high incidence of cardiac dys-
function (‘cirrhotic cardiomyopathy’), and concurrent smoking is a risk
factor for CAD. Preoperative assessment, including echo, where indicated.
Propranolol to reduce portal pressures.
Respiratory
Hypoxia is common and multifactorial in CLD. Ascites causes splinting of
the diaphragm, basal atelectasis and collapse. Excess PEEP will increase
hepatic venous pressure and ICP. Tense ascites may affect respiratory
mechanics; consider percutaneous drainage.
Pulmonary hypertension
Consider echo if suspicion of pulmonary hypertension (see % pp. 139–44).
Encephalopathy
This may be precipitated by sedatives, GI bleeding, infection, surgical op-
erations, trauma, hypokalaemia, constipation or acute severe liver failure.
Anaesthetic management of patients with liver disease 209
Coagulopathy
Very common in liver disease; the liver synthesises all clotting factors,
except factor VIII. Coagulopathy is attributed to several mechanisms (d
synthesis of clotting factors and clearance of activated clotting factors,
quantitative and qualitative platelet abnormalities and hyperfibrinolysis).
Consider vitamin K. Reversal of coagulopathy with FFP, cryoprecipitate and
platelets directed by thromboelastography (TEG®)or similar point-of-care
testing (POCT). Ensure adequate provision is made for cross (X)-matched
blood and clotting products.
Renal
CO monitoring/goal-directed fluid therapy (GDFT) may be useful. Tense
ascites may impair renal blood flow and give a falsely high CVP. Avoid hypo-
tension and nephrotoxic drugs, and aim for urine output >1mL/kg/h.
Portal hypertension
Use of oesophageal Doppler/TOE/oesophageal temperature probes is
contraindicated. Treatment with β-blockers may contribute to periopera-
tive hypotension. A low CVP may reduce the risk of variceal or GI bleeding.
Ascites
Consider draining preoperatively as hypotension, hypoventilation and as-
piration are all i with tense ascites.
Hypoglycaemia
Patients with liver disease have impaired hepatic glycogen storage and are
prone to hypoglycaemia. Check blood glucose levels regularly. Give 10%
glucose infusions if <2mmol/L, and monitor plasma K+.
Immune function
Infections of the respiratory and urinary tracts are common. In the pres-
ence of ascites, spontaneous bacterial peritonitis may cause significant
sepsis—have a low index of suspicion. Intraoperative antibiotic prophylaxis
should be given where indicated.
Fluid resuscitation
Sodium chloride 0.9% is recommended 1st line, and sodium bicarbonate
may be considered if significant acidosis. Addition of glucose-containing
fluids if hypoglycaemic. Caution is required as over-resuscitation with crys-
talloid may worsen cerebral oedema.
Other considerations
IM and SC injections risk haematoma formation if coagulopathic or
thrombocytopenic. Care with positioning; the skin may be fragile. Muscle
wasting may leave patients prone to neuropraxia and pressure damage.
Postoperative considerations
• Patients with advanced liver disease will need postoperative intensive
care or high dependency care.
• Postoperative decompensation of CLD carries a high mortality.
• Constipating analgesics, such as opioids, should be prescribed with
concurrent lactulose to prevent encephalopathy.
• Postoperative ileus may also precipitate encephalopathy in cirrhotic patients.
• Complications include delayed wound healing, sepsis, renal impairment
and bleeding.
021
Induction Propofol,
thiopental,
etomidate
Maintenance Desflurane, Enflurane Halothane
sevoflurane, (possibly)*
isoflurane, N2O
Muscle Atracurium, Rocuronium,
relaxants cisatracurium vecuronium,
suxamethonium
Opioids Remifentanil Fentanyl, alfentanil,
morphine, pethidine
Analgesics Paracetamol NSAIDs, lidocaine,
bupivacaine
*
Halothane has been rarely reported to cause hepatitis (see % p. 213).
21
Halothane hepatitis
The use of halothane has been largely superseded by other volatile agents,
so it is becoming a historical phenomenon. Halothane has been linked to
postoperative liver dysfunction. Two syndromes are recognised:
• The first is associated with a transient rise in LFTs and low morbidity,
often after initial exposure.
• The second is thought to occur after repeated exposure and has an
‘immune’ mechanism with the development of fulminant hepatic
failure and high mortality. It is rare, with an incidence of 1 in 35 000
anaesthetics.
• Antibodies specific to fulminant hepatic failure patients exposed to
halothane are found in 70% of such patients. It is postulated that a
halothane oxidative metabolite binds to liver cytochromes to form a
hapten and induces a hypersensitivity reaction. All patients exposed to
halothane have altered liver proteins, but it is unknown why only a few
develop liver failure.
Postoperative liver dysfunction or jaundice 213
Further reading
Hickman L, Tanner L, Christein J, et al. (2019). Non-hepatic abdominal surgery in patients with cir-
rhotic liver disease. Gastrointest Surg, 23, 634.
Northup PG, Friedman LS, Kamath PS (2019). AGA clinical practice update on surgical risk as-
sessment and perioperative management in cirrhosis: expert review. Clin Gastroenterol Hepatol,
17, 595.
Hernaez R, Solà E, Moreau R, et al. (2017). Acute-on-chronic liver failure: an update. Gut, 66, 541–53.
Machicao VI, Balakrishnan M, Fallon MB (2014). Pulmonary complications in chronic liver disease.
Hepatology, 59, 1627–37.
Lee WM, Stravitz RT, Larson AM (2012). Introduction to the revised American Association for the
Study of Liver Diseases Position Paper on acute liver failure 2011. Hepatology, 55, 965.
Argo CK, Balogun RA (2009). Blood products, volume control, and renal support in the coagulopathy
of liver disease. Clin Liver Dis, 13, 73.
Trotter JF (2009). Practical management of acute liver failure on ITU. Curr Opin Crit Care, 15, 163–7.
Chapter 9 215
See also:
% Endocrine surgery pp. 709–21
621
Diabetes mellitus
Insulin is necessary, even when fasting, to maintain glucose homeostasis and
balance stress hormones (e.g. adrenaline). It has two classes of action:
• Excitatory: stimulating glucose uptake and lipid synthesis
• Inhibitory (physiologically more important): inhibits lipolysis, proteolysis,
glycogenolysis, gluconeogenesis and ketogenesis.
Lack of insulin is associated with hyperglycaemia, osmotic diuresis, dehy-
dration, hyperosmolarity, hyperviscosity predisposing to thrombosis and
i rates of wound infection. Sustained hyperglycaemia is associated with
i mortality, hospital stay and complication rates.
DM is present in 10–15% of the surgical population.
• Type 1 diabetes (20%): immune-mediated and leads to absolute
insulin deficiency. Patients cannot tolerate prolonged periods without
exogenous insulin. Glycogenolysis and gluconeogenesis occur, resulting
in hyperglycaemia and ketosis. Treatment is with insulin.
• Type 2 diabetes (80%): a disease of adult onset, associated with
insulin resistance. Patients produce some endogenous insulin and their
metabolic state often improves with fasting. Treatment may be diet
control, oral hypoglycaemics and/or insulin.
General considerations
Many diabetic patients are well informed about their condition and have
undergone previous surgery; discuss management with them. Hospital dia-
betes teams can be useful for advice. The overall aims of perioperative
diabetic management are to maintain physiological glucose levels (above
hypoglycaemic levels, but below those at which deleterious effects of
hyperglycaemia become evident) and prevent hypokalaemia, hypomagnes-
aemia and hypophosphataemia.
Preoperative assessment
• CVS: IHD (sometimes asymptomatic), cerebrovascular disease, MI and
cardiomyopathy are all associated with DM. Autonomic neuropathy can
lead to tachy-or bradycardia and postural hypotension.
• Renal: 40% of diabetics develop microalbuminuria, which is associated
with hypertension, IHD and retinopathy. This may be reduced by
treatment with ACE inhibitors.
• Respiratory: perioperative chest infections are more common,
especially if other risk factors such as smoking and obesity.
• Airway: thickening of soft tissues (glycosylation) occurs, especially in
ligaments around joints, leading to limited joint mobility syndrome.
Intubation may be difficult if the neck is affected or there is insufficient
mouth opening.
• GI: 50% of patients have delayed gastric emptying ± reflux.
• i risk of wound infection.
• Peripheral neuropathy is common; document any existing sensory loss if
regional technique planned.
Diabetes mellitus 217
Investigations
• Measure glycosylated Hb (HbA1c), a measure of recent glycaemic
control (normal 20–48mmol/mol, 4–6.5%). If HbA1c is >69mmol/mol
(8.5%), refer to the team that manages their diabetes for optimisation.
Surgery may then proceed with caution. A value >85mmol/mol (10%)
suggests inadequate control. Refer to the diabetes team, and only
proceed if surgery is urgent or if they feel the patient’s control is as
good as it can be.
• Patients with hypoglycaemic unawareness should be referred to the
diabetes specialist team, irrespective of HbA1c.
Preoperative management
• Make an individualised diabetes management plan, agreed with the
patient, for the preadmission and perioperative period.
• Place the patient 1st on the operating list, if possible.
• Individuals with type 1 diabetes should NEVER go without insulin, as
they are at risk of diabetic ketoacidosis.
• The Enhanced Recovery Partnership Programme recommends high-
carbohydrate drinks prior to surgery. This may compromise blood
sugar control and is not recommended for people with insulin-treated
diabetes.
• Patients with a planned short starvation period (no more than one
missed meal in total) should be managed by modification of their usual
diabetes regime, avoiding a variable-rate IV insulin infusion (VRIII)
wherever possible.
• Patients expected to miss >1 meal should have a VRIII.
• For suggested perioperative management of insulin, see Table 9.1.
For suggested perioperative management of non-insulin diabetic
medication, see Table 9.2.
Perioperative management
• Monitor blood glucose on admission, and hourly during the day of
surgery. Aim for blood glucose level of 6–10mmol/L; 4–12mmol/L is
acceptable.
• If blood glucose is >12mmol/L either pre-or post-surgery, check
capillary blood ketones or urinary ketones. If capillary blood ketones
are >3mmol/L or urinary ketones > +++, cancel surgery.
• Consider an RSI if gastric stasis is suspected.
• Regional techniques may be useful for extremity surgery and to reduce
the risk of undetected hypoglycaemia.
• Autonomic dysfunction may exacerbate the hypotensive effect of
spinals and epidurals.
Patients undergoing surgery with a long starvation period
(i.e. two or more missed meals)
• A number of glucose, K+ and insulin regimes have been described
in the past (e.g. Alberti), but the VRIII is widely used and should be
commenced on admission.
• If the patient is already on a long-acting insulin analogue, this should be
continued at 80% the usual dose, even if planning to use a VRIII through
the perioperative period.
821
Table 9.1 Perioperative management of insulin therapy when no more than one
missed meal
Blood glucose Initial rate of insulin infusion Insulin infusion rate if blood
(mmol/L) (units/h) glucose not <10mmol/L (units/h)
<4.0 0.5—if a long-acting insulin has been continued, stop and treat
as for hypoglycaemia
4.1–7.0 1.0 2.0
7.1–9.0 2.0 3.0
9.1–11.0 3.0 4.0
11.1–14.0 4.0 5.0
14.1–17.0 5.0 6.0
17.1–20.0 6.0 8.0
>20 Check infusion running, and seek diabetes team or medical
advice)
20
Acromegaly
A rare clinical syndrome caused by overproduction of growth hormone
from the anterior pituitary. Patients may present for pituitary surgery (see
% pp. 567–8) or require surgery unrelated to their pituitary pathology.
Preoperative assessment
• Cardiac assessment for hypertension (30%), IHD, cardiomyopathy,
heart failure, conduction defects and valvular disease.
• Possible difficult airway management and intubation due to large
head and tongue, hypertrophy of the larynx and trachea, vocal cord
thickening and strictures and chondrocalcinosis of the larynx. Consider
direct/indirect laryngoscopy preoperatively if vocal cord or laryngeal
pathology is suspected.
• Enlargement of the thyroid (25%) may compress the trachea.
• Twenty-five per cent of patients have diabetes.
• Snoring and daytime somnolence may indicate sleep apnoea (70%).
Chronic OSA can cause elevated PAP.
• Kyphoscoliosis may worsen respiratory function.
• Medications: somatostatin analogues (octreotide, lanreotide) may cause
vomiting and diarrhoea. Bromocriptine, a long-acting dopamine agonist,
is often used to lower growth hormone levels and can cause severe
postural hypotension.
• Symptoms and signs of raised ICP or nerve compression (e.g. carpal
tunnel syndrome).
Investigations
• ECG as routine. Echocardiogram if patient symptomatic or has
murmurs.
• CXR if cardiorespiratory problems.
• Blood glucose.
Conduct of anaesthesia
• Large face masks, long-bladed laryngoscopes and gum elastic
bougies may make airway management and intubation easier. Use a
videolaryngoscope (VL) if available. AFOI is the technique of choice
for patients with anticipated difficult intubation. More problems
experienced with extubation than intubation.
• A long table may be required.
• Nerve compression syndromes are common, so take care to protect
vulnerable areas (ulnar nerve at the elbow, median nerve at the wrist,
and common peroneal nerve below the knee).
Further reading
Menon R, Murphy P, Lindley A (2011). Anaesthesia and pituitary disease. Contin Educ Anaesth Crit
Care Pain, 11, 133–7.
Nemergut EC, Dumont AS, Barry UJ, et al. (2005). Perioperative management of patients under-
going transsphenoidal pituitary surgery. Anesth Analg, 101, 1170–81.
Thyroid disease 223
Thyroid disease
May present for thyroidectomy (see % pp. 710–13) or non-thyroid surgery.
General considerations for non-thyroid surgery
Hypothyroidism
• Commonly due to autoimmune thyroid destruction.
• CVS complications include d blood volume, d CO (up to 50%),
bradycardia, hypotension and IHD. Pericardial effusions also occur.
• Respiratory muscle weakness, impaired hypoxic/hypercapnic drive
and OSA.
• Also associated with anaemia, hypoglycaemia, hyponatraemia,
i thrombotic tendency, impaired hepatic drug metabolism and renal
clearance affecting drug clearance.
• Reduced gastric motility and i postoperative ileus.
• If clinical evidence of hypothyroidism, delay elective surgery to obtain
a euthyroid state. Liaise with an endocrinologist. Suggest levothyroxine
(T4), starting dose 50 micrograms, increasing to 100–200 micrograms
PO over several weeks. The elderly are susceptible to angina and heart
failure after thyroxine replacement due to i cardiac work. Start with
25 micrograms T4, and increase by 25 micrograms at 3-to 4-weekly
intervals.
• If surgery is urgent, use liothyronine (T3), 10–50 micrograms slow IV
injection with ECG monitoring (consider half dose if suspected cardiac
disease).
• Euthyroid sick syndrome refers to suppression of serum thyroid
hormone occurring in euthyroid patients due to concurrent illness.
Subclinical hypothyroidism is a risk factor for postoperative AF, but
there is no clear evidence hormone replacement should be given in this
situation.
• Myxoedema coma is an emergency with mortality of up to 80%.
Presents with confusion, drowsiness, bradycardia, hypotension and
hypothermia. May be precipitated by infection or cold and require IV
thyroxine replacement.
Hyperthyroidism (thyrotoxicosis)
• Typically presents with weight loss, hypertension, sweating and cardiac
arrhythmias (especially AF). Treatment is with carbimazole (30–45mg
PO daily for 6–8w). This inhibits iodination of tyrosyl residues in
thyroglobulin. Occasionally, in severe cases with a large thyroid, Lugol’s
iodine is substituted 10d preoperatively to reduce gland vascularity.
• β-blockade is started if there are signs of tremor or palpitations.
Non-cardioselective β-blockers (propranolol 30–60mg tds) are most
effective. β1-adrenergic blockade treats tachycardia and β2-adrenergic
blockade prevents the peripheral conversion of T4 to T3. Calcium
channel blockers are an alternative for those with reactive airway
disease.
24
Preoperative assessment
• Elective surgery should only occur when patient is euthyroid (HR
<80bpm, no hand tremor). Patients with subclinical hypothyroidism
usually have no anaesthetic problems and no delay is needed.5
• A goitre can cause respiratory obstruction, so look for tracheal
deviation and retrosternal extension. Look for evidence of tracheal
compression with shortness of breath (may be positional), dysphagia
and stridor (occurs with 50% compression). Infiltrating carcinoma may
make any neck movement difficult and is an independent predictor of
difficult intubation.
• SVC obstruction can occur. Look for distended neck veins that do not
change with respiration.
• Check for other autoimmune disorders.
Investigations
(See % pp. 710–11.)
Conduct of anaesthesia
Hypothyroid patients
• Give all drugs slowly. Susceptible to profound hypotension, which may
be relatively resistant to the effects of catecholamine therapy.
• Actively warm as low metabolic rate predisposes to hypothermia.
• Tendency to hypoventilate; controlled ventilation is recommended.
• Drug metabolism is slower, so reduce the dose of relaxants and opioids
and monitor twitch response.
Hyperthyroid patients
• Continue β-blockade to reduce the possibility of a thyroid storm.
• Consider invasive arterial BP monitoring.
Special considerations
Thyroid storm
• A life-threatening exacerbation of the hyperthyroid state, with evidence
of decompensation in one or more organ systems (mortality 20–30%).
• Usually presents 6–24h post-surgery with fever (>40°C), sweating,
sinus tachycardia (>140bpm), coma, nausea, vomiting and diarrhoea.
• If presents intraoperatively, may be difficult to distinguish from MH.
Higher mixed venous partial pressure of CO2 and higher creatine kinase
(CK) in MH.
• Rehydrate with IV 0.9% sodium chloride and glucose.
• Treat hyperthermia with tepid sponging and paracetamol. Do not
give NSAIDs or aspirin, as they displace thyroid hormone from serum
binding sites.
• Give propranolol (1mg increments, up to 10mg), with CVS monitoring,
to decrease the pulse rate to <90bpm. Alternatively, give esmolol
(loading dose 250–500 micrograms/kg, followed by 50–100
micrograms/kg/min).
• Give hydrocortisone (200mg IV qds) to treat adrenal insufficiency and
to decrease T4 release and conversion to T3 at very high levels.
Thyroid disease 225
Parathyroid disorders
General considerations
The parathyroid glands secrete parathyroid hormone (PTH), which acts on
the bones and kidneys to increase serum Ca2+ and decrease serum phos-
phate. It stimulates osteoclasts to release Ca2+ and phosphate into the ECF
and simultaneously increases phosphate excretion and Ca2+ reabsorption in
the kidney. Patients may present for parathyroidectomy (see % pp. 714–15)
and non-parathyroid-related surgery.
Hyperparathyroidism
• 1° hyperthyroidism: usually an adenoma causing high PTH, high
Ca2+ and low phosphate. Associated with familial multiple endocrine
neoplasia (MEN) type 1. Tumours rarely palpable and are located at
surgery. Methylthioninium chloride (methylene blue) up to 1mg/kg is
given preoperatively to localise the parathyroid gland.
• Fifty per cent of cases are asymptomatic, and presentation is often
subtle. May present with anorexia, dyspepsia, nausea, vomiting and
constipation, hypertension, shortened QT interval, polydipsia, polyuria,
renal calculi, depression, poor memory and drowsiness.
Secondary hyperparathyroidism
• Results from compensatory parathyroid hypertrophy due to chronic
low Ca2+. Complicates CKD.
• Parathyroid hyperplasia causes high PTH, normal or low Ca2+ level and
a high phosphate level.
• Usually presents as excessive bone resorption (seen earliest in the radial
aspect of the middle phalanx of the 2nd digit) or calcification of the
vascular system, organs and soft tissues.
• Treat medically with dietary phosphate restriction and calcium and
vitamin D supplements. Medical therapy fails in 5–10% of patients on
long-term dialysis and surgery becomes necessary.
• Risks of surgery are bleeding, recurrent hyperparathyroidism,
hypoparathyroidism and injury to the recurrent laryngeal nerves.
Patients should undergo dialysis within 1d of surgery and then 48h
postoperatively or as required.
• Watch for postoperative hypocalcaemia and hypomagnesaemia.
Tertiary hyperparathyroidism
• Parathyroid hyperplasia progresses to autonomous secretion, behaving
like an adenoma. Excessive secretion of PTH continues, despite
correction of renal failure. Only a few cases require operation.
Hypercalcaemic crisis
• Occurs most commonly in the elderly with undiagnosed
hyperparathyroidism and with malignant disease. Dehydration
results in anorexia and nausea/vomiting which exacerbates the cycle.
Characterised by weakness, lethargy, mental changes, abdominal pain
and coma.
• Serum Ca2+ >4.5mmol/L is life-threatening and can be rapidly, but
transiently lowered with phosphate (500mL of 0.1M neutral solution
over 6–8h).
Parathyroid disorders 227
Adrenocortical insufficiency
Primary adrenocortical insufficiency (Addison’s disease)
Destruction of adrenal cortex by autoimmune disease (75%), infection
(tuberculosis (TB)), septicaemia, acquired immune deficiency syndrome
(AIDS), haemorrhage, metastases, and surgery. Associated with gluco-
corticoid and mineralocorticoid deficiency.
Secondary adrenocortical insufficiency
Insufficient adrenocorticotrophic hormone (ACTH) to stimulate the ad-
renal cortex due to pituitary suppression by exogenous steroids or gen-
eralised hypopituitarism usually from pituitary or hypothalamic tumours.
Associated with glucocorticoid deficiency only.
Clinical features of adrenal insufficiency
Weakness, fatigue (100%), nausea, vomiting, diarrhoea, weight loss (60%),
myalgia and joint pain. Some features more pronounced or found only in
Addison’s disease: skin hyperpigmentation (90%), postural hypotension
(90%) and salt craving. Skin pallor found only in 2° insufficiency.
Acute adrenal crisis
Medical emergency characterised by dizziness, weakness, sweating, abdom-
inal pain, nausea and vomiting or coma.
Causes may be inadequate stress-related steroid replacement in patients
with chronic adrenal insufficiency, adrenal haemorrhage or pituitary apo-
plexy (apoplexy is defined as a sudden neurological impairment, usually due
to a vascular process, i.e. infarction or haemorrhage).
Investigations
• Serum shows: low glucose, low Na+ (90%) and raised K+ (70%). Ca2+,
urea and creatinine are raised in Addison’s disease only.
• Table 9.4 shows biochemical diagnosis of adrenal insufficiency.
Treatment
• Hydrocortisone, 20mg in the morning and 10mg at night PO.
• Fludrocortisone, 0.1mg PO, to replace aldosterone in Addison’s disease.
Perioperative management of patients with Addison’s
disease
• Joint care with an endocrinologist is advisable.
• Give all medication on the morning of surgery.
• For any nil-by-mouth regime, give IV 0.9% sodium chloride to prevent
dehydration and maintain mineralocorticoid stability.
• Hydrocortisone 100mg before surgery, then continuous infusion at rate
of 200mg/24h intraoperatively. Postoperatively, the infusion can be
reduced to 100mg/24h infusion or give 50mg 6-hourly.
• Once eating and drinking, start double normal dose for 48h, extended
to 1w if recovery complicated.
• It is worth noting that 20mg hydrocortisone is equivalent to 0.05mg
fludrocortisone, so with hydrocortisone doses of 50mg or more,
mineralocorticoid replacement in 1° adrenal insufficiency can be reduced.
• If any postoperative complications arise, e.g. fever, delay the return to
normal dose.
• Four-hourly blood glucose and daily electrolytes.
Adrenocortical insufficiency 229
*
Serum cortisol at 0 and 30min after 250 micrograms of Synacthen® IV.
**
Serum glucose and cortisol at 0, 15, 30, 45, 60 and 90min after insulin (0.1–0.15 units/kg IV).
Test only valid if symptomatic hypoglycaemia (serum glucose <2.2mmol/L) is achieved. Gold
standard test—close supervision mandatory.
Intraoperative Postoperative
Major 100mg hydrocortisone at Reduce infusion rate by
surgery and induction, then initiate infusion at 50% and normal dose
CS rate 200mg/24h. Alternatively, when eating
6–8mg dexamethasone at Complicated recovery:
induction will suffice for 24h continue double normal
dose for 2–7d or until
complications resolve
Body As above Double regular dose for 2d
surface +
intermediate
surgery
Bowel HPA suppression possible: Double normal dose for 24h
procedures IV fluids + 100mg
hydrocortisone IV for bowel
prep and induction
HPA suppression unlikely:
continue normal dose
(equivalent IV dose if nil by
mouth)
Labour Hydrocortisone 100mg IV at
onset of labour, followed by
infusion at rate 200mg/24h
Source: data from Woodcock, T et al. (2020) Guidelines for the management of glucocorticoids
during the peri-operative period for patients with adrenal insufficiency. Anaesthesia, 75:654–63.
Hypothalamic–pituitary–adrenal suppression
• Endogenous cortisol (hydrocortisone) production is of the order of
25–30mg/24h (following a circadian pattern). During stress induced by
major surgery, it rises to 75–100mg/d and can remain elevated for a
variable period of time (up to 72h following cardiac surgery).
• Prednisolone is a synthetic glucocorticoid with the general properties of
corticosteroids. Prednisolone exceeds hydrocortisone in glucocorticoid
and anti-inflammatory activity, being 3–4 times more potent on a
weight basis than the parent hormone; however, it is less active than
The patient on steroids 231
Further reading
Woodcock T, Barker P, Daniel S, et al. (2020). Guidelines for the management of glucocorticoids
during the peri-operative period for patients with adrenal insufficiency. Anaesthesia, 75, 654–63.
Liu MM, Reidy AB, Saatee S, et al. (2017). Perioperative steroid management: approaches based on
current evidence. Anesthesiology, 127, 166–72.
23
Cushing’s syndrome
Cushing’s syndrome describes excess plasma cortisol. Commonly caused
by overtreatment with steroids. The 2nd commonest cause is a pituitary ad-
enoma (Cushing’s disease). Ectopic ACTH (e.g. oat cell carcinoma of lung),
adrenal adenoma and adrenal carcinoma are also possible causes.
Clinical features
• Round ‘moon’ face, truncal obesity, bruised and fragile skin
• Proximal myopathy and osteoporosis
• High Na+, bicarbonate (HCO3–) and glucose; low K+ and Ca2+.
Diagnosis
• High plasma cortisol with loss of diurnal variation (peak 6 a.m., trough
midnight). Normal cortisol range 7140–700nmol/L dependent on time
of day and clinical context.
• i urinary 17-(OH)-steroids.
• Loss of suppression with dexamethasone 2mg.
• ACTH level high with ectopic ACTH, normal/high in pituitary disease
and low with adrenal disease or ectopic cortisol administration.
Preoperative assessment
• Many patients have ECG abnormalities (high-voltage QRS and inverted
T waves), which may make IHD difficult to exclude. These will revert to
normal after curative surgery.
• Eighty-five per cent of patients are hypertensive, often poorly
controlled, and LVH should be looked for.
• Sleep apnoea and gastro-oesophageal reflux are common and difficult
intubation should be anticipated if facial adipose tissue i.
• Sixty per cent of patients have diabetes or impaired glucose tolerance
and a VRIII may be appropriate (see % p. 219).
• Obesity may make venous access difficult.
• Patients are at risk of peptic ulcer disease, so give prophylactic antacid
medication.
Conduct of anaesthesia
• Position the patient carefully intraoperatively due to i risk of pressure
sores and fractures 2° to fragile skin and osteoporosis.
Further reading
Nieman LK, Biller BMK, Findling JW, et al. (2015). Treatment of Cushing’s syndrome: an Endocrine
society clinical guideline. J Clin Endocrinol Metab, 100, 2807–31.
Domi R (2011). Cushing's surgery: role of the anesthesiologist. Indian J Endocrinol Metab, 15, 322–8.
Conn’s syndrome 233
Conn’s syndrome
Excess of aldosterone produced from an adenoma (60%) or benign hyper-
plasia of the adrenal gland (35–40%) or an adrenal carcinoma (rare).
General considerations
Aldosterone promotes active reabsorption of Na+ and excretion of K+
through the renal tubules. Water is retained with Na+, resulting in an in-
crease in ECF volume. To a lesser extent, there is also tubular secretion of
H+ ions and Mg2+, resulting in a metabolic alkalosis.
Clinical features
• Refractory hypertension, hypervolaemia, metabolic alkalosis.
• Spontaneous hypokalaemia (K+ <3.5mmol/L); moderately severe
hypokalaemia (K+ <3.0mmol/L) during diuretic therapy despite PO K+.
• Muscle weakness, especially in ethnic Chinese, 2° to hypokalaemia.
• Nephrogenic diabetes insipidus 2° to renal tubular damage.
• Impaired glucose tolerance in 750% of patients.
Preoperative assessment for adrenalectomy
• Spironolactone, a competitive aldosterone antagonist, is given
to reverse the metabolic and electrolyte effects and restore
normovolaemia. Doses of up to 400mg/d may be required.
• The patient should have normal serum K+ and HCO3– if possible.
• Hypertension is usually mild and well controlled on spironolactone.
• Calcium channel blockers, such as nifedipine, are effective
antihypertensive agents with aldosterone-secreting adenomas.
Investigations
• Aldosterone (pg/mL) to renin (nanograms/mL/h) ratio >400.
• 2° hyperaldosteronism: raised serum aldosterone, but normal ratio.
• Important to distinguish between adenoma and hyperplasia as adenoma
is usually treated surgically and hyperplasia medically.
• Adrenal vein sampling, radiolabelling, CT and MRI are all used.
Conduct of anaesthesia for adrenalectomy
Unilateral adrenalectomy should ideally be performed laparoscopically.
Handling of the adrenal gland during surgery can cause CVS instability but is
not as severe as with a phaeochromocytoma (see % pp. 716–19).
• A short-acting α-blocker should be available (phentolamine 1mg
boluses IV).
• Check blood glucose perioperatively.
• Chronic hypokalaemia has an antagonistic action upon insulin secretion/
release and may result in abnormal glucose tolerance with the stress of
surgery.
Postoperative care
• K+ supplements and spironolactone should be discontinued
postoperatively.
• Give hydrocortisone IV postoperatively until the patient can tolerate
oral hydrocortisone and fludrocortisone.
• Hypertension may persist after removal of the adenoma, presumably
due to permanent changes in vascular resistance.
234
Apudomas
Tumours of amine precursor uptake and decarboxylation (APUD) cells
which are present in the anterior pituitary gland, thyroid, adrenal me-
dulla, GI tract, pancreatic islets, carotid bodies and lungs. Apudomas in-
clude phaeochromocytoma, carcinoid tumour, gastrinoma, VIPomas and
insulinoma and may occur as part of the MEN syndrome. In 2017, the
European Neuroendocrine Society released guidance on perioperative
management of neuroendocrine tumours.1
Phaeochromocytoma
(See % pp. 716–19.)
Carcinoid tumours
• Carcinoid tumours are derived from argentaffin cells and produce
peptides and amines. They occur in the GI tract (75%), bronchus,
pancreas and gonads. Mainly benign, but of those that are malignant,
only about a quarter release vasoactive substances into the systemic
circulation, leading to the carcinoid syndrome.
• Mediators are metabolised in the liver; carcinoid syndrome thus
occurs if: (1) liver metastasis; (2) tumour drainage bypasses the portal
circulation; and (3) precursors are so copious they overwhelm hepatic
enzyme capacity, e.g. high lymph node metastasis burden.
• Niacin deficiency or pellagra can occur due to the consumption of
niacin in serotonin production.
• Vasoactive substances include serotonin, bradykinin, histamine,
substance P, prostaglandins and vasoactive intestinal peptide (VIP).
• Patients with an asymptomatic carcinoid tumour have simple carcinoid
disease and do not present particular anaesthetic difficulties.
• Patients with carcinoid syndrome can be extremely difficult to manage
perioperatively.
• Symptoms such as flushing (multiple episodes a day) are predictive of
sequelae such as carcinoid heart disease.
Carcinoid syndrome
• Affects about 10% of patients with carcinoid tumours.
• Patients may have symptoms related to the tumour (e.g. intestinal
obstruction or haemoptysis).
• Vasoactive peptides result in intermittent flushing, especially of the
head, neck and torso (90%), or diarrhoea (78%), which may lead to
dehydration and electrolyte disturbances.
• Other symptoms include bronchospasm (20%), hypotension,
hypertension, tachycardia and hyperglycaemia.
• Twenty per cent of patients have heart disease related to carcinoid.
Endocardial fibrosis of the pulmonary and tricuspid valves leads to right
heart failure, so consider an echocardiogram preoperatively. ECG may
show RV hypertrophy.
NT-proBNP has been shown to be predictive of both heart disease and
mortality.
• Check FBC, electrolytes, LFTs and clotting if metastases present.
• X-match blood.
(See % pp. 720–1 for conduct of anaesthesia.)
236
Gastrinoma
• Excess production of gastrin by benign adenoma, malignancy or
hyperplasia of D cells of the pancreatic islets.
• Gastrin stimulates acid production from gastric parietal cells. Leads to
Zollinger–Ellison syndrome, severe peptic ulceration and diarrhoea.
• May also have GI bleeds, perforation, electrolyte disturbance and
volume depletion.
• Treatment includes high-dose PPIs (e.g. omeprazole), H2 receptor
antagonists and octreotide.
• May present for surgery related to gastrinoma, e.g. perforation, or
pancreatic resection of the tumour or a totally unrelated pathology.
Actively look for anaemia from gastric ulceration and coagulopathy from
liver dysfunction.
• Patients require perioperative invasive pressure monitoring for major
surgery.
• Continue omeprazole postoperatively (up to 60–80mg/day), as the
gastric mucosa may have become hypertrophied, producing excess acid.
VIPoma
• Rare tumour secreting VIP which leads to Verner–Morrison syndrome.
• Characterised by profuse watery diarrhoea, intestinal ileus, abdominal
distension, confusion, hypokalaemia, achlorhydria, hypomagnesaemia,
hyperglycaemia, metabolic alkalosis and tetany.
• VIP inhibits gastrin release; therefore, give H2 receptor-blocking drugs
preoperatively to prevent rebound gastric acid hypersecretion.
• Will often require a period of resuscitation with correction of fluid
losses and electrolytes prior to surgery.
• Treat medically with somatostatin analogues (octreotide). If this fails, try
steroids (such as methylprednisolone) and indometacin (a prostaglandin
inhibitor).
• Sixty per cent malignant with liver metastases, so all warrant resection.
• Use invasive pressure monitoring for major surgery.
• ABG to check the acid–base status and electrolytes.
Insulinoma
• Rare tumour of β cells of the pancreas which secrete insulin.
• Whipple’s triad of clinical presentation: fasting hypoglycaemia,
symptoms of hypoglycaemia and relief of symptoms when glucose
is given.
• Diagnosis also made by a fasting blood glucose <2.2mmol/L, i insulin,
i C-peptide and no plasma sulfonylurea.
• Patients often have to eat high-carbohydrate diets and limit exercise to
avoid hypoglycaemia; this predisposes to obesity and its sequelae.
• Medical treatment is used to reduce symptoms. Diazoxide (a non-
diuretic benzothiazide which inhibits the release of insulin and stimulates
glycogenolysis) has been used but has unpredictable efficacy and is
avoided in hypoglycaemic presentations. Can cause significant fluid
retention and oedema.
• Octreotide is also used. It binds with somatostatin receptors on
insulinomas and decreases insulin secretion in 40–60% of patients; it
can, however, worsen hypoglycaemia and should be monitored.
Apudomas 237
References
1 Kaltsas G, Caplin M, Davies P, Ferone D, et al.; Antibes Consensus Conference participants
(2017). ENETS Consensus Guidelines for the Standards of Care in Neuroendocrine Tumors:
pre-and perioperative therapy in patients with neuroendocrine tumors. Neuroendocrinology, 105,
245–54.
238
Hypokalaemia
Defined as plasma K+ <3.5mmol/L.
• Mild • 3.0–3.5mmol/L
• Moderate • 2.5–3.0mmol/L
• Severe • <2.5mmol/L
Causes
• d intake.
• i K+ loss: vomiting or nasogastric (NG) suctioning, diarrhoea, pyloric
stenosis, diuretics, renal tubular acidosis, hyperaldosteronism, Mg2+
depletion, leukaemia.
• Intercompartmental shift: insulin, alkalosis (pH increase of 0.1 decreases
K+ by 0.6mmol/L), β2-agonists and steroids.
Clinical manifestations
• ECG changes: T wave flattening and inversion, prominent U wave, ST-
segment depression, prolonged P–R interval.
• Dysrhythmias, d cardiac contractility.
• Skeletal muscle weakness, tetany, ileus, polyuria, impaired renal
concentrating ability, d insulin secretion, d growth hormone secretion,
d aldosterone secretion, negative nitrogen balance.
• Encephalopathy in patients with liver disease.
Management
• Check U&E, creatinine, Ca2+, phosphate, Mg2+, HCO3– and glucose if
other electrolyte disturbances suspected. Hypokalaemia resistant to
treatment may be due to concurrent hypomagnesaemia.
• Exclude Cushing’s and Conn’s syndromes.
• Oral replacement is safest, up to 200mmol/d, e.g. KCl (Sando-K®) two
tablets qds = 96mmol K+.
• IV replacement: essential for patients with cardiac manifestations or
skeletal muscle weakness or where oral replacement not appropriate.
• Aim to increase K+ to 4.0mmol/L if treating cardiac manifestations.
• Maximum concentration for peripheral administration is 40mmol/L
(greater concentrations than this can lead to venous necrosis); 40mmol
KCl can be given in 100mL of 0.9% sodium chloride over 1h, but only
via an infusion device, with ECG monitoring, in an HDU/ICU/theatre
environment and via a central vein. Plasma K+ should be measured at
least hourly during rapid replacement. K+ depletion sufficient to cause
0.3mmol/L drop in serum K+ requires a loss of 7100mmol of K+ from
total body store.
Hypokalaemia 239
Anaesthetic considerations
Predominant issue is risk of arrhythmia. Hypokalaemia is significantly as-
sociated with postoperative gastric transit delay, i.e. ileus, its own source
of morbidity.2
• Classically, K+ <3.0mmol/L has led to postponement of elective
procedures (some controversy exists about this in the fit, non-digitalised
patient who may well tolerate chronically lower K+ levels, e.g. 2.5mmol/
L, without adverse events).
• For emergency surgery, if possible, replace K+ in the 24h prior to
surgery. Aim for levels of 3.5–4.0mmol/L. If this is not possible, use an
IV replacement regime, as documented earlier, intra-/perioperatively.
• If HCO3– is raised, then the loss is probably long-standing with low
intracellular K+ and will take days to replace.
• May increase sensitivity to NMB; therefore, need to monitor.
• i risk of digoxin toxicity at low K+ levels. Aim for K+ of 4.0mmol/L in a
digitalised patient.
Further reading
Freshwater-Turner D (2006). Sodium, potassium and the anaesthetist. Anaesthesia UK. M https://
www.frca.co.uk/article.aspx?articleid=100676
References
2 Zhu Q, Li X, Tan F, et al. (2018). Prevalence and risk factors for hypokalemia in patients sched-
uled for laparoscopic colorectal resection and its association with post-operative recovery. BMC
Gastroenterol, 18, 152.
240
Hyperkalaemia
Defined as plasma K+ >5.5mmol/L.
• Mild • 5.5–6.0mmol/L
• Moderate • 6.1–7.0mmol/L
• Severe • >7.0mmol/L
Causes
• i intake, e.g. IV administration, rapid blood transfusion.
• i urinary excretion, e.g. renal failure (acute or chronic), adrenocortical
insufficiency, drugs (K+-sparing diuretics, ACE inhibitors,
ciclosporin, etc.).
• Intercompartmental shift of K+, e.g. acidosis (H+ is taken into the cell,
in exchange for K+), rhabdomyolysis, trauma, MH, suxamethonium
(especially with burns or denervation injuries), familial periodic paralysis.
• Pseudohyperkalaemia due to in vitro haemolysis.
• Commonest risk factors are AKI, cardiovascular disease, CKD, diabetes
and drugs affecting CVS/renal–aldosterone–angiotensin system.
Clinical manifestations
• ECG changes, progressing through peaked T waves, widened QRS,
prolonged P–R interval, loss of P wave, loss of R wave amplitude, ST
depression, VF, asystole. ECG changes potentiated by low Ca2+, low Na+
and acidosis.
• Muscle weakness at K+ >8.0mmol/L.
• Nausea, vomiting, diarrhoea.
Management
• Treatment should be initiated if K+ >6.5mmol/L or ECG changes
present.
• Unlike hypokalaemia, the incidence of serious cardiac compromise
is high and therefore, intervention is important. Treat the cause, if
possible.
• Ensure IV access and cardiac monitor.
• Insulin 10 units in 50mL of 50% glucose IV over 30–60min. This has
the fastest onset of action and is very effective in reducing serum K+ by
shifting K+ into the cells. Beware rebound occurs within 2h.
• β2-agonist, salbutamol 5–10mg nebulised, but beware tachycardia.
Should see a response at 30min and has a longer duration of action than
insulin.
• 5–10mL of 10% calcium gluconate or 3–5mL of 10% calcium chloride.
Ca2+ stabilises the myocardium by increasing the threshold potential.
Rapid onset, short-lived.
• If acidotic, give HCO3– 50mmol IV.
• Ion exchange resin: calcium polystyrene sulfonate (e.g. Resonium
calcium) 5g PO or 30g per rectum (PR) 8-hourly. This binds K+ in
the gut.
• If initial management fails, consider dialysis or haemofiltration.
Hyperkalaemia 241
Anaesthetic considerations
• Do not consider elective surgery. If life-threatening surgery, treat
hyperkalaemia first.
• Avoid Hartmann’s solution and suxamethonium; rocuronium is the
preferred choice, although suxamethonium has been used safely with K+
of 5.5.3 Monitor NMB, since effects may be accentuated.
• Avoid hypothermia and acidosis.
• Control ventilation to prevent respiratory acidosis.
• Monitor K+ regularly.
Further reading
Kovesdy CP (2017). Updates in hyperkalemia: outcomes and therapeutic strategies. Rev Endocr
Metab Disord, 18, 41–7.
References
3 Schow AJ, Lubarsky DA, Olson RP, et al. (2002). Can succinylcholine be used safely in
hyperkalaemic patients? Anesth Analg, 95, 119–22.
24
Hyponatraemia
Defined as serum Na+ <135mmol/L.
• Mild 125–134mmol/L
• Moderate 120–124mmol/L
• Severe <120mmol/L
ECF volume is directly proportional to total body Na+ content. Renal Na+
excretion ultimately controls the ECF volume and total body Na+ content.
To identify the causes of abnormalities of Na+, assess plasma and urinary
Na+ levels and the patient’s state of hydration. Causes are summarised in
Fig. 9.1. Presentation depends on speed of onset, rather than on absolute
Na+ level—it is rare to get clinical signs if Na+ >125mmol/L.
Signs
Neuropsychiatric symptoms, nausea/vomiting, muscular weakness, head-
ache, lethargy, seizures, coma and respiratory depression.
Treatment of acute symptomatic hyponatraemia (<48h)
• Aim to raise serum Na+ by 2mmol/L/h until symptoms resolve.
Complete correction is unnecessary. May need to infuse hypertonic
(3%) sodium chloride at a rate of 1.2–2.4mL/kg/h through a large vein
(can be i to 4–6mL/kg/h if seizures/coma). Care needed—measure
Na+ levels hourly.
• In cases of fluid excess, give furosemide 20mg IV.
Treatment of chronic hyponatraemia
• Asymptomatic, fluid-restrict to 1L/d.
• Symptomatic (>48h): aim to correct serum Na+ by 5–10mmol/d. Rapid
correction (serum Na+ rise of >0.5mmol/L/h) can lead to central
pontine myelinolysis, subdural haemorrhage and cardiac failure.
• Hypovolaemic: correct with 0.9% sodium chloride (removes ADH
response that accentuates Na+/water imbalance).
• Hypervolaemic: fluid-restrict and give furosemide. For syndrome of
inappropriate antidiuretic hormone (secretion) (SIADH), also give
demeclocycline 300–600mg/d.
• Consult with an endocrinologist and treat the underlying cause.
Anaesthetic implications
• No elective surgery if Na+ <120mmol/L or symptomatic
hyponatraemia. If surgery urgent, consult endocrinologist and assess
risk/benefit ratio.
Further reading
Leise MD, Findlay JY (2017). Hyponatremia in the perioperative period: when and how to correct.
Clin Liver Dis, 9, 111–14.
Sterns RH (2015). Disorders of plasma sodium—causes, consequences and correction. N Engl J
Med, 372, 55–65.
Serum sodium
<135mmol/L
Hypovolaemic Hypervolaemic
Euvolaemic
Urinary sodium >20mmol/L
SIADH
GLUCOCORTICOID DEFICIENCY Urinary sodium
Urinary sodium ≤20mmol/L Urinary sodium Urinary sodium ≤20mmol/L
DIURETICS
PRERENAL LOSSES e.g. >20mmol/L >20mmol/L HEART FAILURE
MALIGNANCY
GI: fistula, diarrhoea, RENAL LOSS, e.g. RENAL FAILURE CIRRHOSIS
vomiting Renal failure HYPOTHYROIDISM
Urine osmolarity < serum osmolarity
Skin: sweat, burns Adrenocorticoid NEPHROTIC SYNDROME
POOR SODIUM OR EXCESS
Cirrhosis insufficiency PREGNANCY
WATER CONSUMPTION
Diuretics TURP SYNDROME
Hypernatraemia
Defined as serum Na+ >145mmol/L.
• Mild 145–150mmol/L
• Moderate 151–160mmol/L
• Severe >160mmol/L
Caused by excessive salt intake or, more frequently, inadequate water in-
take. Important to assess the volume status.
Causes
Hypovolaemic
Renal (loop/osmotic diuretics, intrinsic renal disease, post-obstruction) and
extrarenal (diarrhoea/vomiting, burns, excessive sweating, fistulae).
Euvolaemic
Diabetes insipidus, insensible losses.
Hypervolaemic
Na+ ingestion/administration of hypertonic sodium chloride, Conn’s syn-
drome, Cushing’s syndrome.
Presentation
• CNS symptoms likely if serum Na+ >155mmol/L due to hyperosmolar
state and cellular dehydration, e.g. thirst, confusion, seizures and coma.
• Features depend on the cause, e.g. water deficiency will present with
hypotension, tachycardia and d skin turgor.
Management
• Correct over at least 48h to prevent occurrence of cerebral oedema
and convulsions.
• Treat the underlying cause. Give oral fluids (water), if possible.
• Hypovolaemic (Na+ deficiency): 0.9% sodium chloride until
hypovolaemia corrected, then consider 0.45% sodium chloride.
• Euvolaemia (water depletion): estimate the total body water (TBW)
deficit; treat with 5% glucose.
• Hypervolaemic (Na+ excess): diuretics, e.g. furosemide 20mg IV and 5%
glucose; dialysis if required.
• Diabetes insipidus: replace urinary losses, and give desmopressin (1–4
micrograms daily SC/IM/IV).
Anaesthetic implications
• No elective surgery if Na+ >155mmol/L or hypovolaemic.
• Urgent surgery: consider CVP monitoring and be aware of dangers of
rapid normalisation of electrolytes.
Further reading
Bagshaw SM, Townsend DR, McDermid RC (2009). Disorders of sodium and water balance in hos-
pitalized patients. Can J Anaesth, 56, 151–67.
Chapter 10 245
Rheumatoid arthritis
RA is a chronic, systemic inflammatory disorder, mainly involving synovial
joints, but with extra-articular effects. Overall prevalence in the UK is 1.5
per 100 000 in ♂, and 3.6 per 100 000 in ♀, with a peak incidence in the
7th decade. It also affects children as Still’s disease. There is a higher-than-
average mortality due to both the disease itself and the presence of con-
current disorders.
Preoperative assessment
Articular
• Temporomandibular: assess for limited mouth opening.
• Cricoarytenoid: fixation of the cricoarytenoid joints may lead to voice
changes or even rarely to stridor from glottic stenosis. The larynx can
also be obstructed by amyloid or rheumatoid nodules. Minimal oedema
may lead to airway obstruction postoperatively.
• Atlantoaxial subluxation occurs in 725% of severe rheumatoid
patients, but of these, only a quarter will have neurological signs or
symptoms. Risk factors include disease duration >8y, glucocorticoid
use, seropositivity and nodular and erosive peripheral joint disease.
Enquire about tingling hands or neck pain, and assess the range of neck
movement (Table 10.1).
• Subaxial subluxation (i.e. below C2): >2mm loss of alignment is
significant. Look for this particularly if the patient has undergone
previous fusion at a higher level.
• Other joints: assess joint deformities with a view to positioning and
possible regional anaesthesia. Manual dexterity may be important if
planning to use standard PCA apparatus after surgery.
Non-articular
• CVS: i risk of CAD. Systemic vasculitis may lead to arterial occlusion in
various organs and Raynaud’s. They may have myocardial fibrosis and
amyloid or nodular involvement. Pericarditis and pericardial effusions
uncommon. Aortic incompetence and endocarditis rare. At risk of VTE.
• Respiratory: interstitial lung disease leading to restrictive defects may
also be 2° to drugs (fibrosing alveolitis, pneumonitis). Pulmonary
nodules. Pleural disease (pleuritis and effusions) and airway involvement
(obliterative bronchiolitis). Costochondral disease may reduce chest
wall compliance.
• Haematological: normocytic, normochromic anaemia of chronic
disease. Drug-associated myelosuppression and NSAID-associated
blood loss. Felty’s syndrome is a combination of splenomegaly
and neutropenia and may be associated with anaemia and
thrombocytopenia.
• Nervous system: central (due to axial involvement) and peripheral
compression neuropathies (e.g. carpal tunnel syndrome).
• Sjögren’s syndrome and resultant dry eyes put patients at risk of corneal
ulceration under anaesthesia.
• Infections: common from the disease itself and drug effects.
• Renal and hepatic: CKD commonly from drugs, less frequently from
glomerulonephritis. d albumin, i fibrinogen and α-1 acid glycoprotein
(acute phase protein).
• Fragile skin and difficult venous access.
Rheumatoid arthritis 247
Investigations
• Rheumatologist or spinal surgeon involvement is recommended
in patients with neurological symptoms or signs and in those with
persistent neck pain. Preoperative cervical spine flexion/extension
views are controversial. Stabilisation surgery may be necessary before
elective surgery is undertaken. Specialist radiological advice should be
sought.
• PFTs should be carried out for patients with suspected respiratory
involvement.
• Nasendoscopy preoperatively if suggestion of cricoarytenoid arthritis.
• Echocardiography is needed if there is valvular or pericardial
involvement and in symptomatic cardiac disease.
Drugs in the perioperative period
• Steroid use should be minimised prior to surgery. Steroid
supplementation if indicated (see % pp. 230–1).
• NSAIDs: continue to enable early mobilisation. Stop if postoperative
bleeding is a potential problem, hypotension or deterioration in renal
function.
• DMARDs: these drugs include gold, penicillamine and
immunosuppressant drugs such as methotrexate, azathioprine,
cyclophosphamide, ciclosporin, leflunomide and sulfasalazine. Continue
as little evidence that omission reduces postoperative complications
(wound infections). If leucopenic or for high-risk procedures, consult
with the rheumatologist.
248
Ankylosing spondylitis
Inflammatory arthritis of the sacroiliac joints and spine, leading to ankylosis
and ‘bamboo spine’. Associated with HLA-B27 in >90% of cases. More
common in ♂, with peak age onset in the 3rd decade.
Articular
• Progressive kyphosis and fixation of the spine may hinder intubation.
Conventional intubation and tracheostomy may be impossible.
Atlantoaxial subluxation and myelopathy can occur rarely. There may
be limited mouth opening from temporomandibular involvement.
Use of intubating laryngeal mask airway (LMA) or videolaryngoscopy
described, but fibreoptic intubation usually preferred.
• At risk of occult cervical fracture with minimal trauma, so ensure the
head is supported and not left self-supporting.
• Cricoarytenoid arthritis may make cords susceptible to trauma and
oedema.
• Spinal anaesthesia is often difficult; consider using a paramedian
approach. Possible i risk of epidural haematoma with epidural block.
• Restrictive pulmonary disease from diminished chest expansion and
spinal mobility. Effective external cardiac massage may be impossible.
• Deformity leads to difficulty with positioning, particularly if a prone
position is required.
Non-articular
• Apical fibrosis, which contributes to the restrictive lung defect.
• AR (1%). Mitral valve involvement and conduction defects are rare.
• Amyloid may cause renal involvement.
• Cauda equina syndrome may occur in long-standing cases.
• Side effects of NSAIDs and biological and non-biological DMARDs (see
% pp. 247–8 and pp. 1155–6).
250
Scoliosis
Progressive lateral curvature of the spine with added rotation. Scoliosis may
lead to an increasing restrictive ventilatory defect which, in turn, leads to
hypoxia, hypercapnia and pulmonary hypertension. Scoliosis may be idio-
pathic (775%) or 2° to other conditions with anaesthetic implications:
• Muscular dystrophies
• Poliomyelitis
• Cerebral palsy
• Friedreich’s ataxia
• Marfan syndrome and Ehlers–Danlos syndrome.
Conduct of anaesthesia
• Formal PFTs. Cobb angle exceeding 65° is likely to be associated with
compromised respiratory function.
• Check for pulmonary hypertension and right heart failure.
• Some muscular dystrophies may be associated with cardiac
abnormalities. Consider echocardiography (see % p. 318).
• May be difficult laryngoscopy.
• Neuraxial anaesthesia more difficult.
• Intraoperative spinal cord monitoring is recommended for all spinal
deformity corrective surgery (see % pp. 629–33).
• Invasive arterial monitoring and potential significant blood loss.
• Multimodal analgesia, including regional techniques (e.g. paravertebral
blocks) where possible.
• Plan for high dependency or intensive care in complex cases.
25
Achondroplasia
The commonest form of dwarfism is caused by premature ossification of
bones, combined with normal periosteal bone formation, giving a charac-
teristic appearance of short limbs and a relatively normal cranium. The fol-
lowing should be noted:
• Large head and tongue, mid-facial hypoplasia, obesity and small
larynx may lead to difficulties managing the airway. Laryngoscopy may
additionally be compromised by pectus carinatum.
• Foramen magnum stenosis is common. Avoid hyperextension during
intubation.
• Central and peripheral venous access is often difficult.
• Use an appropriately sized BP cuff.
• OSA is common (see % pp. 73–5).
• Restrictive ventilatory defects may occur and can lead to pulmonary
hypertension.
• Regional techniques may be difficult.
• The back may be normal. The epidural space is often narrowed with
spinal canal stenosis. The volume of LA needed for a subarachnoid
and epidural block is reduced. Epidural over spinal anaesthesia may be
preferred due to ability to titrate to desired height.
• The patient is of normal intelligence.
Further reading
Holroyd CR, Seth R, Bukhari M, et al. (2019). British Society for Rheumatology biologic DMARD
safety guidelines in inflammatory arthritis. Rheumatology, 58, 220–6.
Spiegel J, Hellman M (2015). Achondroplasia: implications and management strategies in anesthesia.
Anaesthesia News. M https://www.anesthesiologynews.com/Review-Articles/Article/10-15/
Achondroplasia-Implications-and-Management-Strategies-in-Anesthesia/33892/ses=ogst
Samanta R, Shoukrey K, Griffiths R (2011). Rheumatoid arthritis and anaesthesia. Anaesthesia, 66,
1146–59.
Ben-Menachem E (2010). Systemic lupus erythematosus: a review for anesthesiologists. Anesth Analg,
111, 665–76.
Woodward LJ, Kam PCA (2009). Ankylosing spondylitis: recent developments and anaesthetic im-
plications. Anaesthesia, 64, 540–8.
Mitra S, Nilanjan D, Gomber K (2007). Emergency caesarian section in a patient with achondroplasia:
an anaesthetic dilemma. J Anesth Clin Pharmacol, 23, 315–18.
Chapter 11 253
Haematology
Peter Valentine and Pete Ford
Anaemia 254
Sickle-cell disease 257
Porphyria 260
Rare blood disorders 263
Disorders of coagulation 265
Haemophilia and related disorders 267
Thrombocytopenia 268
Anticoagulants 269
Antiplatelet drugs 277
Fibrinolytic drugs 280
Haemostatic drug therapy 281
Disseminated intravascular coagulation 283
Coagulation tests 284
Hypercoagulability syndromes 288
254
Anaemia
Anaemia is defined as Hb below normal for age and sex. Conventionally,
this is <130g/dL in an adult ♂ and <120g/dL in an adult ♀. Common
causes of anaemia in the surgical patient are:
• Blood loss: acute or chronic (usually resulting in iron deficiency)
• Bone marrow failure: infiltration by tumour or suppression by drugs
• Megaloblastic anaemias: folate or vitamin B12 deficiency
• Complex anaemias: effects on production and breakdown, e.g. renal
failure, RA and hypothyroidism
• Haemolytic anaemias: either inherited (thalassaemia, sickle-cell disease
(SCD), spherocytosis) or acquired (autoimmune, drugs, infections), or
physical (mechanical heart valves, disseminated intravascular coagulation
(DIC), prolonged marching known as ‘march haemoglobinuria’).
• Chronic disease or inflammation leads to i hepcidin release from the
liver which inhibits iron absorption from the gut despite normal to high
ferritin. Unlikely to respond to oral iron therapy.
Clinical
• Associated with fatigue, dyspnoea, palpitations, headaches and angina.
Severity often reflects the speed of onset more than the degree of
anaemia, as there is less time for adaptation.
• Common causes should be elicited, including relevant family history;
always enquire about NSAIDs and alcohol.
• Respiratory and cardiovascular pathology may be worsened by the
anaemia or make its impact greater.
Investigations
• Measure Hb prior to surgery in appropriate patients (see % p. 28),
including all those at risk of anaemia undergoing major surgery and
patients with significant comorbidities, especially heart or lung
disease.
• Much can be deduced from Hb and mean corpuscular volume (MCV)
alone but in many instances a blood film gives additional useful
information.
• Confirmatory tests, such as ferritin, cobalamin (B12) and folate levels,
reticulocyte count, direct Coombs’ test, erythrocyte sedimentation rate
(ESR), liver and renal function and bone marrow cytology, should be
requested, as appropriate.
Preparation
Patients scheduled for elective surgery should have FBC checked in the
weeks approaching the operation so that abnormalities can be investigated
and corrected in time (Fig. 11.1).
• Where surgery can be safely postponed, it is more appropriate and
safer to treat the underlying cause and raise the Hb slowly with simple,
effective measures, e.g. PO or IV iron and B12 injections. Transfusing a
patient with pernicious anaemia may precipitate heart failure.
Fig. 11.1 Algorithm for classification of perioperative anaemia. Reproduced from Klein AA, et al. (2016). International consensus
statement on the peri-operative management of anaemia and iron deficiency. Anaesthesia, 72, 233–47, with permission from John Wiley &
Anaemia
IV iron preparations are now available that can be given over a few min-
utes and will render a patient immediately iron-replete; typical Hb increase
10–20mg/L after 10d (see also % pp. 54–6).
• Many IV preparations exist. A common preparation is iron isomaltoside
(Monofer®); a single dose of 20mg/kg (typically 1000mg) will render a
patient iron-replete with a 15min infusion and with minimal side effects.
Check your local protocol or discuss with a haematologist.
Perioperative blood transfusion
(See also % pp. 450–9.)
Recent RCTs have confirmed that transfusion is not required for mild an-
aemia, even in the presence of CVS disease. In some of these trials, the use
of a lower ‘transfusion trigger’ has been associated with lower mortality.
Coexisting disease, chronicity of anaemia and the expected perioperative
blood loss all inform the decision of whether to transfuse or not. The fol-
lowing are accepted levels for transfusion:
• Red cell transfusion is indicated if the Hb level is <70g/L.
• Checking a HemoCue® gives comparable results to a Coulter counter
and can help to avoid a transfusion if >80g/L.
• For patients with IHD:
• Mild (angina rarely): accept Hb 70–80g/L
• Moderate (angina regularly, but stable): accept Hb 80–90g/L
• Severe (recent MI, unstable angina): accept Hb 100g/dL or higher.
Sickle-cell disease 257
Sickle-cell disease
Sickle-cell disease (SCD) is caused by inheriting sickling haemoglobinopathies,
either in the homozygous (HbSS; sickle-cell anaemia) or heterozygous
(HbAS; sickle-cell trait) state, or in combination with another Hb β chain
abnormality such as Hb C (HbSC disease), Hb D (HbSD disease) or β-
thalassaemia (HbS/β-thal). It is estimated that there are now over 15
000 patients with SCD in Britain. SCD is endemic in parts of Africa, the
Mediterranean, the Middle East and India. The highest incidence is from
equatorial Africa; all patients from areas with a high prevalence should have
a sickle test preoperatively.
The pathology of SCD is primarily a result of vaso-occlusion by sickled
red cells, leading to haemolysis and tissue infarction. This can be precipi-
tated by hypoxia, hypothermia, pyrexia, acidosis, dehydration or infection.
Other variant haemoglobins Hb C and Hb D-Punjab, in association with
HbS, enhance the sickling process, whereas HbF (fetal Hb) impedes it.
• Susceptibility to sickling is proportional to the concentration of
HbS. In the heterozygous state (sickle-cell trait), sickling is extremely
uncommon as HbS concentration is <50%.
• These patients have a positive sickle solubility test (Sickledex®),
but normal blood film and Hb level. This can be confirmed by Hb
electrophoresis or, in an emergency, a normal blood film should suffice.
• These patients do not need special treatment, other than avoidance of
extreme hypoxia, dehydration, infection, acidosis and hypothermia.
Clinical features
The manifestations of SCD do not become apparent before 3–4mo of age,
when the main switch from fetal to adult Hb occurs.
• There is great variability, not only between patients, but also within
individual patients at different periods of life. Many remain well most of
the time.
• Vaso-occlusive crises are the commonest cause of morbidity and
mortality. The presentation may be dramatic with an acute abdomen,
‘acute chest syndrome’ (acute pneumonia-like), CVE, priapism and
painful dactylitis. By the time patients reach adulthood, most will
have small, fibrotic spleens and are functionally asplenic, with the
associated risk of overwhelming septicaemia. A less acute complication
is proliferative retinopathy due to retinal vessel occlusion and
neovascularisation (more common in HbSC disease).
• Aplastic crises are characterised by temporary shutdown of the
marrow, manifested by a precipitous fall in Hb and an absence of
reticulocytes. Infection with parvovirus B19 and/or folate deficiency are
the two precipitating factors.
• Sequestration crises occur mainly in children. Sudden massive pooling of
red cells in the spleen can cause hypotension and severe exacerbation
of anaemia, with fatal consequences, unless transfusion is given in time.
• Haemolytic crises manifest by a fall in Hb and a rise in reticulocytes/
bilirubin, and usually accompany vaso-occlusive crises. Chronic
haemolysis leads to gallstones in virtually all patients with SCD, though
many remain asymptomatic.
258
Laboratory features
• Hb is usually 6–9g/dL (often lower than suggested by the clinical
picture). Reticulocytes are almost always i, and the film shows sickled
cells and target cells. Howell–Jolly bodies are present if the spleen
is atrophic. Leucocytosis and thrombocytosis are common reactive
features. In the sickle-cell trait, the Hb and film are normal.
• Screening tests for sickling which rely on deoxygenation of HbS are
positive in both HbSS and HbAS.
• Hb electrophoresis distinguishes SS, AS and other haemoglobinopathies.
Measurement of the HbS level is important in certain clinical situations
where a level of <30% is aimed for. It is not necessary to wait for the
results of electrophoresis before embarking on emergency surgery.
Clinical history, Hb level, a positive sickle test and the blood picture
usually allow distinction between SCD and the sickle-cell trait.
Management
As no effective routine treatment exists for SCD, care is directed towards
prophylaxis, support and treatment of complications. Folic acid supple-
ments, pneumococcal and Haemophilus influenzae type b (Hib) vaccinations
and penicillin prophylaxis (to protect from the susceptibility to infection
caused by d splenic function) are recommended from an early age, prefer-
ably within a comprehensive care programme.
• For crises: rest, rehydration with PO/IV fluids, antibiotics if infection is
suspected; maintain PaO2; keep warm; prompt and effective analgesia
(traditionally diamorphine/morphine is used over pethidine; regional
anaesthesia very effective).
• Blood transfusions may be lifesaving, but the indications are limited.1
Exchange transfusions have a role in some vaso-occlusive crises (acute
chest syndrome, CVE). Always discuss with a haematologist. For
patients with high perioperative risk, transfusing to achieve an HbS level
of <30% may decrease complications but is controversial.
Preoperative preparation
Always seek expert advice from a haematologist well before surgery. A
sample for group and antibody screening should be sent well in advance,
as previously transfused sickle-cell patients often have red cell antibodies.
Perioperative and postoperative care
Special attention must be given to hypoxia, dehydration, infection, acidosis,
hypothermia and pain. These considerations should be continued well into
the postoperative period.
• Dehydration: allow oral fluids as late as possible, and pre-and
postoperative IV fluids.
• Hypoxia: pulse SpO2 and prophylactic O2.
• Prophylactic antibiotic cover should always be considered because of
i susceptibility to infection.
• Positive pressure ventilation may be required to achieve normocapnia
and avoid acidosis.
• Hypothermia should be avoided by warming the operating room,
using a fluid warmer and active warming such as a Bair Hugger®. Core
temperature should be monitored.
• Regional anaesthesia is not contraindicated, and tourniquets can be
used if limbs are meticulously exsanguinated prior to inflation.
Sickle-cell disease 259
HbSC disease
• Results from compound heterozygosity for HbS and HbC.
• Affects 0.1% of African Americans.
• Causes SCD, but phenotype may be milder than homozygous HbSS.
• Patients develop anaemia, splenomegaly, jaundice, aseptic necrosis of
the femoral head, hepatic disease, retinal disease and bone marrow and
splenic infarcts.
• Myocardial necrosis has been described after GA.
• Management principles are as for SCD.
• Patients with HbSC disease are more prone to retinal disease and often
maintain splenic function into adult life.
260
Porphyria
The porphyrias are a group of diseases in which there is an enzyme defect
in the synthesis of the haem moiety, leading to an accumulation of pre-
cursors that are oxidised into porphyrins. There are hepatic and erythro-
poietic varieties. There are eight different forms of porphyria. There are
three autosomal dominant acute hepatic forms, with typically 50% reduc-
tion in usual enzyme activity, that affect the administration of anaesthesia.
Acute intermittent porphyria
The commonest and most severe form of acute porphyria. Common in
Sweden. i urinary porphobilinogen and d-aminolaevulinic acid.
Variegate porphyria
Common in Afrikaners. i Copro-and protoporphyrin in the stool. Dermal
photosensitivity.
Hereditary coproporphyria
Very rare. i urinary porphyrins. Dermal photosensitivity.
Porphyric crises
• Attacks occur most frequently in women in the 3rd to 4th decades.
• Fifty per cent of normal enzyme activity is usually enough to maintain
haemostasis. i demand for haem increases flow through pathway and
increases aminolaevulinic acid and porphyrin production, leading to
symptoms. Factors increasing haem demand, including haemorrhage,
induction of P450 enzymes, stress and dehydration, should be avoided.
• Acute porphyric crises may be precipitated by drugs, stress, infection,
alcohol, menstruation, pregnancy, starvation and dehydration.
• Symptoms include acute abdominal pain, vomiting, motor and sensory
peripheral neuropathy, autonomic dysfunction, cranial nerve palsies,
mental disturbances, coma, convulsions and pyrexia.
General principles
• Patients may never have had an attack; therefore, a positive family
history must be taken seriously.
• Individuals may have normal biochemical tests between attacks.
• Patients may present with unrelated pathology, e.g. appendicitis.
• Symptoms may mimic surgical pathologies, e.g. acute abdominal pain,
acute neurology.
• Any patient giving a strong family history of porphyria must be treated
as potentially at risk. Latent carriers may exhibit no signs and be
potentially negative to biochemical screening, but still be at risk from
acute attacks.
Anaesthetic management
Many commonly used drugs are thought to have the potential to trigger
porphyric crises. However, it is difficult to be definitive, as crises can also be
triggered by infection or stress, which often occur simultaneously. Table 11.1
lists the relative safety of commonly used anaesthetic drugs in patients with
porphyria. The website M www.drugs-porphyria.org contains more com-
plete and up-to-date prescribing information.
Porphyria 261
Disorders of coagulation
(For regional anaesthesia and coagulation abnormalities, see % p. 1110.)
The classic description of the clotting cascade was initially proposed in
1964 by Macfarlane and was generally accepted for over 50y. This histor-
ical description involves two pathways, an extrinsic pathway and an intrinsic
pathway, that both converge on a common pathway which leads to the for-
mation of a fibrin clot. Both pathways are complex and involve sequential
proteolytic activation of proenzymes by plasma proteases (clotting factors),
resulting in the formation of thrombin, which then splits the fibrinogen mol-
ecule into fibrin monomers.
With further advances in the knowledge of in vivo blood coagulation, a
cell-based model of coagulation was developed, proposing that coagulation
takes place on different cell surfaces in four overlapping steps:
• Initiation
• Amplification
• Propagation
• Termination.
The cell-based model allows a more thorough understanding of how coagu-
lation works in vivo and sheds light on the pathophysiological mechanism for
certain coagulation disorders. Congenital disorders of clotting may not be
present until challenged by trauma or surgery in adult life.
• Acquired disorders are due to d synthesis of coagulation factors,
i consumption (e.g. DIC, massive blood loss) and i production of
substances that interfere with factor function.
• A family history may be elicited—haemophilia A and B (sex-linked
recessive), von Willebrand’s disease (autosomal dominant with variable
penetrance)—but cannot be relied upon. Family history is absent in 30%
of haemophilia cases.
• Response to previous haemostatic challenges (tonsillectomy, dental
extractions) may indicate the severity of the coagulopathy; for
example, in severe haemophilia A (factor VIII <2%), bleeding occurs
spontaneously; in mild haemophilia A (factor VIII 5–30%), bleeding
occurs only after trauma.
• Concurrent and past medical problems, such as liver disease,
malabsorption (vitamin K deficiency), infection, malignancy (DIC) and
autoimmune disease (SLE, RA), as well as medications (anticoagulants,
aspirin and NSAIDs), may be relevant.
• Abnormalities due to liver disease and vitamin K deficiency; give
daily vitamin K (phytomenadione) 10mg IV slowly. FFP (15mL/kg)
may be needed, in addition, if the presenting symptom is bleeding.
Coagulation tests may be misleading in the presence of liver disease,
overemphasising the bleeding risk; consider using TEG® to evaluate the
true underlying coagulopathy.3
For blood test results in common coagulation disorders, see Table 11.3.
26
Thrombocytopenia
Defined as a platelet count <150 × 109/L.
• Spontaneous bleeding is uncommon, until the count is < 20 × 109/L.
Causes of thrombocytopenia include:
• Failure of platelet production: selective (hereditary, drugs, alcohol,
viral infection) or general marrow failure (aplasia, cytotoxic drugs,
radiotherapy, infiltration, fibrosis, myelodysplasia, megaloblastic
anaemia)
• i platelet consumption: with an immune basis (idiopathic
thrombocytopenic purpura (ITP), drugs, viral infections, SLE,
lymphoproliferative disorders) or without an immune basis (DIC, TTP,
cardiopulmonary bypass)
• Dilution, following massive transfusion of stored blood
• Splenic pooling (hypersplenism).
Preoperative preparation
Unexplained thrombocytopenia should be investigated before elective
surgery, as the appropriate precautions will be determined by the
underlying cause.
• Minor procedures may be performed without platelet support,
provided adequate pressure is applied to the wound.
• For invasive procedures such as central line insertion, transbronchial
biopsy, liver biopsy or laparotomy, platelets should be >50 × 109/L.
• For epidural or spinal anaesthesia, a platelet count of 80 × 109/L is
adequate (see % p. 841).
• For operations in critical sites, such as the brain or eyes, the platelet
count should be raised to 100 × 109/L.
• In ITP, platelet transfusions should be reserved for major haemorrhage,
since platelet survival is extremely short-lived. Preparation for surgery
entails the use of steroids or high-dose immunoglobulins initially.
• In TTP, platelets are relatively contraindicated. Treatment should consist
of plasma or plasma exchange, steroids and, where platelets >50 ×
109/L, LMWH and aspirin.4
Postoperative management
If microvascular bleeding continues, despite a platelet count of >50 × 109/
L, suspect DIC. If confirmed by coagulation tests, give FFP and cryoprecipi-
tate, as appropriate.
• IM injections, aspirin and NSAIDs should be avoided.
• Desmopressin 0.3 micrograms/kg in 50–100mL of 0.9% sodium
chloride over 30min may improve platelet function in renal failure.
Anticoagulants 269
Anticoagulants
Anticoagulants are used to reduce thromboembolic risk. However, in pa-
tients requiring surgery, they i the risk of major bleeding. It is important
to know the indication for anticoagulation and weigh the risk of VTE if it is
stopped vs the risk of significant bleeding if it is continued.
The commonest indications for anticoagulation are AF, mechanical heart
valves, previous VTE, thrombophilia, cancer or other prothrombotic state.
Of these, AF is the commonest. Based on current evidence, patients are
now treated with a broad range of anticoagulants based on their own in-
dividual risk factors. Direct oral anticoagulants are now generally favoured
over warfarin.5 A meta-analysis of 12 studies in 2015 showed an overall
improvement in CVE prevention, a reduction in intracranial haemorrhage
and a reduction in mortality when direct oral anticoagulants were used,
compared to warfarin, for patients with AF and one other risk factor.6 They
also require no monitoring, unlike warfarin.
CHA2DS2-VASc
AF increases a patient’s risk of CVE and the CHA2DS2-VASc score is used to
quantify this risk (Table 11.4). It is used to inform the discussion regarding the
risks and benefits of long-term anticoagulation. Patients are scored 0–9. The
score is also an indication of annual CVE risk (e.g. score of 1 = annual CVE
risk 1.3%; score of 4 = annual CVE risk 4%; score of 9 = annual CVE risk of
15.2%). Anticoagulation should be considered in anyone with a score of ≥1
(except when the only risk factor is ♀ sex), although antiplatelets may suffice
with scores ≤2. A balanced decision for treatment must also include assess-
ment of the patient’s annual risk of a major bleed 2° to the anticoagulation.
Perioperative risk
Weighing up the risks of stopping anticoagulation or not requires know-
ledge of the surgery and how likely major or significant blood loss is, as well
as a calculation of the patient’s thrombotic risk.
Surgical bleeding risk is divided into:
• Low risk (e.g. dental and minor skin procedures)
• Moderate risk (e.g. general surgery, joint replacement, genitourinary or
maxillofacial surgery)
• High risk, both of bleeding or bleeding into an enclosed space (cardiac,
complex general, vascular, posterior chamber ophthalmic, spinal and
intracranial surgery).
270
Condition Points
C Congestive heart failure (or LV systolic dysfunction) 1
H Hypertension: BP consistently above 140/90mmHg (or treated 1
hypertension on medication)
A2 Age ≥75y 2
D Diabetes mellitus 1
S2 Prior CVE or transient ischaemic attack or thromboembolism 2
V Vascular disease (e.g. peripheral artery disease, myocardial 1
infarction, aortic plaque)
A Age 65–74 1
Sc ♀ sex 1
Reprinted from Chest, 137, Lip G, Refining clinical risk stratification for predicting stroke and
thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart
Survey on atrial fibrillation, 263–72, Copyright © 2010, with permission from The American
College of Chest Physicians. Published by Elsevier Inc.
As a general rule, the risk from a major perioperative bleeding event is likely
to be less than that from thrombosis. Consider, for example, that the risk
of major bleeding on antithrombotic agents is estimated at 6–10%, whereas
the mortality associated with:8
• Embolic CVE is 37%
• Mechanical heart valve thrombosis is 17.5%
• VTE (DVT or PE ) is 5–10%.
Fig. 11.2 illustrates perioperative management of a warfarinised patient
relative to surgical bleeding risk and their risk of VTE.
• If using continuous IV infusion (IVI) of UFH for patients with a high risk
of bleeding, start at 1000 units/h and adjust to keep the APTT between
1.5 and 2.5 (Fig. 11.2).
• Direct oral anticoagulants do not require bridging, but timing of the last
preoperative dose is variable and covered later in the chapter.
• It is worth noting that the perioperative risk of arterial
thromboembolism in patients who have AF and no anticoagulation
is 71%.
• Perioperatively, additional methods of VTE prophylaxis should be
considered (e.g. compression stockings and pumps) in all patients at risk
of VTE despite anticoagulation (see % pp. 59–61).
Timing of surgery
Consider whether the surgery can be delayed in order to reduce the risk of
VTE and associated morbidity and mortality.
• Prematurely stopping anticoagulation after VTE within the 1st month
confers an estimated 30d risk of recurrent VTE of 40%. This falls to an
annual risk of 15% after 3mo.
• Vena cava filters should be considered in patients who have had VTE
<4w ago and require interruption of their anticoagulation or in whom
postoperative anticoagulation may be delayed >12h.
Warfarin
Warfarin, a vitamin K antagonist, was the original anticoagulant used in
patients with AF and remains the only treatment with established safety
for patients with AF and rheumatic heart disease and/or mechanical heart
valve prosthesis.
• Warfarin results in synthesis of non-functional vitamin K-dependent
factors (II, VII, IX and X, proteins C and S), prolonging PT, but may take
up to 48h to become effective.
• Warfarin is highly effective but has a narrow therapeutic window,
requiring regular testing and dose adjustment.
• Warfarin is associated with haemorrhagic CVE, and intracranial and GI
haemorrhage.
• The INR compares a patient’s PT to a control, indicating the degree of
anticoagulation.
• It reduces the risk of CVE by 67% and mortality by 25%, compared with
control (aspirin or no therapy).
• Once the INR is <2, alternative pre-and postoperative prophylaxis
should be considered.
Recommended INR targets
• INR 2–2.5 for prophylaxis of DVT
• INR 2.5 for treatment of DVT/PE, prophylaxis in AF and
cardioversion
• INR 3.5 for recurrent DVT/PE or mechanical heart valves
Antiplatelet drugs
Antiplatelet drugs decrease platelet aggregation and inhibit thrombus for-
mation in the arterial circulation where anticoagulants have little effect.
Their indications include 1° or 2° prevention of CVE and CVS disease.
There are now many antiplatelet medications available, some of which are
summarised in Table 11.7.10
Aspirin
Aspirin irreversibly acetylates the active site of cyclo-oxygenase (COX) 1
(2 at higher doses), which blocks the production of thromboxane A2, a
powerful promoter of platelet aggregation. Recovery of platelet function
requires formation of new platelets. Low-dose aspirin is a mainstay for 2°
prevention of thrombotic vascular events in vascular and cardiac disease.
Also used in angina, post-coronary artery bypass surgery, intermittent clau-
dication, AF and 1° prevention of IHD. Once stopped, it takes around 7–
9d for platelet function to return to normal. This risk of bleeding must be
balanced against the possibility of precipitating a thromboembolic event,
particularly in patients with unstable angina.
Dipyridamole
A nucleoside transport and phosphodiesterase inhibitor, dipyridamole is an
antiplatelet and a vasodilator. It is used in 2° prevention of CVE or with
low-dose aspirin for post-coronary artery surgery and valve replacement. It
has an elimination half-life of 10h. There is variability in the literature as to
when, if at all, dipyridamole needs to be stopped prior to surgery. The AoA
states that it does not need to be stopped at all prior to regional blocks, but
other sources recommend it should be stopped anywhere from 24h to 7d.
Check your local policy.
Adenosine diphosphate/P2Y12 inhibitors
P2Y12 is the chemoreceptor responsible for adenosine diphosphate (ADP)
stimulation of the glycoprotein IIb/IIIa receptor. Stimulation of IIb/IIIa re-
ceptors leads to enhanced platelet degranulation, thromboxane release
and prolonged platelet aggregation. Antagonism of the P2Y12 receptor may
be irreversible with clopidogrel or prasugrel, or reversible with ticagrelor
or cangrelor. Often used with aspirin as DAPT for acute coronary syn-
drome, but also after PCI, CABG, AF in patients unable or unwilling to
take anticoagulants, CVE (not prasugrel) and peripheral vascular disease.
Clopidogrel remains the commonest agent, but guidelines are continu-
ally being revised. Recent evidence suggests that prasugrel and ticagrelor
may be more effective than clopidogrel, but with a higher risk of bleeding.
Cangrelor is given IV and may be an option for patients requiring PCI who
have not been loaded with oral therapy.
Glycoprotein IIb/IIIa inhibitors
These medications compete with fibrinogen and vWF for IIb/IIIa receptors.
They prevent both platelet crosslinking and platelet-derived thrombus for-
mation. They are all given IV and are potent inhibitors of platelet activity.
Abciximab is a large monoclonal antibody with a high affinity for binding
to the glycoprotein IIb/IIIa receptor. It has the longest duration of action
and has a UK licence as an adjunct to aspirin and UFH in PCI. While its
biological half-life is 12–24h, due to slow clearance, its functional half-life is
278
Fibrinolytic drugs
These drugs act as thrombolytics by activating plasminogen to plasmin; this
degrades fibrin and therefore dissolves thrombi.
• Newer drugs, such as reteplase and tenecteplase, are given by bolus
injection, making them ideal for early community injection.
• Alteplase (recombinant tissue plasminogen activator (rt-PA)) and
streptokinase are given by continuous infusions.
• Used for AMI where benefits outweigh risks, e.g. when PCI not
available.
• Benefit greatest with early injection, ECG changes with ST-elevation or
new bundle branch block and anterior infarction.
• Alteplase, reteplase and streptokinase need to be given within 12h
of symptom onset, ideally within 1h; use after 12h requires specialist
advice. Tenecteplase should be given as early as possible and usually
within 6h of symptom onset.
• Should be used in combination with antithrombin (LMWH) and
antiplatelet (aspirin) therapy to reduce early reinfarction.
• Alteplase, streptokinase and urokinase can be used for other
thromboembolic disorders such as DVT and PE. Alteplase is also used
for acute ischaemic CVE. Treatment must be started promptly.
• Contraindications include any risk of bleeding, especially trauma
(including prolonged CPR), recent surgery and GI tract and intracerebral
pathology.
• Streptokinase can cause allergic reactions and should be used only once.
Antibodies can inactivate the drug.
• Serious bleeding calls for the discontinuation of therapy and may require
coagulation factors. Cryoprecipitate (high levels of factor VIII and
fibrinogen) and FFP (factors V and VIII), as well as platelets, may all be
required. Antifibrinolytic drugs, such as aminocaproic acid or tranexamic
acid, may also be useful.
• Bleeding times are prolonged for up to 24h after these drugs. In
emergency surgery, reversal will be required.
• Urokinase is also licensed to restore the patency of occluded IV
catheters and cannulae blocked with fibrin clots. Inject directly into the
catheter or cannula 5000–25 000 units dissolved in a suitable volume
of 0.9% sodium chloride to fill the catheter or cannula lumen; leave for
20–60min, then aspirate the lysate; repeat, if necessary.
Haemostatic drug therapy 281
Factor VIIa
Recombinant factor VIIa (rFVIIa) acts at the ‘tissue factor–factor VIIa’ com-
plex at the site of endothelial damage.
• This effect appears localised to the area where the vessel is damaged,
leading to few systemic side effects.
• Numerous case reports have shown rFVIIa to have potent haemostatic
effects, even when other treatments have failed, regardless of the cause
of bleeding. Its use to stop bleeding during operations is off-licence,
however. These potential benefits have to be weighed up against
its thrombogenic risk; a Cochrane review (updated February 2011)
concluded the data supporting the off-licence use of rFVIIa were weak,
and the use of rFVIIa outside its current licensed use—haemophilia and
inhibitory alloantibodies and for prophylaxis and treatment of patients
with congenital factor VII deficiency—should be restricted to clinical
trials.
• Dosing and mode of delivery (IV bolus or continuous infusion) have still
not been established (20–40 micrograms/kg has been used).
Prothrombin complex concentrates
Dried prothrombin complex is prepared from human plasma and contains
factor IX, together with variable amounts of factors II, VII and X. Often
referred to as 4-factor PCC.
• Indications are treatment and prophylaxis of congenital or acquired
deficiency of factors II, VII, IX and X (such as during warfarin
treatment).
• Contraindications are angina, recent MI and history of HIT.
• Side effects include thrombosis and hypersensitivity, including
anaphylaxis.
Disseminated intravascular coagulation 283
Coagulation tests
Standard laboratory coagulation tests typically look at isolated areas of the
clotting cascade and can be related to intrinsic and extrinsic pathways in the
classical coagulation model. In the bleeding coagulopathic patient, pH, tem-
perature and ionised Ca2+ can also be measured for correction.
• PT: the time in s for clot to form, following addition of thromboplastin
and Ca2+ to citrated plasma. Detects deficiencies or inhibitors of factors
II, V, VII and X, and fibrinogen. Normal range: 11–13.5s.
• INR: comparison of PT with laboratory reference sample to allow easy
standardisation. Detects deficiencies or inhibitors of factors II, V, VII and
X, and fibrinogen. Used for monitoring warfarin. Normal range: 0.8–1.1.
• APTT: time for clot to form after an intrinsic factor activator (i.e. kaolin)
and Ca2+ added to citrated plasma. Detects deficiencies or inhibitors of
factors XII, XI, X, IX, VIII, V and II, and fibrinogen. Normal range: 25–35s.
• Fibrinogen: usually calculated from a coagulation assay, e.g. Clauss assay
(thrombin added to dilute plasma until clot forms). Normal range: 2–4g/L.
POCT provides rapid and accurate information typically in theatre or the
ICU, allowing targeted, rather than empirical, treatment. There are three
main types of point-of-care coagulation testing:
• Coagulation time analysers, e.g. PT/APTT/ACT
• Viscoelastic clot strength analysers, e.g. TEG® and ROTEM®
• Platelet function analysers.
Coagulation time analysers
• PT and APTT can be measured by a small portable analyser. A drop of
whole blood is added to a cuvette. This can be useful for monitoring
warfarin status or heparin therapy.
• ACT is used in patients treated with high concentrations of UFH. A
drop of whole blood is added to a cuvette and the sample activated
using kaolin or celite. Often used in CPB surgery. Normal range: 70–
120s. For CPB, the target ACT is usually in the range of 400s.
Viscoelastic tests: thromboelastography/
thromboelastometry
Two analysers TEG® and ROTEM® are available and measure the
strength and elastic properties of clotting whole blood. TEG® uses
thromboelastography, while ROTEM® uses rotational thromboelastometry.
These viscoelastic tests give functional information on the time taken for
clot formation to begin, the speed and strength of clot formation and clot
lysis. Unfortunately, the standard tests are unable to test platelet function.
The potent platelet activation by thrombin overwhelms the effects of the
weaker platelet activators (ADP and arachidonic acid) on which antiplatelet
medications work. Newer Platelet Mapping Assays can be used with some
viscoelastic tests to allow assessment of antiplatelet drugs.
Techniques to assess the viscoelastic properties of clotting can involve
a rotating cup into which a wire is inserted, a spinning wire in a cup and,
more recently, subjecting the blood to vibration whereby the vertical move-
ment of the blood meniscus is measured under LED illumination. A number
of different reagents are used in both techniques, but no matter the tech-
nique, the same trace is produced which facilitates targeted correction of
coagulopathy (Fig. 11.3). The nomenclature and normal values differ be-
tween the two techniques (Table 11.8).
Coagulation tests 285
TEG®
TEG® uses kaolin as the reagent and tests the intrinsic pathway.
• Rapid TEG® (rTEG®) takes just 15min, compared with over 30min
for a standard trace, and uses kaolin and tissue factor to activate the
extrinsic pathway, which speeds up the test. In this test, the R-value is
replaced by the TEG-ACT value which is measured in s, rather than in
minutes. The remainder of the TEG parameters do not differ from the
standard test.
• Functional fibrinogen includes tissue factor and a platelet inhibitor
(abciximab) which removes the platelet contribution to clot strength, so
that the fibrinogen component can be seen independently.
• Platelet Mapping is a new addition to the TEG® repertoire and is
explained below.
ROTEM®
ROTEM® has a number of different tests:
• INTEM uses phospholipid and ellagic acid to test the intrinsic pathway
and is similar to APTT.
• EXTEM also uses tissue factor to test the extrinsic pathway and is
similar to PT.
• FIBTEM uses a platelet inhibitor (cytochalasin D) to inhibit the platelet
contribution and isolate the fibrinogen contribution to clot strength.
• HEPTEM is essentially the same as INTEM, but with the addition of
heparinase which eliminates heparin from the sample, uncovering any
other underlying coagulopathy.
• APTEM uses aprotinin to rule out excessive fibrinolysis which could be
an indication for tranexamic acid.
• ECATEM is prolonged in patients on direct thrombin inhibitors. Using
ecarin, a prothrombin activator, it is similar to the ecarin clotting
time test.
286
TEG® ROTEM®
Clotting time (time to R 4–8min
*
CT:
2mm amplitude) INTEM** 137–246s
EXTEM** 42–74s
Clot kinetics (2–20mm K* 1–4min CFT:
amplitude) INTEM** 40–100s
EXTEM** 46–148s
Clot strength (α angle) α* 47–74° INTEM** 71–82°
EXTEM** 63–81°
Maximum strength MA* 55–73mm MCF:
INTEM** 52–72mm
EXTEM** 49–71mm
Clot lysis CL30, CL60 LI30, ML
*
Kaolin activated.
**
Citrated.
CFT, clot formation time; CL30, clot lysis at 30min; CL60, clot lysis at 60min; CT, clotting time;
K, kinetics; LI30, lysis index at 30min; MA, maximum amplitude; MCF, maximum clot firmness;
ML, maximum lysis; R, reaction time.
Interpretation
Interpretation of a ROTEM® or TEG® is similar to learning how to interpret
an ECG. A stepwise approach is used initially and later pattern recognition
(Fig. 11.4).
Prolongation of clotting time/clot formation time or reaction/kinetics times
Has the patient had heparin? A HEPTEM assay will be able to rule this out.
If heparin has been given and reversal is required, consider protamine. If no
heparin, the results are due to clotting deficiencies, so consider FFP.
Reduced maximum amplitude or maximum clot firmness
Perform a FIBTEM or a functional fibrinogen test. Is maximum amplitude
or maximum clot firmness reduced using these tests? If so, the result is
due to fibrinogen deficiency, so consider using cryoprecipitate or fibrinogen
concentrate. If not, the result is due to platelet deficiency, so correct with
platelet transfusion.
Increased CL30/CL60 or LI30/LI60
There is excessive fibrinolysis, so consider an antifibrinolytic. An APTEM
test will inhibit fibrinolysis, bringing LI30 and LI60 back to normal limits,
confirming the result.
Coagulation tests 287
Anticoagulants/haemophilia
Factor deficiency
R; K: prolonged;
MA; Angle: decreased
Platelet blockers
Thrombocytopenia/thrombocytopathy
R; normal; K: prolonged;
MA: decreased
D.I.C
Stage 1
Hypercoagulable state with
secondary fibrinolysis
Stage 2
Hypercoagulable state
Hypercoagulability syndromes
Polycythaemia
A pattern of RBC changes that usually results in Hb >17.5g/dL in ♂ and
>15.5g/dL in ♀. This is accompanied by a corresponding increase in the red
cell count to 6.0 and 5.5 × 1012/L and an Hct of 55% and 47%, respectively.
Causes
• 1°: polycythaemia vera (PV)
• 2°: due to compensatory erythropoietin (EPO) increase (high altitude,
cardiorespiratory diseases—especially cyanotic, heavy smoking,
methaemoglobinaemia) or inappropriate EPO increase (renal diseases:
hydronephrosis, cysts, carcinoma; massive uterine fibromyomata;
hepatocellular carcinoma; cerebellar haemangioblastoma)
• Relative: stress or spurious polycythaemia. Dehydration or vomiting
• Plasma loss: burns, enteropathy.
Polycythaemia vera
Presenting features include headaches, dyspnoea, chest pain, vertigo, prur-
itus, epigastric pain, hypertension, gout and thrombotic episodes (particu-
larly retinal).
• Splenomegaly is typical.
• Thrombocythaemia occurs in 50% of cases.
• Differential diagnosis is with other causes of polycythaemia. These can
be excluded by history, examination and blood tests, including bone
marrow aspiration, ABGs and EPO levels.
• Genetic testing can reveal the JAK2 mutation in 90–95% of patients with
PV, and in 50% of patients with myelofibrosis.
• Therapy is aimed at maintaining a normal blood count by venesection
and myelosuppression with drugs.
• Thrombosis is a potential cause of death, and 10% of cases develop
myelofibrosis and rarely acute leukaemia.
Essential thrombocythaemia
Megakaryocyte proliferation and overproduction of platelets are the dom-
inant features, with a sustained platelet count >450 × 109/L.
• Closely related to PV, with recurrent haemorrhage and thrombosis as
the principal clinical features.
• Abnormal large platelets or megakaryocyte fragments may be seen on a
blood film.
• Differential diagnosis is from other causes of a raised platelet count,
e.g. haemorrhage, chronic infection, malignancy, PV, myelosclerosis and
chronic granulocytic leukaemia.
• Platelet function tests are consistently abnormal.
• Hydroxycarbamide is the mainstay of therapy, but some treatments are
more toxic.
Hypercoagulability syndromes 289
Antiphospholipid syndrome
This is a rare, but increasingly recognised syndrome resulting in arterial or
venous thrombosis or recurrent miscarriage, with a positive laboratory test
for antiphospholipid antibody and/or lupus anticoagulant. It may present
with another autoimmune disease such as SLE (2°) or as a 1° disease. The
main feature of the disease is thrombosis, with a spectrum from subacute
migraine and visual disturbances to accelerated cardiac failure and major
CVE. Arterial thrombosis helps distinguish this from other hypercoagulable
states. Paradoxically, the LA leads to a prolongation of coagulation tests,
such as the APTT, but detailed testing is needed before the diagnosis can
be confirmed. Patients may present for surgery because of complications
(miscarriage, thrombosis) or for incidental procedures. Initially, patients are
started on aspirin, but after a confirmed episode of thrombosis, they usually
remain on lifelong warfarin. High risk of thrombosis in these patients means
that if warfarin needs to be stopped for surgery, IV heparin should be com-
menced both pre-and postoperatively.
Anaesthesia and surgery in the hypercoagulable patient
There are no published guidelines, but it seems prudent that elective pa-
tients who are polycythaemic should be venesected to a normal blood
count to decrease the risk of perioperative thrombosis.
• Antithrombotic stockings and intermittent compression devices should
be used with SC heparin.
• Haematological advice may be required.
290
Further reading
McIlmoyle K, Tran H (2018). Perioperative management of oral anticoagulation. BJA Educ, 18,
259–64.
Keeling D, Tait RC, Watson H; British Committee of Standards for Haematology (2016). Peri-
operative management of anticoagulation and antiplatelet therapy. Br J Haematol, 175, 602–13.
Klein AA, Arnold P, Bingham RM, et al. (2016). AAGBI guidelines: the use of blood components and
their alternatives 2016. Anaesthesia, 71, 829–42.
Dimitrova G, Tulman DB, Bergese SD (2012). Perioperative management of antiplatelet therapy in
patients with drug-eluting stents. HSR Proc Intensive Care Cardiovasc Anesth, 4, 153–67.
Association of Anaesthetists of Great Britain and Ireland (2005). Blood transfusion and the anaes-
thetist: blood component therapy. M https://www.e-safe-anaesthesia.org/sessions/02_05/pdf/
bloodtransfusion06.pdf
References
1 Davis BA, Allard S, Qureshi A, et al. (2017). Guidelines on red cell transfusion in sickle cell dis-
ease. Part I: principles and laboratory aspects. Br J Haematol, 176, 179–91.
2 Foedinger A, Luger TJ (2016). Glucose- phosphate dehydrogenase deficiency. Anästh
6-
Intensivmed, 57, S115–38.
3 Stravitz RT, Lisman T, Luketic VA, et al. (2012). Minimal effects of acute liver injury/acute liver
failure on hemostasis as assessed by thromboelastography. J Hepatol, 56, 129–36.
4 Scully M, Hunt BJ, Benjamin S, et al. (2012). Guidelines on the diagnosis and management of
thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J Haematol,
158, 323–35.
5 Hicks T, Stewart F, Eisinga A (2016). NOACs versus warfarin for stroke prevention in patients
with AF: a systematic review and meta-analysis. Open Heart, 3, e279.
6 Douketis JD, Spyropoulos AC, Spencer FA, et al. (2012). Perioperative management of
antithrombotic therapy. Chest, 141, e326S–50S.
7 Kearon C, Akl EA, Ornelas J, et al. (2016). Antithrombotic therapy for VTE disease. Chest, 149,
315–52.
8 Hornor MA, Duane TM, Ehlers AP, et al. (2018). American College of Surgeons’ Guidelines for
the perioperative management of antithrombotic medication. J Am Coll Surg, 227, 521–36.
9 Koster A, Faraoni D, Levy JH (2018). Argatroban and bivalirudin for perioperative anticoagulation
in cardiac surgery. Anesthesiology, 128, 390–400.
10 Oprea AD, Popescu WM (2013). Perioperative management of antiplatelet therapy. Br J Anaesth,
111, 3–17.
11 Wijns W, Kolh P, Danchin N, et al. (2010). Guidelines on myocardial revascularization: The Task
Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the
European Association for CardioThoracic Surgery (EACTS). Eur Heart J, 31, 2501–55.
12 Kristensen SD, Knuuti J, Saraste A, et al. (2014). 2014 ESC/ESA Guidelines on non-cardiac sur-
gery: cardiovascular assessment and management. Eur Heart J, 35, 2383–431.
13 Roberts I, Shakur H, Coats T, et al. (2013). The CRASH-2 trial: a randomised controlled trial and
economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and
transfusion requirement in bleeding trauma patients. Health Technol Assess, 17, 1–79.
14 The CRASH-3 Trial Collaborators (2019). Effects of tranexamic acid on death, disability, vascular
occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3):
a randomised, placebo-controlled trial. Lancet, 394, 1713.
15 Fergusson DA, Hebert P, Mazer D, et al. (2008). A comparison of aprotinin and lysine analogues
in high-risk cardiac surgery. N Engl J Med, 358, 2319–31.
16 Henry D, Carless P, Fergusson D, Laupacis A (2009). The safety of aprotinin and lysine-derived
antifibrinolytic drugs in cardiac surgery: a meta-analysis. CMAJ, 180, 183–93.
Chapter 12 291
Parkinson’s disease
General considerations
Parkinson’s disease (PD) is a multisystem neurological disorder character-
ised by a triad of muscle rigidity, bradykinesia and a resting tremor. Loss of
dopaminergic neurones in the substantia nigra of the basal ganglia results in
a dopamine deficiency and excessive thalamic inhibition. This leads to the
classical symptoms seen. The disease affects over 100 000 people in the
UK, with a prevalence of 71% in those aged over 65, and is associated with
an i risk of perioperative morbidity and mortality. The disease is incurable
and progress cannot be slowed; treatment is aimed at relieving symptoms
with either medication or surgical intervention such as insertion of a deep
brain stimulator.
Drug therapies
• The goal of drug therapy is to increase the amount of dopamine readily
available within the CNS (Table 12.1) and to reduce cholinergic activity. This
can be achieved either by administering a dopamine agonist or by inhibiting
the enzymatic breakdown of dopamine in the CNS by monoamine oxidase
B (MAO-B) or catechol-O-methyltransferase (COMT).
• Drug therapy is, however, limited by severe side effects (nausea and
confusion), especially in the elderly. Up to 20% of patients will remain
unresponsive to drug therapy.
• Dopamine is administered as a prodrug (such as levodopa) to allow it to
cross the blood–brain barrier, and must be administered with a DOPA
decarboxylase inhibitor (such as carbidopa) to prevent peripheral
metabolism.
• Anticholinergic drugs are used when symptoms are mild and tremor
predominates, and can be useful in drug-induced parkinsonism.
Preoperative assessment
Patients with PD have i perioperative morbidity and mortality, as well as
an i length of stay.
In addition, the complexity of the timing and administration of drug ther-
apies necessitates a multidisciplinary approach during the perioperative
period, including from a PD specialist.
Important points:
• A history of dysphagia or excessive salivation (sialorrhoea) is suggestive
of upper airway dysfunction and indicates an i risk of failing to protect
the airway during the perioperative period. This may manifest as
aspiration, laryngospasm or postoperative pulmonary complications
such as infection.
• Respiratory function may be further impaired by rigidity and
bradykinesia, as well as sputum retention.
• Cardiovascular instability can result from arrhythmias or orthostatic
hypotension 2° to the disease itself or as a side effect of medications.
• The management of medication administration must be clear and
appropriate preparations made to be able to source and administer the
drug; where enteral medications cannot be given, substitutive parenteral
therapy must be instigated (see % p. 292).
• The patient should be warned that, even with extensive planning,
perioperative management of their parkinsonism may not be optimal
and distressing symptoms may recur. Delirium is also common, with
reported rates as high as 60%.
Drugs to avoid
• Several drugs commonly used in the perioperative period are
contraindicated in PD as they can significantly worsen symptoms or
cause harmful interactions.
• Antiemetics (prochlorperazine, droperidol, metoclopramide) antagonise
dopamine and exacerbate symptoms.
• Pethidine interacts with selegiline which can lead to serotonin syndrome
(see % p. 332).
• Synthetic opioids cause presynaptic inhibition of dopamine and cause
dose-related muscle rigidity.
• Clonidine can cause profound hypotension by enhancing the relative
hypovolaemia.
Conduct of anaesthesia
• Medications for PD should continue uninterrupted until the start of
anaesthesia. Distressing symptoms may develop as little as 3h after a
missed dose and acute withdrawal of drugs may precipitate symptoms
resembling neuroleptic malignant syndrome.
• Consider antisialagogue premedication in the presence of significant
sialorrhoea such as glycopyrronium (200–400 micrograms IM).
• Patients with PD have a high incidence of dysphagia, gastroparesis and
gastro-oesophageal reflux. Consideration therefore should be given to
securing the airway with RSI and intubation.
• Fixed flexion deformity of the neck can occur.
294
Special considerations
• Implantation of deep brain stimulators is increasingly being performed
in patients with advanced disease. Should the patient then require
further unrelated surgery, standard precautions for implantable devices
should be used such as using bipolar diathermy. The device should be
turned off prior to anaesthesia and checked postoperatively.
• Postoperative delirium is common in patients with PD and may
be delayed. A thorough assessment should be made for potential
triggers such as hypoxia or urinary retention. Non-pharmacological
management, such as orientation measures, are preferable to
pharmacological treatment. However, if required, low doses of
benzodiazepines or quetiapine can be given. Dopamine antagonists such
as haloperidol must be avoided.
Further reading
Roberts DP, Lewis SJG (2018). Considerations for general anaesthesia in Parkinson’s disease. J Clin
Neurosci, 48, 34–41.
Chambers DJ, Sebastian J, Ahearn DJ (2017). Parkinson’s disease. BJA Educ, 17, 145–9.
296
Cerebrovascular events
CVEs are a leading cause of death and disability worldwide. In the UK, 1.2
million people have a history of CVE. Around 85% of CVEs are ischaemic in
nature, and 15% are haemorrhagic. The resulting clinical outcome can range
from no deficit, a relatively mild focal neurological deficit to profound dis-
ability. Given the ongoing improvement in outcomes following CVEs, these
patients are increasingly likely to present for surgery and, as such, require
careful perioperative management.
H The most important risk factor for a perioperative CVE is a
previous CVE.
General considerations
Outcome following a perioperative CVE is poor and optimal 2° prevention
measures are extremely important to maximise recovery. Perioperative
hypotension can, for example, precipitate a watershed infarct at a vulner-
able boundary between vascular territories.
When to operate following a CVE
• The risk of major adverse cardiovascular events is markedly i following
CVE. This risk decreases with time and plateaus after 9mo but remains
elevated compared to a patient who has never suffered a CVE.1
• If possible, delay surgery for 9mo after a CVE, unless the benefits of
earlier surgery outweigh the risks.
• TIAs require urgent investigation by a CVE physician and non-
emergency surgery should be delayed until this is completed.
• Emergency surgery should not be delayed; surgery within 3d of a CVE
may have a better outcome than surgery at d3–14 due to delayed
impairment of cerebral autoregulation.2
Preoperative assessment
• Common associations with CVEs are older age, frailty, hypertension,
diabetes, respiratory disease, and cardiac disease.
• Medication and lifestyle changes should all be encouraged, including:
cessation of smoking, anticoagulation for valvular heart disease and
AF, lipid-lowering medications, glycaemic control and healthy diet to
normal BMI.
• For the symptomatic patient with known carotid artery stenosis of
>60%, discussion with a vascular surgeon regarding consideration for
endarterectomy may be appropriate.
• Physical disability may mean that impaired cardiorespiratory reserve is
not immediately obvious.
• Neurological examination is necessary prior to anaesthesia so that any
new perioperative neurological deficit can be identified early.
• Ischaemic CVEs are associated with AF. An ECG is required to
determine the underlying cardiac rhythm. Rate control may be required.
• Assess for bulbar involvement. Tracheal intubation may be needed and
the risk of postoperative pulmonary complications is raised.
• If patients are taking oral anticoagulation, INR, eGFR or CC will be
needed to inform preoperative cessation of these drugs.
• Post-CVE epilepsy occurs in 710% of patients. Antiepileptic drugs should
be continued in the perioperative period.
Cerebrovascular events 297
Mechanical thrombectomy
• Mechanical thrombectomy or clot retrieval is an intervention that can
remove an obstructing embolus from the affected vessel.
• A minimally invasive angiographic technique is used with a catheter
passed via the groin or wrist to the site of the embolus.
• If performed promptly, the neurological deficit can be minimised or
even reversed completely.
• The procedure can be carried out under GA or sedation. GA may be
preferred if there is bulbar involvement, agitation or a reduced level
of consciousness (e.g. basilar artery thrombus).
• Patient outcome correlates with BP management, not the anaesthetic
technique. Hypotension is particularly poorly tolerated. Systolic
pressure should be maintained at 140–180mmHg, with diastolic
pressure <105mmHg.5
Postoperative care
• Reinstate anticoagulants as soon as the surgical team allows.
• Intraoperative BP targets should continue postoperatively.
• Consider critical care admission for comorbid patients or those with
bulbar involvement.
Haemorrhagic CVE
• This may be due to aneurysmal subarachnoid haemorrhage,
spontaneous intracerebral haemorrhage, rupture of an arteriovenous
malformation, haemorrhage into a tumour or cerebral amyloid
angiopathy.
• Hypertension is the commonest risk factor for spontaneous
intracerebral haemorrhage.
• Other risk factors include DM, cigarette smoking and alcohol excess.
• Patients who survive the acute phase may be significantly impaired
with weakness, contractures and/or cognitive deficits.
• BP following intracerebral haemorrhage should be maintained
<140mmHg systolic.6
• When bleeding has occurred due to an aneurysmal rupture, systolic
BP should be maintained between 110 and 160mmHg until the
aneurysm is secured.7
(See also % p. 576.)
Cerebrovascular events 299
References
1 Jorgensen ME, Torp-Pedersen C, Gislason GH, et al. (2014). Time elapsed after ischaemic CVE
and risk of adverse cardiovascular events and mortality following elective noncardiac surgery.
JAMA, 312, 269–77.
2 Christiansen M, Andersson C, Gislason GH, et al. (2017). Risks of cardiovascular adverse events
and death in patients with previous CVE undergoing emergency noncardiac, nonintracranial sur-
gery: the importance of operative timing. Anesthesiology, 127, 9–19.
3 Mehdi Z, Birns J, Partridge J, et al. (2016). Perioperative management of patients with a history of
CVE or transient ischaemic attack undergoing elective non-cardiac surgery. Clin Med, 16, 535–40.
4 Minhas JS, Rook W, Panerai RB, et al. (2020). Pathophysiological and clinical considerations in the
perioperative care of patients with a previous ischaemic CVE: a multidisciplinary narrative review.
Br J Anaesth, 124, 183–96.
5 Talke PO, Sharma D, Heyer EJ, et al. (2014). Society for Neuroscience in Anesthesiology and
Critical Care Expert Consensus Statement: anesthetic management of endovascular treatment
for acute ischaemic CVE: endorsed by the Society of Neurointerventional Surgery and the
Neurocritical Care Society. J Neurosurg Anesthesiol, 26, 95–108.
6 Hemphill JC, Greenberg SM, Anderson CS, et al. (2015). Guidelines for the management of spon-
taneous intracerebral hemorrhage: a guideline for healthcare professionals from the American
Heart Association/American CVE Association. Stroke, 46, 2032–60.
7 Nathanson MH, Andrzejowski J, Dinsmore J, et al. (2020). Guidelines for safe transfer of the
brain-injured patient: trauma and CVE, 2019: guidelines from the Association of Anaesthetists and
the Neuro Anaesthesia and Critical Care Society. Anaesthesia, 75, 234–46.
30
Epilepsy
Epilepsy is characterised by a predisposition of the brain to generate ab-
normal, synchonous, neuronal activity. The clinical manifestations vary
widely and can be focal or generalised, with consciousness maintained or
impaired. Epilepsy may be idiopathic or 2° to a structural, metabolic or trau-
matic cause. Antiepileptic drug therapy is used to reduce and/or control
the rate of seizures. Surgery or implantation of neuromodulatory devices
(such as a vagus nerve stimulator) may be required in refractory cases.
General considerations
• It is vital that antiepileptic drug therapy is maintained throughout the
perioperative period, through either enteral or parenteral routes.
Preoperative assessment
• The nature, timing and frequency of seizures should be recorded, along
with a full drug history and timing of antiepileptic drug therapy. This
can help to determine strategies to minimise disruptions in treatment
regimes.
• Any associated medical conditions must also be assessed.
• If there is suboptimal control of seizures or in those where return to
therapy may be delayed after surgery, consult their specialist.
• Consider drug titres in patients as a baseline prior to major surgery or if
control is suboptimal.
Conduct of anaesthesia
• Perioperatively antiepileptic drugs may need to be given, parenterally if
possible
• Specific drug considerations are considered in Table 12.2.
• Check electrolyte and glucose levels as derangement reduces seizure
threshold, as does hypocapnia.
• IV induction can be performed with propofol or thiopental as both
have anticonvulsant properties at doses used for GA. Ketamine has
proconvulsant properties when used at low doses, but anticonvulsant
properties at GA doses.
• Regional anaesthesia may help to minimise disruption in antiepileptic
drug regimes and can also negate the possibility of missed seizure
activity occurring under GA. LAs can readily cross the blood–brain
barrier and result in seizure activity if maximum doses are exceeded.
• Carefully assess any abnormal movements on induction or emergence
as misdiagnosing dystonic movements or shivering as epilepsy can have
profound implications for the patient (Box 12.1).
Drug Notes
Pethidine and tramadol Both lower the seizure threshold and should
be avoided
Alfentanil Enhances EEG activity and prolongs seizures in
electroconvulsive therapy; avoid or use with
caution
Ketamine Proconvulsant at low doses, but anticonvulsant
at anaesthetic doses (>1mg/kg IV)
Etomidate Avoid as associated with postoperative
seizures. Prolongs seizure duration in
electroconvulsive therapy
Metoclopramide, High incidence of dystonic reactions which
prochlorperazine, droperidol may lead to confusion with epileptic activity
Enflurane Associated with postoperative seizures (no
longer available in the UK)
Aminosteroid neuromuscular Hepatic enzyme induction by antiepileptic
blockers (e.g. vecuronium, drugs may shorten duration of action
rocuronium)
Effect Consequence
Enzyme inducers (e.g. Reduce serum concentration of certain drugs,
carbamazepine, phenytoin, e.g. valproate, lamotrigine, steroids, oral
phenobarbital) contraceptives, amiodarone, digoxin, warfarin
Enzyme inhibitors (e.g. valproate Increase serum concentration of certain
and stiripentol) drugs, e.g. lamotrigine, phenobarbital,
nimodipine, amitriptyline, warfarin
Metabolism inhibited by other Clarithromycin and erythromycin
drugs increase serum concentration of
carbamazepine
Amiodarone increases serum
concentration of phenytoin
May cause toxic levels of antiepileptic drugs
Metabolism induced by other Oral contraceptives markedly reduce serum
drugs lamotrigine concentrations, which may result
in subtherapeutic levels
Pharmacokinetic effects on Continuous NG feed impairs gastric
absorption, distribution or phenytoin absorption
excretion Highly protein-bound drugs (valproate,
phenytoin) may displace other drugs
from protein-binding sites—rarely of
clinical importance
Effect on NMBAs Antiepileptic drugs may potentiate the
effect of non-depolarising neuromuscular
blockers when administered acutely, yet
cause resistance to their effects in chronic
use. Caused by a combination of effects such
as enzyme induction and upregulation of
acetylcholine receptors
Impaired clearance of Renal/hepatic failure, hypoalbuminaemia
antiepileptic drugs
Further reading
Carter EL, Adapa RM (2015). Adult epilepsy and anaesthesia. BJA Educ, 15, 111–17.
Perks A, Cheema S, Mohanra JR (2012). Anaesthesia and epilepsy. Br J Anaesth, 108, 562–71.
Johannessen SI, Johannessen Landmark C (2010). Antiepileptic drug interactions: principles and clin-
ical implications. Curr Neuropharmacol, 8, 254–67.
Anaesthesia in spinal cord lesions 303
Autonomic dysreflexia
Autonomic dysreflexia is a potentially life-threatening condition, charac-
terised by an inappropriate autonomic response to a stimulus below the
level of the spinal cord lesion. It is seen in up to 50–70% of patients with
a spinal cord injury at or above T6. The incidence is greater with higher
lesions and complete cord injury. It may occur as early as 3w following
the initial injury.
Common precipitants include: pain, bladder distension, urinary tract in-
fections, catheter insertion and faecal impaction.
306
Suxamethonium
Following a spinal cord injury, upper motor neurone denervation results in
nicotinic acetylcholine receptors propagating beyond the motor endplate
of the neuromuscular junction. Suxamethonium administration can cause
an elevated release of K+ due to the i number of receptors being de-
polarised. Life-threatening hyperkalaemia can occur. Suxamethonium is
contraindicated from 72h to 6mo after injury.
Conduct of anaesthesia
• Patients are likely to have undergone multiple previous anaesthesia;
review previous anaesthetic charts.
• If surgery is planned for an insensate region, autonomic dysreflexia may
still be precipitated, even if pain is not. It may be possible to undergo
the procedure without anaesthesia, but vigilance for the sequelae of
autonomic dysreflexia must be maintained.
• Autonomic dysreflexia and IHD are common. Consider invasive arterial
BP monitoring, especially if significant fluid shifts are anticipated.
• Laryngoscopy may be difficult if there has been cervical fixation.
• Spinals and epidurals are advantageous in reducing postoperative
ventilation and autonomic dysreflexia. Less cardiovascular instability
as sympathetic tone is already reduced. May be unreliable and can be
difficult to determine the level of block achieved in complete spinal cord
Anaesthesia in spinal cord lesions 307
Neuromuscular disorders
Neuromuscular disorders can be categorised into acquired or hereditary
conditions, and the anatomical site affected (Table 12.6). Common condi-
tions will be discussed in more detail.
Multiple sclerosis
Multiple sclerosis is an autoimmune disease of the CNS characterised
by the development of inflammatory plaques, demyelination and axonal
damage to the brain and spinal cord. Onset usually occurs in early adult-
hood; the disease may relapse and remit or follow a chronic progressive
course. Treatment aims are to limit progression and manage symptoms.
General considerations
• Patients are frequently on multiple medications. Immunosuppressants to
manage disease progression (e.g. steroids, interferon beta), analgesics
for neuropathic pain and antispasmodics. Perioperative management
and potential interactions must be considered.
• Symptoms range from isolated visual disturbances to severe weakness
and typically recur and relapse. Profound spasticity, respiratory failure
and bulbar palsy can occur in end-stage disease.
• Demyelinated axons are sensitive to heat; an increase in temperature
may cause a marked deterioration in symptoms.
Preoperative assessment and investigation
• A documented, detailed preoperative neurological examination is
essential, especially if a regional technique is planned.
• Assess the current state of the disease and consider delaying elective
surgery if the patient is actively relapsing.
• Review any change in respiratory function. Bulbar palsy causes an i risk
of aspiration and reduced airway reflexes in the postoperative period.
Critical care may be required.
Conduct of anaesthesia
• GA itself does not affect the course of multiple sclerosis.
• Demyelinated axons are more susceptible to LA toxicity. Use the lowest
possible dose of LA, in combination with adjuncts such as low-dose
opioids.
• Peripartum use of spinal or epidural techniques does not appear to
affect the occurrence of a postpartum relapse. Prior full neurological
examination and discussion with the patient are required to prevent the
patient from incorrectly attributing a postpartum relapse to anaesthesia.
• Suxamethonium should be avoided when severe weakness and
spasticity are present as it may result in life-threatening hyperkalaemia.
• Response to non-depolarising drugs is normal.
• Autonomic dysfunction can lead to haemodynamic instability.
• Pyrexia should be avoided, if possible, and treated aggressively with
cooling measures.
Further reading
Kopp SL, Jacob AK, Hebl JR (2015). Regional anesthesia in patients with preexisting neurologic dis-
ease. Reg Anesth Pain Med, 40, 467–78.
231
Guillain–Barré syndrome
Guillain–Barré syndrome is a rare disease (1:100 000) forming part of a
group of neuropathic conditions characterised by progressive weakness
and absent reflexes. The most common presentation is an acute inflam-
matory demyelinating polyneuropathy presenting with progressive motor
weakness. Less common subtypes or variants are listed in Table 12.7. The
anaesthetic implications related to NDMRs persist after recovery of symp-
toms and therefore they should be used with caution in patients with a
history of Guillain–Barré syndrome.
Guillain–Barré syndrome often occurs as an autoimmune response fol-
lowing a viral or bacterial illness within the preceding month. Weakness
is classically ascending and symmetrical, with associated areflexia. Sensory
and autonomic dysfunction can also occur. Severity can range from mild to
severe debilitation. Diagnosis is based on clinical features, CSF testing (high
protein, low WCC) and nerve conduction studies.
In patients with Guillain–Barré syndrome:
• 725% will require intubation and mechanical ventilation
• 710% will die from associated complications
• 710% will suffer long-term neurological complications and physical
dependence.
Treatment is generally supportive, however, regardless of subtype. Specific
interventions such as immunoglobulins or plasmapheresis may be used
to reduce neural inflammation and expedite recovery. Steroids are not
indicated.
General considerations
The main systemic effects of Guillain–Barré syndrome and the subsequent
anaesthetic implications are summarised in Table 12.8.
Guillain–Barré syndrome 313
Cardiovascular
Autonomic Over-or underactivity of both sympathetic and
dysfunction parasympathetic nervous systems:
• Tachyarrhythmias, AV block, prolonged QT and
asystole
• Haemodynamic instability during induction,
positive pressure ventilation or postural changes
• Ileus, urinary retention and abnormal sweating
Consider invasive cardiovascular monitoring and large-
bore IV access
Respiratory
Weakness of PFTs preoperatively
respiratory muscles
Risk of aspiration—consider RSI
Difficulty clearing secretions: risk of pulmonary
infection
Difficulty weaning from ventilatory support:
postoperative ventilation ± tracheostomy
Neurological
Bulbar and facial i risk of aspiration and upper airway collapse
palsy
Neuropathic pain Difficult perioperative analgesic management—
multimodal approach recommended
Neurological deficits Document any pre-existing deficit if performing regional
anaesthesia
Myasthenia gravis
Myasthenia gravis is an autoimmune condition characterised by muscle
weakness and fatigability on repetitive exertion. It is caused by antibodies
acting at the nicotinic acetylcholine receptor on the postsynaptic mem-
brane of the neuromuscular junction. Fewer functioning receptors are then
available for acetylcholine to bind to, resulting in impaired generation of
action potentials and subsequent muscle weakness. Disease onset shows a
bimodal distribution, primarily in younger women and older men. Thymus
hyperplasia may have a role.
Symptoms range from mild ptosis to life-threatening bulbar and respira-
tory insufficiency. Weakness illustrates fatigability. Ptosis is often the 1st sign.
Diagnosis is made with blood tests for acetylcholine receptor antibodies,
edrophonium administration or the ice-pack test. The mainstay of chronic
management is oral anticholinesterase medication. Some patients may
require immunosuppressant therapy with steroids, plasma exchange or IV
immunoglobulins. A myasthenic crisis is an exacerbation of the disease that
necessitates mechanical ventilation due to respiratory or bulbar impairment.
General considerations
• Optimal management of the disease in the perioperative period is
imperative. Involvement of a neurologist may help symptom control and
to reduce the risk of a myasthenic crisis.
• Patients who have recently undergone plasmapheresis will
have depleted plasma-esterase levels, prolonging the effect of
suxamethonium, mivacurium, ester-linked LAs and remifentanil.
Preoperative assessment
• Take a full drug history and determine the effect of a missed dose of
anticholinesterase (missing a dose may precipitate severe symptoms).
Plan how anticholinesterase therapy will be administered in the
perioperative period (Table 12.9).
• Assess weakness and the duration and progression of symptoms.
Isolated, long-standing ocular symptoms are less likely to progress.
• Assess bulbar and respiratory function. Intubation and ventilatory
support may be required.
Conduct of anaesthesia
• Maintain anticholinesterase therapy up to the time of induction.
• Avoid premedication with agents that may worsen symptoms of
myasthenia or cause sedation.
• Intubate if FVC <15mL/kg.
• Use short-acting anaesthetic agents to minimise respiratory depression
on emergence.
• LA or regional anaesthesia should be used where possible.
• Patients are resistant to suxamethonium. It can be used, but an i dose
is required (1.5–2.0mg/kg). Do not administer any other neuromuscular
blocker until no fade is present on quantitative nerve monitoring.
• Non-depolarising drugs: doses of 10–20% normal are often adequate.
Monitor response with a quantitative nerve stimulator.
• Use short-acting non-depolarising relaxants that are metabolised
spontaneously or reversed by sugammadex.
• Neostigmine use may trigger a cholinergic crisis, especially if the patient
is taking other anticholinergic medications.
• Avoid ester-linked LAs, such as prilocaine, as anticholinesterase therapy
may interfere with metabolism.
• Aminoglycosides, macrolides and fluoroquinolones all have
neuromuscular-blocking activity.
• Magnesium reduces presynaptic acetylcholine release at the
neuromuscular junction.
• IV lidocaine infusions may cause weakness.
• Steroids may worsen weakness in high doses.
• Ca2+ channel and β-blockers, gabapentinoids, phenothiazines and
phenytoin can all affect neuromuscular function and care should be taken.
• Use multimodal analgesia to minimise the use of opioids.
• Extubate only if neuromuscular function is adequate.
• Consider admission to critical care for ongoing respiratory support.
Postoperative care
• Reinstitution of drug therapy is vital. An NGT may be required if bulbar
symptoms prevent swallowing.
• In the event of GI failure, instigate parenteral therapy and seek expert
opinion from a neurologist.
• Close monitoring of respiratory function is mandatory, ideally with
serial VC measurements.
• Blood gases and SpO2 may be normal up to the point of respiratory
failure.
Special considerations
Myasthenic crisis vs cholinergic crisis
• Myasthenic crisis occurs when a patient with myasthenia receives
insufficient medication and a cholinergic crisis occurs when the patient
receives too much anticholinesterase therapy. They have similar
presentations; both may cause paralysis, bronchospasm, respiratory
failure and diaphoresis.
• Can be distinguished with a small dose of edrophonium which improves
a myasthenic crisis, but this can precipitate respiratory failure in
cholinergic crises.
• In a cholinergic crisis (e.g. organophosphate poisoning), too much
acetylcholine at the nicotinic receptor produces flaccid paralysis
and parasympathetic effects from the muscarinic receptors such
as salivation, lacrimation, and GI upset. Treatment is IV atropine or
glycopyrronium bromide to counteract the muscarinic effects.
• Myasthenic crises can also be triggered by trauma, infection or
metabolic disturbances and can result in bulbar and respiratory muscle
weakness which improves with anticholinesterase treatment.
Thymectomy
• Current evidence favours thymectomy in myasthenic patients; clinical
outcome is improved with a reduction in myasthenic crises and the need
for immunosuppressive therapy.
• Trans-sternal, transcervical or thoracoscopic approaches can be used.
• Anaesthetic management for thymectomy follows the general principles
outlined above.
Lambert–Eaton myasthenic syndrome
Lambert–Eaton myasthenic syndrome is a rare autoimmune disorder that
causes proximal muscle weakness. It is associated with malignancy, particu-
larly small cell lung cancer.
• Antibodies to voltage-gated Ca2+ channels impair acetylcholine release
from the presynaptic junction into the synaptic cleft.
• Unlike in myasthenia, muscle weakness is improved by exercise and
anticholinesterase medication is less effective.
• Amifampridine is a treatment that enhances acetylcholine release at the
neuromuscular junction.
• Autonomic dysfunction and bulbar involvement may occur in advanced
disease.
• Patients with Lambert–Eaton myasthenic syndrome are extremely
sensitive to both depolarising and non-depolarising NMBAs. These
should be used with caution and in reduced doses.
• Postoperative issues are similar to those in patients with myasthenia
gravis.
Further reading
Wolfe GI, Kaminski HJ, Aban IB, et al. (2016). Randomized trial of thymectomy in myasthenia gravis.
N Engl J Med, 375, 511–22.
Muscular dystrophies 317
Muscular dystrophies
Muscular dystrophies are a collective group of progressive muscle dis-
orders, most often caused by defective or absent glycoproteins in the
muscle membrane such as dystrophin. There are >30 forms of muscular
dystrophies. Inheritance follows one of three patterns:
• X-linked recessive: Duchenne muscular dystrophy, Becker muscular
dystrophy, scapuloperoneal muscular dystrophy
• Autosomal recessive: most ‘limb girdle’ types, scapulohumeral
muscular dystrophy, congenital muscular dystrophy, childhood muscular
dystrophy
• Autosomal dominant: facioscapulohumeral muscular dystrophy, some
oculopharyngeal/ocular muscle dystrophies.
Duchenne muscular dystrophy and myotonic dystrophy are discussed
below. Table 12.10 summarises features of some of the other muscular
dystrophies.
Duchenne muscular dystrophy
Duchenne muscular dystrophy is the most common muscular dystrophy
(incidence of 1:5000 ♂ newborns) and is rapidly progressive. It is caused
by an alteration in the gene for dystrophin, a cytoskeletal protein that con-
tributes to the strength, stability and functionality of myofibrils. This leads
to disruption of the integrity of the sarcolemma and, consequently, myo-
fibril atrophy, necrosis and fibrosis. Although primarily an X-linked condi-
tion affecting ♂ , some ♀ carriers are symptomatic, exhibiting a milder
phenotype.
General considerations
• Muscle weakness typically manifests between the ages of 2 and 5.
• It is characterised by a waddling gait, asymmetrical lower limb strength,
delayed motor milestones, calf hypertrophy and falls.
• Proximal muscles are involved before distal, and lower limb extremities
are affected before upper limb.
• Affected ♂ are usually wheelchair-bound by the age of 12 and suffer
from concomitant scoliosis and contractures. Death occurs from cardiac
or respiratory failure typically in 20–30s.
• Key aspects of management are physiotherapy and treatment with
glucocorticoids to slow progression of muscular weakness.
• MD patients may test positive for MH, but this can be a false positive.
Treat as MH susceptible (see % pp. 1096–8).
Physiological considerations
• Cardiovascular: dilated cardiomyopathy (up to 50% of those aged 15 or
over will have dilated cardiomyopathy), myocardial degeneration, heart
failure and arrhythmias (AF/atrial flutter, ventricular tachycardia (VT) or
VF). Signs and symptoms of heart failure in non-ambulatory individuals
are often subtle.
• Respiratory: progressive respiratory muscle weakness, mucus plugging,
atelectasis, pneumonia and restrictive respiratory failure. Management
includes physiotherapy with assisted coughing, assisted ventilation,
subsequent daytime ventilation and tracheostomy.
• Musculoskeletal: severe kyphoscoliosis, muscular contractures and
osteoporosis (worsened by glucocorticoid use).
831
Myotonic dystrophy
Myotonic dystrophy is an autosomal dominant disorder that usually pre-
sents in the 2nd or 3rd decade of life. It exhibits symptoms and signs of
both dystrophies and myotonias. Abnormal Na+ or chloride channels in the
musculature result in the discharge of repetitive action potentials, leading
to sustained muscle contraction in response to stimulation. The disease is
progressive and has multisystem effects. Life expectancy depends on the
subtype of disease and may be normal or reduced.
General considerations
Clinical features are highly variable but include:
• Degradation of cardiac conduction system leading to dysrhythmias and
AV block. Mitral valve prolapse and cardiomyopathy possible
• Respiratory insufficiency due to atrophy of respiratory muscles and
diaphragm, impaired cough, OSA and central respiratory depression
• Muscular atrophy, particularly facial and peripheral muscles
• Dysphagia, dysmotility, reduced gastric emptying and bulbar palsy—
i risk of aspiration
• Possible cognitive impairment after 2nd decade of life
• DM, hypothyroidism, adrenal insufficiency and gonadal atrophy
• Pregnancy may aggravate the disease, and an elective CS is often
required due to uterine muscle dysfunction.
Preoperative assessment
• Assess respiratory function with spirometry; consider CXR and arterial
blood gases if significant impairment suspected.
• ECG ± echocardiography to look for dysrhythmias and cardiac
dysfunction. An implantable pacemaker may be in situ.
• Serum thyroid function tests, glucose and cortisol measurements.
Conduct of anaesthesia
H It is vitally important to avoid factors that may precipitate sustained
muscular contraction.
These include: hypothermia, drugs, shivering, mechanical or electrical
muscle stimulation including diathermy and NMBA monitoring.
• Premedication with a prokinetic and/or antacid is helpful as patients are
at risk of aspiration; RSI may be required.
• Patients are sensitive to sedatives, so use sparingly.
• Avoid suxamethonium as it may cause sustained muscle contractures,
rhabdomyolysis and hyperkalaemia. Rocuronium allows use of
sugammadex for reversal, allowing complete reversal of NMBA and
avoiding the risk of drug-induced muscle contraction. Atracurium can
also be used. Do not use nerve stimulator or anticholinesterase as these
may provoke muscle contraction.
• Inhalational anaesthetic agents have been implicated in rhabdomyolysis
and MH-like reactions. Consider TIVA. If using inhalational maintenance,
avoid high concentrations which may affect cardiac contractility and
conduction.
• Induction agents cause profound CVS depression.
320
Rare conditions
There are many rare neurological conditions that require a considered
approach to anaesthesia. A brief discussion of several key conditions is
outlined below.
Creutzfeldt–Jakob disease
This is a neurodegenerative, prion-related disease that may be sporadic,
inherited or transmitted through contaminated surgical instruments, trans-
fused human tissue or dietary exposure to the bovine form of the disease.
There is a rapid cognitive and neurological decline over months, leading to
death. Anaesthetic considerations are based on the severity of neurological
impairment. While there are no particular isolation precautions required,
airway equipment must be single-use only and surgical instruments should
be disposed of following the procedure, as autoclaving does not destroy
transmissible prions.
Charcot–Marie–Tooth
A condition characterised by chronic peripheral neuromuscular denerv-
ation. Most forms are inherited in an autosomal dominant pattern. Muscle
atrophy results in spinal and limb deformities; restrictive lung disease, dif-
ficult airway management and postoperative respiratory failure may result.
Avoid suxamethonium due to the risk of severe hyperkalaemia. NDMRs
may have a prolonged action; consider using a reversible agent.
Critical illness polyneuromyopathy
Critical illness polyneuromyopathy describes an overlapping syndrome of
diffuse, symmetrical, flaccid muscle weakness that occurs in critically ill pa-
tients and can contribute to failure to wean from mechanical ventilation.
There is no specific treatment other than best supportive care, treating
the underlying condition and minimising risk factors during critical illness.
There are no specific concerns regarding the conduct of anaesthesia.
Suxamethonium should be avoided.
Familial periodic paralysis
Hyperkalaemic periodic paralysis
An autosomal dominant condition in which episodes of flaccid paralysis are
triggered by hyperkalaemia and stress states such as cold and hunger. Loop
diuretics can be used for preoperative K+ reduction. Avoid medications
that increase serum K+ such as suxamethonium. Volatile agents are safe to
use. Physiological stress should be avoided by maintaining normothermia,
minimising fasting and infusing glucose-containing fluids during surgery.
Assess for paralysis on emergence from anaesthesia; patients may remain
paralysed for a prolonged period postoperatively and require mechanical
ventilation.
Hypokalaemic periodic paralysis
This is an autosomal dominant condition. Patients present with se-
vere muscle weakness 2° to hypokalaemia. The focus of treatment is on
maintaining a normal serum K+ level and avoiding hypothermia. Paralysis
should be assessed for on emergence from anaesthesia.
Rare conditions 323
324
Epilepsy N N/i Avoid drugs that reduce seizure threshold. Hepatic enzyme
induction may reduce duration of NDMRs
Neurological and muscular disorders
Myotonic dystrophy 0 d 0 Avoid cold, shivering and mechanical and electrical stimulation
Muscular dystrophy 0 d Respiratory and cardiac compromise
Psychiatric disorders
Aidan O’Donnell
Psychiatric disorders 328
Antidepressant drugs 330
Antipsychotic drugs 334
Agitated patients on the ward 335
Substance abuse disorder 336
Electroconvulsive therapy 339
See also
% Long-term opioid use and the opioid-dependent patient
pp. 1176–8
328
Psychiatric disorders
The anaesthetic implications of psychiatric illness include:
• Where capacity of the patient to give informed consent may be
impaired (e.g. dementia, mania, psychosis)
• Where the psychiatric illness itself also causes physical illness (e.g.
anorexia nervosa)
• Where the psychiatric medication may interact with anaesthetic drugs
and techniques (e.g. antidepressants).
Some form of psychiatric illness is present in about 10% of the UK popu-
lation at any time, but most patients are usually well-controlled. The com-
monest psychiatric disorder is depression. Many patients are on long-term
drug therapy, which should be continued perioperatively where possible.
Major psychiatric illness affects about 1% of the population and carries a
significant risk of self-harm or suicide. Misuse of alcohol and drugs is also
common among the psychiatric population. The stress of hospitalisation for
surgery may exacerbate coexisting psychiatric problems.
Consent
The ability to give consent is assumed unless proven otherwise, as laid
out in the Mental Capacity Act (England and Wales, 2005) and the Adults
with Incapacity Act (Scotland, 2000). Patients who are detained under the
Mental Health Act (1983) may be compelled to accept psychiatric treat-
ment (but not other types of treatment) under the terms of the Act. In the
UK and other countries, someone with ‘Lasting Power of Attorney’, previ-
ously Enduring Power of Attorney, may legally give (or withhold) consent
on behalf of a patient who has been deemed to lack capacity. Check for an
advanced decision/directive (‘living will’) as this may supersede or limit the
powers of the Lasting Power of Attorney.1
Anxiety
Preoperative anxiety is common and can be managed with explanation, re-
assurance, oral premedication, IV sedation (e.g. midazolam 1–2mg) or a
combination of these. Anxiety disorder may be acute or chronic, or occur
as part of other disorders (e.g. depression). Extreme agitation may make
cannulation difficult. Patients may hyperventilate. Higher doses of induction
agents may be required.
Attention-deficit hyperactivity disorder (ADHD)
This condition is present in 1.4–3% of children; more common in boys.
Behavioural problems may make children uncooperative at induction, and
disrupted behaviour can be worse for a few days afterward. Children with
severe ADHD are often prescribed methylphenidate, an amphetamine-
like drug, which could theoretically cause them to require i doses of an-
aesthetics. In practice, anaesthesia in this group of children is manageable
without special precautions, and their stability is helped by continuing their
usual medications2 (see also % p. 914).
Psychiatric disorders 329
Dementia
Dementia refers to an irreversible global deterioration in higher mental
functioning. Fifty per cent of cases are due to Alzheimer’s disease.3
• Prevalence: 1% aged 65–74, rising to 10% aged >75 and 25% aged >85y.
Slightly more common in women.
• Mean life expectancy is 77y from diagnosis.
• Patients may be unable to give informed consent. In the absence of
a Lasting Power of Attorney, clear documentation of the patient’s
incapacity and reasons to proceed (e.g. the patient’s best interests)
should be made.
• Patients can be confused and may be agitated (occasionally violent) or
profoundly withdrawn.
• Patients with mild to moderate dementia are commonly treated with
anticholinesterase drugs such as donepezil, rivastigmine or galantamine.
These may prolong the action of suxamethonium and partially
antagonise the effects of non-depolarising NMB drugs.
• Regional anaesthesia may still be desirable if significant comorbidity;
ketamine (e.g. 5–20mg IV) may facilitate this and preserves airway
reflexes and BP (titrate to effect). (Midazolam may cause disinhibition,
which may paradoxically worsen agitation.)
• The association between postoperative neurocognitive disorder
(POND) and dementia remains unclear, but dementia is considered a
risk factor for the development of POND (see % p. 90).
Anorexia nervosa
Anorexia nervosa is a chronic, severe multisystem disorder, which carries
the highest morbidity and mortality rate of any psychiatric disorder (see
% pp. 86–7).
30
Antidepressant drugs
The aetiology of depression is complex and multifactorial. The monoamine
theory of depression postulates that depression is caused by functional de-
ficiency of serotonin and noradrenaline in the CNS. Manipulation of CNS
monoamines remains the most successful pharmacological approach to de-
pression. Several families of drugs have this effect.4,5
Tricyclic antidepressants
TCAs, such as amitriptyline or imipramine, have largely been superseded by
selective serotonin reuptake inhibitors (SSRIs) (fewer side effects and safer
in overdose) for the treatment of depression. However, TCAs may be used
in the treatment of other problems, e.g. chronic pain. They need to be given
for 2–4w to become effective.
• TCAs block the reuptake of monoamines (e.g. serotonin,
noradrenaline) from the synaptic cleft by competing for a transport
protein.
• Most have atropine-like side effects: dry mouth, blurred vision, urinary
retention and constipation. Other common side effects are sedation,
postural hypotension and delayed gastric emptying.
• They are strongly bound to plasma proteins, and their effects may be
enhanced by competing drugs (e.g. aspirin, warfarin, digoxin).
• In overdose, TCAs cause agitation, delirium, respiratory depression
and coma. Cardiac arrhythmias with prolongation of the QT interval
are frequent. There is no specific antidote, and treatment is supportive,
although intensive care may be required. Alkalinisation of plasma
reduces the amount of free drug.
• TCAs should not be withdrawn perioperatively.
• i sensitivity to catecholamines may result in hypertension and
arrhythmias, following the administration of sympathomimetic drugs
(adrenaline, noradrenaline). Indirect sympathomimetics (e.g. ephedrine,
metaraminol) should be used with caution.
• Anticholinergic drugs (e.g. atropine) which cross the blood–brain
barrier may contribute to postoperative confusion.
• Co-administered tramadol increases the risk of serotonin syndrome.
• St John’s wort (Hypericum perforatum) contains alkaloids which resemble
TCAs in structure and is useful and safe in mild depression, but can also
contribute to serotonin syndrome (see % p. 332).
Selective serotonin reuptake inhibitors
SSRIs are the most commonly prescribed antidepressants worldwide and
are also prescribed for other conditions, e.g. panic disorder, obsessive–
compulsive disorder. They are highly specific inhibitors of presynaptic
reuptake of serotonin from the synaptic cleft and are much less toxic in
overdose than TCAs. Common examples include fluoxetine, sertraline and
citalopram.
• Common side effects affect the GI tract (nausea, vomiting, diarrhoea,
upper GI bleeding) and the CNS (insomnia, agitation, tremor, headache,
sexual dysfunction). CVS side effects are rare (occasional reports of
bradycardia).
• SSRIs may precipitate coronary vasoconstriction in those with IHD.
• Check Na+, especially in the elderly, as SSRIs have been known to cause
hyponatraemia 2° to SIADH (see % p. 242).
Antidepressant drugs 331
Antipsychotic drugs
Antipsychotic drugs
Antipsychotic drugs (formerly known as neuroleptics) include haloperidol,
chlorpromazine, olanzapine, quetiapine and risperidone, and are used in the
treatment of schizophrenia and similar disorders. Their main action is antag-
onism at CNS dopamine (D2) receptors, but most antagonise other recep-
tors, including histamine (H1), serotonin (5-HT2), acetylcholine (muscarinic)
and α-adrenergic receptors. Many have antiemetic effects.4,5
• Common side effects include sedation, extrapyramidal motor
disturbances and tardive dyskinesia with chronic use. Less common
side effects include gynaecomastia, weight gain, postural hypotension,
antimuscarinic effects, obstructive jaundice and agranulocytosis (rare,
but severe).
• Many drugs prolong the QT interval, especially when combined with
other drugs which may do the same (e.g. antidepressants).
• Clozapine is associated with a risk of agranulocytosis.
• Abrupt withdrawal of antipsychotic medication is dangerous.
• Antipsychotic drugs potentiate sedative and hypotensive effects of
anaesthetic agents (including opioids).
Neuroleptic malignant syndrome
A rare idiosyncratic reaction to antipsychotic drugs which resembles MH
and serotonin syndrome (see % p. 332) (Table 13.1). Typical patients are
young ♂ . Features include hyperthermia, tachycardia, extrapyramidal dys-
function (rigidity, dystonia) and autonomic dysfunction (sweating, labile BP,
salivation, urinary incontinence). CK and WCC are raised. Patients should
be treated in the ICU. Mortality approaches 20%.6
Agitated patients on the ward 335
Alcohol10,11
Alcohol use is common and causes problems as a result of both acute in-
toxication and the health effects of chronic consumption. Ask all adults
about alcohol consumption. Surgery should be avoided, if possible, in the
acutely intoxicated as consent is difficult.
• Ketoacidosis may present after binge drinking, in association with
vomiting and fasting. Blood alcohol levels may already have normalised.
• Acute intoxication may cause vomiting, dehydration, hypoglycaemia
and delayed gastric emptying. Careful rehydration, with attention to
electrolytes and glucose, and RSI are advised.
• Chronic alcohol excess induces tolerance to GA and is associated with
an increase in postoperative complications, including infection.
• Alcoholic cardiomyopathy is characterised by a dilated, hypokinetic LV
and d EF. Patients may present with CCF and oedema, exacerbated by
low serum albumin. Consider echocardiography.
• Alcoholic liver disease: the earliest form is reversible fatty liver,
progressing to alcoholic hepatitis (abdominal pain, weight loss, jaundice,
fever) and later cirrhosis (jaundice, ascites, portal hypertension, hepatic
failure). Correct clotting abnormalities preoperatively. X-match blood.
Patients with liver failure may require intensive care if surgery is planned
(see also % pp. 205–10).
• Consider IV thiamine to reduce the risk of Wernicke’s encephalopathy.
• Anticipate alcohol withdrawal symptoms. Most patients can tolerate
24h abstinence perioperatively—many hospitals have benzodiazepine
regimens to prevent withdrawal syndrome.
• Seizures are most commonly seen 6–48h after cessation of drinking,
typically tonic–clonic. Several fits over a period of a few days are
common. Low K+ and Mg2+ predispose. Seizures may be preceded
by disorientation and agitation (delirium tremens). Treat with
benzodiazepines, e.g. diazepam 10mg IV, repeated as required.
Electroconvulsive therapy 339
Electroconvulsive therapy
Procedure Electrically induced seizure
Time 5–10min
Pain ±
Position Supine
Blood loss Nil
Practical technique Short IV GA, face mask only, bite-block
General considerations
Electroconvulsive therapy (ECT) is safe and effective in the treatment of
mental disorders, most commonly severe depression unresponsive to
drugs, or where there is self-neglect or a high risk of suicide. ECT is com-
monly carried out in an isolated site—ensure skilled assistance, adequate
monitoring and resuscitation facilities. Anaesthetic equipment may be older
or unfamiliar.12
Physiological effects of electroconvulsive therapy
During the seizure, there is parasympathetic hyperactivity, bradycardia and
hypotension, lasting about 15s, followed by a more prolonged (5min) sym-
pathetic stimulation: tachycardia, hypertension, dysrhythmias and i myo-
cardial O2 requirement. During this time, there is also i ICP, cerebral blood
flow and cerebral O2 requirement. There may also be hypersalivation,
i intragastric pressure, i intraocular pressure (IOP) and occasionally
incontinence.13
Preoperative
A careful preoperative assessment (including investigations) should be
undertaken, as for any GA. Consent is normally arranged by the psychiatry
team. ECT is typically given twice weekly for several weeks, reducing in
frequency as the patient improves. Read the notes for documentation of
previous problems.
• Absolute contraindications: recent MI or CVE, phaeochromocytoma,
intracranial mass lesion, intracranial or aortic aneurysm.
• Relative contraindications: uncontrolled angina, CCF, severe
osteoporosis, major bone fracture, glaucoma, retinal detachment. ECT
during pregnancy is acceptable.
• Avoid sedative premedication, which is anticonvulsant.
• Glycopyrronium (0.1–0.3mg IV) may be used to reduce secretions and
to counteract bradycardia. Consider antacids if history of reflux.
Perioperative
Efficacy of ECT is dependent on seizure quality, as measured by EEG-
derived variables, rather than just on duration. There is no further benefit
beyond about 60s of seizure time. Good technique provides short GA,
muscle relaxation to lessen the risk of trauma, attenuation of physiological
effects and rapid recovery.12,13,14
• Thorough preoxygenation is recommended.
• All GAs shorten the seizure in a dose-related fashion; use light doses.
340
References
1 Yentis SM, Hartle AJ, Barker IR, et al. (2017). AAGBI: consent for anaesthesia 2017: Association
of Anaesthetists of Great Britain and Ireland. Anaesthesia, 72, 93–105.
2 Cartabuke RS, Tobias JD, Rice J, et al. (2017). Hemodynamic profile and behavioral character-
istics during induction of anesthesia in pediatric patients with attention deficit hyperactivity dis-
order. Paediatr Anaesth, 27, 417–24.
3 Needham MJ, Webb CE, Bryden DC (2017). Postoperative cognitive dysfunction and dementia:
what we need to know and do. Br J Anaesth, 119(S1), i115–25.
4 Saraghi M, Golden LR, Hersh EV (2017). Anesthetic considerations for patients on antidepres-
sant therapy—Part I. Anesth Prog, 64, 253–61.
5 Peck T, Wong A, Norman E (2010). Anaesthetic implications of psychoactive drugs. Contin Educ
Anaesth Crit Care Pain, 10, 177–81.
6 Bartakke A, Corredor C, van Rensburg A (2020). Serotonin syndrome in the perioperative
period. BJA Educ, 20, 10–17.
7 Flood S, Bodenham A (2010). Lithium: mimicry, mania, and muscle relaxants. Contin Educ Anaesth
Crit Care Pain, 10, 77–80.
8 Beaulieu P (2017). Anesthetic implications of recreational drug use. Can J Anesth, 64, 1236–64.
9 Roberts TN, Thompson JP (2013). Illegal substances in anaesthetic and intensive care practices.
Contin Educ Anaesth Crit Care Pain, 13, 42–6.
10 Blincoe T, Chambler D (2019). Alcohol and anaesthesia. Br J Hosp Med, 80, 485.
11 Chapman R, Plaat F (2009). Alcohol and anaesthesia. Contin Educ Anaesth Crit Care Pain, 9, 10–13.
12 Bwalya GM, Bajekal R, Waite J (2019). Anaesthesia for electroconvulsive therapy. In: Ferrier
IN, Waite J (eds). The ECT Handbook, 4th edn. Cambridge: Cambridge University Press; pp.
202–10.
13 Uppal V, Dourish J, Macfarlane A (2010). Anaesthesia for electroconvulsive therapy. Contin Educ
Anaesth Crit Care Pain, 10, 192–6.
14 Weiss A, Hussain S, Ng B, et al. (2019). Royal Australian and New Zealand College of
Psychiatrists professional practice guidelines for the administration of electroconvulsive therapy.
Aust N Z J Psychiatry, 7, 609–23.
342
Chapter 14 343
343
Getting started
Mincho Marroquin- Harris
Getting started 344
Anaesthetic gases 345
Anaesthetic machine 348
Breathing systems 350
Ventilation 352
Airway equipment 355
Long-term venous access 359
34
Getting started
A thorough working knowledge of anaesthetic equipment is essential for
safe and effective anaesthetic practice. Although many different types of
equipment are in use throughout the world, a few basic principles underlie
the functions of nearly all of them.
Anaesthetic gases 345
Anaesthetic gases
Piped medical gases and scavenging system (PMGSS)
The PMGSS is part of the hospital infrastructure and supplies clinical areas
with compressed O2 and vacuum. Operating theatres are also supplied with
N2O, medical air and gas scavenging.
• The PMGSS is a system of seamless copper alloy pipes. Pipes are
cleaned, degreased and free of particulate matter. Colour-coding is used
on the outside of pipes at set intervals. These pipes supply the terminal
gas outlets in clinical areas.
• Terminal outlets are labelled and colour-coded, and have self-sealing
Schrader valves to prevent gas leakage. Each gas has a specific outlet
shape and diameter to prevent misconnection of equipment to the
wrong outlet.
• Alarms are activated in case of gas failure with low pressure (<370kPa)
and at high pressures (>500kPa).
• Isolation valves located in theatre complexes allow PMGSS to be turned
off in case of leak, fire or other emergency.
• Most incidents occur just following installation rather than during long-
term use. Consequently, after installation or modifications, an inspection
process is performed to ensure the correct gases are being supplied to
wall outlets.
• Safety standards and colour codes for medical gas supplies for both
pipeline and cylinder storage conform to International Organization
for Standardization (ISO) requirements. The US (and hence the airline
industry) observes its own colour scheme, in which O2 is colour-coded
green.
Oxygen
O2 is stored in bulk for hospital supply, either in a vacuum-insulated evapor-
ator (VIE) or in a cylinder manifold.
Vacuum-insulated evaporator
The VIE is the typical main O2 store for most hospitals and is a large tank of
liquid O2. One litre of liquid O2 can provide >800L of gaseous O2. Typically,
the VIE is sized to hold 200–1000L. In order to maintain its liquid state, the
VIE stores O2 at –183°C at a pressure of 1050kPa. Prior to entering the
PMGSS, O2 flows through a pressure regulator to provide a supply pressure
of 400kPa.
Cylinder manifold
A cylinder manifold consists of two banks of cylinders which are at least size
G (Table 14.1). When one bank of cylinders is exhausted, a reduction in
pressure will automatically open the 2nd bank, ensuring ongoing gas supply.
Cylinder supply
O2 is available in individual portable cylinders of various sizes. Since O2 is a
gas in the cylinder, the gauge pressure is directly proportional to the quan-
tity in the cylinder. Traditional steel cylinders are pressurised to 13 700kPa,
but more modern materials allow higher pressures in the cylinder. A type E
cylinder at 13 700kPa contains 680L of gaseous O2.
346
Nitrous oxide
N2O for hospitals is often stored in a cylinder manifold, though smaller fa-
cilities may mount a N2O cylinder on the back of the anaesthetic machine.
The mains pressure of N2O is 400kPa.
• N2O is stored as a liquid in the cylinder at 4500kPa. The gauge pressure
is not proportional to the quantity in the cylinder.
• High ambient temperatures could cause the N2O cylinder to explode.
Therefore, the cylinder is only partially filled with liquid to allow for
some expansion.
Medical air
Medical air is atmospheric air which is dehydrated and ultrafiltered to re-
move particulates. It can be supplied by an air compressor, in cylinder form
or as ‘synthetic air’ blended from gaseous O2 and nitrogen. It is often sup-
plied at two mains pressures: 700kPa to drive surgical tools, and 400kPa for
medical and anaesthetic uses.
Medical gas cylinders
Under the ISO standard, all medical gas cylinders have a white body. The con-
tents of the cylinder are denoted by the colour of the shoulder (Table 14.1).
Newer materials allow the cylinders to be light and sustain high internal
pressures. A pin-index system prevents the incorrect gas from being con-
nected to the yoke of the anaesthetic machine.
Vacuum system
The vacuum system includes both medical suction and scavenging for anaes-
thetic gases. The suction for both systems is provided by electrical pumps,
so it is susceptible to power outage.
Medical vacuum
Provides high vacuum to suction for sputum or blood. A pressure of –40kPa
or below is provided with a sustained flow of at least 40L/min.
• Suctioned material is collected in a reservoir to prevent contamination
of the PMGSS.
• Loss of suction pressure can occur from disconnection/leak in the
apparatus, blockage of filter or excessive demand.
Anaesthetic gases 347
Anaesthetic machine
The continuous- flow anaesthetic machine receives a supply of high-
pressure gases, reduces the pressure to safe levels and provides accurate
and controlled flow of gases and vapour to the patient via a breathing
system (Fig. 14.1).
High-pressure system
Takes high-pressure gas (from cylinders or wall outlets) and steps it down
to the working pressure of the machine, at the flow-control valves or flow-
meters. In older machines, this is mechanical; newer machines feature elec-
tronic control of the process.
• Gas pressures from the PMGSS are measured and reduced by
regulators. Valves ensure flow is unidirectional.
• Safety features include antihypoxia and low-pressure alarms. If the O2
supply fails, the supply of N2O is also stopped.
Low-pressure system
Extends from the flow-control valves/flowmeters to the common gas
outlet. In modern anaesthetic machines, the flow and composition of gases
are set digitally. Gases are regulated electronically based on feedback from
electronic flow and gas-content sensors. Traditional anaesthetic machines
use flowmeters. Flow is adjusted by a control knob and displayed by the
height of a rotating bobbin in a fluted glass column. Flowmeter controls are
labelled and colour-coded, and the O2 control is distinguishable by touch.
Vaporisers
Provide precise concentrations of volatile agents. Traditional variable-bypass
plenum vaporisers are calibrated mechanical devices. Newer vaporisers are
electronically controlled. Some devices are not vaporisers in the strictest
sense such as the dual-circuit gas-vapour blenders used for desflurane or
the direct-injection devices which inject precise amounts of volatile into the
gas flow under electronic control.
Common gas outlet
This is the final pathway of gases and volatile agents out of the machine.
It is standardised with a 22mm external and 15mm internal connector.
Traditionally, the breathing attachment was connected here, but in many
modern machines, the connection is internal and the common gas outlet
is absent.
Oxygen flush
• Rapidly provides 100% O2 to the common gas outlet at high flow (30–
75L/min). This O2 bypasses the low-pressure system and contains no
anaesthetic gases. The high flow and pressure have the potential for
causing barotrauma.
• Many machines feature an auxiliary O2 outlet with its own flowmeter.
However, the O2 has the same source as the common gas outlet and
should not be used if there is a problem with this supply.
Anaesthetic machine 349
Further reading
Hartle A, Anderson E, Bythell V (2012). Checking anaesthetic equipment 2012. Anaesthesia,
67, 660–8.
350
Breathing systems
For paediatric breathing systems, see % pp. 910–12. In anaesthesia, many
different breathing attachments are used to bridge the gap from the an-
aesthetic machine to the patient. One of the commonest examples in use
is the circle breathing circuit, as it is versatile and efficient (Fig. 14.2). It
comprises an inspiratory limb, an expiratory limb, a reservoir bag, a valve
and a CO2 absorber. Gas flows via the inspiratory limb to the patient via a
Y-piece, then leaves via the expiratory limb. Exhaled gas is recycled through
the CO2 absorber, which allows very economic use of anaesthetic gases
and agents. This, in turn, minimises atmospheric pollution. The recycling of
expired gases allows heat and moisture to be conserved.
Features of the circle system
• Low-resistance corrugated tubing has low compliance and low
resistance. Tubing connectors have standard 22mm (external) and
15mm (internal) dimensions.
• Unidirectional (‘flutter’) valves are present on both limbs and prevent
backflow. Moisture may accumulate on the expiratory valve, making it
sticky.
• The APL valve allows the anaesthetist to adjust the pressure in the
system during manual ventilation.
• The reservoir bag allows hand ventilation, manual appreciation of
airway compliance and visualisation of SV.
• The CO2 absorber (containing pellets of predominantly calcium
hydroxide) is located on the expiratory limb. It chemically removes CO2
in an exothermic reaction which also produces water vapour.
Other adjuncts and considerations
• An O2 analyser is always positioned on the inspiratory limb.
• The heat and moisture exchange (HME) filter was designed to prevent
particulate material from being inadvertently inhaled. Modern filter
technology provides an effective bacterial and viral barrier. The
HME filter minimises loss of heat and moisture to dry fresh gas by
providing up to 70% relative humidity. It functions poorly at high minute
ventilation and low temperatures.
• A CO2 and volatile sampling line often attaches to, or near, the HME
filter .
• At steady state and in ideal conditions, the fresh gas flow (FGF) can be
reduced to provide the patient’s basal O2 requirement (e.g. 250mL/
min) plus some volatile. However, at low flows, most of the gas the
patient receives is their own recycled expired gas. H This can result
in the patient receiving lower FiO2 and anaesthetic agents than those
selected. Some machines offer electronic control of FiO2 and end-tidal
volatile concentrations. Higher FGF is recommended at induction of
anaesthesia to ensure MAC is reached rapidly.
• Paediatric circle systems have a small (e.g. 500mL) reservoir bag and
narrower tubing.
Breathing systems 351
Fig. 14.2 Layout of a circle breathing attachment. Reproduced from Brockwell RC:
Inhaled Anesthetic Delivery Systems. In Miller RD (ed): Anesthesia, 6th ed, p 295. Philadelphia,
Churchill Livingstone, 2004, with permission from Elsevier.
Ventilation
Self-inflating bag
The self-inflating resuscitation bag allows the anaesthetist to deliver positive
pressure ventilation without an O2 source, e.g. ventilation outside of the
operating theatre, resuscitation of a collapsed casualty or in case of venti-
lator malfunction. A self-inflating bag should always be immediately available
in theatre.
• There are several brands with different sized bags, typically adults 1.5–
2L and paediatrics 250mL to 1L bags.
• A unidirectional valve controls the direction of flow and prevents
rebreathing of CO2. There is little apparatus dead space. The casing is
clear, allowing the valve to be assessed during an equipment check.
• A PEEP valve may be applied to the expiratory port.
• The patient end of the self-inflating bag can be connected to anaesthetic
face masks, ETTs or LMAs.
• When a face mask is attached, it is recommended to use 15L/min of O2
which may splint the unidirectional valve slightly open, reducing work of
breathing. Otherwise spontaneous breaths should be assisted due to i
work of breathing through the unidirectional valve.
• The bag reinflates with room air, but an O2 line and a reservoir bag can
be added. High FiO2 is possible with a good seal.
Mechanical ventilation
The goal of mechanical ventilation in the anaesthetised patient is to support
adequate gas exchange and minimise iatrogenic injury.
Modes of ventilation
When patient-centred outcomes are considered, no particular ventilation
mode has been shown to be better than another. Modern ventilators offer
a large variety of electronically controlled modes, the terminology of which
varies between manufacturers. Mandatory modes tend to ignore any re-
spiratory effort from the patient, but triggered (supportive) modes permit
the patient to initiate a breath, which is then augmented by the ventilator.
Volume control ventilation
Volume control ventilation is a mandatory mode of ventilation where the
anaesthetist sets a desired VT and RR. This mode is tolerant of changes in
respiratory compliance, though any d in compliance may lead to i airway
pressures, and volume control ventilation usually delivers higher pressures
for the same VT, compared to pressure control ventilation. The mode is
usually intolerant of leaks.
Pressure control ventilation
Pressure control ventilation is a mandatory mode where the anaesthetist
sets the pressure to be delivered and the RR. This mode is tolerant of small
leaks, but any d in respiratory compliance will lead to d in VT.
Pressure control ventilation, volume guaranteed (PCV-VG)
This is a mandatory mode of ventilation which attempts to provide the
advantages of both pressure control ventilation and volume control ven-
tilation, delivering a set VT at the lowest possible pressure. This allows for
relatively constant VT despite changes in respiratory compliance.
Ventilation 353
Airway equipment
For paediatric airway equipment, see % pp. 908–10.
Endotracheal tube
The ETT remains the gold standard for securing and protecting the airway.
It is usually made of polyvinyl chloride, which is clear. Silicone tubes are
softer to reduce trauma, but opaque. The size of the tube refers to its in-
ternal diameter in mm.
• The proximal end has a standard 15mm connector. The tube has
markings for length. The distal end has a bevelled tip assisting passage
through the vocal cords, and often a Murphy eye to reduce the
likelihood of obstruction against the wall of the airway. ETTs should
have a radio-opaque insert for visualisation on X-ray.
• The cuff is normally the low-pressure, high-volume type. Cuff pressure
can be measured via the pilot balloon and should be 20–30cmH2O. Very
small-diameter tubes (e.g. for neonatal use) usually have no cuff (see %
pp. 922–4). There are many variations on the basic ETT design.
Ring, Adair and Elwyn (RAE) tubes
These are preformed tubes, designed to pass downward over the chin
(oral) or upward over the forehead (nasal), and hence obstruct the surgical
field as little as possible. They can be difficult to pass over a bougie, and the
position of the bend varies by manufacturer.
Nasal tubes tend to be made of silicone to reduce trauma.
Reinforced tubes
These have a metallic coil in the wall of the tube which reduces kinking.
Laser-proof tubes
These are resistant to laser and used for surgery involving laser in the oro-
pharynx. They may have two cuffs in case one is punctured by the laser (see
% pp. 478–9).
Microlaryngeal tubes
These have a smaller outer diameter for the same inner diameter and are
longer. Used for laryngeal surgery.
Neural integrity monitor
Enable monitoring of laryngeal nerve function via EMG and attached
electrodes.
Double-lumen tubes (DLTs)
There are two tubes, within one outer casing, which can be ventilated
together or independently. These tubes allow lung isolation for thoracic
surgery. The sizing and shaping of DLTs are specific to this tube (see %
pp. 535–7).
Laryngectomy and tracheostomy tubes
Short, kink-resistant, J-shaped tubes for placement into a tracheostomy.
Supraglottic airways
Since the introduction of the classic LMA in the late 1980s, there has been
considerable modification and refinement of the basic design, leading to a
wide range of devices becoming available.
The SGA (also referred to as supraglottic airway device (SAD)) consists
of a flexible tube ending in a soft (usually inflatable) cuff designed to form
356
a seal around the larynx without entering it. SGAs are popular due to ease
of placement and avoid many of the drawbacks of intubation, e.g. d sym-
pathetic stimulation, d sore throat, d trauma to teeth and airway struc-
tures, d bronchospasm, d coughing on emergence. With a reasonable seal,
SGAs are suitable for mechanical ventilation. They do not provide protec-
tion from laryngospasm or aspiration. Newer designs incorporate a gastric
channel to d risk of aspiration.
First-generation SGA
One airway tube with the laryngeal mask cuff at the end (Fig. 14.3).
Common variants of the classic LMA include:
• Flexible LMA: longer and narrower, wire-reinforced tube to prevent
kinking, allowing movement away from surgical field
• Intubating LMA (Fastrach®): designed to allow blind intubation of the
trachea by passing a Fastrach® ETT through the airway channel. This
device is rigid and has a preformed 90° curve.
This chapter copyright © Tim Cook, Julius Cranshaw and Emira Kursumovic
362
Airway terminology
There is an increasing focus on standardising airway nomenclature for safer
and more effective communication. All who manage the airway should use,
as far as possible, the same terminology. Some terms are archaic and can
be simplified. Latin or ancient Greek should not be needed! The following
terms are used in this chapter:
• Flexible optical bronchoscope (FOB) in preference to fibreoptic
bronchoscope. The abbreviation is retained, but this better reflects
modern equipment which does not contain fibres.
• Awake tracheal intubation (ATI) in preference to awake fibreoptic
intubation (AFOI). Modern ATI may be performed with many
instruments, including videolaryngoscopes. Few are now fibreoptic.
• Cannot intubate, cannot oxygenate (CICO) in preference to ‘cannot
intubate, cannot ventilate’, ‘total airway failure’ or other similar
descriptors. Safe communication requires all the words are spoken.
‘CICO’ may be used in writing, but in speech, different pronunciations
(khy-kho, si-co, psycho, etc.) and incomprehension hinder a time-critical
message.
• Cricoid force in preference to cricoid pressure. This is applied in units
of force (N or kg) and is correctly described as such.
• Front of neck airway (FONA) and in an emergency, eFONA, in
preference to front of neck access, emergency surgical airway,
infraglottic access, etc.
• Supraglottic airway (SGA) in preference to supraglottic airway
device (SAD).
• Tracheal tube (TT) in preference to endotracheal tube (ETT).
SGAs
For basic information on adult and paediatric airway equipment, see
% pp. 355-8; % pp. 908-10.
The division between first-and second-generation SGAs is pragmatic with
first-generation devices being ‘simple airway tubes’, including the ‘classic
LMA’ and ‘flexible LMA’. Second-generation devices are those with design
features intended to reduce the risk of pulmonary aspiration of gastric con-
tents. These include the ‘LMA ProSeal™’, ‘LMA Supreme™’ and ‘i-gel®’.
Further reading
Chrimes N, Cook TM (2017). Critical airways, critical language. Br J Anaesth, 118, 649–54.
Airway assessment 363
Airway assessment
The difficult airway is the most important cause of anaesthesia-related
morbidity and mortality. Around 30% of deaths attributable to anaesthesia
are associated with problematic airway management. Some catastrophes
are due to suboptimal management in unforeseen circumstances. Others
are due to poor planning in patients with known or predictable difficul-
ties. History, examination and investigations must detect risks to airway
maintenance, ventilation and oxygenation, not just difficult laryngoscopy.
Assessment must inform an airway ‘strategy’ that anticipates and avoids
predicted difficulties, or mitigates adverse effects.
• Beware multiple predictors of difficulty (an indication of high risk).
• Difficulty or failure with one airway management technique is associated
with difficulty and failure with other techniques.
• Intubation is difficult in 71:50 cases (71:10 in ICU) and impossible in
71:200–1500, depending on setting. Beware risk factors for rapid
hypoxaemia (pregnancy, obesity, infants, existing hypoxaemia). These
mandate great care planning intubation and ventilation strategies (e.g.
preoxygenation, peroxygenation, high-pressure airway seal and PEEP).
• Be familiar with your rescue devices: SGAs, VLs, intubation aids and
eFONAs.
Predictors of difficult airway management
History
Question the patient and check health care records, anaesthetic charts,
alerts and databases for previous airway difficulties, including:
• Anaesthesia-associated dental damage or severe sore throat
• Associated syndromes (e.g. Down, Klippel–Feil, craniofacial)
• Acquired difficulties (e.g. pregnancy, obesity, diabetes, RA, ankylosing
spondylitis, acromegaly, Still’s disease, snoring, OSA)
• Iatrogenic problems (e.g. C-spine fusion, oral/pharyngeal radiotherapy,
laryngeal/tracheal/temporomandibular joint (TMJ) surgery).
Examination
• Anatomical impediments (e.g. small mouth, receding chin, high arched
palate, large tongue, bull neck, obesity, large breasts).
• Acquired problems (e.g. head/neck burns, goitre, tumour, haematoma,
infection, abscess, restrictive scars). Reduced mouth opening and
temporomandibular advancement (e.g. dental abscess, quinsy, TMJ
surgery, post-radiotherapy).
• Poor C-spine movement, especially upper extension.
• Poor dentition (e.g. anterior gaps, sharp/loose/protruding/inward/
awkward teeth).
• Orthopaedic/neurosurgical/orthodontic equipment (e.g. neck collar,
halo traction, external fixator, stereotactic locator, dental wiring).
• If using the nasal route for FOB, check patency of nasal passages.
• Facial hair may hide adverse anatomical predictors.
• Some hairstyles cause difficult intubation.
364
Radiology
• Check imaging (including CXR) for potentially difficult anatomy. A
recent, focused CT/MRI will give more valuable information.
• Check C-spine X-rays. Occipito-atlanto-axial disease is more predictive
of difficult direct laryngoscopy than disease below C2.
• Loss of cervical disc space predicts difficult intubation.
• Flexion/extension or dynamic C-spine studies can confirm instability.
Plain X-rays are inadequate predictors of cervical stability.
Predictors of difficult mask ventilation
• Mask ventilation is difficult in 71–3% of cases; impossible in 71:600.
• Age >60yr, ♂ sex, full beard, BMI >35kg/m2, previous difficult tracheal
intubation, snoring, OSA, absence of teeth, thyromental distance <6cm,
modified Mallampati classes 3 and 4 (Fig. 15.1), facial abnormalities, neck
radiotherapy, DIFFMASK score ≥5.1
• The DIFFMASK score uses ten predictors of difficult mask ventilation
and ranges 0–18. Scores 6–10 merit detailed further assessment; higher
scores predict risk.
Predictors of difficult SGA insertion and ventilation
• First-time SGA insertion and ventilation fails in >5% of attempts.
• Difficult SGA placement is associated with: narrow gape (insertion
may be impossible); intraoral/pharyngeal masses (e.g. lingual tonsils);
obesity; and poor dentition.
• Second-generation SGAs are more likely to succeed at first insertion.
Some can aid intubation. Higher laryngeal seal pressures (726–
30cmH2O vs 715–20cmH2O) may enable ventilation of patients with
low chest compliance and use of PEEP. With higher oesophageal seal
pressures and a drain port, they may reduce aspiration risk.
Predictors of difficult direct laryngoscopy
• Direct laryngoscopy needs a line of sight from upper teeth to glottis. It
entails mouth opening, extension of upper C-spine and displacing the
mandibular arch tissues.
• Predictive tests check one or more of these capabilities, but direct
laryngeal view grade (Fig. 15.2) correlates modestly with difficult
intubation. Most failures occur with grade 2 or 3. Functional grades
have therefore been proposed (Fig. 15.3).
• Problems with predictive tests include frequent false positives (a
smaller number are actually difficult) and negatives (most difficulties are
unpredicted). Combining tests exacerbates these problems.
Interincisor gap (II gap)
The distance between the incisors (or alveolar margins) with the mouth
open maximally:
• <3cm predicts difficulty.
• <2.5cm—SGA insertion will also be difficult.
Mandibular protrusion
• Class A: can protrude lower incisors anterior to upper incisors.
• Class B: can protrude lower incisors to, but not beyond, upper incisors.
• Class C: cannot protrude lower incisors to upper incisors.
Classes B and C are associated with difficulty.
Airway assessment 365
Fig. 15.3 Cook’s modified classification of the laryngeal view. Grades 1–4 refer to
Cormack and Lehane’s classification. In Cook’s classification, ‘easy’ views (glottis visible) require
no adjuncts; ‘restricted’ views (posterior laryngeal structures visible or epiglottis liftable) require
a bougie; ‘difficult’ views (epiglottis not liftable or not visible) require advanced techniques to
intubate.
Fig. 15.4 Unanticipated difficult tracheal intubation. Reproduced from Difficult Airway
Society 2015 guidelines for management of unanticipated difficult intubation in adults. Difficult
Airway Society intubation guidelines working group, BJA, 115(6), 827–848. doi:10.1093/bja/
aev371. Permission for the use of these algorithms for commercial purposes must be sought
directly from Difficult Airway Society as they hold the copyrights.
Obstetric considerations
(For failed intubation in obstetric anaesthesia, see % p. 864.)
• The incidence of failed intubation is high (71:300) due to patient,
surgical and environmental factors.
• Consider obstetric difficult airway guidelines. Most advocate ≤2
intubation attempts, with one more reserved for an experienced
practitioner.
• High-flow nasal oxygen (HFNO) delays desaturation after induction of
GA (see also % p. 397).
Follow-up of patients with difficult airways
• Document difficulties and successful and unsuccessful approaches in
health care records.
• Make sure these are easily accessible and prominent (e.g. in ‘Alert’
sections). Complete an ‘airway alert’ form for local and national (e.g.
DAS) databases.
• Advise patients that they may register with independent medical alert
providers. Warn about delayed symptoms of airway trauma and how to
seek help.
Intubating critically ill patients 373
Fig. 15.5 Tracheal intubation in critically ill adults. Reproduced from Difficult Airway
Society 2015 guidelines for management of unanticipated difficult intubation in adults. Difficult
Airway Society intubation guidelines working group, BJA, 115(6), 827–848. doi:10.1093/bja/
aev371. Permission for the use of these algorithms for commercial purposes must be sought
directly from Difficult Airway Society as they hold the copyrights.
Fig. 15.6 Intubating checklist for critically ill adults. Reproduced from Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in
adults. Difficult Airway Society intubation guidelines working group, BJA, 115(6), 827–48. doi:10.1093/bja/aev371. Permission for the use of these algorithms for commercial
Intubating critically ill patients
purposes must be sought directly from Difficult Airway Society as they hold the copyrights.
375
376
Plan A
The goal is timely, atraumatic first-time intubation by optimising position,
NMB, laryngoscopy, teamwork and equipment. This is supported by
maximised preoxygenation and peroxygenation. Beware a low PaO2 after
preoxygenation predicts hypoxaemia after induction.
Preoxygenation
Consider using:
• Tight-fitting mask, O2 at 15L/min with a system enabling some CPAP,
e.g. Water’s circuit (Mapleson C).
• HFNO at 30–70L/min.
• CPAP with 100% O2.
• Non-invasive ventilation with 100% O2.
• Nasal cannula O2 at 5L/min while the patient is awake and 15L/min
when the patient is induced.
Nasal cannulae can prevent mask seal. If a seal is made, simultaneous
HFNO may cause high airway pressure, as HFNO systems have no pres-
sure relief valve.
• HFNO contraindications include basal skull and facial fractures.
• Running HFNO, a breathing system, e.g. Water’s circuit (Mapleson C),
and a ventilator simultaneously requires three near-patient O2 sources.
• Existing CPAP and non-invasive ventilation systems might be left in situ
during induction, but plan when and how to remove masks quickly to
allow laryngoscopy.
Peroxygenation
HFNO or nasal O2 at 15L/min should be provided until intubation is
successful.
Positioning
Raise the bed head up 20–30° to aid oxygenation. Tilting the whole bed
may be safer in known or suspected spinal injury. Start with the ‘sniffing
position’. In obesity, ‘ramp’ the upper body so the external auditory meatus
is level with the sternal notch and the face horizontal.
Induction
• Ketamine may have advantages over other induction agents. Small doses
during preoxygenation may ease cooperation.
• Rapid-acting opioids, such as fentanyl or alfentanil, may aid CVS stability.
• For rapid NMB, rocuronium has advantages over suxamethonium;
fewer contraindications and adverse effects (fasciculations consume
O2). Rocuronium 1.2mg/kg achieves intubating conditions as fast as
suxamethonium 1mg/kg.
• If indicated, ask a trained assistant to apply cricoid force—10N (1kg) on
induction, i to 30N (3kg) after loss of consciousness. Cricoid force may
reduce aspiration and stomach inflation but, especially if excessive, can
impede face mask ventilation, laryngoscopy and passage of the TT. VL
may aid appropriate cricoid force. Remove cricoid force if vomiting and
when inserting an SGA.
• While waiting for effective NMB, sustain oxygenation by ventilation.
Ventilation may also control PaCO2. This might be important in raised
ICP, pregnancy, pulmonary hypertension and acidaemia. Keep airway
pressure low (preferably <20cmH2O) to avoid stomach inflation.
Reduce cricoid force if ventilation is difficult. Have suction ready.
Intubating critically ill patients 377
• Use a laryngoscope and blade with which you have gained confidence.
Ready your second choice. Limit intubation attempts to ≤3. Allow an
expert one attempt. Maintain oxygenation between attempts.
• If direct laryngoscopy is your first approach, ready a GEB, introducer or
stylet. Use carefully. Avoid ‘blind’ insertion.
• Consider VL as your first choice if trained. Switch to VL if you have
difficulty. It is likely VL will improve your view, reduce trauma and
increase success. If trained, use a hyperangulated blade with a stylet
when a Macintosh-style blade fails. Use your assistants. VL with a screen
shared by assistants can direct them to improve OELM, BURP and
cricoid force. Blood, secretions and reflux may hamper VL (and direct
laryngoscopy).
• Reduce or release cricoid force if the view or TT passage is
problematic. Be ready with suction.
• Where there is difficulty, choose a TT type and size allowing the best
laryngeal view, easy passage and least trauma. TTs with subglottic
suction have larger external diameter. The size and type may not be
optimal for long-term ICU ventilation. However, TT exchange after
stabilisation may be safer than failing with a large TT.
• If Plan A fails, declare clearly, ‘Failed intubation!’
• Call for expert help.
• Open and prepare your eFONA kit.
• If Plan A succeeds, planned and preset ventilation strategies may re-
establish and improve oxygenation quickly.
Plan B/C for failed intubation
The goal is successful oxygenation (Plan B). The ‘high’ seal pressure pro-
vided by a second-generation SGA may enable you to ventilate a low-
compliant chest with PEEP. Aspiration risk is reduced.
• Minimise insertion attempts (≤3).
• If an attempt fails, try a new SGA size, type, insertion technique or
operator.
• One failed optimal attempt might enable you to rule out SGA insertion
as a successful approach.
• Attempt mask ventilation (Plan C) between SGA insertion attempts.
Insert a correctly sized OPA. Use a ‘VE’ grip, thumbs caudad on each
side of the mask. Use your fingers to lift the chin. Ask an assistant to
add ‘jaw thrust’. Use a Water’s circuit (Mapleson C) to give 100% O2
with CPAP.
• Minimise mask ventilation attempts (≤3).
• One failed optimal attempt might lead you to abandon mask ventilation
as a successful option.
• Consider a nasal airway, but beware bleeding.
• Allow an expert one attempt at SGA insertion and mask ventilation,
BUT they may choose an immediate eFONA.
• Recognise failure of Plans B and C within 1min.
• Clinical deterioration and worsening oxygenation mandate rapid
transition to eFONA.
• Declare clearly, ‘I cannot intubate and cannot oxygenate. We need an
emergency front of neck airway!’ (Plan D).
378
Further reading
Higgs A, McGrath BA, Goddard C, et al. (2018). Guidelines for the management of tracheal intub-
ation in critically ill adults. Br J Anaesth, 120, 323–52.
Black AE, Flynn PER, Smith HL, et al. (2015). Development of a guideline for the management of the
unanticipated difficult airway in pediatric practice. Paediatr Anaesth, 25, 346–62.
Frerk C, Mitchell VS, McNarry AF, et al. (2015). Difficult Airway Society 2015 guidelines for manage-
ment of unanticipated difficult intubation in adults. Br J Anaesth, 115, 827–48.
Mushambi MC, Kinsella SM, Popat M, et al. (2015). Obstetric Anaesthetists’ Association and Difficult
Airway Society guidelines for the management of difficult and failed tracheal intubation in obstet-
rics. Anaesthesia, 70, 1286–306.
Cook TM, MacDougall-Davis SR. (2012). Complications and failure of airway management. Br J
Anaesth, 109 Suppl 1, i68–85.
Cook TM, Woodall N, Harper J, et al; Fourth National Audit project (2011). Major complications of
airway management in the UK: results of the Fourth National Audit Project of the Royal College
of Anaesthetists and the Difficult Airway Society. Part 2: intensive care and emergency depart-
ments. Br J Anaesth, 106, 632–42.
Nolan JP, Kelly FE (2011). Airway challenges in critical care. Anaesthesia, 66 (Suppl 2), 81–92.
De Jong A, Molinari N, Terzi N, et al. (2013). Article 1. Early identification of patients at risk for
difficult intubation in the intensive care unit: development and validation of the MACOCHA
score in a multicenter cohort study. Am J Respir Crit Care Med, 187, 832–9. doi:10.1164/
rccm.201210- 1851OC
MANAGEMENT OF DIFFICULT INTUBATION 379
Bladed videolaryngoscopes
• Include straight and Macintosh style (enabling direct laryngoscopy) and
hyperangulated blades (which do not). May be single use or reusable.
• Blade design may facilitate standard, midline or paramedian insertion
and enable some airway manipulation, but a stylet or bougie may be
essential to intubate.
• These include C-MAC®, GlideScope®, I-view™ and McGrath™.
Conduited videolaryngoscopes
• Have a channel to guide a TT into the camera view.
• TT size and type relative to the conduit may affect intubation success.
Avoid relatively small TTs. They may ‘cut the angle’ created by the
channel and point posteriorly.
• These include Airtraq™, Pentax AWS®, King Vision™ and Venner A.P.
Advance™.
Optical stylets
• Are preformed rigid or malleable metal guides connecting an imaging
system to an eyepiece or screen.
• A TT is preloaded, manipulated to the glottis and advanced into the
trachea. Stylets require minimal mouth opening but have limited ability
to displace tissues.
• They may be used for ATI or as a ‘light wand’.
• These include Bonfils®, Levitan, Shikani and Trachway®.
Further reading
Cook TM, Kelly FE (2017). A national survey of videolaryngoscopy in the United Kingdom. Br J
Anaesth, 118, 596–600.
Lewis SR, Butler AR, Parker J, et al. (2016). Videolaryngoscopy versus direct laryngoscopy for adult
patients requiring tracheal intubation. Cochrane Database Syst Rev, 11, CD011136.
Zaouter C, Calderon J, Hemmerling TM (2015). Videolaryngoscopy as a new standard of care. Br
J Anaesth, 114, 181–3.
Behringer EC, Kristensen MS (2011). Evidence for benefit vs novelty in new intubation equipment.
Anaesthesia, 66 Suppl 2, 57–64.
Dhara SS (2009). Retrograde tracheal intubation. Anaesthesia, 64, 1094–104.
Waters DJ (1963). Guided blind endotracheal intubation. Anaesthesia, 18, 158–62.
Emergency front of neck airway 381
Scalpel cricothyroidotomy
Equipment: 1. Scalpel (number 10 blade)
2. Bougie
3. Tube (cuffed 6.0mm ID)
This flowchart forms part of the DAS Guidelines for unanticipated difficult
intubation in adults 2015 and should be used in conjunction with the text.
Fig. 15.7 Cannot intubate, cannot oxygenate. Reproduced from Difficult Airway Society
2015 guidelines for management of unanticipated difficult intubation in adults. Difficult Airway
Society intubation guidelines working group, BJA, 115(6), 827–48. doi:10.1093/bja/aev371.
Permission for the use of these algorithms for commercial purposes must be sought directly from
Difficult Airway Society as they hold the copyrights.
Options
• ATI. Consider if mask ventilation will be difficult. However, ATI may be
intolerable to the patient or cause crisis. Coughing, respiratory distress
and passing an FOB, TT or ventilating catheter through a narrowing may
critically increase obstruction (‘cork-in-a-bottle’).
• In specialist hands:
• FOB-guided insertion of a long, narrow TT (e.g. microlaryngeal
tube, endobronchial tube or AIC (6.3mm external diameter)) allows
conventional ventilation.
• Jet catheters (e.g. LazerJet®, Hunsaker) or other narrow catheters,
such as Cook® airway exchange catheters, enable jet ventilation
but risk barotrauma. A route of exhalation is essential. A Tritube®
(4.4mm external diameter) used with a Ventrain® or Evone® ventilator
enables ‘jet’ inspiration and assisted expiration, reducing the chance
of barotrauma.
• If rigid bronchoscopy is available: IV induction and rapid NMB or
inhalational induction, and passage of a rigid bronchoscope. The
bronchoscope also allows resection, laser or stenting.
• Inhalational induction may be very slow and worsen obstruction,
especially in collapsible lesions. Have a backup plan, especially if mask
ventilation is likely to be difficult.
Lower tracheal lesions and bronchial obstruction
Common causes: tumours, trauma and large mediastinal masses. These are
best managed in specialist centres with facilities for CPB but may present to
ED in extremis. Depending on the lesion, laser resection or stenting may be
required to maintain a patent airway.
Options
• Either IV induction with rapid NMB or inhalational induction followed
by passage of a rigid bronchoscope or FOB-guided double-lumen or
endobronchial tube.
Extubation
Have a management plan for extubation, which may need to be delayed.
Prolonged instrumentation may cause upper airway oedema. Transfer to
ICU or HDU is often necessary before extubation.
Further considerations
• A specific tissue diagnosis may enable preoperative shrinking of a lesion
with antibiotics, steroids, chemotherapy or radiotherapy where time
allows.
• Heliox (premixed helium/O2 containing 21–40% O2) improves gas flow
through narrowed airways, but the FiO2 is low. Increasing FiO2 reduces
the effect of the helium. Specific delivery systems and ventilators for
Heliox exist. Heliox can be useful for any obstruction but is usually a
temporary measure while organising definitive management.
Emergency management of the obstructed airway 387
Further reading
Ahmad I, El-Boghdadly K, Bhagrath R, et al. (2019). Difficult airway society guidelines for awake tra-
cheal intubation (ATI) in adults. Anaesthesia, 75, 509–29.
Cook TM, Morgan PJ, Hersch PE (2011). Equal and opposite expert opinion. Airway obstruction
caused by a retrosternal thyroid mass: management and prospective international opinion.
Anaesthesia, 66, 828–36.
Patel A, Pearce A, Pracy P (2011). Head and neck pathology. In: Cook TM, Woodall N, Frerk C
(eds). 4th National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society.
Major complications of airway management in the United Kingdom. Report and findings, March 2011.
London: The Royal College of Anaesthetists; pp. 143–54. M https://www.nationalauditprojects.
org.uk/NAP4_home
Nouraei SA, Giussani DA, Howard DJ, et al. (2008). Physiological comparison of spontaneous and
positive-pressure ventilation in laryngotracheal stenosis. Br J Anaesth, 101, 419–23.
Gerig HJ, Schnider T, Heidegger T (2005). Prophylactic percutaneous transtracheal catheterisa-
tion in the management of patients with anticipated difficult airways: a case series. Anaesthesia,
60, 801–5.
Ovassapian A, Yelich SJ, Dykes MHM, et al. (1983). Fibre-optic nasotracheal intubation—incidence
and causes of failure. Anesth Analg, 63, 692–5.
38
Risks
• RSI with cricoid force increases the risk of difficult intubation, partly due
to pressure of time and incorrect cricoid force.
• Excessive induction agent may cause CVS collapse, especially in the
presence of hypovolaemia or septic shock.
• Inadequate induction agent may cause tachycardia and hypertension.
Thiopental, in particular, risks accidental awareness during GA (AAGA).
Cricoid force
• Applying cricoid force is a skill. It is often poorly taught and practised.
• Learn to identify the cricothyroid membrane. It is usually in the middle
of the neck, below the ‘Adam’s apple’ at the 2nd skin crease. The
cricoid cartilage is immediately below.
• Hold the cricoid cartilage between the thumb and middle finger and
push onto the neck with the index finger.
• Practise applying the correct force. Compress an air-filled, sealed
syringe positioned vertically on the plunger. Compressing 20mL of air to
12mL, or 50mL to 32mL requires 730N (3kg).
• Correct application improves direct laryngoscopy, reduces the risk of
gastric inflation and does not occlude the airway.
• Excessive force >50N (>5kg) produces airway obstruction and makes
intubation more difficult.
• If intubation is difficult, reduce and if necessary, remove cricoid force.
This may improve the laryngeal view and enable intubation. Have
suction ready. If a patient regurgitates, cricoid force may need to be
reapplied.
• BURP may improve the laryngeal view but increases the risk of
obstruction. If ventilation is difficult, remove BURP.
• Release cricoid force if a patient vomits early during induction. Vomiting
does not occur after loss of consciousness.
• Bimanual force (other hand behind the neck) has not been shown to be
of benefit in supine patients and uses up one of the assistant’s hands. It
is not recommended.
• Some patients may only tolerate cricoid force after induction.
• Applying consistent cricoid force is difficult for >5min.
• If intubation fails, cricoid force must be removed to enable SGA
placement.
Controversies
• RSI with cricoid force has not been proven to reduce aspiration.
• Titrating induction agent to loss of consciousness is sometimes
preferred.
• Rapid-acting opioids of short duration are often used to aid
haemodynamic stability and improve intubation conditions, e.g. alfentanil
(10–30 micrograms/kg) or remifentanil (1–2 micrograms/kg) 1min
before induction. Lidocaine (1–1.5mg/kg) is less commonly used.
• Using sufficient opioid to avoid NMB is not commonly practised nor
recommended.
• After RSI for CS, beware neonatal respiratory depression if opioids are
given to the mother on induction.
• It is a fallacy that ‘RSI is safe because the patient will wake if there are
airway complications’. In the event of failed intubation, whatever drug
combination is used, induction agents and NMBAs are very unlikely
390
Inhalational induction
See also % pp. 408–9.
Relative indications
• To avoid IV induction: children, needle phobia, difficult IV access.
• To maintain airway patency and SV during induction:
• Anticipated difficult intubation ± difficult mask ventilation, e.g. acute
epiglottitis, perilaryngeal tumours
• Inhaled foreign body
• Bronchopleural or tracheo-oesophageal fistula.
394
Chapter 15
Airway assessment and management
Fig. 15.8 Difficult Airway Society ATI technique. Reproduced from Ahmad I,. et al. (2019). Difficult airway society guidelines for awake
tracheal intubation (ATI) in adults, Anaesthesia, 75(4), 509–28 with kind permission of the Difficult Airway Society.
Awake tracheal intubation 395
Local anaesthesia
• Specific airway nerve blocks (sphenopalatine, ethmoid,
glossopharyngeal, superior laryngeal, recurrent laryngeal) can be
effective in skilled hands. Topical LA is an alternative.
• The DAS ATI LA technique is outlined in Fig. 15.8. Lidocaine is
potentially safer than other LAs. Nebulised, it has variable success.
Transtracheal LA injection is invasive, effective and ensures careful
examination of the front of the neck. The total dose of lidocaine should
not exceed 9mg/kg, but this is rarely needed.
• Treatments for toxicity must be immediately available.
Postoperative care
• Plan extubation and potential reintubation carefully. If the airway
remains at risk, delay extubation. The TT may need to be exchanged for
another type or size to facilitate intensive care.
• Postoperatively, if you can, check if direct laryngoscopy is possible.
• Keep the patient starved until airway sensation and reflexes have
returned. After lidocaine, this usually takes >2h.
• Reusable FOB, VLs and other instruments must be decontaminated and
disinfected.
Dealing with difficulty
Sedation
• Sedation can help anxiety, discomfort and intolerance but can cause
airway obstruction, cardiorespiratory depression and hypoxia. Sedation
is not a substitute for effective LA.
• A cautious remifentanil or dexmedetomidine infusion may be safer than
propofol.4 Another anaesthetist monitoring sedation improves safety.
Adding another drug (e.g. midazolam) adds risk. Antagonists must be
immediately available if using opioids and benzodiazepines.
Oral route
• Specialised FOB conduits, e.g. the Berman Airway, Ovasappian Airway
and Williams Airway Intubator, protect the FOB and can improve
laryngoscopy. However, they may not fit well and move from the
midline, making laryngoscopy and intubation difficult.
• Awake insertion of an SGA as a conduit has been described.
Nasal route
• This may be the only option with a narrow gape.
• Assess the patency of nasal passages and any history of epistaxis.
• Topical vasoconstrictors (e.g. phenylephrine) reduce bleeding risk.
• Guiding a TT through the nose with an FOB before advancing to the
larynx avoids realising the TT will not pass through the nose later.
• Nasal dilators (e.g. lubricated nasopharyngeal airway or Hegar cervical
dilators) may make TT passage easier but risk epistaxis.
396
Apnoeic oxygenation
• Preceded by effective preoxygenation, administering O2 via a patent
airway prolongs time to desaturation during apnoea.7
• Alveolar O2 diffusing into blood draws O2 from the airways by
convection. Optimising lung volume and blood flow matching, e.g. by
positioning and CPAP, may enhance this process. Air entrainment must
be minimised.
• Insufflation sources for airway surgery include nasal cannulae, a RAE
TT wrapped round the cheek, nasopharyngeal airways and catheters,
dedicated ports on surgical laryngoscopes and bronchoscopes, and
airway and cricothyroid catheters.
• Note that insufflation devices rarely incorporate pressure-limiting
valves. Inadequate O2 egress from the airway can cause barotrauma.
High-flow nasal oxygenation
HFNO systems deliver heated, humidified O2 via nasal cannulae at up to
50–70L/min. Perioperative systems typically provide 100% O2 only. With
SV, HFNO can provide CPAP (75cmH2O) when the mouth is closed.
Anatomical dead space and upper airway resistance are reduced.
Uses of HFNO
To decrease the risk of hypoxia during intubation in
• Anticipated and known difficult airway management
• RSI
• Obesity (BMI >40kg/m2)
• OSA
• Obstetric patients
• Critically ill patients.
With a patent upper airway, HFNO can enable prolonged apnoeic oxy-
genation during airway management. Beware. An airway rescue strategy
is essential.
Tubeless anaesthesia
• Transnasal humidified rapid-insufflation ventilatory exchange (THRIVE),
i.e. continuous HFNO during apnoea, is a method of increasing apnoea
time in patients with difficult airways undergoing ‘tubeless’ upper airway
surgery.
• Sustained oxygenation may exceed 30min, sometimes up to 71h, in
some low-risk patients.
• Patient selection is crucial. Hypoxaemia onset is more rapid with
obesity.
• Although gas mixing by turbulence and cardiogenic airway oscillation
enables some CO2 clearance, some hypercarbia is the norm.
• ETCO2 measurement can be obtained by intermittent ventilation but
values underestimate PaCO2 which rises unpredictably. PaCO2 may be
>10kPa after 20min. Blood gas or transcutaneous CO2 monitoring has
been recommended but is not routine.
398
Contraindications to HFNO
• Maxillofacial trauma (e.g. base of skull, mid-facial fractures)
• Epistaxis
• Nasal obstruction
• Airway laser or diathermy (fire risk)
• Lack of patient cooperation
• Contraindications to CPAP.
A plan for preoxygenation and THRIVE with HFNO
• Set up and warm the system before the patient arrives.
• Apply HFNO at 720L/min immediately on arrival.
• Ask the patient to breathe through their nose, mouth closed.
• Position 20–45° head up.
• Increase O2 flow to 50–70L/min if tolerated.
• After induction and loss of consciousness, maintain oropharyngeal
patency with two-handed jaw thrust.
• Increase O2 flow to 70L/min.
• Place nasal cannulae on the forehead.
• Confirm you can mask ventilate.
• Return the nasal cannulae to the nares.
Special considerations
• To reduce barotrauma risk, make sure the APL valve of any breathing
system is fully open if you apply simultaneous mask O2 and HFNO.
• Even though HFNO may provide prolonged oxygenation, when an
aspiration risk is present or the airway may be lost, secure the airway by
intubation as quickly as feasible.
Further reading
Patel A, Nouraei SA (2015). Transnasal humidified rapid- insufflation ventilatory exchange (THRIVE):
a physiological method of increasing apnoea time in patients with difficult airway. Anaesthesia,
70, 323–9.
Hermez LA, Spence CJ, Payton MJ, et al. (2019). A physiological study to determine the mechanism
of carbon dioxide clearance during apnoea when using transnasal humidified rapid insufflation
ventilatory exchange (THRIVE). Anaesthesia, 74, 441–9.
Lyons C, Callaghan M (2019). Uses and mechanisms of apnoeic oxygenation: a narrative review.
Anaesthesia, 74, 497–507.
Gustafsson IM, Lodenius Å, Tunelli, et al. (2017). Apnoeic oxygenation in adults under general anaes-
thesia using Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE)—a physio-
logical study. Br J Anaesth, 118, 610–17.
Ward JJ (2013). High-flow oxygen administration by nasal cannulae for adult and perinatal patients.
Respir Care, 58, 98–122.
Groves N, Tobin A (2007). High flow nasal oxygen generates positive airway pressure in adult volun-
teers. Aust Crit Care, 20, 126–31.
Extubation after difficult intubation 399
400
Chapter 15
Airway assessment and management
Fig. 15.9 Difficult Airway Society Extubation Guidelines: low-risk algorithm. Reproduced from Popat M, et al. Difficult Airway Society
Guidelines for the management of tracheal extubation. Anaesthesia 2012; 67:318–40, with permission from the Association of Anaesthetists of Great
Britain & Ireland/Blackwell Publishing Ltd.
Fig. 15.10 Difficult Airway Society Extubation Guidelines: at-risk algorithm. Reproduced from Popat M, et al. Difficult Airway Society
Guidelines for the management of tracheal extubation. Anaesthesia 2012; 67:318–40, with permission from the Association of Anaesthetists of Great
Extubation after difficult intubation
References
1 Lundstrom L, Rosenstock C, Wetterslev J, et al. (2019). The DIFFMASK score for predicting diffi-
cult facemask ventilation: a cohort study of 46,804 patients. Anaesthesia, 74, 1267–76.
2 Detsky ME, Jivraj N, Adhikari NK, et al. (2019). Will this patient be difficult to intubate?: the ra-
tional clinical examination systematic review [published correction appears in JAMA (2020) 323,
1194]. JAMA, 321, 493–503. doi:10.1001/jama.2018.21413
3 De Jong A, Molinari N, Terzi N, et al. (2013). Article 1. Early identification of patients at risk
for difficult intubation in the intensive care unit: development and validation of the MACOCHA
score in a multicenter cohort study. Am J Respir Crit Care Med, 187, 832–9. doi:10.1164/
rccm.201210-1851OC
4 Ahmad I, El-Boghdadly K, Bhagrath R, et al. (2020). Difficult Airway Society guidelines for awake
tracheal intubation (ATI) in adults. Anaesthesia, 75, 509–28.
5 Nolan JP, Kelly FE (2011). Airway challenges in critical care. Anaesthesia, 66 (Suppl 2), 81–92.
6 Brimacombe J, Keller C, Vosoba Judd D (2004). Gum elastic bougie-guided insertion of the
ProSeal™ Laryngeal Mask Airway Is superior to the digital and introducer tool techniques.
Anesthesiology, 100, 25–9.
7 Patel A, Nouraei SA (2015). Transnasal humidified rapid- insufflation ventilatory exchange
(THRIVE): a physiological method of increasing apnoea time in patients with difficult airway.
Anaesthesia, 70, 323–9.
Chapter 16 405
405
Conduct of anaesthesia
John Newland and Heng-Yi (Henry) Wu
Induction of general anaesthesia 406
Maintenance and TIVA 410
Sedation 419
Neuromuscular blockade 420
Neuromuscular function monitoring 423
Reversal of neuromuscular blockade 425
Depth of anaesthesia monitoring 426
Cardiac output monitoring 430
Temperature control 434
Patient positioning for surgery 435
See also
% Conduct of anaesthesia pp. 913–25
406
Intravenous induction
IV induction is faster and more reliable than inhalational induction and is
generally preferred in adults.
• Multiple drugs are often co-administered to reduce dose-dependent
side effects of each individual drug.
Induction agents
• Propofol (1–2.5mg/kg) is the commonest agent used. It provides rapid
onset and emergence, making it suitable for day case surgery. It has
antiemetic properties and can be used for maintenance of anaesthesia.
Propofol obtunds airway reflexes and as such, it is the ideal drug to use
with an SGA. Moderate hepatic or renal impairment do not alter its
pharmacokinetics significantly.
• Ketamine (1–2mg/kg IV or 5–10mg/kg IM) has multiple administration
routes available, making it very versatile. Despite having a direct
myocardial depressant effect, sympathetic stimulation results in a largely
cardiovascularly stable induction. Airway reflexes and respiratory drive
are preserved, but i salivation can lead to upper airway obstruction. It
is frequently used in the ED and the prehospital environment.
• Thiopental (2–5mg/kg) produces a smooth induction of anaesthesia
with a well-defined endpoint, usually within 30s. Airway reflexes are
largely preserved, making it less suitable for use with an SGA. Intra-
arterial injection can cause tissue necrosis.
• Etomidate (0.3mg/kg) is useful for induction of haemodynamically
unstable patients as it causes the least cardiovascular depression of all
the IV induction agents. Controversy exists around its use as it causes
reversible adrenocortical suppression for 12–24h. A single induction
dose is safe, but continuous infusions may lead to an increase in
mortality in critically ill patients.
Titrating propofol
Propofol causes the greatest fall in BP of all IV induction agents, primarily
due to vasodilation. It therefore requires careful titration of a ‘sleep dose’,
with consideration of factors such as patient weight, age, CO and arm–
brain circulation time.
• In low CO states (shocked patients or the elderly), the body
compensates by diverting a higher proportion of the CO to the brain,
reducing flow to other areas of the body. This results in a smaller initial
volume of distribution and a greater proportion of the drug diverted
towards the cerebral circulation. Furthermore, the time taken for the
drug to reach the brain is prolonged. Thus, a slow titration of a reduced
dose is the safer way to induce these patients.
Opioids
Opioids work synergistically with propofol to allow a dose reduction, as
well as obtund the autonomic response to airway instrumentation.
• Timing of administration should take into consideration time to peak
effect. Fentanyl (1–2 micrograms/kg) should be administered 3–5min
prior to the induction agent, whereas alfentanil (10–30 micrograms/kg)
or remifentanil can be administered concurrently due to their faster
onset of action.
408
Adjuncts
• Midazolam (0.5–5mg) is commonly used as a co-induction agent
to reduce the propofol dose required, therefore minimising the
cardiovascular effects of propofol. It can also reduce the incidence
of PONV.
• Lidocaine (0.5–1.5mg/kg) can reduce the induction dose, as well as
blunt stimulus from airway instrumentation. A small amount (20–40mg)
can be added to 200mg of propofol to reduce pain on injection.
Neuromuscular-blocking agents
NMBAs (see % pp. 420–2) are generally used to facilitate intubation, but
care must be taken to avoid awareness. As such, NMBAs should only be
given after loss of consciousness.
Rapid sequence induction
An RSI (see % pp. 388–90) is performed in those with a high aspiration
risk. This technique involves delivering a predetermined dose, rather than
a sleep dose, of IV induction agent, avoiding titration. This is immediately
followed by an NMBA and early intubation.
• Opioids, particularly alfentanil, can be considered for use in RSI.
Other considerations
• Adequate depth of anaesthesia needs to be achieved prior to insertion
of an SGA to avoid biting, hiccupping, breath-holding or laryngospasm.
Reduce opioid dose to facilitate SV.
• Spontaneous breathing induction of anaesthesia with slow incremental
titration of a TCI of propofol is a useful technique, particularly in airway
surgery.
• In those with actual, or potential for, haemodynamic instability,
preloading with IV fluid and co-administration of a vasopressor infusion
may be necessary.
• High-dose opioid, including remifentanil, may be used to blunt the
sympathetic response to laryngoscopy.
Inhalational induction
(See also % p. 919.) Indications for inhalational induction (see % pp. 391–2)
include:
• Avoiding awake IV access, e.g. in children, needle-phobic patients and
patients with difficult IV access
• To maintain SV during induction (TIVA is becoming more popular for
this indication).
Inhalational induction, whether of a child or an adult, requires cooperation
from the patient. Age-appropriate explanation and interaction form part of
the ‘art of anaesthesia’.
• Sevoflurane is the commonest agent used and the best tolerated. A
50:50 mix of N2O:O2 improves tolerance and speeds onset.
• If inhalational induction is used for difficult IV access, have a skilled
assistant present to secure cannulation early.
Induction of general anaesthesia 409
Paediatric considerations
Parental understanding and support are essential, as their assistance is often
very useful. Warn parents about the excitation phase, with noisy breathing
and movement to be expected.
• Optimal positioning will depend on child size. Between ages 2 and 5,
the child can be sat on the parent’s lap, with the parent cuddling/gently
restraining the child during induction. For older and younger children,
the operating table or bed may be more appropriate.
• A close-fitting face mask speeds up induction; however, in those
children not wanting to accept a mask, a cupped hand to deliver the
fresh gas supply can be used initially before moving to a mask.
• Slowly uptitrating sevoflurane is better tolerated in children.
Difficulties with inhalational induction
• In adults, it can take a long time to achieve adequate depth of
anaesthesia. It can be further slowed by a leak around the mask, airway
obstruction, breath-holding and high CO.
• The excitement stage may be long and associated with complications
such as airway obstruction. Induction will only progress past this phase
if the airway remains patent. Application of PEEP/CPAP/gentle assisted
ventilation can be useful if airway obstruction occurs.
• H The traditional view that inhalational induction is safe because if the
airway obstructs, anaesthesia will lighten is false. The NAP4 report1
highlighted that in practice, when total airway obstruction occurs,
patients do not exhale the volatile and hypoxia rapidly ensues. If
this technique is used for a difficult airway, have backup airway plans
prepared.
Further reading
King A (2019). Induction of general anesthesia: overview. [In UpToDate database on the Internet] M
https://www.uptodate.com/contents/induction-of-general-anesthesia-overview
041
Paralysis
The depth of anaesthesia for maintenance requires consideration of
whether NMBAs are used. Without NMBAs, maintenance anaesthesia
needs to be dosed higher to inhibit spinal reflexes and prevent movement.
When using NMBAs, a lower dose is required to maintain unconsciousness
and prevent awareness only. However, NMBAs are a known risk factor for
awareness as movement, a marker of light depth of anaesthesia, is inhibited.
Combined technique
All maintenance anaesthetic agents have dose-dependent cardiovascular ef-
fects and variable offset times. Combined techniques, using inhalational and
IV techniques, can be used to minimise the total dose of any one agent, thus
minimising side effects and potentially hastening emergence, particularly in
long procedures. However, this does increase complexity and the risk of
error, possibly increasing the likelihood of awareness from underdosing or
cardiovascular compromise from a ‘double anaesthetic’. Depth of anaes-
thesia monitoring (see % pp. 426–9) should be considered if this technique
is employed, particularly when using NMBAs.
Inhalational anaesthesia
Volatile agents remain key components of modern GA. They are proven to
be safe, easy to use and effective. There are, however, disadvantages, many
being dose-dependent (Table 16.1).
TIVA
TIVA utilises IV agents alone, avoiding the use of inhalational agents.
Although theoretically any combination of induction agent and opioid can
be used, in practice, the commonest agent used is propofol alongside an
opioid. Pharmacokinetic models for TCI have resulted in i use of TIVA in
various clinical settings (Table 16.2).
Choice of agent
Ideal TIVA agents have fast onset and offset to allow rapid titration and
recovery. Generally, the offset of IV agents slows as the duration of the
infusion increases, which is reflected in the context- sensitive half-time
(CSHT). Propofol and remifentanil exhibit short CSHTs and thus are the
closest to ideal TIVA agents available. Opioids serve two purposes during
TIVA. They provide analgesia and allow a reduction in the required dose
of propofol due to their synergistic effect. If remifentanil is used, a longer-
acting opioid should be given 30–40min prior to stopping the infusion to
cover postoperative pain.
Administering TIVA
There are several effective ways to perform TIVA. The use of TCI is recom-
mended over other methods, if available.
Anaesthetist-administered boluses
Can be useful for very short procedures but often results in excessive drug
at the time of bolus or inadequate effect prior to the next bolus. This oscil-
lation can lead to cardiovascular instability and/or awareness.
Manually controlled infusion regimes
These regimes allow anaesthetists to utilise a ‘multicompartmental model’
without the use of pharmacokinetic infusion pumps. They are not appro-
priate for all patients. Boluses and infusion rates may need to be altered to
achieve adequate depth of anaesthesia (Table 16.3).
41
Table 16.3 Suggested manual infusion regimes for propofol and remifentanil
Propofol
Known as the 50mL of 1% 1mg/kg induction bolus
‘Bristol’ regime propofol 10mg/kg/h for 10min
Achieves a plasma (500mg) 8mg/kg/h for 10min
propofol concentration 6mg/kg/h for maintenance
of 73 micrograms/mL
Remifentanil
Achieves a remifentanil Remifentanil 50 0.5 micrograms/kg/min for 3min
plasma concentration of micrograms/mL 0.25 micrograms/kg/min for
76 nanograms/mL maintenance
Target-controlled infusions
TCIs allow accurate maintenance of concentrations of anaesthetic agents.
The technique requires an infusion pump programmed with a pharmacokin-
etic model. Instead of selecting a set rate, a target concentration is set, with
a target of either plasma (Cpt) or effect site (Cet). The pump will automat-
ically adjust its infusion rate to achieve a predicted target site concentration.
Basic pharmacokinetics
A multicompartment model is often used to describe the redistribution and
elimination of drugs such as propofol. The drug is delivered into a central
compartment (V1), with the initial induction bolus calculated according to
the estimated volume of V1. The drug is then distributed to compartments
V2 and V3. Movement of the drug between compartments is governed by
rate constants (K) (Fig. 16.1).
• Although the various compartments are often equated to biological
compartments within the human body, such as blood vessel rich/
poor, this is technically incorrect. Compartments and rate constants
are purely a mathematical construct used to predict target site
concentrations, with the models validated in small populations of
patients.
• Depending on which model is used, compartmental size and rate
constants can be either fixed or variable. Variable parameters are
determined by patient data entered into the pump.
Plasma vs effect site targeting
Cpt achieves and maintains a predetermined target plasma concentration
of drug as rapidly as possible without overshooting. Plasma concentration
will not approximate effect site (CNS) concentration until a steady state is
reached, which can take a number of minutes. Thus, onset of anaesthesia
using Cpt is slow. This can be overcome by targeting a higher Cpt transi-
ently during induction, then reducing it to the desired maintenance level.
Cet achieves a faster effect site concentration by overshooting the plasma
concentration and, as such, is more useful for rapidly achieving the desired
depth of anaesthesia.
Maintenance and TIVA 415
Drug administered
V2 K12 K13
V1 V3
Rapidly
Central Slowly equilibrating
equilibrating
K21 compartment
K31 compartment
compartment
K1e
K10
Ve Ke0
Drug eliminated Effect site
Starting infusions
• Use a TIVA checklist for safety (Table 16.4).
• Timing of when to start each infusion should be guided by time to
peak effect. If using Cet, both remifentanil and propofol can be started
simultaneously. If using Cpt, remifentanil will equilibrate at the effect
site long before propofol, potentially leading to an apnoeic (but aware)
patient. In this instance, propofol should be started first.
• Some anaesthetists employ a stepwise increase of target concentrations,
starting at 0.5–1.0 micrograms/mL of propofol and increasing by 0.5–
1.0 micrograms/mL increments once the target site has equilibrated.
This method avoids a large initial bolus and the associated CVS
instability. It also allows identification of the Cet at which the patient
becomes unrousable. The target concentration is i above this level for
a layer of safety, but it does guide the minimal level that will be required
to keep the patient anaesthetised.
Maintenance
When used correctly, TCI accurately predicts measured plasma concentra-
tions of drugs in most patients. However, due to pharmacodynamic vari-
ation, target concentrations must still be titrated to achieve the required
effect in any individual. Targets need to be adjusted based on age, ASA
status, adjuvant agents used, degree of surgical stimulation and processed
EEG (Table 16.5).
When to stop the infusions
This is a balance between maintaining adequate anaesthesia and facilitating
rapid emergence. TCI targets can be gradually d near the end of surgery,
but caution must be exercised as wound closure can sometimes be a signifi-
cant noxious stimulus.
641
Infusion Prior to using pumps, ensure they are serviced, plugged into the
pumps mains power and charged.
checked Ensure low-and high-pressure alarms are set—this can warn of
disconnection or a blocked cannula, respectively.
A well- Ideally insert the line yourself and avoid sites where a tissued
functioning line is hard to detect, e.g. antecubital fossa. Secure the line firmly
IV line to the patient’s skin.
Keep the line visible throughout the case to allow early
identification of disconnection, leakage or a tissued cannula.
TIVA Use a dedicated TIVA administering set which incorporates:
administering • Antisiphon valves on the drug lines
tubing • A non-return valve on the IV fluid line
• Minimal dead space between the patient and where the drugs
and IV fluid mix
• Luer lock rather than Luer slip connections.
Drug Have drugs already drawn up in preparation for syringe
preparation exchanges.
Monitoring Consider processed EEG, particularly if NMBAs are used.
Practical Ensure the infusion continues after altering pump settings or a
aspects syringe exchange.
Specific to Be aware that most TCI pumps will forget their programming
running TCI with complete failure of both mains and battery power.
Have a backup plan in the event of pump failure.
Ensure the right model is used for the right drug.
Ensure drug dilutions and syringe size and type are correctly
entered into the pump.
Double-check patient data are entered correctly.
Ensure targets are suitable for the patient’s age and ASA status.
Further reading
Al-Rifai Z, Mulvey D (2016). Principles of total intravenous anaesthesia: practical aspects of using
total intravenous anaesthesia. BJA Educ, 16, 276–80. doi: 10.1093/bjaed/mkv074
Al-Rifai Z, Mulvey D (2016). Principles of total intravenous anaesthesia: basic pharmacokinetics and
model descriptions. BJA Educ, 16, 92–7. doi: 10.1093/bjaceaccp/mkv021
Campbell M, Pierce JMT (2015). Atmospheric science, anaesthesia, and the environment. BJA Educ,
15, 173–9. doi: 10.1093/bjaceaccp/mku033
Sedation 419
Sedation
See % Premedicants, p. 66; for premedication in children, see % pp. 917–18.
Sedation refers to the use of drugs to produce anxiolysis, analgesia and a
degree of amnesia, to allow patients to tolerate uncomfortable treatments
or investigations without resorting to GA. Anaesthetists are well placed to
provide effective and safe sedation. When offered by non-anaesthetists, the
level of training, techniques used and degree of observation of the patient
are highly variable.
• There is a perception that sedation is less stressful or safer than GA.
Sedation may be requested in isolated areas such as radiology or the
ED. Standards of equipment, assistance and monitoring may not be the
same as in theatre. Nonetheless, sedation has the potential to pose
significant risks.
• Sedation is a continuum from alertness to GA. Therefore, definitions of
levels of sedation are somewhat arbitrary.
Minimal sedation
Minimal sedation is where a mild anxiolytic is provided. The patient remains
conscious and has normal response to verbal stimulation.
Conscious sedation
Conscious sedation refers to a state where the patient may have their
eyes closed but will still obey commands or respond to verbal interaction.
Respiration is usually preserved.
Deep sedation
The patient responds only to repeated or painful stimuli, by purposeful
movement (not simply withdrawal). Manoeuvres may be required to keep
the airway open. This state is close to GA and may inadvertently turn into it.
Good practice
It is good practice to perform a full anaesthetic assessment on someone
requiring sedation. Insert a cannula and apply routine monitoring. An anaes-
thetic assistant is likely to be helpful.
• Titrate drugs slowly to effect. Short-acting benzodiazepines are effective
for anxiolysis and amnesia, but have no analgesic effect. Opioids have
synergistic effects if used with them. TCI propofol is a good choice, as it
is highly titrable if the patient becomes too deep.
• Often the most stimulating part is near the beginning, e.g. injection of
LA into a sensitive area.
• Sedation is often carried out on elderly patients with significant
comorbidities. Sedation in the elderly may produce paradoxical
disinhibition and agitation.
• Communication is reassuring to the patient and allows monitoring of
their conscious level.
Further reading
Blayney MR (2012). Procedural sedation for adult patients: an overview. Contin Educ Anaesth Crit Care
Pain, 12, 176–81. doi:10.1093/bjaceaccp/mks016
420
Neuromuscular blockade
Depolarising agents
Suxamethonium is the only depolarising NMBA in clinical use. Given IV
(dose 1–2mg/kg), it has a fast onset of action (<1min), making it the ideal
agent when performing an RSI or for use in an airway emergency. Its short
duration of action (5–10min) also means that it is well suited for procedures
that require a brief period of muscle relaxation (e.g. ECT). Suxamethonium
can also be given IM (dose 2–4mg/kg) in the absence of IV access.
Metabolism is by plasma cholinesterase, a hepatically synthesised circu-
lating enzyme. Acquired factors that reduce the level of circulating plasma
cholinesterase (e.g. hepatic diseases, malnutrition) or reduce plasma cholin-
esterase activity (e.g. presence of anticholinesterase drugs, pregnancy) can
therefore lead to an increase in duration of action.
Congenital factors, such as variants in the genes that encode the plasma
cholinesterase enzyme, can reduce its activity and prolong the duration of
action of suxamethonium (Table 16.6).9
Adverse effects of suxamethonium may be predictable or unpredictable.
Neo, neostigmine; PTC, post-tetanic count; SGX, sugammadex; TOFC, train-of-four count;
TOFR, train-of-four ratio.
426
Raw EEG
BIS
98 Awake
80 Sedation
60
Surgical
anaesthesia
40
Burst
20
suppression
0 Isoelectricity
Fig. 16.2 EEG changes and corresponding BIS values with increasing depth of
anaesthesia.
Fluid-responsive Non-fluid-responsive
Fluid administration will Fluid administration
improve cardiac output ineffective or potentially
harmful
Stroke volume/
cardiac output
Preload
Bioimpedance/bioreactance
Cyclical changes in blood flow within the thorax induce changes in impedance
to alternating electrical current, which can be measured using electrodes.
Newer devices use bioreactance, which is less susceptible to interference and
shows good correlation with pulmonary artery flotation catheters (PAFCs).
Parameters of volume responsiveness
Most CO monitors display a multitude of measured and derived haemo-
dynamic parameters. These can be either static or dynamic.
Static parameters
• These parameters include stroke volume, CO, CVP, pulmonary artery
occlusion pressure (PAOP), mixed venous O2 saturations, SVR, etc.
Unfortunately, the absolute values for these parameters fail to predict volume
responsiveness in the majority of patients. However, they can be reliably used
to observe trends and the effect of interventions such as fluid administration.
Dynamic parameters
• These include stroke volume variation (SVV) and pulse pressure variation
(PPV). Changes in intrathoracic pressure due to IPPV induce changes
in the stroke volume and pulse pressure as a result of a reduction in
preload. The greater the change in stroke volume or pressure, the
greater the likelihood that the patient is intravascularly deplete.
• Dynamic parameters are superior to static parameters when
determining volume responsiveness; however, the reliability of these
variables can be adversely affected by arrhythmias, right heart failure,
spontaneous breathing and VT <8mL/kg.
Fluid administration
The interpretation of data from CO monitoring should be made in light
of clinical examination and investigations such as serum lactate and base
deficit trends.
• When trying to optimise stroke volume, fluid is usually administered in boluses
over 5min, in volumes of around 3mL/kg (200–250mL) (Table 16.11).
• The response to a passive leg raise (or head-down position) is also
a reversible way to demonstrate whether the patient is likely to be
volume-responsive.
Temperature control
Core body temperature in an awake patient is tightly controlled between
36.7°C and 37.1°C. Deviation above or below these temperatures causes
the hypothalamus to initiate behavioural and autonomic mechanisms to re-
store normothermia. This tight regulation is lost under GA and neuraxial
anaesthesia due to:
• Drug-induced vasodilation
• Abolition of behavioural responses to thermal discomfort and
• Resetting of the threshold temperatures in which autonomic responses
are activated, resulting in a widened range.
The anaesthetised patient is prone to hypothermia (defined as core body
temperature <36°C). This typically occurs in a triphasic pattern.
Phase 1
Rapid loss of 71°C within the first 30–45min of anaesthesia due to heat re-
distribution from the core compartment to the peripheries.
Phase 2
Loss of 71°C over 2–3h from radiation (40%), convection (30%), evapor-
ation (25%) and conduction (5%).
Phase 3
A plateau occurs when heat loss is finally matched by heat production as
maximal vasoconstriction is activated.
Hypothermia in the perioperative period is not benign. Adverse conse-
quences include:
• Coagulopathy and an i need for transfusion
• i risk of surgical site infection
• i rate of MACE
• Reduced rate of drug metabolism (e.g. prolonged NMB and delayed
emergence from anaesthesia).
Measures to reduce the risk of perioperative hypothermia include:
• Identifing high-risk patients (high ASA grade, low BMI, undergoing major
surgery and using a combined general/neuraxial technique) and treating
hypothermia before commencing anaesthesia
• Monitoring core body temperature (distal oesophagus, nasopharynx,
tympanic membrane or bladder) at 30min intervals
• Maintaining ambient temperature in preop areas and operating theatres,
prewarming fluids to 37°C for IV administration or internal irrigation
and humidifying respiratory gases using an HME filter
• Active cutaneous warming, most commonly achieved using a forced
air device, which should be used for all procedures with anaesthesia
time >30min
• Active internal warming techniques, such as CPB and peritoneal
lavage, are invasive and therefore are not indicated for most routine
operations.
Patient positioning for surgery 435
Fig. 16.4 Supine position. Image courtesy of Medical photography, Waikato District
Health Board.
436
Fig. 16.5 Lithotomy position. Image courtesy of Medical photography, Waikato District
Health Board.
Fig. 16.6 Lloyd-Davies position. Image courtesy of Medical photography, Waikato District
Health Board.
Fig. 16.7 Lateral decubitus position. Image courtesy of Medical photography, Waikato
District Health Board.
Fig. 16.8 Prone position. Image courtesy of Medical photography, Waikato District
Health Board.
40
Fig. 16.9 Sitting position. Image courtesy of Medical photography, Waikato District
Health Board.
Anaesthetic factors
• Use of volatile anaesthesia (2× risk). Note this risk increases in a dose-
dependent manner and risk peaks in the first 2–6h following surgery
• Duration of anaesthesia (1.5× risk if exceeding 90min)
• Postoperative opioid use (1.5× risk). Note that this is independent of
the opioid administered
• Use of N2O (1.5× risk).
Note: NGT placement, muscle relaxant reversal and use of supplemental
O2 have no proven association with PONV.
Surgical factors
• Laparoscopic surgery, gynaecological surgery and cholecystectomy.
Note: head and neck, breast, abdominal, posterior cranial fossa and oph-
thalmic surgery are all associated with i PONV but have not been proven
to be independent risk factors.
Simplified risk scores for predicting PONV
• The Apfel PONV risk score assesses four domains: ♀ gender, history
of PONV and/or motion sickness, non-smoking status and predicted
postoperative use of opioids. When zero, one, two, three or four factors
are present, the risk of PONV is 10%, 20%, 40%, 60% and 80%, respectively.
• The Koivuranta PONV risk score assesses five domains: ♀ gender,
non-smoking status, history of PONV, history of motion sickness and
duration of surgery >60min. If zero, one, two, three, four or five risk
factors are present, the incidence of PONV is 17%, 18%, 43%, 54%,
74% and 87%, respectively.
• The POVOC PONV risk score for paediatric patients assesses five
domains: duration of surgery ≥30min, age ≥3y, strabismus surgery and
history of PONV in the child or of PONV in his/her relatives. When
zero, one, two, three or four risk factors are present, the incidence is
9%, 10%, 30%, 55% and 70%, respectively.
• The Apfel PDNV score assesses five domains: ♀ gender, age <50y,
history of PONV, opioid use in the post-anaesthesia care unit and
nausea in the post-anaesthesia care unit. When zero, one, two, three,
four or five factors are present, the risk of PONV is 10%, 20%, 30%,
50%, 60% and 80%, respectively.
Prevention and prophylaxis
Risk assessment
• If low risk (0–1 risk factors), consider no prophylaxis.
• If moderate risk (2–3 risk factors), consider 1–2 interventions.
• If high risk (4+ risk factors), consider >2 interventions, including
regional anaesthesia.
Methods to reduce PONV
• Prophylactic antiemetic administration (Table 16.12).
• Avoid GA and opioids by using LA or regional anaesthesia (9×
reduced risk).
• Avoid volatile and N2O by using propofol for induction and maintenance
(number needed to treat (NNT) = 5).
• Use multimodal analgesia to reduce opioid requirement.
Non-pharmacological methods to reduce PONV include adequate hydra-
tion, and acupuncture at P6 point, on the volar wrist (NNT = 5).
4
444
Dexamethasone Steroid 4–8mg IV at 4 4mg equal in effect to 1.25mg of droperidol and 4mg of ondansetron.
induction Reduces postoperative opioid use. Does not increase risk of wound
Single dose only infection, may cause lability in blood glucose readings in diabetic patients
Droperidol Butyrophenone 0.625–1.25mg IV at 5 Superior to metoclopramide. Similar effect on corrected QT (QTc) interval
D2 antagonist induction to ondansetron; however, when used together, does not significantly further
Q8H increase QTc. Haloperidol at low doses (<2mg) has similar antiemetic
efficacy. May cause sedation, anxiety, extrapyramidal signs (EPS) and
abnormal LFTs
Ondansetron 5HT3 antagonist 4–8mg IV at end of 6 Less effective than aprepitant and palonosetron. Similar activity to
surgery granisetron, tropisetron and dolasetron. Constipation and headache are
Conduct of anaesthesia
Treatment principles
Using combination therapy with drugs targeting different receptor classes is
the most effective strategy due to their additive effect.
• Ondansetron, dexamethasone and droperidol are the most studied and
are widely considered to be 1st-line antiemetics in both the prophylaxis
and treatment of nausea and vomiting.
• In the context of failed prophylaxis, repeating doses of prophylactic
antiemetics already administered is of no benefit. Choose a drug from
another class.
Postoperative nausea and vomiting 447
Further reading
Gan TJ, Diemunsch P, Habib AS, et al. (2014). Consensus guidelines for the management of
postoperative nausea and vomiting. Anesth Analg, 118, 85–113.
Apfel CC, Meyer A, Orhan-Sungur M, Jalota L, Whelan RP, Jukar-Rao S (2012). Supplemental intra-
venous crystalloids for the prevention of postoperative nausea and vomiting: quantitative review.
Br J Anaesth, 108, 893–902.
Apfel CC, Philip BK, Cakmakkaya OS, et al. (2012). Who is at risk for postdischarge nausea and
vomiting after ambulatory surgery? Anesthesiology, 117, 475–86.
Lee A, Fan LT (2009). Stimulation of the wrist acupuncture point P6 for preventing postoperative
nausea and vomiting. Cochrane Database Syst Rev, 2, CD003281.
Apfel CC, Kranke P, Eberhardt LH, Roos A, Roewer N (2002). Comparison of predictive models for
postoperative nausea and vomiting. Br J Anaesth, 88, 234–40.
References
1 Cook T, Woodall N, Frerk C (eds); 4th National Audit Project of The Royal College of
Anaesthetists and the Difficult Airway Society (2011). Major complications of airway manage-
ment in the United Kingdom. London: Royal College of Anaesthetists.
2 Campbell M, Pierce JMT (2015). Atmospheric science, anaesthesia, and the environment. BJA
Educ, 15, 173–9. doi:10.1093/bjaceaccp/mku033
3 The Lancet, Health and Climate Change Commission. Countdown on health and climate change.
M https://www.thelancet.com/commissions/climate-change
4 National Health Service. NHS Long Term Plan 2019. M https://www.longtermplan.nhs.uk/
online-version/appendix/health-and-the-environment/
5 Kuvadia M, Cummis CE, Liguori G, et al. (2020). ‘Green-gional’ anesthesia: the non-polluting
benefits of regional anesthesia to decrease greenhouse gases and attenuate climate change. Reg
Anesth Pain Med, 45, 744–5.
6 Sherman J, Le C, Lamers V, Eckelman M (2012). Life cycle greenhouse gas emissions of anesthetic
drugs. Anesth Analg, 114, 1086–90.
7 NHS Sustainable Development Unit (2018). Reducing the use of natural resources in health and
social care, 2018 report. M https://www.sduhealth.org.uk/policy-strategy/reporting/natural-
resource-footprint-2018.aspx
8 McGain F, Muret J, Lawson C, Sherman F (2020). Environmental sustainability within anaesthesia
and critical care. Br J Anaesth, 125, 680–92.
9 Lin T, Smith T, Pinnock C (eds) (2016). Fundamentals of Anaesthesia, 4th edn. Cambridge:
Cambridge University Press. M https://www.cambridge.org/core/books/fundamentals-of-
anaesthesia/5BB9DCFBF693F77E4B21E5E37CD81B52
10 Harper NJN, Cook TM, Garcez T, et al. (2018). Anaesthesia, surgery, and life-threatening allergic
reactions: epidemiology and clinical features of perioperative anaphylaxis in the 6th National
Audit Project (NAP6). Br J Anaesth, 121, 159–71.
11 Sadleir PHM, Clarke RC, Bunning DL, Platt PR (2013). Anaphylaxis to neuromuscular blocking
drugs: incidence and cross-reactivity in Western Australia from 2002 to 2011. Br J Anaesth,
110, 981–7.
12 Ortega R, Brull SJ, Prielipp R, Gutierrez A, De La Cruz R, Conley CM (2018). Monitoring neuro-
muscular function. N Engl J Med, 378, e6.
13 Naguib M, Brull SJ, Johnson KB (2017). Conceptual and technical insights into the basis of neuro-
muscular monitoring. Anaesthesia, 72(S1), 16–37.
14 Mashour GA, Avidan MS (2015). Intraoperative awareness: controversies and non-controversies.
Br J Anaesth, 115 Suppl 1, i20–6.
15 Pandit JJ, Andrade J, Bogod DG, et al. (2014). 5th National Audit Project (NAP5) on accidental
awareness during general anaesthesia: summary of main findings and risk factors. Br J Anaesth,
113, 549–59.
16 Wildes TS, Winter AC, Maybrier HR, et al. (2016). Protocol for the Electroencephalography
Guidance of Anesthesia to Alleviate Geriatric Syndromes (ENGAGES) study: a pragmatic,
randomised clinical trial. BMJ Open, 6, e011505. M https://bmjopen.bmj.com/content/6/6/
e011505
17 Avidan MS, Jacobsohn E, Glick D, et al. (2011). Prevention of intraoperative awareness in a high-
risk surgical population. N Engl J Med, 365, 591–600.
18 Avidan MS, Zhang L, Burnside BA, et al. (2008). Anesthesia awareness and the bispectral index.
N Engl J Med, 358, 1097–108.
19 Mashour GA, Shanks A, Tremper KK, et al. (2012). Prevention of intraoperative awareness with
explicit recall in an unselected surgical population: a randomized comparative effectiveness trial.
Anesthesiology, 117, 717–25.
48
20 Myles PS, Leslie K, McNeil J, Forbes A, Chan MTV (2004). Bispectral index monitoring to prevent
awareness during anaesthesia: the B-Aware randomised controlled trial. Lancet, 363, 1757–63.
21 Gustafsson UO, Scott MJ, Hubner M, et al. (2019). Guidelines for perioperative care in elective
colorectal surgery: Enhanced Recovery After Surgery (ERAS®) Society recommendations: 2018.
World J Surg, 43, 659.
22 Watson X, Cecconi M (2017). Haemodynamic monitoring in the peri-operative period: the past,
the present and the future. Anaesthesia, 72, 7–15.
23 Myles PS, Bellomo R, Corcoran T, et al. (2018). Restrictive versus liberal fluid therapy for major
abdominal surgery. N Engl J Med, 378, 2263–74.
24 Kobe J, Mishra N, Arya VK, Al‑Moustadi W, Nates W, Kumar B (2019). Cardiac output moni-
toring: technology and choice. Ann Card Anaesth, 22, 6–17.
25 Stornelli N, Wydra FB, Mitchell JJ, Stahel PF, Fabbri S (2016). The dangers of lithotomy posi-
tioning in the operating room: case report of bilateral lower extremity compartment syndrome
after a 90-minutes surgical procedure. Patient Saf Surg, 10, 18.
26 [No authors listed] (2019). Practice advisory for perioperative visual loss associated with spine
surgery 2019: an updated report by the American Society of Anesthesiologists Task Force on
Perioperative Visual Loss, the North American Neuro-Ophthalmology Society, and the Society
for Neuroscience in Anesthesiology and Critical Care. Anesthesiology, 130, 12–30.
27 Higgins JD, Frank RM, Hamamoto JT, Provencher MT, Romeo AA, Verma NN (2017). Shoulder
arthroscopy in the beach chair position. Arthrosc Tech, 6, e1153–8.
Chapter 17 449
449
Blood products
The goal of transfusion is to efficiently correct tissue hypoperfusion,
coagulopathy or anaemic hypoxaemia, while minimising the risk of
transfusion-related adverse outcomes for patients. Blood products are
largely obtained through voluntary donation prior to undergoing expensive
and labour-intensive processing, storage and dispensing. Consideration of
both the intrinsic and financial values of blood products is appropriate. In
this spirit, we aim to give the right blood products to the right patients at
the right time in the right amount.
Donation and testing
Whole blood donation
Each donor provides 500mL of blood. A total of 470mL goes on to be pro-
cessed while 30mL is utilised for routine testing. Donors can typically give
blood four times annually.1
Apheresis donation
A cell separator is used to collect plasma, platelets, white cells or haemato-
poietic progenitor cells. Donor red cells are returned to the donor. Donors
may give these fractions every 2w.1
Testing
Donated blood is tested for ABO/rhesus D (RhD) blood groups and
screened for infectious diseases (HIV, hepatitis B, hepatitis C, human T
cell lymphotropic virus (HTLV)-1/2 and syphilis). Donations at risk of mal-
aria or Chagas disease are tested for Plasmodium and Trypanosoma cruzi.
Cytomegalovirus (CMV) antibody-negative components derived from CMV
antibody-negative donors are available for immunosuppressed patients and
neonates.
Blood processing
Whole blood is a heterogeneous suspension of cellular and protein elem-
ents in plasma. Donated blood is usually processed into a range of blood
components and fractionated products (Table 17.1).2 In low-and middle-
income countries, and in military surgery, whole blood is often used.
Prestorage leucodepletion
Filtration reduces the risk of bloodborne infections such as HTLV-1/2 and
CMV. Leucodepletion may also prevent alloimmunisation, febrile reactions
and transfusion-related acute lung injury (TRALI).
Centrifugation and cryoprecipitation
Separates red cells, platelets, plasma and protein components.
Irradiation
Gamma or X-ray irradiation eliminates lymphocytes for patients at risk of
transfusion-associated graft-versus-host disease (TA-GvHD).
Viral inactivation
Plasma-derived products (e.g. FFP and cryoprecipitate) to be used in those
born after 1996 in the UK are sourced from outside the UK and have under-
gone viral inactivation with either solvent detergent or methylene blue.2
Blood products 451
Compatibility testing
This involves either a serological crossmatch to ensure compatibility or an
electronic crossmatch on the basis of the antibody screen.
Transfusion compatibility
ABO compatibility
Normal individuals produce immunoglobulin M (IgM) antibodies against the
A or B antigens which are not expressed on their cells. ABO compatibility
prevents acute haemolytic transfusion reactions caused by recipient IgM
antibodies binding A or B antigens on donor red cells.1
• Red cells express ABO antigens and recipients must be transfused with
ABO-compatible units to prevent serious harm or death.1
• Platelets weakly express ABO antigens. Therefore, recipients should be
transfused with ABO-compatible units. Non-ABO-compatible units of
platelets can be used in the event of life-threatening haemorrhage, but
these platelets will have a reduced lifespan in vivo.1
• Cryoprecipitate and FFP contain anti-B or anti-A IgM antibodies,
depending on the donor blood group. For donated plasma to be
compatible, it must not contain IgM antibodies against antigens
expressed on recipient cells.1
(See Table 17.3.)
RhD compatibility
Immunoglobulin G antibodies against the RhD antigen (also known as anti-
D) only form as a result of allogeneic exposure (e.g. transfusion or preg-
nancy). Compatibility testing prevents exposing RhD-negative recipients to
the RhD antigen in transfused units.1
• Red cells express RhD antigens. This is of particular importance for all
♀ of reproductive potential to prevent future haemolytic disease of
the newborn (due to maternal anti-D harming RhD-positive fetuses).
RhD-positive blood may be provided for RhD-negative ♂ or ♀ beyond
reproductive age if blood bank reserves of RhD-negative blood are
depleted.1
• Platelets do not express RhD antigens. However, units should be RhD-
compatible with the recipient as the RhD antigen is highly immunogenic
and residual red cells in the units may sensitise RhD-negative patients.1
• Cryoprecipitate and FFP may contain red cell fragments; however,
these are far less immunogenic than whole red cells. Therefore,
cryoprecipitate and FFP of any RhD type can be safely given.1
Positive antibody screens
Patients with positive antibody screens may require specific antigen-negative
blood components. Not all antibodies detected are of clinical significance,
and discussions with blood bank and a transfusion specialist are warranted.
Uncrossmatched blood
Immediate dispensing of emergency O RhD-negative blood is reserved
for haemorrhagic emergencies in the absence of a group and screen.2
Obtaining blood samples for transfusion X-matching is a priority early in
haemorrhage management. Group-specific blood (ABO/RhD) can be is-
sued significantly quicker than fully grouped and screened blood (15min vs
45min). Although it has undergone limited testing, group-specific blood is
an alternative to using O RhD-negative blood when transfusion is required
urgently but not immediately.
Transfusion indications and triggers
Clinical judgement, lab results, POCT and best available evidence deter-
mine the blood components to be prescribed, as well as the timing, dose
and rate of administration. Consideration should also be given to risks,
benefits and available alternatives to transfusion.
Globally, red cell transfusion policies have become increasingly restrictive
in response to emerging evidence of harm associated with unnecessary
transfusion. FFP should not be given for prolonged PT or INR in the ab-
sence of bleeding. For transfusion triggers, see Table 17.4 (red cell),2,4 Table
17.5 (cryoprecipitate),2 Table 17.6 (platelet)2,4 and Table 17.7 (FFP).2
Blood products 455
Transfusion risks
Transfusion safety requires robust and reliable systems from the point of
blood donation to the point of administration. Timely reporting of adverse
events to blood banks is an essential step to aid systems improvement for
the future. Adverse events include:1
Common
• Febrile non-haemolytic transfusion reaction (1–3:100) occurs within
30min of transfusion and is mediated by either cytokines or alloimmune
reactions to contaminant leucocytes. Simple cooling and paracetamol
are sufficient for mild reactions (<1.5°C rise in temperature). Mitigated
by slowing infusions.
• Minor allergy (1–5:500) commonly presents with mucocutaneous
manifestations, flushing, angio-oedema or urticaria due to recipient
antibodies against leucocyte antigens or plasma proteins.
• Hypotension (1–2:1000). Idiosyncratic reaction, possibly related to
bradykinin in transfused blood to recipients on ACE inhibitors. Defined
as a 30mmHg drop in systolic BP.
• Transfusion-associated circulatory overload (1–10:1000). Incidence is
determined by both the volume transfused and patient comorbidity.
• Hypothermia. Prevalent in rapid infusions of large volumes of
blood products. Can worsen all physiological processes, including
cardiovascular function and coagulation.
• Immunosuppression. Transfusion may influence the recurrence or
spread of malignancies, as well as the incidence of postoperative
bacterial infections through immunomodulation.
Rare
• Acute haemolytic transfusion reaction (1–8:100 000). Severe, life-
threatening reaction occurring within 24h of red cell transfusion due to
ABO incompatibility. Rarely may result from Kell, Duffy or Kidd antigen
incompatibility. Recipient antibodies bind to and haemolyse transfused
erythrocytes, causing complement activation, inflammation, DIC and
shock. Signs and symptoms may be indistinguishable from bacterial
sepsis or anaphylaxis.
Blood products 457
Massive transfusion
Introduction
More than 5 units of PRBCs in <4h or >10 units of PRBCs administered to
a patient within 24h is considered a massive transfusion.
• Goals of therapy are to expand circulating volume rapidly, economically
and without adverse effects.
• The current standard of care in the resuscitation of severe
haemorrhage is administration of blood components (platelets, plasma
and PRBCs) in a 1:1:1 ratio.13
Physiology of massive haemorrhage and transfusion14
• Rapid, large-volume haemorrhage results in systemic hypoperfusion and
reduced O2 delivery to tissues, causing acidosis.
• Acidosis, hypothermia and coagulopathy are known as the ‘triad of
death’ in massive haemorrhage. Each individually causes worsening of
the other two components of the triad.
• Hypoperfusion also activates the protein C pathway, deactivating
factors Va and VIIIa and initiating fibrinolysis and coagulopathy.
• Consumption of clotting factors may lead to DIC.
• Administration of cold IV fluids and exposure of the patient for vascular
access and resuscitation may lead to hypothermia.
• Hypothermia and acidosis reduce myocardial contractility, precipitate
bradycardia and dysrhythmias and cause vasodilation and hypotension.
They also reduce activity of clotting factors and platelets, with clotting
factor function d by 10% for every 0.1 reduction in pH.
• Transfused red cells are not as effective at O2 delivery as endogenous
red cells.
Resuscitation priorities during massive haemorrhage and
transfusion1
(See also % p. 971.)
Adequate staffing and assistance
• Call for additional senior surgical and anaesthetic help.
• Nominate a crisis leader to manage and assign roles to staff present.
• Notify blood bank and declare need for massive transfusion; this will
result in more blood bank staff dedicated to X-matching and thawing
blood products in readiness for use.
• A dedicated ‘runner’ to obtain blood products from the blood bank.
• Additional staff to check/administer blood products as they arrive.
• Additional theatre staff to set up key equipment.
Maintain circulating volume
• Obtain rapid source control of haemorrhage (e.g. surgical, endoscopic,
interventional radiology).
• Immediately request 3 units of PRBCs; use O-negative emergency
blood if X-matched blood not immediately available.
• Obtain large-bore IV access; give crystalloid until blood arrives.
• Increase FiO2 to 100% to improve tissue O2 delivery. Consider reducing
dose of anaesthetic agent administered.
Massive transfusion 461
Jehovah’s Witnesses
There are over 8 million members of the Jehovah’s Witness movement
worldwide.15,16,17 Most Jehovah’s Witnesses refuse receipt of ‘primary blood
components’ (whole blood, including autologous preoperative donation,
PRBCs, platelets, white cells and FFP). The acceptance of ‘blood fractions’
is variable and up to each individual’s interpretation of the church’s teach-
ings. Blood fractions, or derivatives, include cryoprecipitate, clotting factor
concentrates, albumin and immunoglobulin. So long as lines are primed
with non-blood fluids, intraoperative cell salvage is often acceptable, as are
apheresis, haemodialysis, CPB and normovolaemic haemodilution. IV iron
and tranexamic acid are pharmacological agents that present no quandary
and may reduce postoperative anaemia. Determining and documenting pre-
cisely which products, components and techniques a Jehovah’s Witness pa-
tient is willing to accept are therefore of critical importance when planning
for surgery.16,17
Ethical and legal considerations
Competent patients
Competent patients have the right to autonomously decline transfusion.
For this to be informed consent, an anaesthetist is obliged to inform pa-
tients of the risks, benefits and alternatives to their decision, including the
probable outcomes of doing nothing. Clinicians must also be satisfied that
a patient’s decision is free from coercion,16 which may require consenting a
patient individually, away from family or associates. Administration of blood
products to a competent patient who has refused blood transfusion is un-
lawful and may lead to professional and criminal proceedings against the
doctor.17
Advance directives
Advance directives state a patient’s acceptance or otherwise of specific
medical interventions for situations in which they would be unable to pro-
vide consent. They must contain clear and medically interpretable instruc-
tions about the treatments which are acceptable or unacceptable. They
must also be clear that these directives are to apply even if a patient’s life
is at risk.17 Advance directives may be issued by a church; however, these
often lack sufficient medical detail.16 Many hospitals will therefore have
checklist-styled forms to clearly document a patient’s consent.
Emergency surgery
Conscious and competent patients
Conscious and competent patients must be provided the opportunity
for informed consent and have their wishes regarding blood transfusion
acceptance—or refusal—respected.16,17
Unconscious or incompetent patients
Unconscious or incompetent Jehovah’s Witness patients present uncer-
tainty. In emergency situations where a patient’s wishes are unknown, doc-
tors must act in the best interests of the incompetent patient, which may
include providing blood transfusion.17 Opinions of relatives or associates
that the patient would not accept a blood transfusion are insufficient, and
advance directives should be sought and verified. If the proposed treatment
Jehovah’s Witnesses 463
Fluid therapy
Routine fasting for minor surgery is usually well tolerated by healthy patients
with minimal disturbance to fluid status or electrolyte levels.18 The magni-
tude of disturbance to fluid and electrolyte homeostasis is dependent on
fasting times, the extent of surgery, age, patient comorbidity and the nature
and severity of acute pathology present. Disease, anaesthesia, trauma and
surgery precipitate a combined metabolic, neuroendocrine, immunological
and inflammatory stress response which readily disrupts fluid homeostasis
(Table 17.8). Concepts such as liberal, restrictive and goal-directed fluid
therapy have all gained popularity within the last two decades at various
times. Clarity around the optimal strategy for a given patient, with a given
pathology and a given collection of comorbidities, undergoing a given sur-
gery remains elusive, however.
Normal fluid and electrolyte balance
Under normal homeostatic conditions, net input and output of fluid and
electrolytes are equal. Mean 24h water intake, around 2500mL, roughly
constitutes 1500mL of fluid, 750mL of food and 250mL of metabolic water.
Output is balanced with 1500mL as urine, 100mL in faeces and 900mL as
insensible loss. Daily requirements of electrolytes are listed in Table 17.8.
Fluid compartments
Water constitutes 60% total body weight (600mL/kg). TBW comprises:
• Intracellular fluid: 66% total body weight (400mL/kg)
• ECF: 33% total body weight (200mL/kg)
• Interstitial fluid: 75% ECF (150mL/kg)
• Plasma: 25% ECF (50mL/kg).
The glycocalyx
• Structure: membrane-bound, carbohydrate-rich proteoglycan and
glycoprotein layer on the luminal surface of vascular endothelium.
• Function: vascular permeability, coagulation, inflammation, antioxidation
and regulating transluminal oncotic pressures.19 A non-circulating
volume of 700–1000mL of plasma volume is fixed within the endothelial
glycocalyx. Theoretically, isotonic crystalloid will distribute through this,
while colloid fluids will not.
Fluid therapy 465
Colloids
(See Table 17.10.)
Colloids are homogeneous, non- crystalline substances, consisting of
large molecules which persist in the vascular compartment to expand the
functional plasma volume (lasting several hours to several days). Duration
of action is determined by physicochemical properties, integrity of the
glycocalyx/capillary membrane and pharmacokinetics of metabolism and
clearance.
Human albumin solution
• Molecular weight (MW) 69 000.
• Available as a 4–5% solution for the treatment of hypovolaemia, and as
a salt-poor 20% solution for the treatment of hypoalbuminaemia.
• Like other blood products, HAS is manufactured from fractionation
of whole blood. Concern of theoretical transmission of variant
Creutzfeldt–Jakob disease (vCJD) in the UK has resulted in this product
currently being imported from the US, and it is thus expensive.
• Albumin has not been shown to improve survival in either all-comer
admissions to intensive care28 or in the treatment of severe sepsis.29
• Used in the treatment of hypovolaemic shock, although post hoc
analysis of the SAFE trial demonstrated an association with i mortality
when albumin was used, rather than 0.9% sodium chloride, in the
resuscitation of critically ill patients with traumatic brain injuries.30
• Also used as a priming fluid in CPB and as a replacement solution in
plasma exchange.
Gelatins
Examples: Gelofusine® 4%, Physiogel®, Gelafundin® 4%:
• Succinylated gelatins (MW 30 000), presented in sodium chloride
solution.
• Manufactured from bovine collagen from bovine spongiform
encephalopathy-free herds. There have been no reports of vCJD.
• Initially these have a powerful osmotic effect. Administration may
rarely lead to histamine release, causing bronchospasm, urticarial rash,
hypotension and tachycardia. May trigger anaphylaxis.
• Therapeutic maximal dose is limited by haemodilution.
Hydroxyethyl starches
• Starch solutions have been associated with considerable side effects,
including accumulation, pruritus, renal impairment,31 coagulopathy,
haemorrhage, anaphylaxis and death.
• Hydroxyethyl starch products were withdrawn in the UK in 2013
because of safety concerns over their use as resuscitation fluids in
critically ill patients and patients with pre-existing renal dysfunction.
Liberal vs restrictive fluids
Over the last two decades, styles of administering fluids have varied be-
tween liberal strategies (designed to replace ‘3rd space’ fluid shifts and ‘in-
sensible’ losses from surgery) and restrictive strategies, aiming to achieve
‘zero balance’, or zero weight gain due to postoperative fluid retention.32
Many ERAS pathways incorporate restrictive strategies. However, both lib-
eral and restrictive strategies have been associated with problems.
• From this point of uncertainty, the RELIEF trial by Myles et al. in 2018
has offered some guidance to clinicians.33 This multicentre trial of 3000
patients undergoing major abdominal surgery had a restrictive arm and
a liberal arm during and up to 24h after surgery. AKI and renal
replacement therapy rates were lower in the liberal arm, although
disability-free survival was the same in both groups.
• There is now support for ‘moderately liberal’ fluid regimens for major
abdominal surgery requiring 10–12mL/kg/h of IV fluid administered
intraoperatively and 1.5mL/kg/h in the following 24h post-surgery.
Other major surgeries which do not result in major fluid shifts are
unlikely to require as much fluid.33,34
Goal-directed fluid therapy
GDFT uses a combination of fluids and inotropic agents administered in a
predetermined algorithm to optimise blood flow to organs.
IV fluids and inotropes are sequentially administered to achieve specific
haemodynamic endpoints (CVP, MAP, stroke volume, CO, cardiac index,
etc.). Although appealing, GDFT has not resulted in significant benefits for
patients. Clinical benefits seen in small trials have not been corroborated in
later literature. Nonetheless, GDFT remains in many ERAS protocols for
abdominal surgery worldwide.
Fluid therapy 469
References
1 New Zealand Blood Service (2016). Transfusion Medicine Handbook, 3 rd edn. Auckland: New
Zealand Blood Service.
2 Klein AA, Arnold P, Bingham RM, et al. (2016). AAGBI guidelines: the use of blood components
and their alternatives 2016. Anaesthesia, 71, 829–42.
3 Curry N, Foley C, Wong H, et al. (2018). Early fibrinogen concentrate therapy for major haem-
orrhage in trauma (E-FIT 1): results from a UK multi-centre, randomised, double blind, placebo-
controlled pilot trial. Crit Care, 22, 164.
4 Muñoz M, Acheson AG, Bisbe E, et al. (2019). An international consensus statement on the man-
agement of postoperative anaemia after major surgical procedures. Anaesthesia, 73, 1418–31.
5 Mueller MM, Van Remoortel H, Meybohm P, et al. (2019). Patient blood management: recom-
mendations from the 2018 Frankfurt Consensus Conference. JAMA, 321, 983–97.
6 Desai N, Schofield N, Richards T (2018). Perioperative patient blood management to improve
outcomes. Anesth Analg, 127, 1211–20.
7 Franchini M, Marano G, Veropalumbo E, et al. (2019). Patient blood management: a revolu-
tionary approach to transfusion medicine. Blood Transfus, 17, 191–5.
8 World Health Organization (2011). Haemoglobin concentrations for the diagnosis of anaemia and
assessment of severity. M http://www.who.int/vmnis/indicators/haemoglobin.pdf
9 CRASH-2 trial collaborators; Shakur H, Roberts I, Bautista R, et al. (2010). Effects of tranexamic
acid on death, vascular occlusive events and blood transfusion in trauma patients with significant
haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet, 376, 23–32.
10 Ker K, Beecer D, Roberts I (2013). Topical application of tranexamic acid for the reduction of
bleeding. Cochrane Database Syst Rev, 7, CD010562.
11 Klein AA, Bailey CR, Charlton AJ, et al. (2018). Association of Anaesthetists guidelines: cell sal-
vage for peri-operative blood conservation. Anaesthesia, 73, 1141–50.
12 Kha KS, Moore PAS, Wilson MJ, et al. (2017). Cell salvage and donor blood transfusion during
cesarean section: a pragmatic, multicentre randomised controlled trial (SALVO). PLoS Med, 14,
e1002471.
13 Holcomb JB, Tilley BC, Baraniuk S, et al. (2015). Transfusion of plasma, platelets and red blood
cells in a 1:1:1 vs 1:1:2 and mortality in patients with severe trauma: the PROPPR randomized
clinical trial. JAMA, 313, 471–82.
14 Chang R, Cardenas JC, Wade CE, Holcomb JC (2016). Advances in the understanding of trauma-
induced coagulopathy. Blood, 128, 1043–9.
15 Lima GL, Byk J (2018). Trauma and early blood transfusion: the challenging hemorrhage manage-
ment in Jehovah's Witnesses. Rev Col Bras Cir, 45, e1974.
16 West JM (2014). Ethical issues in the care of Jehovah’s Witnesses. Curr Opin Anesthesiol,
27, 170–6.
17 Klein AA, Bailey CR, Charlton A, et al. (2019). Association of Anaesthetists: anaesthesia and peri-
operativecare for Jehovah’s Witnesses and patients who refuse blood. Anaesthesia, 74, 74–82.
18 Jacob M, Chappell D, Conzen P, Finsterer U, Rehm M (2008). Blood volume is normal after pre-
operative overnight fasting. Acta Anaesthesiol Scand, 52, 522–9.
19 Astapenko D, Benes J, Pouska J, Lehmann C, Islam S, Cerny V (2019). Endothelial glycocalyx
in acute care surgery— what anaesthesiologists need to know for clinical practice. BMC
Anesthesiology, 19, 238.
20 Bentzer P, Griesdale DE, Boyd J, MacLean K, Sirounis D, Ayas NT (2016). Will this hemodynam-
ically unstable patient respond to a bolus of intravenous fluids? JAMA, 316, 1298–309.
21 Marik PE, Baram M, Vahid B (2008). Does central venous pressure predict fluid responsiveness?
A systematic review of the literature and the tale of seven mares. Chest, 134, 172–8.
22 Biais M, de Courson H, Lanchon R, et al. (2017). Mini-fluid challenge of 100 ml of crystalloid
predicts fluid responsiveness in the operating room. Anesthesiology, 127, 450–6.
23 Young P, Bailey M, Beasley R, et al. (2015). SPLIT: effect of a buffered crystalloid solution vs saline
on acute kidney injury among patients in the intensive care unit. JAMA, 314, 1701–10.
24 Shaw AD, Bagshaw SM, Goldstein SL, et al. (2012). Major complications, mortality, and re-
source utilization after open abdominal surgery: 0.9% saline compared to Plasmalyte. Ann Surg,
255, 821–9.
25 Burdett E, Dushianthan A, Bennett-Guerrero E, et al. (2012). Perioperative buffered versus non-
buffered fluid administration for surgery in adults. Cochrane Database Syst Rev, 12, CD004089.
470
26 Self WH, Semler MW, Wanderer JP, et al. (2018). SALT-ED: balanced crystalloids versus saline in
noncritically ill adults. N Engl J Med, 378, 819–28.
27 Semler MW, Self WH, Wanderer JP, et al. (2018). SMART: balanced crystalloids versus saline in
critically ill adults. N Engl J Med, 378, 829–39.
28 The SAFE Study Investigators (2004). SAFE: a comparison of albumin and saline for fluid resusci-
tation in the intensive care unit. N Engl J Med, 350, 2247–56.
29 Caironi P, Tognoni G, Masson S, et al. (2014). ALBIOS: albumin replacement in patients with
severe sepsis or septic shock. N Engl J Med, 370, 1412–21.
30 The SAFE Study Investigators (2007). SAFE: saline or albumin for fluid resuscitation in patients
with traumatic brain injury. N Engl J Med, 357, 874–84.
31 Myburgh JA, Finfer S, Bellomo R, et al. (2012). CHEST: hydroxyethyl starch or saline for fluid
resuscitation in intensive care. N Engl J Med, 367, 1901–11.
32 Brandstrup B, Svendsen PE, Rasmussen M, et al. (2012). Which goal for fluid therapy during
colorectal surgery is followed by the best outcome: near maximal stroke volume or zero fluid
balance? Br J Anaesth, 109, 191–9.
33 Myles PS, Bellomo R, Corcoran T, et al.; Australian and New Zealand College of Anaesthetists
Clinical Trials Network and the Australian and New Zealand Intensive Care Society Clinical Trials
Group (2018). Restrictive versus liberal fluid therapy for major abdominal surgery. N Engl J Med,
378, 2263–74.
34 Miller TE, Myles PS (2019). Perioperative fluid therapy for major surgery. Anesthesiology, 130,
825–32.
Chapter 18 471
471
Specific circumstances
Matthew Evans and Leigh Kelligher
Oncological impact of anaesthesia 472
Oncological considerations 474
Susanna Ritchie-McLean
General principles of laser surgery 476
Safety in laser surgery 478
Jakob Mathiszig-Lee
Robotic surgery 480
Mary Stocker
Day surgery 483
Conduct of day case anaesthesia 487
Laura Bainbridge
Neurological determination of death 493
Organ donation surgery after brain death 497
Major anaesthetic mishaps: what to do in the aftermath 503
472
and opioids in breast cancer patients. The definitive case for the benefit of
propofol over volatile anaesthesia in cancer surgery is yet to be made; how-
ever, it should be noted that no evidence exists showing propofol is worse.
Opioid analgesia
Opioid analgesics mediate their effect principally via the mu-opioid re-
ceptor. This receptor is known to be overexpressed on many cancer cell
types and is postulated to play a role in tumour growth and development.
High levels of mu-opioid receptor expression have been correlated with
worse oncological outcomes in clinical studies. It has therefore been postu-
lated that perioperative opioids may be tumorigenic via their action on, and
induction of, the mu-opioid receptor. The clinical evidence to date does not
support this and it remains a theoretical risk.
Regional anaesthesia
Following on from the theoretical risk of opioid analgesics, it has been
postulated that, by minimising surgical stress and reducing opioid usage,
regional anaesthesia may be beneficial in oncological surgery. Current evi-
dence is mixed and the use of regional anaesthesia for this purpose alone
cannot be recommended.
NSAIDs
Via inhibition of COX, NSAIDs reduce the expression of a number of
growth factors, including prostaglandin E2, which has been implicated
in a variety of tumorigenic processes. It is postulated that perioperative
NSAID use may therefore reduce the risk of tumour recurrence/metas-
tasis. Clinical evidence of a significant effect following perioperative NSAID
administration is lacking.
Dexamethasone
Steroids are known to be immunosuppressive and therefore, it has been
questioned whether the use of dexamethasone perioperatively is appro-
priate in cancer surgery. There is no clinical evidence to support this hy-
pothesis at the time of writing.
Recommendations for practice
While there is biological plausibility for some of the interventions above
being recommended/avoided in cancer surgery, definitive evidence—and
therefore evidence-based guidance for practice—is still some way off.
The best approach has to be a pragmatic one, taking into account the
patient’s needs and preferences and the options available. The overall
guiding principle must be to adopt a strategy that minimises the physiological
insult and stress of surgery and produces a rapid, high-quality recovery and
return to premorbid function, allowing the patient to move on to the next
phase of their cancer treatment in the optimum time frame. Initiatives such
as ERAS, or other fast-track recovery programmes, utilising many of the
interventions described above, produce good short-term postoperative re-
covery and may also be beneficial for oncological outcomes.
47
Oncological considerations
General considerations
Cardiac injury
May be induced by drugs (anthracyclines, fluorouracil, trastuzumab) or the
stress of chemotherapy on a compromised heart. Anthracycline-induced
cardiac failure may be irreversible and has a mortality of above 30%.
Bleomycin Exposure as part of chemotherapy conveys the potential risk of
rapidly progressive pulmonary toxicity. Pulmonary toxicity occurs in 10% of
patients exposed to bleomycin, with acute, followed by chronic, fibrosing
alveolitis. Avoidance of high inspired O2 concentrations and careful fluid
management are recommended. Bleomycin is notably administered in germ
cell tumours and Hodgkin lymphoma.
Cytokine release syndrome An acute systemic inflammatory response to
immunotherapies, including chimeric antigen receptor T- cell therapy,
heralded by fever. Associated features may range from mild flu- like
symptoms to severe life-threatening circulatory collapse.
Hepatic veno-occlusive disease A progressive obliteration of venous channels
in the liver.
Tumour lysis syndrome Can follow initial chemotherapy (typically for
lymphoma and high-count leukaemias). Mass cell death leads to acute renal
impairment, with hyperkalaemia, hyperuricaemia, hyperphosphataemia and
hypocalcaemia.
Mediastinal masses (Particularly in leukaemia or lymphoma patients)
can cause complete airway collapse under anaesthesia, even in the
asymptomatic. Warning signs include stridor, wheeze, orthopnoea and SVC
obstruction.
SVC obstruction Can arise from compression by a tumour or lymph
nodes (usually bronchogenic carcinoma) or direct vessel invasion. Pleural
effusions and ascites are common in ovarian cancer, metastatic disease and
mesothelioma.
Paraneoplastic syndromes
Occur in 10% of cancer patients1 (especially lung, lymphoma, breast, pros-
tate, ovarian and pancreatic tumours). Anaesthetic considerations:
• Lambert-Eaton myasthenic syndrome is common in small-cell lung
cancer and breast, thymus and GI tract tumours (see % p. 316).
• Cushing’s syndrome may occur in tumours of the lung, pancreas,
thymus and ovary (see % p. 232).
• Hypercalcaemia may be caused by bony metastases or PTH-like
compounds.
• Hyponatraemia and SIADH-like syndromes may be caused by small-cell
lung cancer and also lymphoma, leukaemia and pancreatic/carcinoid
tumours (see % p. 242).
• Cachexia can be caused by vomiting, loss of appetite or other GI
disturbances. Hypoalbuminaemia (<35g/L) is a risk factor for poor
outcomes.2
Oncological considerations 475
Fig. 18.1 A LaserJet ETT, with a side port for CO2 sampling. Courtesy Aidan
O’Donnell.
Further reading
Magee P (2018). Physics for anaesthesia. Magnetic resonance imaging; depth of anaesthesia moni-
toring; LASER; and light spectroscopy. BJA Educ, 18, 102–8. doi:10.1016/j.bjae.2017.12.004
Pearson KL (2017). Anaesthesia for laryngo-tracheal surgery, including tubeless field techniques. BJA
Educ, 17, 242–8. doi:10.1093/bjaed/mkx004
Kitching AJ, Edge CJ (2003). Lasers and surgery. Contin Educ Anaesth Crit Care Pain, 3, 143–6.
doi:10.1093/bjacepd/mkg143
480
Robotic surgery
The number of procedures undertaken robotically around the world con-
tinues to grow, with an increasing variety of surgery now possible with ro-
botic systems (Table 18.2).
• Advantages for the surgeon include i comfort while operating, 3D
video, filtering out of any tremor and scaling of movement to allow for
precision work.
• Patient-based advantages include a better cosmetic result from
minimally invasive approaches, reduced pain from port sites and
reduced length of stay.
• The effect of robotic surgery on outcomes is controversial and
procedure-specific. While some papers suggest better oncological
outcomes from robotic procedures, there have been warnings about
poorer survival from other robotic procedures for cancer.
• The i cost and length of time it takes to complete robotic surgery
are an important consideration for institutions, particularly at the
establishment of any robotic programme.
• The considerations for the anaesthetist are largely due to positioning,
length of procedure and the significantly reduced access to the patient
caused by most robotic systems. The docking and undocking of a robot
often takes significant time and rapid removal is rarely possible.
Preoperative
It is important to clarify with the surgeon how they will need the patient
positioned as it is likely to be much more extreme or different from a non-
robotic procedure. A high-quality team brief is critical to the smooth run-
ning of a robotic theatre.
• The docking of the robot is one of the rate-limiting steps of robotic
surgery and so it is useful to ensure a consistent theatre team to reduce
the delay this incurs to a minimum.
• The preassessment of the patient should be as normal. However,
for procedures where prolonged steep head-down is anticipated, a
note should be made of significant glaucoma as this may lead to an i
incidence of ophthalmic complications, including visual loss.
Robotic surgery 481
Day surgery
Organisation
A surgical ‘day case’ is a patient who is admitted, operated upon, and dis-
charged on the same calendar day. In the UK (unlike the US), a 24h stay
is not classed as day surgery, as this requires overnight admission and a
hospital bed.
The surgery must have been planned as day surgery. Patients who are
booked as inpatients but are successfully discharged on the day of surgery
will not appear in hospital day case statistics. Booking potential day case pa-
tients via an inpatient pathway can result in patient cancellation due to lack
of availability of a postoperative bed which would not have been required
if a day surgery pathway was planned from the outset.
Organisation is the key to efficient, good-quality day surgery and requires
close cooperation between all agencies involved, including surgeons, anaes-
thetists, day unit staff, GPs, patients and their carers.
Facilities An efficient organisation requires ‘ring-fenced’ theatres and ward
space. Day surgery can be managed successfully in a variety of hospital
configurations; however, day cases on inpatient wards and theatres have
a higher admission rate and will suffer cancellation when there are bed
shortages. Self-contained units with their own facilities, but within an acute
hospital, offer the best option.
Escalation It is essential that day surgery facilities will not be used to
accommodate overnight patients at times of hospital escalation. At times
of escalation, it is even more important that the day surgery unit continues
to function efficiently and hence enable the majority of elective surgery to
proceed uninterrupted.
Staff Adequately trained and experienced staff should perform day case
anaesthesia and surgery to minimise unplanned admissions. The day surgery
environment provides many opportunities for training of junior staff, but
supervision and guidance from senior clinicians are essential. The unit
should be staffed with nurses and operating department practitioners who
are in themselves expert day surgery practitioners, invested in the success
of the day surgery team.
Day surgery procedures
The British Association of Day Surgery has produced a directory which
details over 200 procedures now deemed appropriate to be undertaken
on a day case basis. Day surgery is no longer confined to minor procedures
but embraces the majority of elective surgery and a large percentage of
urgent surgery. There is no time limit for surgical duration; however, consid-
eration must be given when scheduling an operating theatre list to potential
postoperative recovery times for more complex surgery, such that longer
procedures will usually be undertaken in the morning or early afternoon.
For a procedure to be appropriate for day surgery, the following criteria
must be met:
48
Postoperative
• Balanced analgesia with paracetamol, NSAIDs, LA and short-acting
opioids is usually adequate. If more analgesia is needed, it is imperative
to use it early; consider IV fentanyl 50–100 micrograms.
• Give PO morphine or other agents such as tramadol if stronger
analgesia is required. Remember that morphine in doses above 0.1mg/
kg increases the admission rate.
• Antispasmodic agents, such as hyoscine, and physical therapies, such as
hot water bottles, may help, particularly for cramping lower abdominal
pain following gynaecological surgery.
Postoperative nausea and vomiting
(See also % pp. 442–8.)
• A multifactorial approach to the prevention of PONV should be used.
The Apfel scoring system may significantly overestimate the risk of
PONV if the anaesthetic techniques described above are employed.
Patients experiencing PONV must be actively managed before
discharge home.
• For high-risk patients, LA techniques or GA using TIVA, avoidance of
opioids, multimodal analgesic therapy, good hydration (IV fluids) and
minimal fluid fast are appropriate. Dexamethasone 8mg, in combination
with cyclizine 50mg, or a 5-HT3 antagonist are effective prophylactic
agents. This is an approach that works well and leaves only a small
number of patients requiring rescue treatment postoperatively.
Regional anaesthesia
(See also % Chapter 40.)
The i use of ultrasound enables many procedures to be undertaken
under purely regional anaesthesia with huge efficiency gains, particularly
if entire lists are undertaken this way. It is reasonable to discharge pa-
tients with working plexus blocks, thus allowing the benefit of prolonged
postoperative analgesia. Remember that patients need special instructions
on the care of the anaesthetised part so as to avoid inadvertent damage.
This would include a sling for patients with brachial plexus blocks.
Local anaesthesia
Surgeons should be encouraged to use liberal infiltration of LA for any in-
cision ‘if you cut it, block it’. For many procedures such as inguinal hernia
repair or breast cancer surgery, surgical infiltration is as effective as re-
gional anaesthesia. It can also be more efficient and associated with fewer
complications.
Specific blocks
Field block performed by the surgeon Excellent for LA hernia repair, as
provides postoperative analgesia and obviates the need for GA. LA for
inguinal surgery is best placed by the surgeon under direct vision. Attempt
at ilioinguinal nerve block by anaesthetists has a high incidence of blockade
of the femoral nerve, with subsequent unplanned admission due to difficulty
mobilising.
Conduct of day case anaesthesia 489
PERINEAL SURGERY
Haemorrhoids, fissure, fistula,
Saddle block? abscess, EUA
Yes Perianal abscess
Prilocaine
No 10–20mg Circumcision/meatoplasty
(0.5–1mL)
Vulval surgery
>T10 block?
GENERAL Epigastric/
Yes
umbilical hernia
No Prilocaine GYNAE Diagnostic
60mg+ laparoscopy
(3mL+)
UROLOGY Ureteroscopy
+/– stent and laser
>1 h?
Yes
Prilocaine GENERAL Inguinal/femoral
No hernia
40–60mg
(2–3mL) Recurrent or bilateral hernia
Discharge organisation
Written and verbal discharge information must be provided. It is essen-
tial that patients are given the contact number of someone in the hospital,
should they require advice overnight. This may be the day surgery unit
within opening hours and either a surgical ward or senior surgical nurse
overnight. It is not appropriate for patients to be directed to out-of-hours
GP services or emergency departments.
Conduct of day case anaesthesia 491
Postoperative admission
The most common reasons for overnight admission are:
• The patient not fulfilling discharge criteria before the unit closes
• Observation after surgical or anaesthetic complications
• Unexpectedly more extensive surgery
• Uncontrolled pain or PONV.
Overall, unanticipated admission rates will depend upon the surgical case
mix undertaken. With increasingly complex procedures entering the day
surgery arena, timely discharge is more challenging to achieve, and consid-
eration to the development of a procedure-specific anaesthetic guideline
is required. Examples of procedures where this has been found useful in-
clude joint replacements, hysterectomy, laparoscopic cholecystectomy and
tonsillectomy.
Follow-up, audit and benchmarking
Patient follow-up is an essential part of the day surgery pathway to en-
sure patients are comfortable and satisfied postoperatively. The most ef-
fective method of undertaking this is via a postoperative telephone service.
A structured questionnaire should be undertaken covering the following:
• Postoperative pain score
• PONV score
• Patient satisfaction
• Satisfaction with the day surgery pathway
• Requirement for any postoperative advice or support.
This service provides detailed audit information, analysis of which drives
continuous service improvement. It also provides the opportunity for pa-
tient support, should they have any queries or concerns following their
procedure.
492
Further reading
Association of Anaesthetists, British Association of Day Surgery (2019). Guidelines for day case sur-
gery 2019. M https://anaesthetists.org/Portals/0/Images/Guidelines%20cover%20images/
Guideline_day_case_surgery_2019.pdf?ver=2019-05-05-075731-563
Fox B (2019). Spinal Anaesthesia for Day Surgery Patients: A Practical Guide, 4th edn. London: British
Association of Day Surgery.
Jackson I, McWhinnie D, Skues M (2012). The pathway to success— management of the
day surgical patient. M https://publications.bads.co.uk/the-pathway-to-success---
management-of-the-day-surgical-patient-17-p.asp
Smith I, McWhinnie D, Jackson I, eds. (2012). Day Case Surgery (Oxford Specialist Handbooks).
Oxford: Oxford University Press.
Association of Anaesthetists of Great Britain and Ireland (2010). Pre-operative assessment and patient
preparation—the role of the anaesthetist. London: Association of Anaesthetists of Great Britain
and Ireland.
Chung F, Mezei G (1999). Adverse outcomes in ambulatory anesthesia. Can J Anaesth, 46, RI8–26.
British Association of Day Surgery. M http://www.bads.co.uk [for updates, a series of handbooks
on topics referred to in this chapter, and new day surgery links].
Society for Ambulatory Anesthesia. M http://www.sambahq.org
Neurological determination of death 493
Other considerations
• The tests must be performed twice, each by a different doctor.
• The diagnosis should not normally be considered until at least 6h after
the onset of an apnoeic coma or 24h after the restoration of circulation
if the cause was a cardiac arrest.
• If prolonged hypothermia (<34°C for >6h) has occurred, the
tests should be performed at least 24h after the restoration of
normothermia.
• Death is confirmed after the 2nd set of tests, but in the UK, the time of
death is recorded as the completion of the 1st set.
• The coroner (Procurator Fiscal in Scotland) should be informed in the
usual referral manner. If organ donation is contemplated, this should be
discussed.
• Care of the relatives is essential at this time, irrespective of whether the
patient is to be an organ donor or not.
• Observations that are incompatible with the diagnosis of brainstem
death include seizures, decorticate and decerebrate posturing and limb
movements elicited with stimulation in the cranial nerve distribution
• Observations that are compatible with brainstem death include spinal
reflexes, blushing and the absence of diabetes insipidus.
• Spinal reflexes can be spontaneous or in response to stimulus. They do
not occur in the motor distribution of the cranial nerves or in response
to stimulation within the cranial nerve distribution.
Circulatory determination of death
For organ donation following circulatory determination of death, the fol-
lowing observations are required:
• The person responsible for confirming death must observe apnoea,
unconsciousness and the absence of pulsatility on an arterial line trace
or of electrical activity on ECG for 5min.
• After 5min of continued cardiorespiratory arrest, death is confirmed
if there is no pupillary response to light, no corneal response and no
motor response to supraorbital pressure.
Further reading
Smith M (2018). Brain death. In: Bersten AD, Handy JM (eds). Oh’s Intensive Care Manual, 8th edn.
Elsevier. pp. 673–80.
Smith M (2015). Brain death: the United Kingdom perspective. Semin Neuro, 35, 145–51.
doi:10.1055/s-0035-1547534
Oram J, Murphy P (2011). Diagnosis of death. Contin Educ Anaesth Crit Care Pain, 11, 77–81.
doi:10.1093/bjaceaccp/mkr008
Academy of Medical Royal Colleges (2008). A code of practice for the diagnosis and confirmation
of death. M https://www.aomrc.org.uk/reports-guidance/ukdec-reports-and-guidance/
code-practice-diagnosis-confirmation-death/
Organ donation surgery after brain death 497
Target parameters
MAP 60–80mmHg
Pulse 60–120/min
Cardiac index >2.1L/min/m2
Core temperature 36–37.5°C
Hb >70g/L for CV stable donor
>90g/L for unstable donor
SpO2 >95% with lowest FiO2 to maintain PaO2 >10kPa
VT 6–8mL/kg
PaCO2 NHS guidelines: 5–6.5kPa as long as pH>7.25
ANZICS and US guidelines: 4.7–6.0kPa
(35–45mmHg)
Plateau pressure <30cmH2O
Urine output 0.5–2mL/kg/h
Perioperative
• The WHO Surgical Safety Checklist (or similar) should be applied.
• During the organ retrieval operation, the anaesthetist should aim to
maintain physiological stability in the donor to ensure the donated
organs are in optimal condition for transplantation.
• Standard monitoring is required, plus an arterial line, core temperature
and urine output.
• Patients who are brain-dead cannot experience pain and lack
consciousness and so a true ‘anaesthetic’ is not required. However,
spinal cord function remains intact and administration of NMBAs, volatile
agents and, at times, an opioid is required to prevent spinal reflex motor
responses and reduce spinal sympathetic responses (tachycardia and
hypertension) that can occur spontaneously or during surgical stimulation.
• Opioids are sometimes given to suppress catecholamine-mediated
sympathetic activity, although they may not be sufficient. GTN or a β-
blocker may also be needed to treat hypertension.
• Spinal reflexes in the limbs can be distressing for observers and could
potentially lead to contamination of the operative field. Excessive
sympathetic responses can result in myocardial injury or excessive
bleeding, with subsequent haemodynamic instability and detrimental
effects on graft function.
• Large and frequent haemodynamic fluctuations occur due to compression
of the IVC, manipulation of the adrenal glands and blood/fluid loss.
Hypotension is treated with crystalloids, blood products, vasopressin
infusion and inotropes as indicated. There is no role for synthetic colloids as
these may impair graft function. Have 4 units of RBCs available in theatre.
• Broad-spectrum antibiotics are given as per local transplant protocol.
• Cardiothoracic and abdominal surgeons work concurrently to mobilise
the organs.
Organ donation surgery after brain death 501
Further reading
Australian and New Zealand Intensive Care Society (2019). The statement on death and
organ donation, 4th edn. M https://www.anzics.com.au/wp-content/uploads/2020/07/
ANZICS-Statement-on-Death-and-Organ-Donation-Edition-4.pdf
Martin-Loeches I, Sandiumenge A, Charpentier J, et al. (2019). Management of donation after brain
death in the ICU:the potential donor is identified, what’s next? Intensive Care Med, 45, 322–30.
doi:10.1007/s00134-019-05574-5
Pasternak JJ (2019). Neuroanesthesiology update. J Neurosurg Anesthesiol, 31, 178–98. doi:10.1097/
ANA.000000000000058
Streat SJ (2018). Organ donation. In: Bersten AD, Handy JM (eds). Oh’s Intensive Care Manual, 8th
edn. Elsevier. pp. 1205–14.
Anderson TA, Bekker P, Vagefi PA (2015). Anesthetic considerations in organ procurement surgery:
a narrative review. Can J Anesth, 62, 529–39. doi:10.1007/s12630-015-0345-8
Manara AR, Murphy PG, O’Callaghan G (2012). Donation after circulatory death. Br J Anaesth, 108
(S1), i108–21. doi:10.1093/bja/aer357
McKeown DW, Bonser RS, Kellum JA (2012). Management of the heart-beating brain-dead organ
donor. Br J Anaesth, 108, i96–107. doi:10.1093/bja/aer351
Academy of Medical Royal Colleges. UK Donation Ethics Committee. M https://www.aomrc.org.uk/
all-publications/reports-guidance/ukdec/
NHS Blood and Transplant Service. M https://www.odt.nhs.uk/
Major anaesthetic mishaps: what to do in the aftermath 503
Caring for the family A formal meeting with the family needs to be arranged
immediately. Bad news must not be broken over the phone, although they
should be informed there has been a complication and that they need
to come to the hospital immediately. It is advisable they bring a support
person. If English is not the family’s first language, a translator must be used.
Breaking bad news can be challenging, especially for those who do not
do it very often. This involves a team approach and should include senior
members of the anaesthetic, nursing and surgical teams.
Prior to meeting with the family, a brief premeeting should occur with
the attendees to identify who will be the 1° spokesperson; if the patient has
survived, this role may be most appropriately performed by the intensivist
now caring for the patient. At the premeeting, a summary of the events and
facts to be discussed should be agreed upon. Information that is unknown
should be acknowledged.
The meeting should take place in a quiet room where interruptions will
not occur. All members of the team should be introduced, as well as all
family members. It is important the bad news is delivered succinctly at the
beginning, in easy-to-understand, non-medical language. Apologising to the
family that this event has occurred is not an admission of guilt, but a sign of
both empathy and caring and may provide comfort to a grieving family. A
bad news meeting can be emotionally draining for all concerned and only
a small proportion of the information presented may be retained. If the
family asks questions to which you do not know the answer, reply honestly
and tell them if and how you will find out this information. A record of the
meeting must be documented in the clinical notes and should include who
attended, what was covered and what follow-up is planned.
Caring for the team Ideally, after a major event, the theatre should be
immediately closed and subsequent cases cancelled or performed by
another team. A ‘hot’ debriefing session should be facilitated as soon as
possible. This allows staff to talk about what has happened and aims to
defuse emotions. It is also used to let staff know what other resources
are available to them, e.g. counselling or further more formal debriefing
sessions.
Caring for the anaesthetist It is essential that the anaesthetic department
provides support for the anaesthetist.
Surveys reveal >70% of anaesthetists who experience a catastrophic
perioperative event will have a high degree of emotional impact, experi-
encing guilt, anxiety, sleeplessness, fear of judgement by colleagues and of
litigation, anger and reliving the event.3 They may also suffer from phys-
ical effects such as tiredness, muscle tension and nausea. These are a nat-
ural consequence of such an event but should lessen within a week or so.
Depending on the event and the individual, time off work to emotionally
recover may be helpful and on return to work, additional support may be
needed.
Support from a mentor should be sought or arranged by the clinical lead
as soon as possible. Discussing the events in an open, non-judgemental
manner can assist the anaesthetist in coming to terms with what has
Major anaesthetic mishaps: what to do in the aftermath 505
Criminal prosecution Police investigations are unusual. They occur if there are
suspicious circumstances, if it is felt that a clinician has been grossly negligent
or as a recommendation following a coronial inquest. Any communications
with the police should be done in conjunction with your medical defence
organisation. These investigations are invariably extremely slow and can
take months or even years to complete. Any doctor involved in this must
be offered support as this process is incredibly stressful.
Civil litigation Following a major anaesthetic mishap, a civil case for negligence
can potentially be brought against the doctor or the hospital. This is an
exceedingly slow process and can drag on for years.
Further reading
Clegg I, MacKinnon R (2014). Strategies for handling the aftermath of intraoperative death. Contin
Educ Anaesth Crit Care Pain, 14, 159–62. doi:10.1093/bjaceaccp/mkt050
Association of Anaesthetists (2005). Catastrophes in anaesthetic practice—dealing with the aftermath.
M http://dx.doi.org/10.21466/g.CIAP.2005
Bacon AK, Morris RW, Runciman WB, et al. (2005). Crisis management during anaesthesia: re-
covering from a crisis. Qual Saf Health Care, 14, e25. doi:10.1136/qshc.2002.004333
White SM (2003). Death on the table. Anaesthesia 58, 515–19. doi:10.1046/j.1365-2044.2003.03241.x
Aitkenhead AR (1997). Anaesthetic disasters: handling the aftermath. Anaesthesia, 52, 477–82.
References
3 Gazoni FM, Amato PE, Malik ZM, et al. (2012). The impact of perioperative catastrophes on an-
esthesiologists: results of a national survey. Anesth Analg, 114, 596–603. doi:10.1213/ANE.0b013
e318227524e
Chapter 19 507
507
Cardiac anaesthesia
Kelly Byrne, Kate Goldstone and Peter Simmons
Perioperative considerations 508
Intraoperative transoesophageal echocardiography 510
Cardiopulmonary bypass 511
Myocardial protection during CPB 512
Cardiac anaesthesia: routine elective surgery 513
Surgery specific considerations 516
Deep hypothermic circulatory arrest 521
Intra-aortic balloon pump 523
Cardiac surgery, pulmonary hypertension, the right
ventricle 524
Controversies in cardiac surgery 526
See also
% Anaesthesia for transcatheter aortic valve implantation p. 834
508
Preoperative considerations
As with all anaesthetic assessment, it is crucial in cardiac surgery to under-
stand the indications for the surgery and the expected benefits, so an
effective risk–benefit analysis can be undertaken. Most successful cardio-
thoracic units will use a multidisciplinary team approach where the best
option for the patient is considered among cardiologists, surgeons, an-
aesthetists and critical care specialists. Decisions regarding the choice be-
tween a percutaneous intervention and surgery are not as clear-cut as they
were previously, and may depend on institutional expertise or protocols.
Increasingly, there are two potential intervention pathways for patients
to consider. There are well-described guidelines for the indications for
CABG and the timing of valve replacement or repair. According to cur-
rent guidelines, CABG has a survival benefit over PCI in patients with left
main stem disease, severe (>70% stenosis) three-vessel disease, reduced
EF, DM and patients with a SYNTAX score (used to score the complexity
of CAD) >22.1
Valve replacement should be considered in symptomatic patients, pa-
tients where the valve disease is severe and the patient is considered low
risk for surgery and those where there has been myocardial change as a
result of the valve lesion, even in the absence of symptoms, e.g. ventricular
dilation in AR or MR.2
In addition to the routine preoperative assessment, careful attention
should be paid to:
• Recent MI and stability of ischaemic symptoms
• History of heart failure
• Bleeding history
• Current rhythm and history of arrhythmia
• Other organ dysfunction, and reserve including cerebral reserve
• Previous cardiac surgery or interventions
• Previous radiotherapy to the chest
• Assessment of LV function (usually via echocardiography, occasionally
LV ventriculogram during angiogram)
• Other important echocardiographic findings (significant valvular heart
disease, presence of i pulmonary pressures, RV dysfunction)
• Configuration of CAD if present
• Exercise tolerance—gives an indication of cardiorespiratory reserve
• Routine investigations, including the following:
• Bloods: FBC, U&E/eGFR, LFTs, coagulation, group and screen (G&S)
• ECG, CXR, echocardiography, angiogram (or CT angiogram)
• Additional tests (e.g. iron studies, cardiac biomarkers, HbA1c, PFTs,
carotid artery doppler)
• A history of dysphagia, hiatus hernia or surgery on the oesophagus,
relevant and important for any patient requiring TOE insertion.
Preoperative considerations 509
Medications
• ACE inhibitors and ARBs are stopped perioperatively in many centres.
• Check that antiplatelet and anticoagulant drugs (including novel oral
anticoagulants) have been stopped appropriately. Platelet assays can be
undertaken to determine whether any residual activity remains.
• With cardiac preadmission clinics and day of surgery admissions, many
centres do not premedicate patients the night prior to surgery.
• Patients often receive midazolam after IV cannula placed in theatre.
• A cautious approach should be taken if administering premedication in
patients with pulmonary hypertension/RV dysfunction, or severe AS.
Risk stratification
The EuroSCORE II and Society of Thoracic Surgeons (STS) scoring sys-
tems are frequently used cardiac risk models (Table 19.1). They predict an
individual’s mortality after cardiac surgery. These risk calculators are avail-
able online at:
• M http://riskcalc.sts.org/stswebriskcalc/calculate
• M http://www.euroscore.org/calc.html
Some preoperative interventions aim to improve an individual’s risk profile,
such as:
• IABP for those with critical CAD
• Placement of defibrillation pads in those with a history of VF arrest
• Preoperative pulmonary vasodilators in those with i PAP
• Awareness that patients with critical mitral stenosis and AS tolerate AF
poorly.
Intraoperative transoesophageal
echocardiography
TOE has become standard practice during cardiac surgery in many centres,
although this is not completely without controversy. While generally
very safe, there is a 0.2% chance of complications during intraoperative
TOE, ranging from minor abrasions to oesophageal rupture (0–0.3%).3
Oesophageal rupture can be fatal and is i in elderly ♀.
Class I indications
Valve repair or replacement, unexplained haemodynamic instability.
Absolute contraindications
• Perforated viscus, oesophageal stricture, oesophageal tumour,
oesophageal perforation, laceration, oesophageal diverticulum, active
upper GI bleed.
A comprehensive perioperative TOE includes 28 standard 2D TOE views.3
(See Fig. 19.1.)
RCA RCA or Cx
LAD LAD or Cx
cx RCA or LAD
Mid
Fig. 19.1 This image demonstrates the typical distributions of the right coronary
artery (RCA), left anterior descending (LAD) and circumflex (Cx) artery supply
to the left ventricle, as seen on 2D TOE. Modified with permission from Lang RM
et al. Recommendations for chamber quantification: a report from the American Society of
Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing
Group, developed in conjunction with the European Association of Echocardiograpy, a branch of
the European Society of Cardiology. J Am Soc Echocardiogr. 2005; 18:1440–63, with permission
from Elsevier.
Cardiopulmonary bypass 511
Cardiopulmonary bypass
• CPB replaces the function of the heart and lungs while the heart is
arrested, allowing for a bloodless, motionless surgical field.
• The pump (roller or centrifugal) requires full anticoagulation of the
patient with systemic heparin.
• The pump is primed with crystalloid, heparin, mannitol, HAS and
HCO3–. The pump delivers non-pulsatile flow of around 2.4L/min/
m3 (correlating with a normal cardiac index), maintaining a MAP of
between 50 and 70mmHg.
• Volume can be added to the pump via the reservoir or removed by
ultrafiltration to maintain an Hct of 20–30%.
• CPB causes platelet dysfunction, haemolysis and consumption of
coagulation factors. This is minimal for the first 2h but increases with
prolonged duration.
• Membranous oxygenators are incorporated into the CPB circuit,
providing oxygenation via diffusion down a concentration gradient
over a large surface area; increasing gas flow removes more CO2, and
increasing the O2 concentration increases alveolar partial pressure of
oxygen (PAO2).
(See Fig. 19.2.)
Patient
Arterial
cannula Venous
drain
Filter
O2 Reservoir
Pump
Fig. 19.2 Schematic of CPB circuit. Venous blood drains into a reservoir bucket; a
pump controls onward flow through the oxygenator and a bubble filter ensures no
gas embolises into the systemic circulation via the arterial cannula.
251
Surgery-specific considerations
For the following specific procedures, the same considerations apply as for
routine cardiac surgery, with the addition of the following points.
Off-pump coronary artery bypass grafting
Advantages of off-pump coronary artery bypass grafting (OPCABG) are
perceived to be avoiding manipulation of the great vessels, therefore re-
ducing the risk of atheroma embolisation, and avoiding the physiological
insult of CPB.
Perioperatively
• Line placement is the same as on-pump CABG.
• Active warming device(s) are required to maintain normothermia.
• The surgeon performs bypass grafts on a beating heart aided by
stabilising and suction devices (Octopus® and Starfish® devices) to
position the heart and isolate the target vessel. Intracoronary shunts
help minimise intraoperative ischaemia.
• Significant haemodynamic instability can occur with lifting of the heart,
particularly to access the posterior heart for grafting the left circumflex
or crux of the right coronary artery.
• Techniques to counter BP changes: vasopressors (phenylephrine may
allow more rapid titration than noradrenaline); crystalloid to augment
preload; positioning of the bed head down/up to increase/reduce
venous return; atropine to prevent vagally mediated bradycardia; low-
dose inotrope to support severe LV impairment; IABP for left main
stem disease.
• Heparin 150 units/kg is given, aiming for an ACT of 7300. Reversal of
heparin at the end varies by surgeon preference.
• TOE useful for pre-and post-graft assessments. Images often poor
intraoperatively due to anatomical distortion. Refractory hypotension
may be due to severe MR when heart lifted.
• Be prepared to transition rapidly to bypass if patient is unstable. Rate of
conversion from off-to on-pump CABG varies in publications (1–15%).7
Emergency conversion (after distal anastomoses have been started) is
associated with i morbidity and mortality.
Postoperatively
• OPCABG may result in a d blood transfusion rate, compared with
CABG, as well as d length of ICU stay. OPCABG is associated with a
lower rate of successful revascularisation, although this is not associated
with an i risk of postoperative MACE.
• No reduction in CVE has been demonstrated in trials comparing
OPCABG to on-pump CABG.7,8
• Debate remains regarding long-term mortality outcomes for OPCABG
vs on-pump CABG, with some analyses reporting no difference and
others showing a small, significant trend towards a mortality benefit at
>5y for on-pump CABG.7
Surgery-specific considerations 517
Perioperatively
• Ensure large-bore IV access in case of massive haemorrhage.
• Place external defibrillation pads prior to induction because of i risk
of ventricular arrhythmias and difficulty accessing the chest for internal
defibrillation.
• Ensure availability of immediate access to PRBCs.
• Femoral or axillary cannulation may precede sternotomy if surgeon
considers patient very high risk for re-entry (institution of peripheral
bypass allows greater control of haemorrhage/ischaemia but requires
sternal re-entry to be performed with systemic heparinisation).
• Sternal re-entry may be complicated by adhesions between the sternum
and key cardiovascular structures such as the RV, grafts or great vessels.
Injury can cause haemorrhage, ischaemia, arrhythmias or cardiac arrest.
• Longer surgical and CPB time resulting in i risk of transfusion and
coagulopathy. POCT is to guide therapy.
• Myocardial protection in redo surgery is more difficult in the presence
of a functioning internal mammary artery graft. Supplementing
antegrade cardioplegia with retrograde cardioplegia with temporary
occlusion of the internal mammary artery graft may be used to
overcome this.
Valve surgery
Table 19.2 highlights aspects of patient presentation and management spe-
cific to each valve surgery which tailor the standard approach to cardiac
surgery for grafting. (See % pp. 120–7 for haemodynamic goals of specific
valve lesions.)
(Continued)
Surgery-specific considerations 519
(Continued)
520
AF, atrial fibrillation; AR, aortic regurgitation; AS, aortic stenosis; AVR, aortic valve replace-
ment; CO, cardiac output; CPB, cardiopulmonary bypass; HR, heart rate; IHD, ischaemic heart
disease; LAP, left atrial pressure LV, left ventricle/ventricular; LVEF, left ventricular ejection
fraction; LVESD, left ventricular end-systolic diameter; LVH, left ventricular hypertrophy; MAP,
mean arterial pressure; MR, mitral regurgitation; MVR, mitral valve repair or replacement;
PAFC, pulmonary artery flotation catheter; PAP, pulmonary artery pressure; RV, right ventricle/
ventricular; SAM, systolic anterior motion (SAM) of the anterior leaflet of the mitral valve;
SVR, systemic vascular resistance; TOE, transoesophageal echocardiograph; TTE, transthoracic
echocardiography.
Deep hypothermic circulatory arrest 521
Perioperatively
• Acute aortic (Stanford type A) dissection is a cardiac surgical emergency
and the patient can present in extremis.
• Depending on the anatomical location of aortic pathology, tamponade,
cardiogenic shock, myocardial ischaemia, visceral ischaemia or arch
vessel occlusion may be present.
• Without surgery, mortality can be as high as 2% per hour, so expedient
care is imperative.14
• For acute cases, aggressive preoperative BP control is important,
including the use of antihypertensive infusions (GTN/labetalol/
esmolol), to prevent progression of dissection.
• The following monitoring is required:
• Nasopharyngeal temperature (representing brain temperature)
• Core temperature measurement (often urinary catheter)
• Modified EEG monitoring (BIS™/Entropy™)
• Cerebral oximetry—should be available
• Potentially >1 arterial line, dependent on planned CPB cannulation
sites—aiming to monitor proximal (right radial) and distal aortic arch
flow (left radial/femoral).
• Avoidance of hypertension during laryngoscopy and intubation is
essential to prevent aortic rupture.
• Peripheral bypass cannulae may be placed prior to sternotomy,
depending on aortic pathology. TOE can be used to confirm wire
placement within the true lumen of the aorta during femoral arterial
cannulation.
• When DHCA is instituted, drug infusions are stopped.
• On rewarming, infusions are recommenced.
• Consider running a heparinase TEG® once core temperature reaches
36°C to guide transfusion (cryoprecipitate and FFP take time to thaw).
• Inotropic support is often required to allow separation from CPB.
• These patients are at high risk of bleeding.
Postoperatively
• These patients are at high risk of coagulopathy and neurological
disturbance or injury. Prolonged intubation after these procedures is
common.
Intra-aortic balloon pump 523
Thoracic surgery
Charlotte Earnshaw and Kajan Kamalanathan
General principles 530
Enhanced recovery after surgery 532
Miscellaneous thoracic procedures 533
Isolation of the lungs 535
Management of one-lung ventilation 538
Rigid bronchoscopy and stent insertion 540
Superior/cervical mediastinoscopy and endobronchial
ultrasound 541
Lung surgery: wedge resection, lobectomy and
pneumonectomy 542
Lung volume reduction surgery, bullectomy and endobronchial
valves 544
Drainage of empyema and decortication 546
Repair of bronchopleural fistula 547
Pleurectomy/pleurodesis 549
Oesophagectomy 551
Chest injury 553
See also
% Thoracoscopic sympathectomy p. 607
% First rib resection p. 608
% Tracheoesophageal fistula p. 936
% Inhaled foreign body p. 947
% Chest injuries pp. 553–5
530
General principles
Successful thoracic anaesthesia requires the ability to control ventilation of
the patient’s two lungs independently, management of the shared lung and
airway and a clear understanding of planned surgery.
Long-term smoking, bronchial carcinoma, pleural effusion, cardiac dis-
ease, oesophageal obstruction and cachexia are all common and can signifi-
cantly reduce the cardiorespiratory physiological reserve.
General considerations
• Discuss planned procedure and potential problems with the surgeon.
• Smoking cessation, optimising respiratory function and cardiovascular
fitness in preparation for surgery reduce perioperative morbidity.
• Place patients on an ERAS pathway at time of referral (see % pp. 44).
• The lateral decubitus position, with the operating table ‘broken’ to
separate the ribs, is used for the majority of procedures.
• Increasingly, cases are done by video-assisted thoracoscopic surgery
(VATS).
• Postoperative mechanical ventilation stresses pulmonary suture lines
and increases air leaks and risk of chest infection; avoid, if possible.
• Minimise respiratory dysfunction by providing good analgesia and
physiotherapy. Patients go to HDU/specialist ward postoperatively.
• Postoperative O2 is routine to compensate for i V/Q mismatch.
Warmed humidified 40% O2 via a face mask is recommended after
pulmonary surgery.
General preoperative assessment considerations
• Pay attention to functional status and cardiorespiratory reserve.
• Patients with significant cardiac disease form a high-risk group.
• Discuss results of CXR and CT scans with the surgeon, focusing
on airway problems making DLT placement problematic, tumours
impinging on the chest wall and crossing fissures or vessels.
Preoperative assessment for lung resection
Risk assessment is based upon history, examination and assessment of func-
tional status, in combination with spirometry, tests of diffusion capacity (e.g.
DLCO) and calculation of Thoracoscore.
• The Thoracoscore gives an estimate of mortality risk based on a
number of variables (e.g. demographics, degree of dyspnoea and
comorbidities, performance status and type of surgery). It is especially
useful in the consent process. A multidisciplinary team approach is
essential and should involve the patient, anaesthetist, surgeon, clinical
nurse specialists, respiratory physician and radiologist.
• Patients may be classified as:1,2
• Clinically fit—good exercise tolerance, normal spirometry: accept for
surgery
• Major medical problems, minimal exercise capacity, grossly impaired
PFTs: consider alternative treatment
• Reduced exercise capacity (shortness of breath climbing two flights of
stairs) and abnormal spirometry, with or without moderate coexisting
disease: further assessment and careful evaluation of risks/benefits of
surgery.
General principles 531
• PFTs (see % p. 164) are often used to determine suitability for lung
resection surgery by estimating the postoperative lung function. Put
the results in the context of the patient’s general health and proposed
operation.
• Spirometry should be performed in addition to tests of diffusion
capacity (e.g. DLCO). Patients with diffuse alveolar lung disease can
have severely impaired gas transfer with relatively normal spirometry.
• Predicted postoperative (ppo) value of the PFT results is calculated by
the following formula: ppo = preoperative value × (19 –number of
segments resected)/19.
• If preoperative DLCO or ppoFEV1 is <40% predicted normal, the
patient should undergo CPET prior to surgery.
• CPET assesses VO2max which is used to inform the risk of
perioperative morbidity and mortality. Patients with a VO2max 10–
15mL/kg/min are higher risk and should have postoperative HDU
admission. VO2max <10mL/kg/min are very high risk and surgery
may not be appropriate—further discussion is needed with the
multidisciplinary team and with the patient.
• All patients undergoing pneumonectomy or bilobectomy should
have CPET, echocardiography and a postoperative HDU admission.
Ventilation scans may be used to assess for non-functional lung (e.g.
atelectasis beyond an obstructing tumour). All patients with an active
cardiac condition should undergo cardiology review.
Analgesia
• Chronic pain syndrome after thoracic surgery occurs in 25–60% of
patients and the risk is i by high-intensity postoperative pain, so optimal
analgesia is essential.
• Inadequate analgesia increases the neurohumoral stress response,
impairing mobilisation and respiration and increasing complications.
• Combining opioid-sparing agents such as paracetamol, NSAIDs,
clonidine, magnesium, ketamine, glucocorticoids and a regional block is
recommended.3
• Regional anaesthesia typically involves surgically performed internal
intercostal nerve blocks alongside a paravertebral catheter for both
open and video-assisted thoracotomy (equivalent analgesic efficacy to
epidurals, but associated with fewer adverse events and may be better
suited to patients taking anticoagulants or in renal failure).
• Continuous postoperative infusion of levobupivacaine 0.375% for 48–
72h at 0.1mL/kg/h via the paravertebral catheter is advised.
• Limiting the use of PCAs aids enhanced recovery and VATS procedures
are generally less painful.
• Thoracic epidural may be necessary for bilateral procedures (match the
level of block to that of the incision—usually T5/6 or T6/7).4
• Perineural catheters and regional analgesia into the serratus anterior or
erector spinae plane can be considered for single-port VATS and also
provide good analgesia for rib fractures (see % pp. 995–6).
532
(Contd.)
534
• Left-sided DLTs are easier to place and more commonly used. They
can be used for most cases, although for VATS major lung resections,
the opposite side tube to the side of surgery is preferred. This avoids
trauma from the end of the bronchial portion of the tube.
Placement of double-lumen endobronchial tube
• Assess the risks/benefits of using a DLT.6
• Check the DLT prior to use, including checking both cuffs and that all
connections fit together appropriately, including the Y-connector.7
• Most plastic DLTs are supplied with a malleable stylet which can be used
to adjust the curve of the tube to facilitate intubation.
• Commence intubation with the concavity of the endobronchial section
of the DLT facing anteriorly. Once the tip is past the glottis, withdraw
the stylet and rotate the tube 90–180° to bring the oropharyngeal curve
into the sagittal plane. Gently advance while bringing the DLT back into
a neutral position.
• Advance the tube to around 29cm, which is the average depth for
patients who are 170–180cm tall. There is a 1cm change in depth for
every 10cm variation in the patient’s height from this position.8
• Do not simply advance until resistance as this could result in trauma.
• At this stage, treat the DLT as an ordinary ETT. Inflate the tracheal cuff,
check for ETCO2 and confirm placement in both lungs.
• The diameter of a DLT makes intubation more difficult than with a
standard tube, even with a good view of the larynx. Despite a grade 1
view of the larynx, the DLT can end up in the oesophagus, so vigilance
should be maintained throughout.
• Bougies can be used, but check that they are compatible with a DLT.
Other useful equipment for a difficult DLT are a VL and an airway
exchange catheter (AEC).
Confirmation of double-lumen endobronchial tube position (left)
• Clamp the tracheal lumen on the Y-connector and open the port to
feel for a leak. Look at the movement of the chest and check if there is
appropriate unilateral expansion.
• Inflate the bronchial cuff until the leak disappears. Check with the DLT
manufacturer the maximum amount of air that can be placed into the
cuff. Continue to observe movement of the chest and that it is unilateral
and appropriate for the side that has been clamped.
• Another method to check that the DLT is in the correct position is to
auscultate over the side you wish to isolate. Listen while placing the
clamp on and inflating the bronchial cuff; if correct, the chest sounds
should disappear.
• Next, confirm it is possible to isolate and achieve OLV of the opposite
(operative) lung via the tracheal lumen by clamping the opposite side on
the Y-connector.
• ETTs often move when the patient is placed in the lateral position.
Recheck isolation and OLV once in position and before surgery.
Isolation of the lungs 537
Fibreoptic bronchoscope
• Ideally, the position of every DLT should be checked bronchoscopically.
At the very least, a suitable bronchoscope must be immediately
available to assess DLT placement if there are clinical problems with the
tube or with OLV.
• The position of a right-sided tube should always be checked with a
bronchoscope to ensure correct position of the Murphy’s eye.
• It may be necessary to use the bronchoscope to help intubate the
correct bronchus and then railroad the tube over the bronchoscope.
Several bronchoscopic studies have shown that up to 80% of DLTs are
malpositioned to some extent, even when clinical signs are satisfactory.
The upper surface of the bronchial cuff (blue) should lie just below the
carina when visualised via the tracheal lumen.
Bronchial blocker technique
• Bronchial blockers (Univent™ tube or Arndt endobronchial blocker)
are useful in patients who are difficult to intubate, have distorted
tracheobronchial anatomy/tracheostomy and occasions when
isolation of a lobar bronchus is required (localised bronchiectasis
or haemorrhage, lung abscess, bronchopleural fistula, previous lung
resection and poor tolerance of OLV).9
• A balloon-tipped catheter (‘blocker’) is manipulated through an SLT
into the appropriate main (or lobar) bronchus with the aid of a narrow
fibreoptic bronchoscope.
• Good lubrication of both the bronchoscope and blocker is essential.
• The position of the blocker should be rechecked after the patient has
been positioned for surgery. They move out of position easily.
• Placement is usually straightforward in the supine position but can be
awkward in the lateral position.
• The lung or lobe is isolated from ventilation by inflating the balloon
within the bronchus. The lung slowly collapses, as the trapped gas is
absorbed or escapes via the blocker’s narrow central lumen.
• Collapse can be accelerated by ventilating with 100% O2 for a few
minutes and then inflating the blocker at end-expiration when lung
volume is at its minimum.
• Reinflation of the collapsed lung requires deflation of the blocker and
consequent loss of isolation of the lungs. A DLT will maintain separation
of the airways to each lung until extubation.
• During pneumonectomy or sleeve resection (bronchial reanastomosis),
the blocker has to be withdrawn to allow surgical access to the
bronchus.
• There are two modern forms of bronchial blocker: Univent™ tube
(SLT with an internal channel containing an adjustable blocker bearing a
high-volume, low-pressure cuff ) and Arndt wire-guided endobronchial
blocker (Cook™). This is a stiff catheter with a cylindrical cuff and
an adjustable ‘wire’ loop at its tip to guide the blocker along the
fibreoptic bronchoscope into the required bronchus (special adapter
allowing deployment through a conventional single-lumen or cuffed
tracheostomy tube).
538
• Check the tube position with a fibreoptic scope and make sure that the
tube has not moved to obstruct the upper lobe.
• Suction out any secretions.
• Maintain perfusion with fluid and vasopressors.
• Apply PEEP to the ventilated lung, but be aware this can worsen the
shunt.
Actions: the non-ventilated lung
• Insufflate O2 via a suction catheter.
• Apply CPAP via a separate circuit to the non-ventilated lung.
• Requires discussion with surgeon as will make operative view more
difficult, which is particularly a problem during VATS.
• Clamp the PA, but this is only really an option near completion of a
pneumonectomy.
Returning to two-lung ventilation
• Gently suction the non-ventilated lung to clear any blood or pus—use
the long suction catheters supplied with the DLT.
• Close the sealing cap on the lumen to the non-ventilated lung and
remove the clamp on the Y-connector.
• Switch to manual ventilation and reinflate the collapsed lung under
direct vision. Long, sustained ventilation breaths are effective, and
inflation pressures of up to 30cmH2O are often required to fully re-
expand all areas of the lung.
• The surgeon will commonly observe for air leaks at this point and may
ask for a specific Paw to be generated.
• Return the patient to mechanical ventilation and, unless significant
volumes of the lung have been resected, return to the original two-lung
ventilator settings and FiO2.
• Adjust the RR to maintain normocapnia.
• Always be prepared to return to OLV immediately, should problems
occur, e.g. large air leak from the operated lung. It is prudent to keep
your fibreoptic scope nearby until you are completely satisfied with
the lungs.
• Many anaesthetists advocate deflating the bronchial cuff as soon as
possible to prevent bronchial wall necrosis.
540
Preoperative
• Check for airway obstruction: stridor, tracheal tumour on CT scan or
history of foreign body inhalation.
• Suitable as a day case procedure in appropriate patients.
• Warn about postoperative coughing, haemoptysis and sore throat.
• Combined with mediastinoscopy to assess suitability for resection.
• The airway will be unprotected, so patients at risk of regurgitation may
need premedication with omeprazole or ranitidine.
Perioperative
• Give full preoxygenation and check the jet ventilator is working before
anaesthetising the patient.
• It is safer to anaesthetise these patients in theatre with the surgical team
ready to go as soon as the patient is anaesthetised.
• Coordinate low-frequency jet ventilation with surgical activity—the
surgeons will say when not to ventilate.
• Dexamethasone can be given to reduce airway swelling.
Postoperative
• Sit fully upright as soon as awake.
• A blood clot can cause severe lower airway obstruction, requiring
immediate intubation, suction and repeat bronchoscopy.
Special considerations
• A stimulating procedure that can generate a marked hypertensive
response.
• Extreme CVS responses need to be obtunded, and profound relaxation
provided, but with prompt return of laryngeal reflexes and spontaneous
respiration.
• Rarely, a biopsy can precipitate a life-threatening airway bleed.
• Stent insertion can be technically difficult and may involve periodic loss
of airway control.
MEDIASTINOSCOPY AND ENDOBRONCHIAL ULTRASOUND 541
Preoperative
• Suitable as day case procedure in appropriate patients.
• Check for SVC obstruction and tracheal deviation or compression due
to large mediastinal masses.
• Sometimes preceded by rigid bronchoscopy (‘Bronch & Med’).
Perioperative
• Ensure the airway is secure as the head will be obscured by drapes.
• Give boluses of IV fentanyl during surgery.
• Insert a 16-gauge (G) cannula in a lower leg vein after induction (see %
Special considerations, p. 541).
• Beware surgical compression of the trachea (monitor VT and Paw).
Postoperative
• Paracetamol and NSAID. Usual day case precautions.
Special considerations
• There is the potential for massive haemorrhage from the great vessels.
The risk is i in patients with SVC obstruction (hence cannula in the leg).
May require immediate sternotomy.
• Mediastinotomy can cause a pneumothorax, recurrent laryngeal nerve
injury and VAE.
Endobronchial ultrasound
• An alternative method for mediastinal staging of lung cancer. Can be
done with LA ± sedation or GA (TIVA).
• Effectively, this is a flexible bronchoscopy through either a laryngeal
mask or a single-lumen ETT, so be prepared for problems with
ventilation and you may need to hand-ventilate on relatively high flows.
542
Preoperative
• Cancer is the commonest indication for lung resection; others include
benign tumours, bronchiectasis and TB.
• Patients require extensive preoperative assessment to assess
cardiovascular and functional fitness.
• Large majority of wedge resections and lobectomies now performed by
VATS. This can be done with multiple ports or a single port, depending
on the case and surgical preference.
• Assess the airway with respect to placement of the DLT.
• Ensure patient education, commence ERAS protocol and plan the
postoperative analgesia regime.
Perioperative
• Select the appropriate DLT and check lung isolation carefully after
intubation.
• The choice of side of tube to use will be dependent on the case and
surgical technique. For VATS for major lung resections, use opposite
side tube to side of operation to avoid any trauma to bronchus during
surgery.
• Place arterial line for most cases involving OLV.
• OLV facilitates surgery and prevents soiling of the dependent lung.
• Continuous display of the Paw/volume loop is a valuable adjunct to
monitoring and managing OLV.
• Surgical manipulation often causes cardiac and venous compression,
which reduces the CO/BP and may cause arrhythmias.
• Suction the airway to the collapsed lung prior to reinflation.
• The bronchial suture line is ‘leak-tested’ under 0.9% sodium chloride by
manual inflation to 20–30cmH2O.
• Use multimodal analgesia as described previously.
WEDGE RESECTION, LOBECTOMY AND PNEUMONECTOMY 543
Postoperative
• Aim to extubate the patient awake and sitting at the end of the
procedure.
• Prescribe continuous humidified supplementary O2.
• Ensure good analgesia is achieved. Many centres are now using
paravertebral analgesia, rather than epidurals, especially for VATS
cases. Intercostal blocks can also be placed under direct vision by the
surgeons.
• Good regional analgesia may avoid excessive amounts of opioids and
PCA may not be required.
• A CXR is usually required postoperatively.
Special considerations
• Occasionally, patients with bronchial carcinoma may have ‘non-
metastatic’ manifestations (Lambert-Eaton myasthenic syndrome or
ectopic hormone production) (see % p. 316; % p. 232; % pp. 235–7).
• Perioperative mortality from pneumonectomy is 5–13%. ALI occurs in
4% of resections and the mortality rate is 30–50%.13
• Additional risk factors include the inflammatory response to surgery,
chronic alcohol abuse, genetic predisposition, intraoperative plateau
pressures >15cmH2O and >4000mL of IV fluid in first 24h.
• Incidence may be reduced by the intraoperative use of lung-protective
strategies (as established in acute respiratory distress syndrome (ARDS)
management) and GDFT.
• Heparinisation may be required during sleeve lobectomy if vessel
resection is necessary.
54
Postoperative
• Aim to extubate at the end of the procedure. HDU or ICU care will be
required in most cases.
• Watch closely for air leaks and alert surgeons to any concerns.
• Requires excellent pain relief, skilled physiotherapy and a pulmonary
rehabilitation programme.
Special considerations
• Commonest complication is prolonged air leak: >7d in 50% of patients.
• Mortality from recent series is 5–10%.
• The National Emphysema Treatment Trial demonstrated that lung
volume reduction surgery benefits patients with predominantly upper
lobe disease and a low baseline exercise capacity.
• Patients with an isolated congenital bulla or ‘lung cyst’ require the same
careful intraoperative anaesthetic management but are usually much
fitter and do not normally require invasive cardiological assessment.
Endobronchial valves
• These are one-way valves that are placed into specific lung segment
to prevent air moving in during inspiration but allow air and mucus to
leave during expiration. The idea is that this will lead to atelectasis of
emphysematous areas of the lung.16
• This procedure is done bronchoscopically with either sedation or GA.
• There is much less morbidity associated with this technique, compared
to complete lung reduction surgery.
• Interlobar collateral ventilation which occurs in up to two-thirds of
patients with severe emphysema will prevent the use of endobronchial
valves. In this scenario, endobronchial coils may be considered.17
546
Special considerations
• Most fistulae are postoperative complications of pneumonectomy
or lobectomy, but some are 2° to pneumonia, lung abscesses and
empyema.
• Anaesthesia for repair of a bronchopleural fistula is challenging and not
recommended for an ‘occasional’ thoracic anaesthetist!
Pleurectomy/pleurodesis 549
Pleurectomy/pleurodesis
Procedure Stripping of parietal pleura from inside of chest wall
(pleurectomy). Production of adhesions between parietal
and visceral pleura either chemically (talc, tetracycline) or
by physical abrasion (pleurodesis)
Time Pleurectomy 1–2h; pleurodesis 20–40min
Pain +++/++++
Position Lateral decubitus for VATS or open thoracotomy
Blood loss Can bleed from the stripped pleura; G&S
Practical IPPV and OLV advised for open/VATS procedures
techniques
Preoperative
• Patients fall into two groups: the relatively young and fit with recurrent
pneumothoraces (check for asthma) and older patients compromised
by COPD or recurrent pleural effusions (check respiratory reserve).
• Check a recent CXR for pneumothorax and/or effusion.
• Ensure any infection is treated.
• A preoperative intercostal drain is advised if pneumothorax present.
• Check the planned surgical approach.
• Discuss postoperative analgesia and the regional technique.
Perioperative
• Keep Paw as low as possible in patients with a history of pneumothorax.
• Be alert for pneumothoraces, as they can tension rapidly on IPPV, even
with a drain in situ, and can be on the ‘healthy’ side.
• Avoid N2O.
• Aim for full expansion of the lung at the end of the procedure to
oppose the parietal and visceral pleurae.
Postoperative
• Extubate and sit the patient upright before transfer to the recovery
room.
• A CXR is needed to check full lung expansion. Pleural inflammation
usually causes severe pain, particularly when abrasion of the pleura is
performed.
• Multimodal analgesia is again imperative but tend to avoid NSAIDs
which may make pleurodesis less effective due to anti-inflammatory
effects.
• Paravertebral blocks are usually unsuitable due to damage to the pleura.
Intercostal blocks can be sited at the start of the procedure.
50
Special considerations
• Pleurectomy is usually performed for recurrent pneumothorax,
combined with stapling of the lung tissue responsible for recurrent air
leaks (usually apical ‘blebs’ or small bullae).
• Pleurodesis is often used to manage malignant pleural effusions
(mesothelioma, metastatic carcinoma)—there may be large volumes of
fluid causing significant respiratory compromise.
• Patients with massive pleural effusions (more than two-thirds of
the hemithorax on CXR or >2000mL) should have these ‘tapped’
and partially drained at least 12h before surgery, because rapid
intraoperative reinflation of the collapsed lung can precipitate unilateral
postoperative ‘re-expansion’ pulmonary oedema.
• Patients with extensive effusions are also at risk of circulatory collapse
when turned ‘effusion side up’ for surgery. The mechanism is probably
a combination of mediastinal shift and high intrathoracic pressure from
IPPV reducing the venous return and CO. If this occurs, return the
patient to the supine position and drain the effusion before proceeding.
Oesophagectomy 551
Oesophagectomy
Procedure Total or partial excision of oesophagus with mobilisation
of stomach (occasionally colon) into chest
Time 3–6h
Pain +++++
Position Supine with arms by sides and/or lateral decubitus for
thoracotomy
Blood loss 500–1500mL; X-match 2 units
Practical IPPV, OLV via DLT or bronchial blocker, arterial/CVP
techniques lines, urinary catheter, thoracic epidural or paravertebral
catheter for thoracoabdominal incision
Types of procedure
Minimally invasive
Thoracoscopic oesophageal mobilisation, laparoscopic gastric mobilisation
and cervical anastomosis.
Ivor–Lewis
Laparotomy and right thoracotomy, often laparoscopic-assisted.
Transhiatal
Laparotomy and cervical anastomosis.
Thoracoabdominal
Left thoracotomy crossing the costal margin and diaphragm.
McKeown 3-stage
Laparotomy, right thoracotomy and cervical anastomosis.
Preoperative
• Establish the indication for surgery—usually oesophageal cancer, but
occasionally for non-malignant disease (benign stricture, achalasia).
• Preoperative malnutrition or cachexia is common and associated with a
higher risk of postoperative morbidity and mortality.
• Preoperative adjuvant chemotherapy may leave residual
immunosuppression but can dramatically improve dysphagia.
• Some centres utilise enhanced recovery protocols.
• Will need HDU or ICU, depending on local protocols.
Perioperative
• Consider all patients with oesophageal disease to be at risk of
regurgitation; some patients may require a modified RSI.
• If thoracotomy is planned, use a DLT or bronchial blocker.
• Prepare for long surgery, sometimes involving repositioning.
• Multimodal analgesia is necessary, including regional block. NSAIDs
should be avoided, but give intraoperative paracetamol and magnesium.
Consider clonidine, and for shoulder tip pain, tramadol.
• Plan regional anaesthesia according to the surgical approach.
Paravertebral catheter infusion with morphine PCA for the
thoracoabdominal approach. For laparotomy/thoracotomy, a mid-
thoracic epidural is advised for intra-and postoperative use.
52
Chest injury
The emergency diagnosis and initial treatment of major thoracic trauma are
described on % pp. 995–8. This section deals with the anaesthetic manage-
ment of rib fractures and the definitive repair of ruptures of the diaphragm,
oesophagus and tracheobronchial tree.
Rib fractures
• These are common and associated with a high risk of respiratory
complications. Trauma injuries are increasingly being seen in those
aged >65y who have i comorbid burden and polypharmacy, including
anticoagulation.
• Prompt multimodal analgesia including paracetamol, NSAID where
appropriate, oral or PCA opioids and regional block are essential to
improve respiratory mechanics and reduce complications.
• Regional analgesia can be afforded by paravertebral catheter insertion
or fascial plane catheters. An increasing number of ultrasound-guided
erector spinae or serratus anterior plane blocks are being performed,
which are both relatively simple to do, reduce the risk of pneumothorax
and can be performed in coagulopathic patients.
• Plane block catheters can be bolused with 30–40mL of 0.25%
levobupivacaine and then run as 10mL/h of 0.125% levobupivacaine.
• Paravertebral catheter insertion is an alternative and provides a reliable
unilateral block with reduced hypotension, motor blockade and urinary
retention seen with thoracic epidurals, which are no longer considered
the gold standard in traumatic rib fractures.
• Operative fixation may be indicated, especially in those with flail
segments and uncontrollable pain.
• Humidified O2, nebulised 0.9% sodium chloride and respiratory
physiotherapy also help reduce respiratory complications. Non-
invasive ventilation or high-flow O2 reduce atelectasis and improve the
paradoxical movement of a flail segment. IPPV should be avoided, if
possible.
Repair of ruptured diaphragm
• Clinical features and diagnosis are described on % p. 998.
• May present as a chronic condition or as intestinal obstruction of a
herniated bowel, so check preoperative fluid and electrolyte status.
• The defect should be closed promptly, but rarely emergently.
• The surgical approach is via a standard lateral thoracotomy or a
thoracoabdominal incision. DLT facilitates surgical access.
• Management is as for a fundoplication (see % p. 534).
• Avoid N2O, as it distends the bowel and may make reduction of the
hernia more difficult.
• An NGT should be used to decompress the stomach.
Repair of ruptured oesophagus
• Clinical features and diagnosis are described on % p. 997. Surgical
emphysema and empyema are frequently present.
• Other causes of oesophageal rupture include excessive abdominal
straining and uncoordinated vomiting (Boerhaave’s syndrome).
54
Further reading
El-Boghdadly K, Wiles MD (2019). Regional anaesthesia for rib fractures: too many choices, too little
evidence. Anaesthesia, 74, 564–8.
Wilson WC, Benumof JL (2005). Anesthesia for thoracic surgery. In: Miller RD (ed). Miller’s
Anesthesia, 6th edn. Philadelphia, PA: Elsevier Churchill Livingstone; pp. 1847–930.
Ghosh S, Latimer RD (1999). Thoracic Anaesthesia Principles and Practice. London:
Butterworth-Heinemann.
References
1 Lim E, Baldwin D, Beckles M, et al.; British Thoracic Society, Society for Cardiothoracic Surgery
in Great Britain and Ireland (2010). Guidelines on the radical management of patients with lung
cancer. Thorax, 65 (Suppl 3), iii1–27.
2 Hackett S, Jones R, Kapila R (2019). Anaesthesia for pneumonectomy. BJA Educ, 19, 297–300.
3 Short HL, Kamalanathan K (2018). Has analgesia changed for lung resection surgery? Anaesthesia,
73, 444–9.
4 Slinger P, Campos JH (2020). Anaesthesia for thoracic surgery. In: Gropper M, Miller R, Cohen N
(eds). Miller’s Anesthesia, 9th edn. Philadelphia, PA: Elsevier; pp. 1648–716.
5 Batchelor TJP, Rasburn NJ, Abdelnour-Berchtold E, et al. (2019). Guidelines for enhanced re-
covery after lung surgery: recommendations of the Enhanced Recovery After Surgery (ERAS)
Society and the European Society of Thoracic Surgeons (ESTS). Depth of placement of left
double-lumen endobronchial tubes. Eur J Cardiothorac Surg, 55, 91–115.
6 Ashok V, Francis J (2018). A practical approach to one lung ventilation. BJA Educ, 18, 69–74.
7 Dr Gallagher’s Neighborhood. Lung isolation. M https://www.youtube.com/watch?v=9oV_
0AbTW6s
8 Brodsky JB, Benumof JL, Ehrenwerth J, Ozaki GT (1991). Depth of placement of left double-
lumen endobronchial tubes. Anesth Analg, 73, 570–2.
9 Campos JH (2003). Which device should be considered the best for lung isolation: double-lumen
endotracheal tube versus bronchial blockers. Curr Opin Anaesthesiol, 20, 27–31.
10 Wilson WC, Benumof JL (2005). Physiology of one lung ventilation. In: Miller RD (ed). Miller’s
Anesthesia, 6th edn. Philadelphia, PA: Elsevier Churchill Livingstone; pp. 1890–4.
11 Conacher I (1998). Dynamic hyperinflation—the anaesthetist applying a tourniquet to the right
heart. Br J Anaesth, 81, 116–17.
12 Karzai W, Schwarzkopf K (2009). Hypoxemia during one lung ventilation: prediction, prevention
and treatment. Anesthesiology, 110, 1402–11.
13 Slinger PD (2006). Postpneumonectomy pulmonary edema: good news, bad news. Anesthesiology,
105, 2–5.
14 Elayaperumal AK, Jackson RE (2018). Anaesthesia for lung volume reduction surgery and
endobronchial valves. BJA Educ, 18, 193–8.
15 National Institute for Health and Care Excellence (2017). Endobronchial valve insertion to reduce
lung volume in emphysema. Interventional procedures guidance [IPG600]. M https://www.nice.
org.uk/guidance/ipg600
16 Zoumot Z, Davey C, Jordan S, et al. (2017). Endobronchial valves for patients with heteroge-
neous emphysema and without interlobar collateral ventilation: open label treatment following
the BeLieVeR-HIFi study. Thorax, 72, 272–9.
17 Shen KR, Bribriesco A, Crabtree T, et al. (2017). The American Association for Thoracic Surgery
consensus guidelines for the management of empyema. J Thorac Cardiovasc Surg, 153, 129–46.
56
Chapter 21 557
557
Neurosurgery
Gemma Nickols and Amit Goswami
General principles 558
Craniotomy 561
Ventriculoperitoneal shunt 563
Evacuation of traumatic intracranial haematoma 564
Pituitary surgery 567
Posterior fossa surgery 569
Awake craniotomy 572
Intracranial aneurysms 575
Complications of aneurysmal subarachnoid haemorrhage 576
Intracranial aneurysm clipping 578
Endovascular treatment of intracranial aneurysms 580
Endovascular thrombectomy 582
Venous air embolism 584
Resuscitation in neurosurgery 586
See also
% Spinal surgery pp. 629–33
% Cervical spine fracture p. 1020
58
General principles
Intracranial pressure
Normal ICP is 5–15mmHg. Changes in ICP reflect changes in the volume
of intracranial contents held within the confines of the skull (brain sub-
stance 1200–1600mL, blood 100–150mL, CSF 100–150mL, ECF <75mL).
Compensatory mechanisms initially reduce the effect of an intracranial
space-occupying lesion on ICP by displacing the CSF into the spinal sub-
arachnoid space, increasing the absorption of CSF and reducing intracranial
blood volume. Eventually, these mechanisms are overwhelmed, and further
small increases in intracranial volume result in a steep rise in ICP (Fig. 21.1).
If a lesion develops slowly, it may reach a relatively large volume before
causing a significant rise in ICP. Conversely, a small lesion may have devel-
oped quickly, allowing little time for compensation.
80
ICP 60
(mmHg)
40
20
0
Intracranial volume
Craniotomy
Procedure Excision or debulking of tumour, brain
biopsy, drainage of cerebral abscess
Time 1–12h
Pain +/+++
Position Supine, head-up tilt or lateral decubitus
Blood loss 0–2000mL, G&S ± X-match
Practical techniques ETT, IPPV, arterial line
Preoperative
• Assess the patient’s current neurological state, including symptoms and
signs of raised ICP, documenting deficits. Assess the gag reflex.
• Intracranial tumours may be metastatic; 1° sites include lung, breast,
thyroid and bowel.
• Check CT/MRI scans: the duration and complexity of the procedure
are determined by the size, site and vascularity of lesions.
• Patients vomiting or receiving diuretics may have disordered
electrolytes. Patients receiving dexamethasone may be hyperglycaemic.
• Restrict IV fluids if cerebral oedema present. Avoid glucose-containing
solutions, which can cause hyperglycaemia, associated with a worse
outcome after brain injury. They also reduce osmolality, resulting in i
cerebral oedema.
• Mechanical methods of DVT prophylaxis should be utilised.
• Prophylactic or therapeutic anticonvulsants may be required.
Levetiracetam (loading dose 500–1000mg) is now much more
frequently used than phenytoin (loading dose 15mg/kg), with evidence
for better efficacy.
Perioperative
• Patients undergoing burr hole biopsy require standard monitoring.
Those scheduled for craniotomy also need an arterial line, and a urinary
catheter for long procedures and patients on diuretics. Neuromuscular
and core temperature monitoring are desirable. Depth of anaesthesia
monitoring should be considered, especially with TIVA.
• Induce with propofol bolus or TCI infusion (or thiopental 3–5mg/kg if
available), combined with remifentanil infusion or fentanyl. Give slowly
to avoid reducing BP and CPP. A non-depolarising relaxant is used to
facilitate intubation. Remifentanil usually attenuates the hypertensive
response to intubation. Additional agents such as lidocaine 1.5mg/kg or
a β-blocker (labetalol 5mg increments) can be used. Use an armoured
ETT to prevent kinking, and tape in place, as ties may cause venous
obstruction.
• Ensure adequate eye protection to avoid injury.
• Avoid N2O. Maintain anaesthesia using either a volatile agent
(sevoflurane/isoflurane <1 MAC) or TCI propofol. Remifentanil
infusion (micrograms/kg/min) or TCI (nanograms/mL) or intermittent
fentanyl boluses can be titrated to response. Top-up doses of muscle
relaxants are rarely required when remifentanil is used.
562
Ventriculoperitoneal shunt
Procedure CSF drainage for hydrocephalus
Time 45–120min
Pain ++
Position Supine, head-up tilt
Blood loss Minimal
Practical techniques ETT, IPPV
Shunts are inserted for hydrocephalus, with CSF diverted from the cerebral
ventricles to other body cavities, from where it is absorbed. Most com-
monly, a ventriculoperitoneal shunt is created, more rarely a ventriculoatrial
or ventriculopleural shunt. An occipital burr hole enables a tube to be
placed into the lateral ventricle. This is then tunnelled SC down the neck
and trunk, and inserted into the peritoneal cavity through an abdominal
incision. A flushing device can be placed in the burr hole to keep the system
clear, and a valve system is incorporated to prevent CSF draining too rapidly
with changes in posture.
Preoperative
• As for craniotomy (see % pp. 561–2). Assume i ICP in all patients.
• Patients requiring shunts are often children; therefore, usual paediatric
considerations apply.
• Emergency cases may have a full stomach, requiring RSI.
Perioperative
• Shunt procedures are shorter and simpler than craniotomies. Use
routine monitoring. Arterial lines are not usually required, unless
significant comorbidity.
• IV antibiotic treatment or prophylaxis is required and intrathecal
antibiotics are usually administered by the surgeon. Strict antisepsis
protocols are normally followed to reduce the incidence of infection.
• Advancing the trocar to allow tunnelling of the shunt is particularly
stimulating. Additional analgesia and/or muscle relaxation is often
required at this stage.
• Establish warming with forced air warming blanket or underbody heated
mat, as large area of patient often exposed.
Postoperative
• Any deterioration in conscious level is an indication for a CT scan to
exclude shunt malfunction or a subdural haematoma.
Special considerations
• Risk of intracranial haemorrhage if CSF drained too rapidly.
• Shunts often block or become infected, requiring revision.
• Watch for signs of a pneumothorax, as the trocar is placed SC.
564
566
Chapter 21
Neurosurgery
Fig. 21.2 Guidelines for managing adults with severe head injuries in the ICU.
Pituitary surgery 567
Pituitary surgery
Procedure Trans-sphenoidal hypophysectomy
Time 90–300min
Pain ++
Position Supine, head-up tilt
Blood loss Nil usually, but large if venous sinus disrupted, G&S
Practical ETT, IPPV, arterial line
techniques
Postoperative
• Diabetes insipidus may occur within 12–24h of surgery, in up to
50% of patients. It is managed initially with IV desmopressin (0.25–1
micrograms). Can be given PO subsequently if required.
• Cerebrospinal rhinorrhoea may occur. It is usually self-limiting, but
if persistent, intermittent CSF drainage via a lumbar drain may be
required. Occasionally, surgery to repair the CSF leak is required.
Special considerations
Patients with preoperative panhypopituitarism or who develop post-
operative endocrine disturbances should be referred to an endocrinologist
for advice on hormone replacement.
If a craniotomy is planned, rather than a trans-sphenoidal approach, refer
to % pp. 561–2.
Posterior fossa surgery 569
• The posterior fossa lies below the tentorium cerebelli and contains the
pons, medulla and cerebellum. Within the brainstem lie the main motor
and sensory pathways, the lower cranial nerve nuclei and the centres
that control respiration and CVS function.
• An increase in pressure in this area results in d consciousness,
hypertension, bradycardia, respiratory depression and loss of protective
airway reflexes.
• The exit pathways for CSF from the ventricular system are also located
here and obstruction results in hydrocephalus.
• Space-occupying lesions and surgical disturbance in this area can
therefore have a profound physiological impact.
• Common pathologies requiring surgery include tumours, vascular
malformations, cysts, cranial nerve lesions and craniocervical
abnormalities.1
Preoperative
• Patients with posterior fossa lesions may have a reduced level of
consciousness and impaired airway reflexes. Bulbar palsy may lead to
silent aspiration. Pulmonary function must be assessed.
• Patients with pre-existing impaired airway reflexes may require
postoperative ventilation or tracheostomy.
• Assess ICP: may be raised. If hydrocephalus is present, ventricular
drainage may be required before the definitive procedure.
• Assess the fluid status: may be dehydrated if vomiting. A reduced
intravascular volume will result in hypotension on induction or if placed
in the sitting position.
• Check electrolytes and glucose, particularly if taking diuretics or
steroids.
• Assess CVS function, particularly the presence of untreated
hypertension, postural hypotension and septal defects.
Perioperative
• As for craniotomy (see % pp. 561–2).
• Insert an NGT if risk of postoperative bulbar dysfunction.
• Further specialised monitoring is required for posterior fossa surgery,
including monitoring for VAE (see % pp. 584–5) and nerve tract
injury. The appropriate neurophysiological monitor used to detect
a nerve tract injury depends upon the neural pathway at risk during
the procedure. Spontaneous or evoked EMG activity, somatosensory
570
Postoperative
• Most patients can be safely extubated and managed on a neurosurgical
HDU postoperatively.
• Airway obstruction can occur after posterior fossa surgery due to
macroglossia, partial damage to the vagus nerve and excessive flexion of
the cervical spine.
• Surgery on the medulla or high cervical lesions carries a significant risk
of postoperative impairment of the respiratory drive.
• The patient should be admitted to ICU for ventilation if the
preoperative state was poor, the surgical resection was extensive, there
is significant cerebral oedema, there is evidence of an inadequate cough
or there are intraoperative complications.
Special considerations
• Acoustic neuroma: the facial nerve is particularly vulnerable and is
monitored using evoked EMG needles placed over the face. This allows
the surgeon to identify when the nerve is at risk. NMBA should be
used only at induction to allow intubation. Often the 8th nerve function
is also monitored to preserve any residual hearing. This requires a
constant level of anaesthesia, so that neurophysiological changes
can be attributed to surgery, rather than to variations in anaesthetic
depth. These requirements can be easily met using TIVA (propofol and
remifentanil).
• VAE (see % pp. 584–5).
• Postoperative analgesia is managed as for craniotomy.
572
Awake craniotomy
Procedure Excision of tumours in eloquent cortex, epilepsy surgery,
implantation of deep brain stimulator electrodes
Time >1.5h
Pain +/+++
Position See below
Blood loss 100–2000mL, G&S
Practical LMA, arterial line
techniques
Perioperative
The surgery can be simply divided into three phases:
1. From start of surgery to bone flap removal and dural opening
2. Resection of the lesion with functional testing
3. From completion of resection to closure.
• Aims of anaesthesia are to ensure adequate sedation, analgesia,
cardiorespiratory stability, avoidance of hypercapnia, nausea and
vomiting, as well as ensuring an awake and cooperative patient when
required for intraoperative testing.
• Routine monitoring as for craniotomy should be used, including urinary
catheterisation if the procedure is expected to be prolonged.
• The location of the lesion will determine patient position—commonly
the supine or lateral position is used. The patient will need to lie in this
position for a prolonged period of time. Positioning the patient awake,
if possible, can allow the most comfortable position to be achieved.2
• Effective LA is key to successful awake surgery. This can be achieved
through a scalp block or local infiltration by the surgeon.3
• There is no clear consensus as to the best anaesthetic technique.
This decision should be made on a case-by-case basis, dependent
upon patient and surgical factors.2,3 Two common techniques are
discussed below.
• Additional complications of awake surgery include seizures, failure to
complete intraoperative testing and unplanned conversion to GA.3
Asleep–Awake–Asleep
Using an Asleep– Awake– Asleep technique, the patient is given a GA
during the initial phase of the craniotomy. The patient is then woken for
intraoperative testing before being reanaesthetised for closure.
• Either TIVA or a volatile can be used. A commonly used recipe is TIVA
(propofol and remifentanil) using an SGA with IPPV.3
• Benefits include avoidance of complications of the sedation technique
(hypoxia, hypoventilation, airway obstruction) and the ability to
control CO2.2
Conscious sedation technique
Using a conscious sedation technique, the patient is sedated without airway
intervention during the initial phase and then woken up for testing. The pa-
tient can be resedated for closure.
• Commonly used drug infusions include propofol, remifentanil and
dexmedetomidine.3
• Benefits include improved compliance with testing, reduced opioid and
vasoactive requirements and reduced hospital length of stay.3
• Achieving the right balance of sedation can be difficult—too little
sedation can result in pain and discomfort, while too much can result
in hypoventilation ± airway obstruction. Hypercapnia can lead to a
raised ICP.3
574
Postoperative
• A long-acting opioid (morphine, oxycodone) should be administered at
the end of the procedure.
• Other aspects of postoperative care are as for craniotomy (see %
pp. 561–2).
Special considerations
• Discuss the plan for the management of seizures and emergency airway
management in the team brief.
• Ensure that a calm and quiet atmosphere is maintained in theatre.
The patient should be draped in a fashion that allows constant access
to the patient’s airway and minimises the feeling of claustrophobia.
Transparent drapes can be used to achieve this.
Acknowledgement
Text in ‘Awake craniotomy’ reproduced with permission of FinalPush ©
2020.
Intracranial aneurysms 575
Intracranial aneurysms
• Aneurysms occur at vessel junctions. Cerebral arteries have a weaker,
less elastic muscle layer than systemic vessels.
• The commonest sites are the junction between the anterior cerebral
artery and the anterior communicating artery (40%), the bifurcation of
the middle cerebral artery (34%) and the junction between the distal
internal carotid artery and the posterior communicating artery (20%).4
• They are more common in ♀ and 40–60y olds. In 20% of cases,
they are multiple. In the UK, the incidence is 6–12/100 000 per year.
Autopsy studies show unruptured aneurysms are present in 76% of the
population.4,5,6
• Risk factors include hypertension, smoking, positive family history,
polycystic kidney disease, cocaine use and connective tissue disorders
such as Ehlers–Danlos and Marfan syndromes.6
• Aneurysms do not usually rupture until they are >7mm in diameter.
They then present as a subarachnoid or an intracerebral haemorrhage.
• Classic symptoms include sudden onset of severe headache with loss
of consciousness, which may be transient in mild cases. Occasionally, a
patient presents with a focal neurological deficit due to the pressure of
an enlarging aneurysm on surrounding structures.
• The World Federation of Neurosurgeons (WFNS) grade of SAH is
related to morbidity and mortality (Table 21.1).
• Following aneurysm rupture, definitive management is either by
endovascular treatment or surgical clipping. Endovascular treatment,
most commonly coiling, is used for the majority of cases.4
• Current guidance recommends treatment should be performed to
secure the aneurysm within 48h of ictus for patients with WFNS grades
1–3. If presentation is delayed, treatment should occur within 48h of
diagnosis. The timing for treatment in poorer-grade patients is less
clear.5,7
Complications of aneurysmal
subarachnoid haemorrhage
Neurological complications
Rebleeding
• Rebleeding is an independent prognostic factor for poor outcome. The
risk of rebleeding is 5–10% within the first 72h, with the highest risk
period within the first 24h. The overall aim of management is to prevent
rebleeding by securing the aneurysm.5
Delayed cerebral ischaemia
• Vasospasm is defined as arterial narrowing, demonstrated radiologically,
with a corresponding clinical picture. It can be seen in up to 70% of
patients on angiography.4,9
• Delayed cerebral ischaemia is defined as neurological deterioration
caused by ischaemia lasting over an hour that is not attributable to
another cause. While delayed cerebral ischaemia can be caused by
vasospasm, it can also occur independently of vasospasm.4
• Despite treatment, delayed cerebral ischaemia can result in cerebral
infarction and death. It is seen in 722% of patients and is an independent
prognostic factor for poor outcome.5,8
• Peak incidence occurs at 4–10d after the initial bleed.4
Treatment
• Calcium channel blockers: nimodipine is a relatively selective calcium
channel antagonist with effective penetration of the blood–brain barrier.
It is started at the time of diagnosis and continued for 3w (60mg NG/
PO 4-hourly). Alternatively, it can be administered IV (0.5–1mg/
h, increasing to 2mg/h) centrally. Nimodipine may cause systemic
hypotension, which should be managed aggressively with fluids and, if
necessary, vasopressors.
• Classical treatment of delayed cerebral ischaemia involves ‘triple H
therapy’: Hypertension, Hypervolaemia and Haemodilution. Concerns
exist with elements of this treatment, including the risk of pulmonary
oedema as a result of hypervolaemia and reduced O2 carriage resulting
from haemodilution.
• Current recommendations from the American Heart Association/
American Stroke Association are for induced hypertension and
maintenance of euvolaemia in the treatment of delayed cerebral
ischaemia.9
• For severe cases, refractory to medical management, endovascular
therapy can be considered. Evidence exists for the use of both intra-
arterial vasodilators, such as nimodipine and verapamil, and transluminal
balloon angioplasty.7
Hydrocephalus
• Blood in the subarachnoid space may obstruct drainage of CSF and
result in hydrocephalus and raised ICP. About 30% of patients will
develop hydrocephalus requiring CSF diversion.5,8
• Hydrocephalus must be ruled out by a CT scan before attributing
neurological deterioration to delayed cerebral ischaemia.
ANEURYSMAL SUBARACHNOID HAEMORRHAGE 577
• Once the aneurysm has been successfully treated, the femoral sheath
is removed. An artificial collagen plug (e.g. AngioSeal™) can be used to
seal the hole in the artery. Alternatively, haemostasis can be achieved
by applying manual pressure for 15–20min. The patient should remain
anaesthetised until this is achieved.
• Aim for smooth emergence, avoiding coughing and an associated
rise in ICP. This is especially important if the aneurysm has not been
definitively secured.14
Postoperative
• Patients with a reduced postoperative GCS should have a CT scan to
exclude hydrocephalus or vascular complications.
• Analgesic requirements are minimal postoperatively.
Complications
• Peri-procedural aneurysm rupture, and the resultant intracranial
haemorrhage, can be life-threatening. Intracranial hypertension
can cause hypertension, with or without bradycardia. Contrast
extravasation may be seen by the radiologist on imaging.
• Aim to reverse the heparin and reduce MAP to the level before
the bleed.
• Institute treatment of raised ICP (see % pp. 559–60).
• If the extravasated blood load is significant, an EVD may be required,
if not already in place. Craniotomy, evacuation of intracranial
haematoma and aneurysm clipping may also be required.14
• Other complications include intraoperative vasospasm and vascular
occlusion due to arterial thromboemboli and misplaced coils.14
Special considerations
• Unfamiliar environment, remote site, radiation, radiology equipment,
contrast media, heparin, antiplatelet drugs and thrombolysis.
582
Endovascular thrombectomy
Procedure Interventional neuroradiological procedure where oc-
clusive thrombus is aspirated in acute CVE
Time 1–2h
Pain +
Position Supine
Blood loss Usually minimal
Practical LA, conscious sedation, GA (ETT, arterial line)
techniques
Introduction
• Acute ischaemic CVE accounts for 785% of all cases of CVE.15
• A proportion of patients with acute ischaemic CVE will be eligible for
endovascular thrombectomy. This is an interventional procedure where
the thrombus is aspirated, resulting in cerebral reperfusion.15
• The decision to proceed with endovascular thrombectomy is based
on the time since onset of symptoms, severity of CVE, location of the
thrombus within the cerebral circulation and pre-existing functional
status of the patient.15
Preoperative
• This is a true time-critical emergency—the greater the duration of
time before vessel recanalisation, the greater the degree of cerebral
infarction.
• Challenges can include:
• Acute effects such as dysphasia and hemiparesis
• Chronic comorbidities such as hypertension, AF, DM
• Fasting status
• Remote location of the interventional radiology suite.
• Options for anaesthesia include LA, with or without conscious sedation,
and GA.
• Three single-centre RCTs comparing GA with conscious sedation for
endovascular thrombectomy have produced equivocal results. Meta-
analyses of these trials suggest GA is associated with better functional
outcome.15,16,17
Perioperative
• For cases under GA:
• Intubation and ventilation allow airway protection and control
of CO2.
• Co-induction with opioids allows dose-sparing of propofol and
obtunds the pressor response to laryngoscopy.
• Invasive BP monitoring is recommended prior to induction. However,
this should not delay the start of the procedure.
• Either TIVA or a volatile can be used for maintenance.
Endovascular thrombectomy 583
Treatment
• Treatment is supportive.
• Inform the surgeon, who should flood the operative field with fluid. This
stops further entrainment of air and allows the identification of open
veins that can be cauterised or waxed if within bone.
• If possible, position the operative site below the level of the heart to
increase VP.
• Stop N2O immediately if used, and increase the FiO2 to 1.0.
• Consider increasing PEEP (not with patent foramen ovale).
• Support the BP with fluid and vasopressors.
• Attempt to aspirate air from the CVP line. The tip should be placed
close to the junction of the SVC and the right atrium, and ideally
confirmed radiologically prior to surgery.
• If a large volume of air has been entrained and surgical conditions
permit, turn the patient into the left lateral decubitus position to
attempt to keep the air in the right atrium. Or alternatively the
Trendelenburg position. There is little evidence for this.
• Commence CPR, if necessary. This may break down a larger air bubble.
Paradoxical air embolism
• Air emboli may enter the systemic circulation through the Thebesian
veins in the heart, the bronchial vessels or a patent foramen ovale. Such
defects may be small.
• Small volumes of air in the systemic circulation can have disastrous
consequences, resulting in temporary or permanent symptoms of CVE
or ischaemia of other organs.
• Intracardiac septal defects are an absolute contraindication to surgery
in the sitting position. This should be screened preoperatively in
high-risk cases.
586
Resuscitation in neurosurgery
• Cardiac arrest during anaesthesia for non-cardiac surgery occurs with
an incidence of 0.01–0.34%.
• Factors such as type of neurosurgical procedure and patient positioning
can have a significant effect on the occurrence of cardiac arrest.
• Appropriate management may need immediate attention to the
underlying cause.20
Specific factors influencing CPR
The surgical procedure
• Procedures on the anterior hypothalamus, brainstem, cerebello-pontine
angle, pituitary and trigeminal nerve can cause arrhythmias.
• Generally, severe bradycardia with hypotension and potentially asystole
can occur, caused by the trigeminocardiac reflex.
• Caused by surgical traction/instrumentation—temporarily ceasing this
often leads to resolution.
• If bradycardia persists, atropine (500–600 micrograms up to 3mg) can
be administered, or glycopyrronium bromide (200–400 micrograms).
Adrenaline may be required if no response, and CPR if asystole.
• VAE can lead to cardiovascular collapse and cardiac arrest (see %
pp. 584–5).
The position of the patient
• Neurosurgical positioning can present significant challenges during
cardiovascular resuscitation.
• Common positions include supine, lateral/park bench, prone and
occasionally sitting.
• The Mayfield 3-point head fixator is frequently used and the clamp
needs to be released before chest compressions commence, to avoid
damage to the cervical spine and skull (fixed head and mobile torso).
• Patient positioning will need to be adjusted to safely allow CPR and
defibrillation to occur.
• CPR can be commenced in the prone position initially. Adequacy can
be determined from ETCO2 and arterial line monitoring (often in situ).
Turning supine will take time and personnel.
• Defibrillation pad positions: standard pad position if patient supine/
sitting; anteroposterior position if lateral; and posterolateral or biaxillary
position if prone.
Wound management
• The open wound needs to be expediently managed by surgeon.
Special management considerations
• Diagnosis and management of cardiac arrest should be managed
as per advanced life support (ALS) and specific Cardiac Arrest in
Neurosurgery algorithm (Fig. 21.3).
• Variation from the ALS algorithm is an initial dose of adrenaline. Give
IV aliquots of 50–100 micrograms up to 1mg initially. This will prevent
rebound hypertension and potential haemorrhage if resuscitation is
successful. Further doses are given at 1mg.
Resuscitation in neurosurgery 587
Fig. 21.3 Cardiac Arrest in Neurosurgery algorithm. Reproduced with the kind
permission of Resuscitation Council UK
58
Further reading
Pasternak JJ, Lanier WL (2011). Neuroanesthesiology update 2010. J Neurosurg Anesthesiol, 23, 67–99.
[Postgraduate issue on clinical neurosciences] (2007). Br J Anaesth, 99, 1–138.
References
1 Jagannathan S, Krovvidi H (2014). Anaesthetic considerations for posterior fossa surgery. Contin
Educ Anaesth Crit Care Pain, 14, 202–6.
2 Burnand C, Sebastian J (2014). Anaesthesia for awake craniotomy. Contin Educ Anaesth Crit Care
Pain, 4, 6–11.
3 Sewell D, Smith M (2019). Awake craniotomy: anesthetic considerations based on outcome evi-
dence. Curr Opin Anesthesiol, 32, 546–52.
4 Luoma A, Reddy U (2013). Acute management of aneurysmal subarachnoid haemorrhage.
Contin Educ Anaesth Crit Care Pain, 13, 52–8.
5 Gough MJ, Goodwin APL, Shotton H, Butt A, Mason M (2013). Managing the flow? A review of the
care received by patients who were diagnosed with an aneurysmal subarachnoid haemorrhage. A report
by the National Confidential Enquiry into Patient Outcome and Death. M https://www.ncepod.org.
uk/2013report2/downloads/ManagingTheFlow_FullReport.pdf
6 Keyrouz S (2019). Subarachnoid haemorrhage. BMJ Best Practice. M https://bestpractice.bmj.
com/topics/en-gb/415
7 Intercollegiate Stroke Working Party (2016). National clinical guideline for stroke, 5th edn. M
https://www.strokeaudit.org/SupportFiles/Documents/Guidelines/2016-National-Clinical-
Guideline-for-Stroke-5t-(1).aspx
8 Galea JP, Dulhanty L, Patel HC (2017). Predictors of outcome in aneurysmal subarachnoid hem-
orrhage patients: observations from a multicenter data set. Stroke, 48, 2958–63.
9 Li K, Barras CD, Chandra RV, et al. (2019). A review of the management of cerebral vasospasm
after aneurysmal subarachnoid hemorrhage. World Neurosurg, 126, 513–27.
10 Nathanson MH, Moppett I, Wiles M (2011). Neuroanaesthesia. Oxford Specialist Handbooks in
Anaesthesia. Oxford: Oxford University Press.
11 Castioni CA, Amadori A, Bilotta F, et al. (2017). Minerva Anestesiologica, 83, 956–71.
12 Nathanson MH, Andrzejowski J, Dinsmore J, et al. (2020). Guidelines for safe transfer of the
brain-injured patient: trauma and stroke, 2019. Guidelines from the Association of Anaesthetists
and the Neuro Anaesthesia and Critical Care Society. Anaesthesia, 75, 234–46.
13 Moore LE, Teig MK, Tarnal V (2019). Anesthesia for intracranial neurovascular
procedures in adults. M https://www.uptodate.com/contents/
anesthesia-for-intracranial-neurovascular-procedures-in-adults
14 Patel S, Reddy U (2016). Interventional neuroradiology. BJA Educ, 16, 147–52.
15 Dinsmore J, Elwishi M, Kailainathan P (2018). Anaesthesia for endovascular thrombectomy. BJA
Educ, 18, 291–9.
16 Zhang Y, Jia L, Fang F, Ma L, Bowen C, Faramand A (2019). General anesthesia versus conscious
sedation for intracranial mechanical thrombectomy: a systematic review and meta-analysis of
randomized clinical trials. J Am Heart Assoc, 8, e011754.
17 Schönenberger S, Hendén PL, Simonsen CZ, et al. (2019). Association of general anesthesia vs
procedural sedation with functional outcome among patients with acute ischemic stroke under-
going thrombectomy: a systematic review and meta-analysis. JAMA, 322, 1283–93.
18 White PM, Bhalla A, Dinsmore J, et al. (2014). Standards for providing safe ischaemic stroke thromb-
ectomy services. M https://naccsgbi.org.uk/wp-content/uploads/2015/03/Standards_for_
providing_safe_acute_ischaemic_stroke_thrombectomy_services_Oct14-1.pdf
19 Rasmussen M, Schonenbergen S, Henden PL, et al. (2020). Blood pressure thresholds and neuro-
logic outcomes after endovascular therapy for acute ischemic stroke: an analysis of individual
patient data from 3 randomized clinical trials. JAMA Neurol, 77(5), 622–31.
20 Resuscitation Council UK (2014). Management of cardiac arrest during neurosurgery in adults. M
https://www.resus.org.uk/sites/default/files/2020-05/CPR_in_neurosurgical_patients.pdf
Chapter 22 589
Vascular surgery
Mark Stoneham
General principles 590
Abdominal aortic aneurysm repair 592
Emergency open repair of abdominal aortic aneurysm 595
Endovascular stenting of elective or emergency abdominal aortic
aneurysm 597
Thoracoabdominal aortic aneurysm repair 599
Carotid endarterectomy 601
Peripheral revascularisation 604
Axillobifemoral bypass 605
Amputations 606
Thoracoscopic sympathectomy 607
First rib resection 608
Arteriovenous fistula formation 609
Varicose vein surgery 610
See also
% Ascending aorta and aortic arch surgery pp. 521–2
590
General principles
Vascular surgery usually involves operating on arteries diseased by ath-
erosclerosis, causing poor peripheral blood flow (ischaemia) or emboli.
Mortality is high; elective abdominal aortic aneurysm (AAA) surgery has a
mortality of 2.4%,1 while that of ruptured AAA is 30–40%. Operations may
be long and involve blood transfusion, marked fluid shifts and significant im-
pairment of lung function. In the UK, all major vascular operations now take
place in designated ‘vascular centres’.
• Vascular patients are usually elderly arteriopaths with significant
associated disease. Hypertension (66%), IHD (angina, MI), heart failure,
DM and COPD (many are current or ex-smokers) are common.
Many patients are taking aspirin, β-blockers, diuretics, heart failure
medication, insulin and/or oral hypoglycaemics.
• Some patients are anticoagulated; others will receive anticoagulants
perioperatively—consider the pros and cons of regional techniques
carefully (see % p. 591). However, regional techniques can reduce
morbidity and mortality (see % p. 1109).
• Vascular patients tend to have serial operations, so there may be
several previous anaesthetic records to review. A significant minority
of vascular operations occur out of hours and these are often high-risk
procedures in high-risk patients.
• Measure NIBP in both arms as these may differ due to arteriopathy (use
the higher BP side clinically; put your arterial line in this side).
• All patients require prophylactic antibiotic cover.
• Develop a working relationship with your vascular surgeon; you will
have a better chance of being warned of untoward events (e.g. aortic
clamping/unclamping, sudden massive blood loss, etc.). Vascular
surgery is the only anaesthetic subspecialty where the presence of a
specialist consultant vascular anaesthetist has been shown to reduce
long-term mortality of major vascular surgery. The most likely cause for
this is better teamwork.2
Preoperative assessment
• Quantify the extent of any cardiorespiratory disease, both in terms of
the planned surgical procedure and the postoperative period. Carefully
consider (and document) if regional anaesthesia is appropriate.
• Include direct questions about exercise tolerance (walking distance on
the flat, ability to climb stairs) and the ability to lie supine. Look for signs
of cardiac failure.
• Investigations: FBC, U&E, coagulation, LFTs, ECG and CXR.
Premedication
Continue β-blockers and statins perioperatively. Anxiolytic premedication
may be useful for major surgery.
General principles 591
Preoperative
• The elderly often have multiple coexisting diseases.
• The 30d mortality for elective open surgery is 2.4% (predominantly MI
and multiorgan failure).
• A dynamic assessment of the cardiac function is required for all elective
aortic surgery and for any patients with symptomatic/new cardiac
disease. CPET is the ‘gold standard’ for all patients undergoing AAA
repair (see % pp. 33–5). Refer patients with critical IHD to cardiology
for angiography and possible coronary revascularisation before aortic
surgery. Emergent vascular patients may have to undergo surgery
before such dynamic investigations.
• PFTs (including ABG analysis while breathing air) should be performed
in patients with significant respiratory disease.
• Careful preoperative assessment is essential. Scrutinise the ECG for
signs of ischaemia, and check for any renal impairment. Check access
sites for CVC and arterial line.
• HDU/ICU for postoperative care. Alert the patient to this plan,
especially if a period of postoperative IPPV is planned. Preoptimisation
is performed in a few units but is not widespread—patients are
admitted to the HDU/ICU preoperatively to have lines, etc. inserted
and to have the haemodynamic status ‘optimised’.
• Continue the usual cardiac medications perioperatively.
Perioperative
• Have available vasoconstrictors (ephedrine and metaraminol),
vasodilators (GTN) and β-blockers (labetalol).
• Two 14G or greater IV access.
• Monitor intraoperative temperature and be obsessive about
temperature control from the start. Avoid heat loss, as it is easier to
keep a patient’s temperature constant than to try to increase it. Use a
fluid warmer (ideally fast-flow) and a forced air warmer (avoiding the
lower limbs while the aortic cross-clamp is in place, as this may worsen
limb ischaemia).
• There is no good evidence supporting the use of isovolaemic
haemodilution. Cell salvage should be mandatory—there is good
evidence that it reduces usage of allogeneic blood in aortic surgery.
Abdominal aortic aneurysm repair 593
Postoperative
• ICU/HDU is essential postoperatively. HDU may be appropriate for
otherwise fit patients who are warm and haemodynamically stable, and
with a working epidural. Otherwise transfer to ICU intubated.
• Opioid infusion and/or PCA if no epidural. Routine observations of
arterial and CVP monitoring, distal pulses and urine output should be
continued postoperatively to assess haemodynamic stability. There is
potential for large fluid shifts which need replacement.
Special considerations
• Management of epidural: a bolus of epidural diamorphine 2–3mg at
induction will last for 12–24h. Use epidural LA sparingly until the aorta
is closed. It is easier to treat the hypotension of aortic unclamping with
a functioning sympathetic nervous system.
• Renal failure occurs in 1–2% of cases, is multifactorial in origin and is
associated with a mortality of 50% following AAA repair. It is more
likely if the cross-clamp is suprarenal. There is no evidence that
dopamine prevents renal failure, merely acting as an inotrope. Mannitol
is used routinely by some (0.5g/kg during cross-clamp) as a free radical
scavenger and an osmotic diuretic. Avoid hypovolaemia, and monitor
the urine output hourly.
References
3 Lindholm EE, Aune E, Norén CB, et al. (2013). The anesthesia in abdominal aortic surgery
(ABSENT) study: a prospective, randomized, controlled trial comparing troponin T release
with fentanyl- sevoflurane and propofol- remifentanil anesthesia in major vascular surgery.
Anesthesiology, 119, 802–12.
4 Matyal R, Hess PE, Asopa A, Zhao X, Panzica PJ, Mahmood F (2012). Monitoring the variation in
myocardial function with the Doppler-derived myocardial performance index during aortic cross-
clamping. J Cardiothorac Vasc Anesth, 26, 204–8.
Emergency open repair of abdominal aortic aneurysm 595
This technique has become widely adopted in the last 15y. It is certainly
associated with lower operative morbidity and mortality than standard
open AAA repair,6 but it is still unproven whether it lowers the risk of an-
eurysm rupture; thus, postoperatively, patients must be kept under CT
surveillance for the rest of their lives. Significant complications, such as mi-
gration of the stent and endoleak, can develop, as well as rupture of the
original aneurysm sac.
• The procedure is performed in the angiography suite with the
interventional radiologists. In many hospitals, vascular surgeons gain
access to the aorta via the femoral arteries, and the stent is inserted by
an interventional radiologist, although all the procedure may be done
by one or the other. Most straightforward EVAR procedures are done
percutaneously; thus, LA may be suitable.
• During elective EVAR, if the aneurysm ruptures (incidence is around
2%), mortality rises to >50%.
• Preassessment, monitoring and X-matching are all exactly as for an
open repair. However, since the patient will not undergo aortic cross-
clamping, patients who have been refused open surgery because of
significant LV impairment may tolerate EVAR. ICU is usually not needed
postoperatively. Guidelines for who should be offered EVAR or open
repair are still under development.
• GA, regional anaesthesia or LA is appropriate, depending on
preference, although regional anaesthesia/LA may shorten the
procedure and hospital stay.7,8
• Postoperatively, the patient may go to the HDU or the vascular ward
for overnight monitoring. Hospital stay is usually only 24–48h.
• Complex EVAR procedures in which custom-made, fenestrated grafts
allow reconnection of visceral aortic branches may take longer than
standard EVAR and are usually therefore best performed under GA.
• EVAR is also now an increasingly popular technique for patients
presenting with ruptured AAA. A balloon is inserted into the femoral
artery percutaneously and inflated above the rupture which confers
some haemodynamic stability. The IMPROVE Trial showed similar 30d
mortality between open (37.4%) and endovascular (35.4%) techniques,
but with women faring better than men with the EVAR technique.
Hospital costs were marginally lower for the EVAR group.5
598
Thoracoabdominal aortic
aneurysm repair
Procedure Excision of aortic aneurysmal sac extending above the
origin of the renal arteries and replacement with a syn-
thetic graft. May involve thoracotomy and the need for
OLV
Time 3–6h
Pain ++++
Position Supine, arms out (crucifix), may be right lateral if
thoracotomy
Blood loss 1000mL –+++, X-match 8 units, plus platelets and FFP
Practical DLT + IPPV, arterial + CVP lines. Thoracic epidural
techniques
Carotid endarterectomy
Procedure Removal of atheromatous plaque from the internal ca-
rotid artery. The internal carotid artery is clamped and
opened, the plaque removed and the artery closed dir-
ectly or with a patch
Time 1–3h
Pain ++
Position Supine, head-up. Contralateral arm board
Blood loss Minimal, G&S
Practical Cervical plexus block + sedation, or
techniques ETT + IPPV, arterial line
• For patients who do not tolerate being awake, GA is the best option,
although techniques have been described in which the patient is ‘woken
up’ intraoperatively to check neurological function.
Postoperative
• Careful observation in a recovery room for 2–4h is mandatory. HDU is
preferable for patients who develop a neurological deficit.
• Airway oedema is common in both GA and regional cases, due to
dissection around the airway. Cervical haematoma occurs in 5–10% of
cases—remove skin sutures in recovery to allow drainage. Immediate
re-exploration is required for developing airway obstruction. Although
the block may still be working, plan for emergent control of the airway.
• Haemodynamic instability is common postoperatively. Hyperperfusion
syndrome, typically presenting as headaches which may lead ultimately
to haemorrhagic CVE, is caused by areas of the brain previously
‘protected’ by a tight carotid stenosis being suddenly exposed to
hypertensive BP. Thus, BP must be tightly controlled. Careful written
instructions should be given to staff about haemodynamic management.
An example is:
• If systolic BP >160mmHg, give labetalol 5–10mg boluses IV or a
hydralazine infusion
• If systolic BP <100mmHg, give colloid 250mL stat.
• New neurological symptoms and signs require immediate surgical
consultation and investigation.
• Carotid stenting is a developing procedure for symptomatic carotid
patients performed in the radiology suite, in which a stent is placed
under LA into the stenotic carotid artery. Anaesthetic supervision may
be required because of the complications, which include perioperative
CVE and haemodynamic disturbances. CVE rates of carotid stenting
remain higher than of operative intervention.
References
9 GALA Trial Collaborators Group (2008). General anaesthesia versus local anaesthesia for ca-
rotid surgery: a randomized, controlled trial. Lancet, 372, 2132–42.
10 Stoneham MD, Thompson JP (2009). Arterial pressure management and carotid endarterec-
tomy. Br J Anaesth, 102, 442–52.
11 Stoneham MD, Stamou D, Mason J (2015). Regional anaesthesia for carotid surgery. Br J Anaesth,
114, 372–83.
604
Peripheral revascularisation
Procedure Bypass operations for occlusive arterial disease. A vein or
a synthetic graft is used to bypass occluded arteries
Time 1–6h
Pain +++
Position Supine
Blood loss Usually 500–1000mL, X-match 2 units
Practical Combined spinal/epidural with sedation, arterial line.
techniques ETT/IPPV, consider LMA
Axillobifemoral bypass
Procedure Extraperitoneal bypass (trouser graft) from axillary artery
to femoral arteries
Time 2–4h
Pain ++++
Position Supine
Blood loss <1000mL, X-match 2 units
Practical GA—ETT, IPPV, arterial line, consider CVC
techniques
Amputations
(Below/through/above knee, Syme’s, digits, etc.)
Procedure Removal of necrotic or infected tissue due to vascular
ischaemia
Time 30–120min
Pain ++++
Position Supine
Blood loss Usually 200–500mL, G&S
Practical Spinal or epidural with sedation. Sciatic/femoral blocks
techniques ± GA
Preoperative
• Commonly sick, bed-bound diabetic patients with significant CVS
disease who have had repeated revascularisation attempts previously.
• Many will be in considerable discomfort preoperatively (less so the
diabetics) and may be on large doses of enteral or parenteral opioids.
Regional analgesia may give more predictable postoperative relief.
Perioperative
• Spinal anaesthesia ± sedation offers excellent anaesthesia which can
be directed unilaterally. The duration of block (and postoperative
pain relief ) can be extended with intrathecal diamorphine (250–500
micrograms) or intrathecal clonidine (15–30 micrograms).12
• Diabetic patients presenting for amputations commonly have peripheral
neuropathy. As a result, ankle blocks are very successful for minor
amputations of the foot.
• Epidural analgesia offers better postoperative analgesia and can be sited
preoperatively, if required (pre-emptive analgesia).
• GA is an option, but additional regional blockade is advisable (combined
sciatic/femoral blocks will ensure analgesia for up to 24h). A wound
catheter may be placed next to the sciatic nerve by the surgeon for
postoperative infusion of LA (e.g. bupivacaine 0.25% at 10mL/h).
• Occasionally, these patients are septic due to the necrotic tissue. The
only way they will improve is to have the affected part amputated, so
cancellation may not be an option.
Postoperative
• Regional analgesia is the best option; otherwise PCA.
• Phantom limb pain is a problem for 60–70% of amputees at some time. It
must be distinguished from surgical pain. If possible, get pain team input.
• Pre-emptive analgesia (preoperative siting of epidural) is believed by
some to reduce the incidence and severity of chronic pain.
• Combined sciatic/femoral nerve blocks are an alternative to an
epidural, particularly when the patient is receiving anticoagulation.
• Even with perfect regional analgesia, you may need to continue enteral
opioids postoperatively.
References
12 Ypsilantis E, Tang TY (2010). Pre-emptive analgesia for chronic limb pain after amputation for
peripheral vascular disease: a systematic review. Ann Vasc Surg, 24, 1139–46.
Thoracoscopic sympathectomy 607
Thoracoscopic sympathectomy
Procedure For patients with sweaty palms/axillae. The sympathetic
trunk is divided via a thoracoscope inserted through a small
axillary incision
Time 30–60min
Pain ++
Position Supine, affected arm on arm board
Blood loss Minimal
Practical IPPV via DLT, SV via LMA
techniques
• Patients are usually young and fit with hyperhidrosis (sweaty palms and
axillae).
• Surgical technique involves cutting the thoracic sympathetic trunk at T2
or T3 thoracoscopically.
• Traditionally, this is done using one-lung anaesthesia (DLT), with the
patient in the reverse Trendelenburg position.
• A simpler technique involves the patient breathing spontaneously
through an LMA. When the surgeon insufflates CO2 into the pleural
cavity, the lung is pushed away passively, allowing surgery to take place.
The degree of shunt produced is less dramatic than with OLV. Assisted
ventilation must be avoided, except to reinflate the lung manually at the
end. The CO2 insufflator machine regulates intrapleural pressures.
• With either technique, at the conclusion of the procedure, the lung
must be re-expanded (under the surgeon’s direct vision) to prevent a
pneumothorax.
• LA can be deposited by the surgeon directly onto the sympathetic trunk
and into the pleural cavity.
• A postoperative chest radiograph is required to confirm lung reinflation.
• Synchronous bilateral sympathectomy is a much more challenging
operation. This can lead to profound hypoxia when the 2nd lung is
collapsed, due to persistent atelectasis in the 1st lung. It is certainly
inappropriate for all but the very fittest patients.
608
Orthopaedic surgery
Richard Griffiths and David Brooks
General principles 612
Fat embolism syndrome 614
Bone cement implantation syndrome 615
Tourniquets 616
Total hip replacement 618
Revision of total hip replacement 620
Total knee replacement 621
Arthroscopic lower limb procedures 623
Cruciate ligament repair 624
Ankle surgery 625
Foot surgery 627
Spinal surgery 629
Shoulder surgery 634
Total shoulder replacement 637
Elbow replacement surgery 638
Anaesthesia for hand surgery 639
Anaesthesia for femoral neck fracture 642
See also
% Regional anaesthesia pp. 1099–1146
% The major trauma patient pp. 967–1032
% Pelvic injuries p. 1001
% Spinal trauma pp. 1002–3
% Anaesthesia in spinal cord lesions pp. 303–8
% Amputations p. 606
% Congenital talipes equinovarus p. 945
% Femoral osteotomy p. 946
261
General principles
• About 220 000 major joint replacements are performed annually in
England and Wales.1
• The population is ageing and these patients are now likely to be obese
with multiple comorbidities.
• Many operations are amenable to regional anaesthesia and ultrasound-
guided LA blocks (see % p. 613).
• Patient education before surgery, using joint schools, has promoted
patient choice and highlighted areas, such as the anaesthetic technique,
well before the day of surgery.
Preoperative
• Liaison with the surgeon is essential, particularly if undertaking regional
techniques.
• Arthritis often makes assessment of cardiorespiratory fitness difficult.
• If planning a regional technique (particularly CNB), it is important
to consider factors affecting clotting (timing of the last dose of
anticoagulant) and discuss specific risks and benefits with the patient2,3
(see % pp. 1100–1101).
• A high risk of VTE occurs with certain operations requiring
antithromboembolic measures, e.g. LMWH, stockings, foot pumps (see
% pp. 59–61).
Perioperative
• Give IV antibiotic prophylaxis as per local protocols, but be aware of
the potential for anaphylaxis4 (see % pp. 62–3).
• Utmost care with positioning is essential to avoid soft tissue or nerve
injuries. This is a shared responsibility between the anaesthetist and the
surgeon.
• Maintenance of normothermia with blood warmers and forced air
warming blankets can reduce both morbidity and mortality.
• Hypotension should be avoided.5
• Consider invasive monitoring for those patients with CVS disease
and those having revision lower limb surgery, especially if from a
periprosthetic fracture.
• Blood loss may be significant.
• Monitor blood loss accurately. Consider cell salvage, including drain
salvage.
• A urinary catheter should be inserted for long procedures or when
epidurals/spinal opioids are used.
• Local infiltration analgesia (LIA), using low-dose, high-volume LA,
is an effective technique for pain reduction in elective hip and knee
arthroplasty surgery.6
Postoperative
• Good analgesia will have a positive effect on recovery, mobility and
discharge.
• Liaise with the surgeon if prescribing NSAIDs, but use with care in
those over 75 (see % p. 91; % pp. 1155–6).
General principles 613
Regional anaesthesia
• Regional anaesthesia may be used for most joint replacements (alone
or with carefully administered sedation). Benzodiazepines should be
avoided in elderly patients. CNB and major nerve blocks are commonly
performed (see % pp. 1099–146).
• In major orthopaedic surgery, blocks may provide postoperative pain
relief and may reduce PONV.
• There is some evidence that regional anaesthesia, either alone or
in combination with GA, may improve outcome in hip and knee
arthroplasty, although these data are based on large observational
studies.6,7,8
• Good fixation of cement and joint prosthesis requires a dry, bloodless
surgical field. Regional anaesthesia (particularly spinal/epidural) reduces
bleeding at the surgical site, without the need for other pharmacological
hypotensive anaesthetic techniques.
• Surgeons often prefer the operating conditions produced by regional
techniques.8
461
Tourniquets
Tourniquets are commonly used to produce a bloodless field.14
• Only pneumatic tourniquets should be used. Mechanical tourniquets
can cause areas of unpredictably i pressure in underlying tissues.
• Small tourniquets on fingers and toes are dangerous, because they are
easily forgotten. Use a rubber strip with artery forceps.
• Expressive exsanguination using an Esmarch bandage is contraindicated
in cases of tumour or severe infection because of the risks of
dissemination. It is also contraindicated if DVT is suspected; fatal PE has
been reported.15 It also represents a potential risk of LV failure from
fluid overload if compression of both legs is carried out simultaneously
(adds 15% to the circulating volume); therefore, limit to one leg only in
patients at risk. Effective exsanguination can be achieved by arm or leg
elevation for 5min at 90°, without mechanical compression.
• Peripheral arterial disease is a relative contraindication to use.
• Avoid in severe crush injuries.
• Sickle-cell disease: use of tourniquets is controversial. Sickling of RBCs
under anoxic conditions causes thrombosis, but some surgeons use limb
tourniquets after full exsanguination. If employed, use for as short a
time as possible (see also % pp. 257–9).
Site of application
• The upper arm and thigh have sufficient muscle bulk to distribute the
cuff pressure evenly and are the recommended sites.
• For short operations (<1h) in fit patients, a calf tourniquet is preferred
by some surgeons.
Cuff width
• The American Heart Association concluded that if a
sphygmomanometer cuff has a width of 20% greater than the diameter
of the upper arm or 40% of the circumference of the thigh (to a
maximum of 20cm), then the pressure in the underlying central artery
will be equal to that in the cuff. This avoids the need for excessively high
cuff pressures.
• Modern silicone cuffs tend to be smaller than this, measuring 90mm in
width (bladder 70mm) for the arm and 105mm (bladder 75mm) for the leg.
• Cuff length should exceed the circumference of the extremity by
7–15cm. The cuff should be positioned at the point of maximum
circumference of the limb.
• The tissues immediately underlying the cuff should be protected with
cotton wool. This is not necessary with a correctly applied modern
silicone cuff.
Pressure
• Base on patient’s BP measured on the ward preoperatively.
• Upper limb: systolic BP + 50mmHg. Lower limb: twice systolic BP. This
higher pressure is needed because there is often not enough room
above the operating site for a full-sized cuff.
• The use of lower inflation pressures may minimise complications
following the use of tourniquets and speed up postoperative recovery.
In a normotensive patient, a pressure of 200mmHg should be ideal for
the upper limb and 250mmHg for the lower limb.
Tourniquets 617
Tourniquet time
• The minimum time possible should be the aim.
• Notify the surgeon at 1h, and remove as soon as possible after that.
• If the operation is difficult, the time can be extended to 1.5h. Two
hours should be regarded as a maximum, but this will not be safe for all
patients.
• PEs can occur following tourniquet release. When monitored using
TOE, the rate was higher with i tourniquet time.16
Tourniquet pain
• After 30–60min of cuff inflation, a patient may develop an increase
in HR and diastolic BP. This response results from ‘tourniquet pain’.
This also occurs under anaesthesia, although the response is usually
abolished by spinal or epidural techniques.
• In volunteers, when a tourniquet is inflated, a dull pain, associated with
an increase in BP, occurs after 30min.
• Often the physiological changes are resistant to analgesic drugs and i
depth of anaesthesia. β-blockers, in particular labetalol, may be useful.
• Small doses of ketamine given IV (0.25mg/kg) before tourniquet
inflation has been reported to attenuate these BP rises.17,18
861
Aseptic loosening was the commonest indication in 2019 NJR data, and
over 16% of the procedures were for periprosthetic fractures.1
Preoperative
General principles as for total hip replacement, except:
• The operation may take longer, but timings are variable. Discuss with
your surgeon beforehand.
• Blood loss can be significant, with 1L or more commonly lost
perioperatively.
• Postoperative pain can be a significant problem.
Perioperative
• As for 1° hip replacement, including a urinary catheter.
• If significant blood loss is anticipated or the patient’s CVS status
indicates it, insert an arterial line and make use of near-patient
monitoring to assess fluid status and Hb concentration.
• Technique should be planned, according to the length of surgery, the
operative position and patient factors.
• If CNB is contraindicated, consider supplementing GA with nerve
blocks (femoral, 3-in-1 or psoas compartment lumbar plexus).
• Use blood recovery and autologous transfusion wherever possible.
• Perioperative blood transfusion is frequently required, and blood loss
may be substantial. Two units of X-matched blood should be available
in theatre, with the ability to obtain more within 30min.
• Consider IV tranexamic acid.6
Postoperative
• Mobilisation varies with the complexity of the revision and the strength
of reconstruction.
• PCA is a suitable alternative.
• Supplemental O2 is required for 24h or longer, particularly if significant
blood loss or an underlying cardiorespiratory disease.
• Remember thromboembolic prophylaxis (see % pp. 59–61).
Total knee replacement 621
Postoperative
• Postoperative pain is usually the most significant problem, and this is the
main determinant of the anaesthetic technique. Many patients are now
already on opioids, and this makes the management of postoperative
pain more difficult.
• When blood loss into the drains continues to be brisk after the first
500mL, the surgeon will often clamp the drains for a period of time.
• Ideally, rehabilitation should be offered on the day of surgery if
possible.6
Bilateral total knee replacement
• Bilateral knee replacements should only be considered in young, fit,
motivated patients. Elderly patients and those with significant CVS
disease are high risk.
• The advantage is that two admissions/operations are avoided.
• The disadvantage is that bilateral total knee replacement is a major
CVS stress and is associated with unpredictable blood loss and fluid
requirements.
• This can be achieved under regional anaesthesia and bilateral adductor
canal blocks, but frequently GA may be required for over 2h of surgery.
Revision of total knee replacement
• Same as 1° knee replacement, except it takes longer (≥2h).
• The technique is as for 1° knee replacement.
• If done without a tourniquet, then 2 units of blood should be
X-matched.
Arthroscopic lower limb procedures 623
General principles
• The patient population is generally younger than those having joint
replacements.
• Smaller procedures are done as day cases and therefore require a
technique that allows early ambulation and discharge home.
• Virtually all are done on the knee, though arthroscopy is also performed
on the ankle.
• Arthroscopy for knees with osteoarthritis is not supported by evidence
of effectiveness.23
Technique
• Premedication with paracetamol and NSAID.
• GA/LMA is a ‘standard’ day case anaesthetic with IV opioids such as
fentanyl 1 microgram/kg.
• Ambulatory spinal anaesthesia can be achieved with prilocaine due to its
rapid onset, predictable regression and low incidence of adverse effects
(see % p. 490).24
• A tourniquet is often used.
• Prescribe NSAIDs and strong oral analgesics to take home.
• Many surgeons instil 10–20mL of 0.5% bupivacaine ± morphine (10mg)
into the joint cavity for postoperative pain relief.
• Ketamine in low dosage (IV) has been suggested to enhance analgesia
(0.15mg/kg).25
• Ideally, IV morphine should be avoided in day case arthroscopic
procedures due to the high incidence of PONV.
• EUA ± washout can be performed under intra-articular and infiltration
LA alone. Nerve blocks have been used but are limited by the long
duration of action of anaesthesia and the failure to block the site of the
arterial tourniquet.
624
Technique
• These operations are of two main types: using the patellar tendon
only for the repair, and using both the patellar tendon and hamstring
ligaments.
• Usually 12h of analgesia are required prior to mobilisation.
• Nerve blocks have been used but hinder postoperative mobilisation.
• Oral opioids, combined with paracetamol and NSAIDs, are the
mainstay of analgesia.
• If the hamstrings are used, the operation takes longer and there is more
postoperative pain.
Ankle surgery 625
Ankle surgery
General principles
• Four main types of procedure: tendon transfers, open reduction and
internal fixation (ORIF) of fractures, joint arthrodesis and prosthetic
joint replacement (Table 23.2).
• Ankle arthrodesis takes 1–2h. Tendon transfer is generally quicker than
this, and joint replacement may take longer.
• These operations are amenable to regional anaesthetic techniques,
either alone or combined with GA.
• Tourniquets are often used, and tourniquet pain has to be considered
(see % pp. 616–17).
• Patients may be supine, prone or occasionally on their side.
• In the case of ORIF following trauma, surgery may need to be
undertaken urgently if distal circulation is compromised. Beware of the
risk of aspiration from a full stomach, and also take time to ensure that
any other significant injury has been properly managed.
• If regional block is considered for ORIF, check that there is no concern
about the development of compartment syndrome postoperatively, as
the symptoms may be masked by the block (see % p. 1005).
Technique
• Local, regional, general or a combination of techniques can be used for
all procedures on the ankle.
• Nerve blocks under ultrasound guidance are popular and, for ankle
surgery, require sciatic (or popliteal) and femoral (or saphenous) nerve
blockade. The saphenous nerve (terminal branch of the femoral nerve)
supplies the skin down to the medial malleolus of the ankle (see %
p. 1140).
• Nerve blocks following a spinal anaesthetic improve analgesia well into
the 1st postoperative day. GA can also be combined with nerve blocks.
• Care must be taken in trauma cases with fractured ankles, as nerve
blocks may mask compartment syndrome. Always discuss your
proposed technique with the surgeon. The general rule is that nerve
blocks are best avoided in ankle trauma cases. Local infiltration is useful.
• Tendon transfer surgery takes up to 1h and is not particularly painful
postoperatively.
• ORIF may be an emergency if the vascular supply is compromised, and
an RSI is the best anaesthetic option in this situation. A good alternative
for ORIF is spinal anaesthesia. The addition of intrathecal opioid (e.g.
diamorphine 0.25–0.5mg) prolongs the period of analgesia.
• Ankle joint replacement is a procedure that is increasing in popularity.
Usually the procedure is accomplished within 2h.
62
626
Chapter 23
Arthrodesis of ankle joint 1.5–2 +++ Supine Nil with tourniquet GA or spinal with nerve blocks
PCA
Spinal + nerve blocks
Prosthetic replacement 2+ ++/+++ Supine Nil with tourniquet GA + nerve blocks
of ankle joint Spinal + nerve blocks
Foot surgery 627
Foot surgery
General principles
• Most operations are on the forefoot and toes, e.g. 1st metatarsal
osteotomy, Keller’s, excision of ingrowing toenails and terminalisation
of toes. Other operations in the midfoot include tendon transfers and
some osteotomies (Table 23.3).
• The patient population varies, and many are elderly. Those for
terminalisation of toes may well have concomitant problems such as
diabetes and/or CVS disease.
• Osteotomies tend to be painful postoperatively.
• Surgical time is 30min to 1h.
• Many are done as day cases and require early ambulation and discharge
with adequate pain relief.
• Nerve blocks make a valuable contribution to postoperative analgesia,
particularly in osteotomies and nail bed excision, and promote early
ambulation. However, onset time is relatively long and they need to be
performed a full 40min prior to surgery, if planned without GA. With
experience, this can work well, but for the less experienced, it is best to
undertake them primarily for postoperative pain relief in combination
with LMA and GA.
• Patients may find an ankle block painful, so sedation may be required.
• Adrenaline must not be used for ‘ring’ or ‘web-space’ blocks and is best
avoided in ankle blocks if the peripheral circulation is poor.
• Breakthrough pain from the tourniquet can be a problem, especially if
surgery is longer than 45min. Place the tourniquet as distally as possible
to reduce this effect.
Technique
• Regional blocks useful for foot surgery include ring/web-space or ankle
blocks for toe surgery, ankle block for forefoot surgery and sciatic (or
popliteal) nerve block for operations on the midfoot. Most commonly,
these blocks are performed for postoperative pain relief and are
combined with GA (see % pp. 1142–4).
• An alternative in all cases is spinal anaesthesia.
628
628
Chapter 23
Forefoot 1st metatarsal 30–60 +++ Supine Nil GA/LMA with ankle block or infiltration
osteotomy, Keller’s
Midfoot Tendon transfers 30–60 +/++ Supine Nil GA/LMA + local infiltration
Midfoot Osteotomy 30–60 +++ Supine Nil GA/LMA ± sciatic nerve block at knee
Spinal surgery 629
Spinal surgery
Definition
Surgery on the spinal column between the atlanto-occipital junction and
the coccyx.26,27
Can be loosely divided into four categories (Table 23.4):26,27,28
• Decompression of the spinal cord and nerves
• Stabilisation and correction of spinal deformity
• Excision of spinal tumours
• Trauma.
General principles
Children present for scoliosis surgery,28 young and middle-aged adults for
decompressive surgery and older patients for stabilisation.
• Most procedures are in the prone position,29 although anterior and
lateral approaches are used. Some procedures will involve turning the
patient during the operation (see % pp. 435–41).
• Airway access will be limited during surgery and must be secure.
• Prevent excessive abdominal or thoracic pressure due to incorrect
patient positioning, which may compromise ventilation and circulation.
• Surgical blood loss can be considerable. Ensure good vascular access
and accurate measurement of blood loss. Consider tranexamic acid and
cell salvage.
• Long procedures necessitate active prevention of heat loss.
• Assessment of spinal function may be required during the procedure
and monitoring can be affected by the choice of anaesthetic technique.30
• Fastidious attention to detail is necessary to evade the many inherent
complications in spinal surgery.
Anaesthesia
• Thorough preoperative assessment is essential. Any existing
neurological deficit must be documented prior to the induction of
anaesthesia.26,27
• Plans for the recovery period should be made in advance and will be
dictated by local experience. Long cases, those involving excessive
blood loss and major paediatric cases will need postoperative care in
the HDU. Few patients require postoperative ventilatory support.
• Secure venous access is critical. It may be difficult to access the cannula,
so an extension with a three-way tap is recommended. If multiple
infusions are planned, additional cannulae may be prudent.
• Not all cases require invasive arterial pressure monitoring. Indications
include planned postoperative critical care admission, predicted
intraoperative instability, high predicted blood loss and a requirement
for intraoperative blood investigations.
• Central venous access is not required for most cases.
• Choice of anaesthetic will be dictated by personal experience, but
most will choose an IV induction with muscle relaxation and opioid
supplementation. Both volatile anaesthesia and TIVA are frequently
used. Remifentanil is useful perioperatively. The need for intraoperative
neuromonitoring may preclude the use of volatile anaesthetic gases.
630
630
X-match +++++)
Discectomy or Excision of herniated 1–2 Prone Not significant +/++ Microdiscectomy can be done as day case
microdiscectomy intervertebral disc
Cervical discectomy Excision of herniated 2 Prone/head Not significant ++/ May be an emergency with neurological deficit
cervical intervertebral on horseshoe +++
disc or halo
traction pins
Spinal fusion ± Correction of 1–2 Prone 500–2000mL, +++/ May take bone graft from pelvis
decompression spondylolisthesis or (then 1 per X-match 4 units ++++ Metal implantation
Orthopaedic surgery
Shoulder surgery
General considerations
• Shoulder surgery is often excruciatingly painful, more so than many
other day case procedures.31,32
• Pain is not predictable and may last for several days, although it is
undoubtedly worst within the first 48h.
• A multimodal approach to analgesia is crucial.
• Heterogeneous patient population: from young athletic patients with
trauma through to elderly patients with numerous comorbidities such as
RA.31,32
• Arthroscopic procedures are generally less painful than open
procedures. Patients get effective postoperative analgesia if the surgeon
injects LA within the joint space at the end of surgery.
• Bankart’s and capsular shift operations for recurrent dislocations are
more painful for larger, muscular patients, but not generally as painful as
cuff repairs and open acromioplasties.
• Massive cuff repairs are often extremely painful, and an interscalene
block is useful. Consider a PCA, and a loading dose of morphine during
surgery. Consider an interscalene catheter with infusion of LA.33
Arthroscopic shoulder procedures
• Used diagnostically and for surgical procedures.
• Examples: acromioplasty, stabilisation, adhesiolysis and rotator cuff
repair.
• Two to three ports (e.g. posterior port for viewing and anterior or
lateral ports for instrumentation).
• Posterior port may require additional LA infiltration if surgery is
performed under interscalene block alone.32
Open shoulder procedures
• Examples: arthroplasty of the glenohumeral joint, open stabilisation,
open rotator cuff repair, subacromial decompression and procedures
for trauma.32
Preoperative considerations
• Discuss the planned anaesthetic technique with the patient, with
particular emphasis on proposed regional anaesthetic techniques and
their complications.
• Choice of anaesthetic technique will depend on both patient and
surgical factors.
• The RCoA produces patient information leaflets such as Nerve blocks
for surgery on the shoulder, arm or hand which may be provided to the
patient prior to surgery.34
• If surgery is to be performed with the patient conscious or sedated
while employing a regional technique, the patient must understand that
they are not receiving a GA.35
• Patients may not tolerate awake surgery, even with a fully working
block, as instruments and drapes may be close to the face.32
• Patients should be aware of the likely postoperative course and the
intended postoperative pain management regime.
Shoulder surgery 635
In 4373 operations between 2012 and 2019, NJR data show the median age
of patients for 1° elbow replacement was 68y.1
Indications for elbow replacement surgery
• Acute trauma
• Osteoarthritis
• Other inflammatory conditions
• Trauma sequelae
• Essex-Lopresti fracture
• Avascular necrosis.
Types of elbow replacement surgery
• Total prosthetic replacement
• Radial head replacement
• Lateral resurfacing
• Distal humeral hemiarthroplasty.
Anaesthetic technique
• Assess the patient for manifestations of rheumatoid disease (see %
pp. 246–8).
• Insert IV access into the side opposite to surgery.
• Ultrasound-guided regional anaesthetic techniques will provide
intraoperative and postoperative analgesia38 (e.g. supraclavicular (see %
pp. 1120–1) or infraclavicular block (see % pp. 1121–2)).
• Prophylactic antibiotics as per local protocol (see % pp. 62–3).
• A tourniquet is often used; ketamine may help with tourniquet pain.
• Ensure careful positioning to prevent tissue injury and to reduce
postoperative pain from other arthritic areas.
• Postoperative ulnar nerve compression is common and may necessitate
further surgery.
Anaesthesia for hand surgery 639
The majority of hand surgery procedures (Table 23.5) are suitable for LA or
regional anaesthesia as a day case. This can be combined with GA or add-
itional sedation, if required. Some procedures, such as carpal tunnel release
or trigger finger release, can be done under local infiltration alone. IV re-
gional anaesthesia (IVRA), e.g. Bier’s block, is suitable for procedures below
the elbow of 30min or less (see % p. 1127).
An upper arm tourniquet is almost always used for any type of hand
surgery. Positioning and duration of use will be an important determinant
of whether the patient is able to tolerate regional anaesthesia or LA alone.
Patients with a good brachial plexus block will usually tolerate 60–90min of
arm ischaemia.38
An axillary brachial plexus block can provide excellent anaesthesia to
the hand, arm and forearm, although tourniquet pain may be a problem.
Other approaches include infra-and supraclavicular approaches (see
% pp. 1120–1; % pp. 1121–2).38
Preoperative
• Full assessment as for GA. The patient may request a GA, and regional
anaesthesia may fail.
• Check that patients can lie flat for the proposed duration of operation if
planned to be awake.
• Assess movement of the operative arm. Can the patient achieve the
necessary position for regional block or the surgery planned?
• Discuss the planned anaesthetic technique with the patient, with
particular emphasis on proposed regional anaesthetic techniques and
their complications.
• The RCoA produces patient information leaflets such as Nerve blocks
for surgery on the shoulder, arm or hand which may be provided to the
patient prior to surgery.34
• If surgery is to be performed with the patient conscious or sedated
while employing a regional technique, the patient must understand that
they are not receiving a GA.35
Perioperative
• Make sure the patient’s bladder is empty.
• Use full monitoring, whether or not GA/sedation is to be used.
• Prophylactic antibiotics as per local protocol.
• Perform a local block, with the patient awake or lightly sedated.
• Choose an appropriate and familiar block for the planned site of
surgery ± tourniquet.
640
640
Trigger finger release and carpal Tendon or nerve release 5–15 + These procedures can usually be carried out under LIA
tunnel release
Dupuytren’s contractures Usually confined to ulnar and <60 + GA with wrist block or infiltration. Brachial plexus block
(simple) median distribution. Usually <30min with upper arm tourniquet ± GA. Quick procedure:
tourniquet time wrist block with wrist tourniquet
Dupuytren’s contracture Severe disease or redo procedure 60–120 + Prolonged tourniquet time means that a brachial plexus
(complex) may need skin grafting block or a GA with local block is often required
Metacarpophalangeal (MCP) MCP joint replacement usually for 30 per joint ++/+++ Generally frailer patients with systemic disease
joint replacement (e.g. rheumatoid
Orthopaedic surgery
Swanson)
Tenolysis, capsulotomies, These procedures may need patient 15–60 +/++ If hand movement is required, then any block must be
tendon grafts participation to assess the adequacy distal. A wrist block with sedation is usually adequate
of the procedure
Digit reimplantation Microvascular surgery Hours ++ GA is usually required because of the prolonged
procedure. Regional anaesthesia for the sympathectomy
is helpful
Ulnar head excision or Surgery for wrist pain in rheumatoid 30–60 ++/+++ As pain is severe, a single-shot brachial block or catheter
trapeziectomy disease technique is ideal, with or without GA
Anaesthesia for hand surgery 641
Hip fractures are common: 767 000 per annum in the 2020 National Hip
Fracture Database report39 (80% ♀). Every hospital that does hip fracture
surgery should have a National Hip Fracture Database Anaesthesia Lead.
Average age is 84y, and 80% occur in those >75y. In Western society, the
lifetime risk is 18% (women) and 6% (men). The 3mo mortality is 712%,
increasing to 21% at 1y.40
Preoperative
• Physiological reserve is reduced, and comorbidity is common. Ideally,
resuscitation should start as soon as the patient is admitted to hospital.
Thorough preoperative assessment must take place, and surgery should
be scheduled for the earliest possible daytime session.
• Patients should be risk-assessed prior to surgery, e.g. with the
Nottingham Hip Fracture Score, a frailty score and the 4AT delirium
score.2
• Surgical treatment can be either fracture fixation or femoral head
replacement, depending on the nature of the fracture, surgical
preference, previous mobility and life expectancy.
• Determine which procedure is to be performed (Table 23.6). Cannulated
hip screws are quick, largely non-invasive procedures with a small incision
and little blood loss. Cemented/uncemented hemiarthroplasty is a longer
procedure, similar to the femoral part of a 1° hip replacement. DHS/
Richards screw and plate are intermediate procedures.
• Any decision to delay surgery should be based on a realistic attempt
to improve the patient’s medical condition, rather than a fruitless
pursuit of ‘normal’ values. A mild chest infection is unlikely to improve
in a bed-bound elderly patient, whereas frank pneumonia with sepsis
and dyspnoea may respond to rehydration, antibiotics and chest
physiotherapy.
• Surgery should not be delayed pending echocardiography for suspected
valvular disease.2
• Hip fracture surgery should take place within 36h of sustaining a
fracture.2
• Many patients will be taking anticoagulant or antiplatelet therapy; see
the AoA guideline for advice on specific management2 (see % p. 1109).
• Good communication between the surgeons, orthogeriatricians and
anaesthetists is important. There should be a daily multidisciplinary team
discussion of each patient scheduled for surgery.
Table 23.6 Surgical procedures for fractured neck of femur
Operation Description Time (min) Pain (+ to +++++) Position Blood loss/ Notes
X-match
Cannulated screws Screws across femoral neck 20 +++ Supine, hip Nil Minimally invasive, small
(previously ‘Garden screws’) table thigh incision. Can be done
with local/nerve block
and sedation, if necessary.
X-ray-guided
Richards screw and plate Plate along femur, with 30–45 ++ Supine, hip <400mL Somewhat larger thigh
(RSP) compression screw into table incision/blood loss.
femoral head X-ray-guided
Dynamic hip screw (DHS) As RSP 30–45 ++ Supine, hip <400mL As RSP
table
Dynamic compression As RSP 30–45 ++ Supine, hip <400mL As RSP
screw (DCS) table
Total hip replacement As for total hip replacement 60–90 Offered to those who Lateral A recent study shows the
were able to walk incidence of 2° procedures
independently and after 2y does not differ
were not cognitively significantly between patients
impaired prefracture. For who receive total hip
displaced intracapsular arthroplasty and those who
fractures receive hemiarthroplasty42
Intramedullary nail Used for extracapsular 45–60min For extracapsular Supine
fractures fractures
Anaesthesia for femoral neck fracture
643
64
References
1 National Joint Registry (2020). 17th Annual report. National Registry for England, Wales and
Northern Ireland and the Isle of Man. Surgical data to 31 December 2019. https://reports.
njrcentre.org.uk/Portals/0/PDFdownloads/NJR%2017th%20Annual%20Report%202020.pdf
2 Griffiths R, Babu S, Dixon P, et al. (2021). Guideline for the management of hip fractures 2020.
Guideline by the Association of Anaesthetists. Anaesthesia, 76, 225–37.
3 Harrop-Griffiths W, Cook T, Gill H, et al. (2013). Regional anaesthesia and patients with abnor-
malities of coagulation. Anaesthesia, 68, 966–72.
4 Royal College of Anaesthetists (2018). National Audit Project 6 Summary. M https://www.
nationalauditprojects.org.uk/downloads/NAP6%20Chapter%206%20-%20Summary%20of%20
main%20findings.pdf
5 Salmasi V, Maheshwari K, Yang D, et al. (2017). Relationship between intraoperative hypotension,
defined by either reduction from baseline or absolute thresholds, and acute kidney and myocar-
dial injury after noncardiac surgery. Anesthesiology, 126, 47–65.
6 National Institute for Health and Care Excellence (2020). Joint replacement (primary): hip, knee
and shoulder. NICE guideline [NG157]. M https://www.nice.org.uk/guidance/ng157
7 Memtsoudis SG, Sun X, Chiu YL, et al. (2013). Perioperative comparative effectiveness of anes-
thetic technique in orthopedic patients. Anesthesiology, 118, 1046–58.
8 Hunt LP, Ben-Shlomo Y, Clark EM, et al. (2013). 90 day mortality after 409,096 total hip replace-
ments for osteoarthritis, from the NJR for England & Wales: a retrospective analysis. Lancet, 382,
1097–104.
9 Newbigin K, Souza CA, Torres C, et al. (2016). Fat embolism syndrome: state-of-the-art review
focused on pulmonary image findings. Respir Med, 113, 93–100.
10 Gurd AR, Wilson RI (1974). The fat embolism syndrome. J Bone Joint Surg, 56B, 408–16.
11 Donaldson AJ, Thomson HE, Harper NJ, et al. (2009). Bone cement implantation syndrome. Br J
Anaesth, 102, 12–22.
12 Healthcare Quality Improvement Partnership (2014). Falls and Fragility Fracture Audit Programme,
National Hip Fracture Database, Anaesthesia Sprint Audit of Practice (ASAP). M https://www.nhfd.
co.uk/20/hipfractureR.nsf/vwContent/asapReport/$file/onlineASAP.pdf
13 Griffiths R, White SM, Moppett IK, et al. (2015). Safety guideline: reducing the risk from ce-
mented hemiarthroplasty for hip fracture 2015. Anaesthesia, 70, 623–6.
14 Deloughry JL, Griffiths R (2009). Arterial tourniquets. Contin Educ Anaesth Crit Care Pain,
9, 56–60.
15 Boogaerts JG (1999). Lower limb exsanguinations and embolism. Acta Anaesthesiol Belg, 50, 95–8.
16 Hirota K, Hashimoto H, Kabara S, et al. (2001). The relationship between pneumatic tourniquet
time and the amount of pulmonary emboli in patients undergoing knee arthroscopic surgeries.
Anesth Analg, 93, 776–8.
17 Satsumae T, Yamaguchi H, Sakaguchi M, et al. (2001). Preoperative small dose ketamine pre-
vented tourniquet induced arterial pressure increase in orthopaedic patients under general anes-
thesia. Anesth Analg, 92, 1286–9.
18 Kam PC, Kavanaugh R, Yoong FF (2001). The arterial tourniquet: pathophysiological conse-
quences and anaesthetic implications. Anaesthesia, 56, 534–6.
19 Muñoz M, Acheson AG, Auerbach M, et al. (2017). International consensus statement on the
peri-operative management of anaemia and iron deficiency. Anaesthesia, 72, 233–47.
20 Guay J, Johnson RL, Kopp S (2017). Nerve blocks or no nerve blocks for pain control after
elective hip replacement (arthroplasty) surgery in adults. Cochrane Database Syst Rev, 10,
CD011608.
21 Grevstad U, Mathiesen O, Lind T, et al. (2014). Effect of adductor canal block on pain in patients
with severe pain after total knee arthroplasty: a randomized study with individual patient analysis.
Br J Anaesth, 112, 912–19.
22 Andersen LO, Gaarn-Larsen L, Kristensen BB, Husted H, Otte KS, Kehlet H (2010). Analgesic ef-
ficacy of local anaesthetic in knee arthroplasty: volume v concentration. Anaesthesia, 65, 984–90.
23 Bandolier. Surgery for arthritic knees. M http://www.bandolier.org.uk/band102/b102-3.html
24 Rattenberry W, Hertling A, Erskine R (2019). Spinal anaesthesia for ambulatory surgery. BJA
Educ, 19, 321–8.
25 Menigaux C, Guignard B, Fletcher D, et al. (2001). Intraoperative small-dose ketamine enhances
analgesia after outpatient arthroscopy. Anesth Analg, 93, 606–12.
26 Raw DA, Beattie JK, Hunter JM (2003). Anaesthesia for spinal surgery in adults. Br J Anaesth, 91,
886–904.
27 Nowicki RWA (2014). Anaesthesia for major spinal surgery. Contin Educ Anaesth Crit Care Pain,
14, 147–52.
64
28 Young CD, McLuckie D, Spencer AO (2019). Anaesthetic care for surgical management of ado-
lescent idiopathic scoliosis. BJA Educ, 19, 232–7.
29 Feix B, Sturgess J (2014). Anaesthesia in the prone position. Contin Educ Anaesth Crit Care Pain,
14, 291–7.
30 Levin DN, Strantzas S, Steinberg BE (2019). Intraoperative neuromonitoring in paediatric spinal
surgery. BJA Educ, 19, 165–71.
31 Hewson DW, Oldman M, Bedforth NM (2019). Regional anaesthesia for shoulder surgery. BJA
Educ, 19, 98–104.
32 Beecroft C, Coventry DM (2008). Anaesthesia for shoulder surgery. Contin Educ Anaesth Crit
Care Pain, 8, 193–8.
33 Vorobeichik L, Brull R, Bowry R, et al. (2018). Should continuous rather than single-injection
interscalene block be routinely offered for major shoulder surgery? A meta-analysis of the anal-
gesic and side-effects profiles. Br J Anaesth, 120, 679–92.
34 Royal College of Anaesthetists, Association of Anaesthetists, Regional Anaesthesia United
Kingdom (2020). Nerve blocks for surgery on the shoulder, arm or hand. [Information for pa-
tients and families] M https://www.rcoa.ac.uk/sites/default/files/documents/2020-05/10-
NerveBlocks2020web_0.pdf
35 Pandit JJ, Andrade J, Bogod D, et al.; Royal College of Anaesthetists, Association of Anaesthetists
of Great Britain and Ireland (2014). 5th National Audit Project (NAP5) on accidental awareness
during general anaesthesia: summary of main findings and risk factors. Br J Anaesth, 113, 549–59.
36 Kuo L, Hsu W, Chi C, et al. (2018). Tranexamic acid in total shoulder arthroplasty and reverse
shoulder arthroplasty: a systematic review and meta-analysis. BMC Musculoskelet Disord, 19, 60.
37 Pandya J, Johnson T, Low AK (2018). Shoulder replacement for osteoarthritis: a review of sur-
gical management. Maturitas, 108, 71–6.
38 Brown AR (2002). Anaesthesia for procedures of the hand and elbow. Best Pract Res Clin
Anaesthesiol, 16, 227–46.
39 Royal College of Physicians (2020). National Hip Fracture Database Report 2020 annual report
https://www.nhfd.co.uk/files/2020ReportFiles/NHFD_Annual_Report_2020.pdf
40 Parker MJ, Pryor GA, Myles J (2000). 11 year results in 2,846 patients of the Peterborough
hip fracture project: reduced morbidity, mortality and hospital stay. Acta Anaesthesiol Scand,
71, 34–8.
41 Foss NB, Kristensen BB, Bundgaard M, et al. (2007). Fascia iliaca compartment blockade for
acute pain control in hip fracture patients: a randomized, placebo-controlled trial. Anesthesiology,
106, 773–8.
42 HEALTH Investigators; Bhandari M, Einhorn TA, Guyatt G, et al. (2019). Total hip arthroplasty or
hemiarthroplasty for hip fracture. N Engl J Med, 381, 2199–208.
43 Klein AA, Arnold P, Bingham R, et al. (2016), AAGBI guidelines: the use of blood components
and their alternatives 2016. Anaesthesia, 71, 829–42.
44 White SM, Moppett IK, Griffiths R, et al. (2016). Secondary analysis of outcomes after 11,085
hip fracture operations from the prospective UK Anaesthesia Sprint Audit of Practice (ASAP-2).
Anaesthesia, 71, 506–14.
45 Neuman MD, Silber JH, Elkassabany NM, et al. (2012). Comparative effectiveness of regional
versus general anesthesia for hip fracture surgery in adults. Anesthesiology, 117, 72–92.
46 Foss NB, Kristensen MT, Palm H, et al. (2009). Postoperative pain after hip fracture is procedure
specific. Br J Anaesth, 102, 111–16.
47 Cuvillon P, Ripart J, Debureaux S, et al. (2007). [Analgesia after hip fracture repair in elderly pa-
tients: the effect of a continuous femoral nerve block: a prospective and randomised study]. Ann
Fr Anesth Réanim, 26, 2–9.
48 NHS Networks. Hip Fracture Perioperative Network (HipPeN). M http://www.networks.nhs.uk/
nhs-networks/hip-fracture-anaesthesia
Chapter 24 647
647
See also
% Burns: early management pp. 1013–18
648
General principles
The complexity of anaesthesia for plastic and burns surgery ranges from
the routine to the challenging. Some extensive procedures (e.g. free flap
repairs, craniofacial reconstruction) may involve invasive monitoring, exten-
sive blood loss and postoperative intensive care support. See Table 24.1 for
a range of plastic surgical procedures.
Regional techniques and sedation
Minor body surface procedures may be performed under LA infiltration
alone. Significant body surface procedures in those unfit for GA, such as
excision and grafting of skin tumours, can be accomplished using extensive
infiltration of LA and IV sedation. Upper and lower limb surgery is especially
suitable for regional anaesthesia. Consider the surgical site, placement of
tourniquets and the location of split skin grafts (SSGs), if required, when
deciding on the best regional block. Long procedures or those which would
benefit from ongoing regional sympatholysis, such as digit reimplantation,
would benefit from a regional catheter. Sedation to supplement a regional
technique may be required in anxious patients or for longer or extensive
procedures. Use any sedative technique which is familiar and appropriate
for the patient’s physiology, ideally with an agent which is easily titratable.
Propofol (0.5–1.0 micrograms/mL TCI or 10–15mL/h of 1% solution), with
or without supplemental midazolam (1–2mg), is effective. Alternatively,
remifentanil (0.5–1.0 nanograms/mL TCI or 5mL/h of 1mg in 20mL solu-
tion) offers both sedation and analgesia, and respiratory depression can be
avoided if the infusion rate is slowly titrated upward.
The difficult airway
(See also % pp. 363–4.) Patients with head and neck pathology causing
airway difficulty are often encountered. Airway difficulty may arise from
anatomical deformity due to tumour, trauma, infection, previous oper-
ations, radiotherapy or scarring. Competence in difficult airway techniques
(e.g. awake intubation) is required. The ‘shared airway’ is regularly a feature
of head and neck surgery. Discuss with the surgeon which tube you pro-
pose to use and by which route to achieve the best surgical access (oral,
nasal, conversion to tracheostomy) and how the tube will be secured (tied,
taped, stitched).
Poor access to the patient
The operating site may be extensive (e.g. burns debridement) or multiple
(e.g. free flap procedures). This may produce added difficulty with:
• Heat conservation: it may be difficult to achieve enough access to
the patient’s body surface area to maintain temperature. Heated
underblankets are useful.
• Monitoring: ECG leads, the pulse oximeter probe and the BP cuff may
all be difficult to position adequately.
• Vascular access: position cannulae away from the operative field. Use
femoral vessels or the foot, if necessary. Long extension sets may be
required.
General principles 649
Long operations
Patients undergoing complicated reconstructive procedures may be in
theatre for many hours. Give careful consideration to:
Vascular access Check that line placement will not interfere with the site of
surgery. Invasive arterial monitoring is desirable. A central venous line can
assist with estimations of the intravascular volume and provide dependable
venous access in the postoperative period. Site at least one large-bore
peripheral (14–16G) cannula for fluid administration and a small cannula
(20–22G) for other infusions such as TCI and PCA.
Blood loss Ensure blood has been X-matched. The initial dissection is usually
the period of most blood loss, and a moderate hypotensive technique may
help to limit this. Thereafter, losses may be insidious and ongoing. Aim
to keep track by swab weighing, visual estimation and regular Hb or Hct
measurement. Non-invasive CO monitoring can help optimise the fluid
status. Assessment of stroke volume, flow time or SVV, using devices such
as LiDCO™, may give valuable information to the anaesthetist.
Fluid balance Urinary catheterisation is essential. Ensure careful monitoring of
fluid balance, especially in children and patients with poor cardiorespiratory
function.
Body temperature Monitor the core temperature (e.g. rectal, nasopharyngeal,
oesophageal). Maintain the temperature by using low FGFs, an HME filter,
warmed IV fluids, a warm ambient theatre temperature (e.g. 24°C), a
heated mattress or a forced air warming blanket. Take care not to overheat
the patient.
Positioning Ensure that structures, such as the cervical spine and brachial
plexus, are not in positions of stress. Take care with pressure areas. Pad
bony prominences and raise the heels off the table.
VTE DVT prophylaxis is often initiated during surgery. All patients should
have thromboembolism compression stockings and intermittent calf
compression while in theatre, and be assessed for daily LMWH.
NGT Consider emptying the stomach. Children are especially prone to
gastric distension during prolonged procedures.
Eye care Lightly tape and pad the eyes for protection. Avoid excessive
padding, since this may negate the natural protection afforded by the bony
orbit. Prophylactic antibiotic ointment is unnecessary. Do not allow corneal
abrasion to develop from surface drying. A simple eye ointment is helpful if
the eyes are left uncovered.
ETT cuff pressure Cuff pressure will gradually increase if N2O is used.
Where possible, recheck the cuff pressure at intervals during the case.
Postoperative care Discuss the preferred site of postoperative care with the
nursing staff and surgical team. Surgeons often prefer patients to return
to the plastic surgery ward where wound care and nursing observation
may be more attuned to the specifics of the operation. Closer patient
observation, invasive monitoring and regular blood gas estimation may be
more achievable in an ICU/HDU. The site for immediate postoperative
care is principally dictated by the general condition of the patient.
650
Smooth emergence
Avoid the patient coughing and straining at the end of the procedure. This
will put tension on delicate suture lines and increase bleeding and haema-
toma formation, especially for facial procedures. Deep extubation, deep
conversion of ETT to LMA (Bailey manoeuvre), extubation with a run-
ning remifentanil infusion or IV lidocaine 1.0mg/kg bolus 2min prior to
extubation can smooth emergence.
Analgesia
• Most procedures are performed on the body surface. These tend to be
less painful than procedures involving the body cavities and are usually
amenable to LA infiltration or regional block. Continuous catheter
techniques may be useful in limb procedures.
• Patients recovering from head and neck procedures are often
surprisingly comfortable despite extensive surgery.
• Major body cavities and abdominal musculature are usually not involved.
The pain experienced after an abdominoplasty is significantly less than
pain following a laparotomy.
• Plastic surgery procedures seldom involve new fractures of long bones.
• The GI tract is usually unaffected. The oral route for drugs is frequently
available, which may make dosing and administration of analgesics
simpler.
Attention to detail
Successful anaesthesia for plastic surgery requires careful attention to de-
tail. Patients for aesthetic surgery will have high expectations and will be
well informed.
Breast surgery 653
Breast surgery
General considerations
Breast cancer is now the commonest cancer in the UK, and the incidence
has i by >20% over the last 25y. Mortality from breast cancer, however, has
fallen steadily since 1990, probably because of earlier detection and improved
treatment. Over this time, there have been significant advances in more ex-
tensive combined procedures of breast resection and reconstruction. Radical
mastectomy is now rarely indicated, as better efficacy is shown for breast-
conserving treatment, such as wide local excision of tumour, in addition to
chemotherapy or radiotherapy, compared to full mastectomy alone. The min-
imally invasive technique of sentinel lymph node biopsy has now predomin-
antly replaced axillary lymph node dissection for breast cancer staging.
Preoperative
Anxiety is often high. It is important to gain the patient’s confidence at the
preoperative visit, discuss analgesia and prescribe anxiolysis if necessary.
• Adverse effects from any neoadjuvant therapies should be considered
and optimised. Patients who have recently undergone chemotherapy
may be immunocompromised. Check FBC for evidence of bone
marrow suppression and anticipate potentially difficult venous access.
• Reconstructive procedures, mastectomy following radiotherapy,
mastectomy where breasts are large and breast reduction surgery increase
the risk of blood loss. Check Hb and ensure blood is grouped and screened.
Perioperative
LMA and SV are often appropriate for short-to medium-length procedures.
Use intubation and mechanical ventilation for prolonged procedures, the
obese and patients at risk of aspiration.
• Avoid placing venous access on the side of surgery.
• Standard monitoring is appropriate for most procedures. Longer
procedures will require active warming and temperature measurement.
• Additional invasive monitoring may be required for prolonged
reconstructive procedures, including free flap surgery.
• Give multimodal analgesia, including NSAID, systemic opioid and
regional techniques, if possible.
• Breast surgery patients are at high risk of PONV. Avoid causative
agents, and administer prophylactic antiemetics. TIVA may be useful.
• Beware of the blue dyes used in sentinel lymph node biopsy as they
have been associated with anaphylaxis.
Regional analgesia
Regional techniques may offer advantages in some cases; however, the risks
in healthy women undergoing minor procedures may outweigh the benefits.
• Consider regional techniques for more radical procedures, e.g. radical
mastectomy/axillary clearance and breast reconstruction.
• Regional techniques include paravertebral block, thoracic epidural,
interfascial plane (pectoral nerve and serratus anterior plane) blocks,
intercostal blocks and intrapleural block. Beware of the complications
of each technique. An ultrasound-guided approach is advocated.
• Recent evidence suggested that breast surgery supplemented by a
paravertebral block does not reduce the risk of cancer recurrence.1
654
Postoperative
• Minor procedures, including wide local excision with sentinel lymph
node biopsy, could be suitable for day case surgery.
• HDU may be required after extensive procedures.
• If a paravertebral catheter or thoracic epidural is sited, continue infusion
postoperatively.
Special considerations
Patients may present with previous breast surgery and axillary clearance.
Cannulation should be avoided in the arm on the affected side due to the
risk of infection and potential development of lymphoedema. There is
limited evidence of the risk of short-term cannulation on the affected side,
and if venous access is limited, it may be appropriate to use the affected side
and remove at the end of the case.
• Chronic pain, typically presenting in the affected anterior chest wall,
ipsilateral axilla or upper arm, may occur following breast surgery.
Incidence is as high as 20–50% after mastectomy. Intensity of the
pain following extensive surgery, postoperative radiotherapy and
chemotherapy are risk factors.
• Breast reconstruction following mastectomy is common. The two main
methods include implant-based or autologous tissue flap reconstruction.
The tissue flap can be transferred as a free flap or a pedicled flap.
Options for flap reconstructions are listed in Table 24.2.
References
1 Sessler DI, Pei L, Huang Y, et al. (2019). Recurrence of breast cancer after regional or general
anaesthesia: a randomised controlled trial. Lancet, 394, 1807–15.
Breast surgery 655
Breast reduction
Procedure Reduction of breast size by glandular resection. Usually
bilateral
Time 3h
Pain ++
Position Supine, 30° head-up, periodic deck-chair. Arms may be
positioned on boards, or with elbows flexed and hands
placed behind the upper part of the buttocks
Blood loss 500mL, G&S
Practical IPPV via ETT or LMA
techniques
Preoperative
Bilateral breast reduction is not primarily an aesthetic procedure. These
patients may suffer from severe neck and back pain. Participating in ex-
ercise and sport is not possible. There may be symptoms of emotional
disturbance.
• Patients are usually fit; aged 20–40y. Many surgeons exclude patients
with a BMI >30 due to a higher incidence of wound breakdown,
infection and haematoma formation.
• A mastopexy is a surgical procedure for correcting breast ptosis when
breast volume is adequate. Anaesthetic implications are similar. Blood
loss is less.
• Check FBC and G&S. X-matching is generally unnecessary, except for
larger reductions.
• Timing in relation to the menstrual cycle is unimportant.
• All patients should receive DVT prophylaxis (compression stockings,
daily LMWH).
Perioperative
• IPPV may be preferable, since the surgeon often puts pressure on the
chest wall during surgery. IPPV will maintain satisfactory chest expansion
with good aeration and control of PaCO2, and help minimise blood loss.
An LMA may be satisfactory for IPPV.
• Place ECG electrodes on the patient’s back. Lie the patient on
incontinence pads to absorb blood loss.
• Take care to position the patient carefully on the operating table. The
anaesthetic machine is usually at the head end. Ensure that the chest
and arms are symmetrical. Confirm that vascular cannulae are secured
well and padded if the hands are to be positioned behind the buttocks.
Local pressure damage to the skin may otherwise ensue.
• The patient may be placed in a deck-chair position briefly multiple
times throughout the operation to allow the surgeon to check breast
symmetry. The position changes mandate care with securing airway,
vascular access, monitoring and maintenance of CPP.
• Blood loss depends on the surgical technique. Use of cutting diathermy
causes less bleeding than a scalpel. Infiltration with dilute adrenaline-
containing LA helps reduce blood loss. All surgeons have their own
recipe. Check the dosage being used; in practice, this is seldom a
concern (see % p. 1102).
Breast reduction 657
Breast augmentation
Procedure Bilateral or unilateral augmentation of breast size
Time 90min
Pain ++/+++
Position Supine, 30° head-up. Arms may be out on boards, or with
elbows flexed and hands placed behind the upper part of
the buttocks
Blood loss Minimal
Practical SV or IPPV via LMA
techniques
Preoperative
Breast augmentation may be performed for:
• Reconstruction following mastectomy
• Correction of breast asymmetry
• Aesthetic bilateral augmentation.
Patients are usually fit and well.
Perioperative
Position on the operating table as for breast reduction.
• The four 1° augmentation techniques include inframammary,
periareolar, transaxillary and transumbilical.
Postoperative
Postoperative discomfort may be related to the size of the implants. Large
implants cause more tissue stretching and postoperative pain.
• In general, breast augmentation appears to cause more discomfort than
breast reduction. Give regular simple analgesics. Opioid analgesia may
be needed, but PCA techniques are seldom required.
• Haematoma formation may require early return to theatre. Later
complications include infection, capsule formation and rupture.
Special considerations
An association between silicone breast implants and the development of
systemic symptoms of connective tissue diseases has been suggested. This
association has not been proven, following data from large studies.
• Soybean oil-filled implants have been withdrawn from use in the UK.
There are insufficient data concerning the long-term consequences
of soybean oil breakdown. Sodium chloride 0.9% implants are not
perceived as sufficiently realistic and are unpopular with many women.
Free flap surgery 659
Preoperative
A free flap is a transfer of tissue with its blood supply from one part of the
body to another when the vessels are disconnected during the transfer and
microvascularly reanastomosed to a new artery and vein at or near the re-
cipient site. The transferred tissue volume may contain skin, muscle, nerve,
fascia and bone. Free flaps are commonly used to provide tissue cover for
large defects following trauma or resection for malignancy, or when com-
plex tissue is required to regain normal aesthetics or function.
• Surgical success depends on establishing and maintaining adequate
flap perfusion. Hypercoagulable states, such as sickle-cell anaemia and
polycythaemia, are contraindications to surgery. Smokers should be
advised to stop smoking for at least 4w before surgery due to nicotine-
induced vasoconstriction, carbon monoxide (CO)-related tissue
hypoxia and blood hypercoagulability caused by i platelet aggregation.
In oncology patients, consider chemotherapy-related organ system
dysfunction and anticipate difficulty gaining IV access.
• Elderly patients with head and neck cancer are often heavy smokers and
drinkers and may have significant cardiac and respiratory comorbidity, as
well as poor nutritional state. Their airway anatomy may be distorted,
especially with previous head and neck surgery or radiotherapy,
increasing the risk of a difficult intubation.
Perioperative
The physiological aim of anaesthesia is to optimise circulatory flow through
the grafted flap. Anaesthetic management is largely guided by 1st principles
and application of the Hagen–Poiseuille equation:
πPr4
Q=
8ηl
where Q = flow rate, ΔP = pressure gradient, r = vessel radius, l = vessel
length, and η = blood viscosity.
The variables which can be controlled by the anaesthetist are pressure
gradient, viscosity and vessel radius.
• Free flap surgery is a long procedure on multiple body sites and all patients
should have a GA. Pain often originates from the flap donor site or from
SSGs taken to cover deficits in either the donor or the recipient site and a
regional block of these areas adds to effective analgesia. The flap itself is
denervated and insensate and the recipient site is often relatively pain-free.
60
Postoperative
• Aim for a smooth emergence, avoiding any strain on suture lines.
• Vasoconstriction from cold, pain, low circulating volume, hypotension
and hypocapnia will threaten the flap and should be addressed. If
postoperative shivering occurs, exclude hypothermia and consider
treating with a forced air warming device, 0.5–3mg/kg IV tramadol or
20–50mg IV pethidine.
• In addition to regional anaesthesia, oral opioids are usually sufficient.
Consider IV PCA when swallowing is impaired such as with head and
neck flaps. NSAIDs have been associated with flap haematoma, but
selective COX-2 inhibitors, such as celecoxib, have been shown to
be safe.
• Flap observation is a specialised nursing skill and care is often best
provided on the plastic surgery ward. The need to escalate to
critical care will be determined by patient factors. Postoperative flap
observation will evaluate the Doppler signal of the arterial supply, flap
colour, capillary refill time, skin turgor, skin temperature and bleeding on
pinprick. Compromised flaps can be salvaged if early detection occurs.
A revision operation on a compromised flap should employ the same
anaesthetic principles to promote optimum flap perfusion.
Special considerations
• The reimplantation of severed digits or limbs should be managed as for
a free flap. A brachial plexus catheter is helpful in managing reimplanted
digits as it provides a continuous vasodilated limb.
• A pedicle flap is constructed when A–V connections remain intact, but
the raised flap is rotated to fill a neighbouring defect. This procedure
requires the same anaesthetic principles to optimise flap circulation.
• Overall free flap survival is >95%; patients in a poor general condition
with coexisting disease have the highest risk of flap failure.
62
Liposuction
Procedure Vacuum aspiration of SC fat via a small skin incision and a
specialised blunt-ended cannula
Time Variable 30–90min
Pain +
Position Variable, depending on site. Usually supine
Blood loss 1% of the volume of fat aspirated with fluid infiltration
technique
Practical Local infiltration with IV sedation/LMA and SV
techniques
Preoperative
Liposuction is a procedure to manage lipoma, gynaecomastia or reducing
the bulk of transplanted flaps. Alternatively, a cosmetic procedure where
adipose tissue is either removed or used for autologous fat grafting.
• In the obese patient, be aware of altered drug pharmacokinetics and
pharmacodynamic effects and consider associated comorbidities such as
metabolic syndrome, hypertension, DM, IHD and OSA.
• Use caution with patients vulnerable to large doses of adrenaline used
(IHD, MAOI use) or large volume of fluid infiltrated (cardiac or renal
failure).
Perioperative
• The total amount of fat aspirated depends on patient requirement and
surgical judgement.
• Fat is infiltrated with dilute LA with adrenaline. Back-and-forth
movement of the cannula disrupts fatty tissue, which is then aspirated
by either a suction apparatus or a syringe.
• Injection of fluid helps fat breakdown and aids aspiration. A typical
recipe for an SC infiltration solution would be 1000mL of warmed 0.9%
sodium chloride or Hartmann’s solution containing 50–100mL of 1%
lidocaine (0.05–0.1% in final solution) and 1mL of 1:1000 adrenaline.
The ‘Superwet’ technique of 1mL of infiltrate per 1mL of anticipated
aspirate is commonly used.
• The ‘Tumescent’ technique refers to a large volume of LA/adrenaline
infiltrate to produce tissue turgor. Developed as an outpatient
technique and performed without additional anaesthesia or sedation.
A total of 3mL of infiltrate per 1mL of aspirate is often used. There is
little evidence that this technique is superior to the Superwet technique,
and it may produce more complications. It may provide unsatisfactory
anaesthesia when used alone, and sedation or GA may be required.
• Blood loss depends on the volume of LA/adrenaline infiltrate used and
the extent of liposuction required. Loss is 71% of the volume of the
aspirate for the Superwet and Tumescent techniques. This may increase
to 40% without SC infiltration.
• Extensive liposuction physiologically resembles a burn injury, and large
fluid shifts result. Replace aspirate 1:1 with IV crystalloid, although take
caution with the Tumescent technique where there is a net fluid gain.
Patients with heart failure are at risk of pulmonary oedema.
Liposuction 663
Preoperative
Patients for simple excision and grafting of isolated lesions may be other-
wise well.
• Elderly patients for excision/grafting of skin lesions or pretibial
lacerations may be in poor general health. A local or regional technique
may be preferable to GA. Sedation may be necessary for long
procedures or in those unable to lie still.
• Patients with extensive burns for debridement and grafting require
careful assessment.
Perioperative
Full-thickness skin graft
Consists of the epidermis and dermis. Used in small areas where the thick-
ness, appearance and texture of the skin are important. Usually harvested
with a scalpel. FTSG can be harvested using SC LA infiltration with a 27G
needle. The donor site needs to be closed directly. Common sites include:
• Post-auricular skin for grafts to the face
• Groin or antecubital fossa to the hand for management of flexion
contractures.
Split skin graft
Consists of the epidermis and a variable portion of the dermis. Much wider
usage than FTSG. Usually harvested with a skin graft knife or a power-
driven dermatome. Donor sites will heal spontaneously within 2w. Donor
sites are chosen according to the amount of skin required, the colour and
texture match and local convenience. Meshing is used to expand the extent
of the area that the graft is required to cover. Common donor sites are the
thigh, the flexor aspect of the forearm, the upper arm and the abdomen.
SSG can be harvested using LA cream. It should be applied at least 2h in
advance and covered with an occlusive dressing. Anaesthesia does not ex-
tend into the deeper dermis, so the technique is unsuitable for FTSG. The
lateral cutaneous nerve of the thigh (LCNT) or fascia iliaca block provides
useful analgesia of a thigh donor site. If regional block is not possible, then
surgical infiltration of LA will be useful. Excess harvested skin can be stored
at 4°C for 2–3w.
Skin grafting and burns reconstructive surgery 665
Postoperative
The SSG donor site is a painful wound. Supplement with LA (LCNT or
femoral block) where possible. The type of dressing is important for donor
site healing and comfort. Common dressings used are alginate dressings or
an adhesive retention tape (such as Mefix®). Dressings are removed once
the donor site has healed in 2–3w. NSAIDs and simple analgesics are usually
required for 3–4d. Itching follows when the acute pain settles and healing
is under way.
Acute burns surgery
(See also % pp. 1013–18.) Extensive debridement and grafting of burns
are major procedures. Current management is to aim to debride burnt
tissue and cover at the earliest opportunity (often within 48h). Debrided
areas may be covered with autograft (SSG or FTSG taken from healthy skin
on the patient), allograft (skin from cadaveric donors) or a range of com-
plex burns dressings. This converts the burn to a healthy surgical wound.
Potential sources of sepsis are eradicated; fluid shifts are less, and intensive
care management tends to be more stable. Wounds not covered with auto-
graft will require further surgery in the following weeks to cover the wound
fully with the patient’s own skin. This process may take many weeks of
repeated procedures.
• Two anaesthetists may be required. Two surgical teams will
considerably speed up the procedure and help minimise complications.
• Ensure 6–8 units of red cells are X-matched. Debrided tissue bleeds
freely. Losses can be rapid and difficult to estimate, particularly in
small children. Regularly check Hct, and maintain at 730%. Correct
coagulopathy. Massive transfusion may be required.
• Perform a careful airway assessment: intubation is required for all but
the smallest of burn debridements. Face mask ventilation may be made
difficult by facial burns and the presence of feeding tubes. Laryngoscopy
may be compromised by upper airway oedema due to burns and
resuscitation. Securing the airway by tape or ties may not be possible
with facial burns; suturing or even wiring the tube may be necessary.
• Use lung-protective ventilation: ventilation requirements will be high
due to the high metabolic rate. Hypercapnia may have to be tolerated.
• Significant improvements in blood loss and patient comfort are achieved
with surgical infiltration of tumescent solution containing adrenaline and
LA (e.g. bupivacaine) into the tissues being debrided and used as donor
sites. Care should be taken to not exceed toxic LA doses, although
large doses of adrenaline can be infiltrated. Reduction in vasopressor
requirements and lactic acidosis may be seen.
• Temperature control: a large exposed body surface area will lose heat
rapidly by radiation and evaporation. Measure core temperature and
use all methods available for heat conservation. This should include
active warming of fluids, use of an HME filter, underpatient warmer,
forced air warmer and attention to minimising patient exposure.
Ongoing discussion with the operating team can ensure that only
areas currently being operated on remain exposed; other areas can be
covered with sterile insulation (e.g. Gamgee tissue). Little body surface
area may be available for warming blankets; however, these should be
utilised. The ambient temperature in the operating theatre will often
6
Gastrointestinal surgery
Matt Rucklidge and Peter Garnett
Major GI surgery 670
Open GI surgery 672
Summary of open GI procedures 672
Laparoscopic GI surgery 674
Summary of laparoscopic GI procedures 678
Laparoscopic cholecystectomy 680
Laparoscopic appendicectomy 681
Inguinal hernia repair 682
Anal and perianal procedures 683
670
Major GI surgery
General considerations
Major abdominal surgery generates a neuroendocrine, metabolic and in-
flammatory response which may result in adverse physiological changes,
including pulmonary dysfunction, i cardiac demand, pain, nausea and
vomiting. This may result in delayed mobilisation, prolonged hospital stays
and i morbidity and mortality. Principles of prehabilitation and ERAS
should be applied (see % pp. 44–6). Major GI surgery may be performed by
open and minimally invasive (laparoscopic and robotic) techniques.
Preoperative preparation
• History, examination, ECG if indicated, FBC, U&E. Other blood tests,
as indicated by patient comorbidities.
• Assessment of exercise function (e.g. CPET; see % pp. 33–5). Optimise
cardiac and respiratory function.
• Optimise nutrition. Patients with inflammatory bowel disease may be
significantly malnourished and immunosuppressed.
• Discuss multimodal analgesia. Key components for GI surgery include:
abdominal wall blocks and catheters (see % p. 1168), wound catheters,
IV lidocaine infusions (see % p. 1171) and neuraxial blocks (see %
pp. 1114–17).
• Withhold ACE inhibitors/ARBs 24h before surgery. The VISION study
found reduced risk of mortality, CVE and myocardial injury if withheld.1
• Consider premedication with H2 antagonist or PPI if at risk of
regurgitation, and discuss RSI if indicated.
• Determine whether postoperative HDU/ICU care is indicated and
ensure a bed is booked before surgery.
• Balance the health of the patient with the complexity and duration of
the surgical procedure, and consider the additional information invasive
monitoring will provide against the risks involved in placement and
interpretation (Table 25.1).
• Minimise the period of fasting. Continue clear fluids until 2h prior to
surgery and administer oral carbohydrate preload (caution in diabetic
patients).
Perioperative
• Large-bore IV access, with long extension if access to arms restricted.
Arms are commonly placed by the sides in laparoscopic colorectal
surgery, limiting access intraoperatively.
• Perform neuraxial block for postoperative analgesia if indicated, e.g.
spinal with long-acting opioid (e.g. diamorphine or morphine) or low
thoracic epidural.
• Institute invasive monitoring as indicated.
• Consider appropriate line placement for postoperative parenteral
feeding. This may be required in patients undergoing procedures for
inflammatory bowel disease.
• RSI if evidence of bowel obstruction or risk of regurgitation.
• Prophylactic antibiotics before skin incision.
• Consider the need for perioperative steroid supplementation. Steroid
therapy is common in patients with inflammatory bowel disease.
Major GI surgery 671
Minimally invasive Major abdominal surgery with potential fluid shifts, CVS
CO monitoring compromise, likely requirement for perioperative inotropes
Arterial line CVS, respiratory compromise, major blood loss, need for
blood gas sampling
CVP line Need for vasopressors and/or inotropes. Requirement for
postoperative parenteral nutrition
672
Open GI surgery
Despite the increasing range and complexity of abdominal procedures
performed laparoscopically, open techniques remain common and are
listed on % p. 672. Open GI surgery is associated with i pain and tissue
trauma, and may impair postoperative respiratory and GI function, com-
pared with minimally invasive surgical techniques. Some open abdominal
procedures may require the patient to be turned prone intraoperatively
(e.g. abdominoperineal resection).
Laparoscopic GI surgery
Laparoscopic surgery is well established for an increasing range and com-
plexity of elective and emergency procedures. The principles of laparo-
scopic surgery can also be applied to robotically assisted GI procedures.
Laparoscopic and robotic techniques can both be considered minim-
ally invasive surgery. Minimally invasive surgery may have significant
intraoperative effects on cardiopulmonary physiology because of the ef-
fects of the pneumoperitoneum and patient positioning (see Table 25.3).
However, benefits of laparoscopy over laparotomy include:
• Reduced tissue trauma, wound size and postoperative pain
• Improved postoperative respiratory function
• Reduced postoperative ileus
• Earlier mobilisation, shorter hospital stays
• Improved cosmetic results.
Surgical requirements
• Creation of a pneumoperitoneum by insufflation of gas (usually CO2)
into the peritoneal cavity.
• CO2 is non-combustible, colourless, non-toxic and highly soluble, and
is continuously insufflated into the abdomen to maintain a pressure of
10–20mmHg.
• Devices that warm and humidify CO2 for laparoscopic abdominal
procedures are in use, but their effect on clinical outcomes is unclear.
• Adequate NMB is required in laparoscopy to optimise operating
conditions and limit intra-abdominal pressure.
• Muscle relaxation is essential while docked in robotic surgery to avoid
unexpected patient movement and injury.
Patient positioning
• Patient position will be determined by the type of surgery (see %
p. 678).
• Patients placed head-down are at greater risk of pulmonary impairment,
including reduction in FRC, V/Q mismatch and atelectasis. There is an
i risk of endobronchial intubation due to cephalad movement of the
lungs exacerbated by the pneumoperitoneum.
• Long periods positioned steeply head-down can result in facial,
airway and cerebral oedema. This must be considered when planning
extubation.
• Regurgitation of gastric contents in the head-down position can result in
conjunctival chemical injury. Ensure eyes are protected.
• Patients placed head-up are at i risk of reduced BP and CO due to d
venous return. Those most at risk include the hypovolaemic patient, the
elderly and patients with pre-existing CVS disease.
• Patients are at risk of injury from slipping in both head-up and head-
down positions. Consider use of specialised poisoning devices, e.g. non-
slip padding, shoulder supports.
Laparoscopic GI surgery 675
Respiratory CVS
Airway pressure i Venous return d
FRC d SVR i
Pulmonary compliance d CO nd
V/Q mismatch i Risk of arrhythmias i
Neurological GI
ICP ni Risk of regurgitation i
CPP ni
Preoperative
• Contraindications to laparoscopic surgery are relative; risks are i with
IHD, valvular heart disease, i ICP and hypovolaemia.
• All patients must be considered at risk of conversion to an open
procedure, and a plan for analgesia considered.
• Laparoscopic procedures are increasingly performed in obese patients
due to improved postoperative recovery when compared to an open
procedure. However, the deleterious effects of the pneumoperitoneum
and positioning may be exaggerated in this patient group.
Perioperative
• GA with endotracheal intubation, muscle relaxation and controlled
ventilation is considered the safest technique, as it protects against
pulmonary aspiration and enables control of PaCO2.
• Avoid gastric distension during bag–mask ventilation which may increase
the risk of gastric injury during trocar insertion. Consider inserting a
gastric tube if laparoscopic entry via the left upper abdomen (Palmer’s
point) is planned.
• A urinary catheter may be required in lower abdominal procedures to
decompress the bladder and reduce the risk of injury.
• Systemic absorption of CO2 and raised intra-abdominal pressure will
require i minute volume and result in higher intrathoracic pressure.
• Aim for normocapnia, but beware of adverse effects of high
intrathoracic pressure. Controlling ETCO2 during prolonged
procedures, especially in the obese and head-down position, can
be difficult and may occasionally necessitate intermittent release of
intraperitoneal gas or tolerance of a degree of hypercapnia.
• If high inspiratory pressures are encountered, exclude endobronchial
intubation and inadequate NMB. Consider a change to pressure-
controlled ventilation and a reduced I:E ratio (e.g. 1:1).
• Analgesia requirement is dictated by the procedure (see % p. 678).
Pain may be intense intraoperatively, but postoperative pain is generally
much less than for open procedures. Perioperative IV lidocaine infusion
may reduce postoperative pain and bowel dysfunction following
laparoscopic surgery.
• Avoid hypovolaemia as this exaggerates the deleterious CVS effects of
laparoscopy.
• Laparoscopic surgery is associated with a high incidence of nausea
and vomiting. Administer prophylactic antiemetics and prescribe
postoperatively.
• Invasive arterial BP and CVP monitoring may be required for extensive
procedures or for patients with CVS or respiratory compromise.
Causes of hypoxia
• Hypoventilation: inadequate ventilation due to pneumoperitoneum and
head-down positioning.
• Reduced CO: IVC compression, arrhythmias, haemorrhage, myocardial
depression, venous gas embolism, extraperitoneal gas.
• V/Q mismatch: reduced FRC, atelectasis, endobronchial intubation,
venous gas embolism, pulmonary aspiration and rarely pneumothorax.
Laparoscopic GI surgery 677
Postoperative
• At the end of the procedure, encourage the surgeon to expel as much
intraperitoneal gas as possible to reduce postoperative pain.
• LA infiltration of port sites and intraperitoneal administration of LA may
reduce postoperative analgesia requirements.
• Pain varies and is often worst in the first few hours. Shoulder tip pain
due to diaphragmatic irritation may be troublesome but is usually short-
lived. Significant pain extending beyond the 1st day raises the possibility
of intra-abdominal complications.
Special considerations
• An SGA may be used for some laparoscopic procedures. This should
be avoided if the patient has a history of reflux or obesity and the
procedure is anticipated to be difficult or prolonged, especially in the
head-down position.
• Regional anaesthesia is not generally used as the sole anaesthetic
technique because of the high level of block required to cover the
pneumoperitoneum.
678
Laparoscopic cholecystectomy
Procedure Laparoscopic removal of gall bladder
Time 40–80min
Pain ++
Position Supine, 15–20° head-up, slight left tilt
Blood loss Not significant
Practical techniques GA, ETT, IPPV
Preoperative
• Patients are classically, though not always, ‘♀, forty, fair, fat and fertile’.
• Gallstone-associated pancreatitis may make surgery more difficult and
increase the risk of conversion to an open procedure.
• With appropriate patient selection and perioperative techniques, the
procedure can be performed as a day case.
Perioperative
• Avoid gastric distension during bag–mask ventilation which may increase
the risk of gastric injury during trocar insertion. Consider inserting a
gastric tube prior to abdominal access.
• Ensure adequate IV access; haemodynamic changes may be profound
and there is potential for sudden blood loss.
• The combination of pneumoperitoneum and obesity may make
ventilation difficult.
• High risk for PONV. Administer prophylactic antiemetics.
• Short-acting opioids (alfentanil or fentanyl) may counter the
haemodynamic fluctuations and limit postoperative opioid-related side
effects.
• Ask the surgeon to infiltrate the port sites with LA.
• About 5% of cases require conversion to an open procedure.
Postoperative
• Prescribe regular simple analgesics, opioid as required (PRN), antiemetic
and IV fluids until tolerating oral fluids.
Special considerations
• This can be a very stimulating procedure, particularly during diathermy
around the liver.
• LA applied to the gall bladder bed may reduce postoperative analgesic
requirements (e.g. 20mL of 0.25% bupivacaine).
• If conversion to open cholecystectomy, pain can be significant and
a PCA may be required. LA should be infiltrated by surgeons, and a
wound catheter or a subcostal TAP block may be beneficial.
Laparoscopic appendicectomy 681
Laparoscopic appendicectomy
Procedure Resection of appendix
Time 20–40min
Pain ++
Position Supine
Blood loss Not significant
Practical techniques RSI, ETT, IPPV, TAP block
Preoperative
• Patients are often young and fit unless appendix ruptured, in which case
they may be septic and unwell.
• In the unwell patient, resuscitate preoperatively and administer timely
antibiotics.
• Conversion to open appendicectomy is more likely if the appendix is
ruptured.
• Occasionally presents in the elderly. May be the presenting condition of
caecal adenocarcinoma requiring subsequent right hemicolectomy.
Perioperative
• Prophylactic antibiotics.
• RSI. Patients may be unfasted or at risk of aspiration due to delayed
stomach emptying 2° to intra-abdominal pathology.
• Consider NSAID and paracetamol IV.
• Encourage the surgeon to infiltrate LA or perform a right-sided
TAP block.
• Extubate awake (consider left lateral position).
Postoperative
• Prescribe regular simple analgesics and opioid PRN, antiemetics and IV
fluids until tolerating oral fluids.
682
Preoperative
• Patients are usually older adult ♂ or young children.
• Can usually be performed as a day case procedure.
Perioperative
• Inguinal LA field block may be used as a sole technique for surgery or to
complement GA.
• The iliohypogastric and ilioinguinal nerves are easily blocked, 2cm caudal
and medial to the anterior superior iliac spine (ASIS).
• The genitofemoral nerve is located 1–2cm above the midpoint of the
inguinal ligament, deep to the aponeurosis of the external oblique. This
may be left to the surgeon to block, reducing the risk of vascular or
peritoneal puncture.
Special considerations
• Inguinal hernia repair may be performed laparoscopically.
• Patients who are unfit and/or elderly may benefit from hernia repair
under LA. However, some hernias may prove difficult to repair
under LA and a spinal anaesthetic or GA may be preferable to avoid
intraoperative GA conversion. Confirm with the surgeon the suitability
for LA repair.
• A low-dose propofol infusion may be a useful adjunct in cases
performed under LA.
• Other hernia repairs are commonly performed. It is important to
establish the type of hernia repair and anaesthetic requirements. An
incisional hernia repair may vary from a minor repair of a laparoscopic
port site hernia to a complex repair of a large anterior abdominal wall
defect.
Anal and perianal procedures 683
Preoperative
• Assess suitability for SGA/lithotomy/head-down position.
• Consider ETT if the patient is obese or at risk of aspiration.
Perioperative
• Often intensely stimulating procedures, and laryngospasm is common.
Maintain deep anaesthesia and consider short-acting opioids (fentanyl or
alfentanil) and/or N2O.
• Potential for bradycardia or asystole due to increase in vagal tone.
Anticipate and have vagolytic to hand.
• LA infiltration by the surgeon during the procedure often provides
effective pain relief.
Postoperative
• Avoid PR route of drug administration.
• Prescribe regular simple analgesics and opioid PRN.
• Consider aperients for discharge, particularly if opioids used.
Special considerations
• Surgery for pilonidal sinus may require prone positioning. Confirm with
surgeon preoperatively and prepare patient accordingly.
• Avoid spinal anaesthesia followed by immediate head-down tilt.
• A sacral-only spinal block (‘saddle block’) using heavy bupivacaine is a
useful alternative, with little effect on CVS dynamics.
References
1 Roshanov PS, Rochwerg B, Patel A, et al. (2017). Withholding versus continuing angiotensin-
converting enzyme inhibitors or angiotensin II receptor blockers before noncardiac surgery: an
analysis of the vascular events in noncardiac surgery patients cohort evaluation prospective co-
hort. Anesthesiology, 126, 16–27.
2 Sessler D, Bloomstone JA, Aronson S, et al. (2019). Perioperative quality initiative consensus
statement on intraoperative blood pressure, risk and outcomes for elective surgery. Br J Anaesth,
122, 563–74.
3 Myles PS, Bellomo R, Corcoran T, et al. (2018). Restrictive versus liberal fluid therapy for major
abdominal surgery. N Engl J Med, 378, 2263–74.
684
Chapter 26 685
Bariatric surgery
Nicholas Kennedy and Katherine Reeve
Introduction 686
Indications for surgery 687
Risk scoring in bariatric surgery 688
Intragastric balloon insertion/removal 689
Gastric banding 690
Gastric bypass 692
Sleeve gastrectomy 694
68
Introduction
Bariatric surgery describes a variety of procedures that are performed on
people with obesity. Weight loss is achieved by reducing the size of the
stomach with gastric banding, removal of part of the stomach or rerouting
part of the small intestine.
When anaesthetising patients for bariatric surgery, perioperative factors
discussed in % Chapter 2 should be considered.
Bariatric surgery should occur in a multidisciplinary team setting with
rigorous preoperative assessment, intraoperative pathways and consider-
ation for postoperative location and management.
Indications for surgery 687
References
2 Demaria EJ, Murr M, Byrne TK, et al. (2007). Validation of the Obesity Surgery Mortality Risk
Score in a multicenter study proves it stratifies mortality risk in patients undergoing gastric bypass
for morbid obesity. Ann Surg, 246, 578–82.
Intragastric balloon insertion/removal 689
Preoperative
Intragastric balloons are typically inserted in:
• Patients with BMI 25–35kg/m2 as a weight loss adjunct in those who do
not qualify for bariatric surgery. These patients are usually very low risk.
• Very high-BMI patients often >60–70kg/m2, usually with many
significant comorbidities, in whom invasive surgical procedures are
deemed too risky.
Perioperative
• Topical anaesthesia is possible in cooperative patients.
• Low-risk patients are usually suitable for IV sedation, and often an
anaesthetist is not required. Left lateral position is usual for insertion of
the balloon. Balloon removal can be done in a similar fashion.
• IV sedation may be poorly tolerated and risky in high-risk patients
due to hypoventilation, hypoxia and airway obstruction. A GA with
intubation and ventilation may be indicated.
• Very large patients tolerate lying on their side very poorly and are
better dealt with sitting up.
Special considerations
• Intragastric balloon insertion is associated with considerable
nausea immediately postoperatively. Antiemetics should be given
perioperatively and prescribed for the patient to take home. There is
no nausea associated with balloon removal.
• Balloon removal can sometimes be surgically tricky and may take longer.
• Both insertion and removal of balloons can usually be done as day case
procedures, even in high-risk patients.
690
Gastric banding
Procedure Placement of silicone adjustable band around the top of
the stomach to create a small pouch above it. A small in-
jection port is placed SC and connected to the band with
tubing to allow the band to be inflated with 0.9% sodium
chloride to control passage of food past it
Time 45–90min
Pain +
Position Supine, head-up
Blood loss Minimal
Practical GA, ETT, IPPV (with PEEP)
techniques
Preoperative
• Gastric banding is a relatively straightforward laparoscopic procedure
with a very low mortality rate.
• Gastric banding is commonly used for the lower-BMI and lower-risk
bariatric surgical patients. However, some centres use gastric banding
for most of their cases and some patients choose banding, so some
very high-BMI and high-risk patients present.
• Preoperative analgesia with paracetamol is recommended.
Perioperative
• Ensure equipment (e.g. operating table, hover mattress) appropriate for
weight and adequate staff numbers are available.
• Insert two IV cannulae.
• Take extreme care in positioning the patient to avoid damage due to
pressure or overhanging tissue.
• Take precautions to ensure the patient does not slide down the table
when head-up.
• Standard perioperative monitoring. Use forearm BP cuff if upper arm
too large or wrong shape to place a cuff.
• Preoxygenate fully in head-up position.
• Intubation and ventilation are mandatory. Use VT appropriate for IBW
or lean body mass.
• Face mask ventilation can be difficult. Expect rapid desaturation during
apnoea, and have a plan for airway management. RSI is not mandatory.
• Use short-acting anaesthetic agents such as sevoflurane. TIVA with
propofol is a good technique, but correct dosing may be difficult.
• Good NMB is important.
• Antiemetics are important immediately postoperatively to prevent
strain on the band sutures. Give two drugs perioperatively.
• Opioid analgesia is usually required postoperatively; usually fentanyl or
morphine. Limit intraoperative opioid and titrate dosage upwards in
recovery.
• Patients should be woken up and extubated sitting up. Plan for an
electric bed.
• Ensure the surgeon infiltrates all port sites with LA.
Gastric banding 691
Postoperative
• Ensure patients are nursed sitting up in recovery.
• Titrate opioids in recovery.
• Most patients can be safely managed without HDU, but this should be
considered for patients with significant OSA.
• Encourage early mobilisation.
• Thromboprophylaxis as per local protocol.
692
Gastric bypass
Procedure Roux-en-Y gastric bypass. Almost always laparoscopic
Time 90–200min
Pain ++
Position Supine, head-up
Blood loss >500mL, occasionally more due to ooze from splenic
injury or stomach. G&S required
Practical GA, ETT, IPPV (with PEEP)
techniques
Preoperative
• Gastric bypass involves a small bowel anastomosis, formation of a
Roux limb, creation of a gastric pouch and a gastrojejunal anastomosis.
Surgical techniques differ, and it is important to establish in what order
the surgeon will do the procedure.
• Many surgeons ask for a large (typically 34Fr) bougie (or large NGT
or dilator) to be passed orogastrically by the anaesthetist during
pouch formation. This identifies the pouch and prevents stapling of
the oesophagus. The bougie is then pushed distally into the Roux limb
during gastrojejunal anastomosis to allow suturing around it. There are
other techniques involving circular staplers, so ensure you understand
what is used, how it works and when it is needed. Discuss with the
surgeon preoperatively.
Perioperative
• Antiemetics immediately postoperatively to prevent strain on the
anastomosis. Two agents are recommended perioperatively.
Postoperative
• Postoperative CPAP is quite safe. No evidence of damage to the gastric
anastomosis.
Special considerations
• Sometimes surgeons ask for an NGT to be inserted to decompress the
stomach prior to pouch formation. If so, insert it orogastrically, and
remove as soon as the stomach is decompressed. Leaving an NGT in
situ runs the risk of stapling it into the pouch, an avoidable disaster.
• Many surgeons test the gastrojejunal anastomosis for leaks by asking
for an OGT to be passed into the pouch after the anastomosis is
complete. Leak testing is achieved either by injecting air down the
OGT and observing for bubbles in the fluid that has been added via
the laparoscope, or by injecting 760mL of dilute methylthioninium
chloride (methylene blue) into the pouch. Leaks are usually obvious to
see. Beware of the dyed fluid refluxing back into the mouth. Inserting a
sucker into the mouth during this procedure helps prevent the dye from
either being aspirated or refluxing out and onto the patient’s face and
hair! Consider cricoid pressure during this procedure.
Gastric bypass 693
Sleeve gastrectomy
Procedure Stomach divided by stapling to reduce it to about 25%
of its original size. A large portion of the stomach along
the greater curvature is removed through a small inci-
sion. The result is a sleeve or tube-like structure. Almost
always laparoscopic
Time 90–150min
Pain ++
Position Supine, head-up
Blood loss >500mL, occasionally more due to ooze from stomach
staple line. G&S required
Practical GA, ETT, IPPV (with PEEP)
techniques
Preoperative
• Sleeve gastrectomy is becoming increasingly common as the weight loss
procedure of choice.
• Often performed in high-risk patients, instead of a gastric bypass, as it is
an easier and quicker procedure.
• Some surgeons ask for a large (typically 34Fr) bougie (or large NGT
or dilator) to be passed orogastrically by the anaesthetist during the
procedure. This allows the surgeon to staple alongside the bougie,
identify the anatomy and prevent stapling of the oesophagus. Ensure
you understand what is used, how it works and when it is needed.
Discuss with the surgeon preoperatively.
Perioperative
• Antiemetics immediately postoperatively to prevent strain on the
anastomosis. Two agents are recommended perioperatively.
• Avoid hypotension after stomach stapling. This helps identify staple line
bleeding, reducing the risk of postoperative bleeding.
Postoperative
• Postoperative CPAP is safe.
Special considerations
• As per gastric bypass.
Chapter 27 695
Liver procedures
Alwyn Kotze and Nilmini Manawaduge
Anaesthetic management of acute oesophageal bleeding 696
Anaesthesia for transjugular intrahepatic portosystemic shunt
procedure 698
Liver transplantation 699
Hepatic resection 704
69
Salvage interventions
• Interventional radiology may be indicated for patients who rebleed after
endoscopic treatment if appropriate expertise is available. TIPSS is the
treatment of choice.
• Balloon tamponade with an oesophageal and gastric balloon should be
used only where endoscopic and drug treatments have failed. There is
a high risk of fatal complications (aspiration, oesophageal tear/rupture
and airway obstruction) and therefore, this should be used only in
HDU/ICU.
Stabilisation and prevention of rebleeding
• Consider ICU/HDU admission in situations described above or
according to usual physiological criteria.
• Prophylactic β-blockade (propranolol 40–160mg bd) reduces portal
pressure and decreases rebleed rate from 70% to 50%.
698
Liver transplantation
Procedure Transplantation of entire liver
Time 4–10h
Pain Variable, but less than other comparable procedures (e.g.
gastrectomy, thoracotomy). PCA; avoid NSAIDs
Position Supine, one or both arms out
Blood loss Extremely variable. 0–10 000mL, X-match 6 units and con-
sider need for thawing other components before surgery.
Cell salvage and point-of-care coagulation management
vital. Use donated blood and components as necessary
Practical ETT, IPPV
techniques
Introduction
The majority of patients who present for liver transplantation have end-
stage liver disease. The commonest indication worldwide is post-hepatitis
C cirrhosis,12 but alcohol-related cirrhosis and hepatic cancers are the com-
monest aetiologies in the UK.13 Other conditions requiring transplantation
include: 1° sclerosing cholangitis, viral hepatitis (B, C), polycystic liver dis-
ease, 1° biliary cirrhosis and metabolic liver disease.
Transplants are performed semi-electively as graft availability is the rate-
limiting step. Patients with end-stage liver disease are ranked in order of
priority according to a pre-agreed allocation system, then matched to the
1st suitable organ based on considerations including compatibility and graft
size. A minority with fulminant or subacute liver failure are listed ‘super-
urgently’ and receive priority over end-stage liver disease patients. In the
UK, offers are allocated nationally based on the United Kingdom model for
End-Stage Liver Disease (UKELD) and Transplant Benefit Score (TBS) that
considers both risk of death without, and life expectancy gained after liver
transplantation.14
Liver transplantation is performed under GA guided by invasive moni-
toring, with resuscitation facilities (including fluid and donated and/or sal-
vaged blood components) and vasoactive drugs being readily available. Key
anaesthetic objectives are to maintain normal systemic physiology and to
stabilise vital organ function (including graft function) despite unique chal-
lenges at different surgical stages.
Preoperative
Potential recipients are assessed by a multidisciplinary team, including,
as a minimum, a hepatologist, a transplant surgeon and an anaesthetist.
Opinions are sought from others as required (intensivist, dietitian, psych-
ologist, physiotherapist, substance misuse specialist and medical specialties)
before listing. Individual decisions are made based on regularly updated na-
tional selection policies and risk scoring systems (e.g. UKELD/TBS in the
UK or MELD in the US).15,16 Preoperative assessment includes investigation/
treatment of the following.
70
Pre-anhepatic/dissection phase
Bilateral subcostal (‘Mercedes’)/reverse L subcostal incision. The liver,
porta hepatis and surrounding structures are exposed, its anatomy de-
fined and slings placed around the major vessels. Haemorrhage from dis-
section, varices and pre-existing coagulopathy is common. Most bleeding
is venous and can be limited by judicious maintenance of low CVP, as for
liver resection.
Anhepatic phase
Portal and hepatic veins divided. Explantation of native liver and IVC prep-
aration for implantation. New liver inserted. Caval and portal anastomoses
fashioned. Two main techniques are used for hepatectomy and implantation
of the donor liver (Fig. 27.1):
• Cava-cavostomy: division of the hepatic veins with caval preservation,
followed by a ‘piggy back’ implant where the new liver, with its own
attached vena cava, is anastomosed cava-to-cava with the recipient’s
IVC either side-to-side or end-to-side. Surgery is usually performed
with the native vena cava side-clamped, so that venous return is
relatively preserved.
• Classical technique: liver explant with its included portion of the IVC.
Anastomosis of the donor vena cava above and below the liver (‘caval
replacement’). Now less popular as it requires caval cross-clamping
with reduced venous return and consequent refractory hypotension.
Venovenous bypass is employed in some centres to facilitate venous
return (femoral vein to right internal jugular or brachiocephalic vein).
Venovenous bypass uses heparin-bonded extracorporeal circuitry;
systemic anticoagulation is unnecessary.
• Anastomosis fashioned between donor and recipient portal vein.
• While anhepatic, patients with acute liver failure may become
profoundly hypoglycaemic. This is less common in end-stage liver
disease.
• Hypocalcaemia, lactic acidosis, coagulopathy and hypoglycaemia
progressively occur during the anhepatic phase. Regular monitoring and
prompt treatment are essential.
Fig. 27.1 (a) Classical technique; (b) ‘Piggy back’ technique of orthotopic liver
transplantation. This image was published in BJA Education, 17(1), Kashimutt S, Kotze, A.
Anaesthesia for liver transplantation, 35–40, Copyright © The Author 2016.
702
Neohepatic stage
Graft reperfusion, hepatic artery anastomosis and biliary reconstruction.
Reperfusion phase
• Begins with the re-establishment of blood flow through the liver
(portal vein to vena cava). Reperfusion syndrome occurs, with
cytokines release, complement activation and transient reduction
in core temperature. Immediately after reperfusion, there is a rapid
elevation in plasma K+, as it is washed out of the previously ischaemic
graft along with other products of hepatocyte breakdown. At the
start of reperfusion, a bolus dose of 10mmol calcium chloride helps
protect against the cardiac effects of sudden K+ flux. Arrhythmias
are common and cardiac arrest occasionally occurs. Profound
hypotension is common unless the circulation is actively supported with
appropriate fluid and vasoactive drug therapy (e.g. noradrenaline up
to 2 micrograms/kg/min, adrenaline 10 micrograms or phenylephrine
boluses of 500 micrograms to 1mg aliquots). As graft hepatocyte
function returns, electrolyte gradients are restored. Hypotension
at this stage results from myocardial depression and subsequently
vasodilation. Myocardial depression usually resolves within 2 or 3min,
but vasodilation may persist for several hours. In severely ill patients, an
infusion of noradrenaline may subsequently be required. Some centres
use a prophylactic vasopressin analogue, such as terlipressin, before
reperfusion.
• The haemodynamic and biochemical mayhem of reperfusion resolves
rapidly if the graft is functioning. Persisting acidosis or hypocalcaemia are
suggestive of graft 1° non-function, which represents a transplantation
emergency. This may necessitate urgent retransplantation. Early
promising signs of graft function include a rise in body temperature
due to i metabolism, hyperglycaemia from enhanced gluconeogenesis,
normalisation of coagulopathy, bile production and lactate clearance.
Coagulopathy is managed with haemostatic agents (tranexamic acid/
protamine) and blood or blood product transfusion guided by POCT
(TEG®/ROTEM®/point-of-care INR/ABG).
• Following reperfusion, the hepatic artery is reanastomosed, and finally
the bile duct reconstructed by direct duct-to-duct anastomosis/Roux-
en-Y loop.
• Other considerations:
• Induction immunosuppression (e.g. methylprednisolone 0.5–1g) is
administered before graft reperfusion in some centres.
• K+ and Ca2+ should be monitored regularly during surgery and
supplemented, when required, to maintain normal values. Some
centres use Ca2+ infusion (3–5mmol/h) from the dissection phase.
• There is no proven strategy for avoiding renal failure, other than
optimising fluid balance and avoiding nephrotoxins. In patients at
particularly high risk, avoidance of nephrotoxic immunosuppressants
(such as ciclosporin, tacrolimus) in the early postoperative period
may have a role.
Liver transplantation 703
Postoperative
• Patients should be managed in ICU. Early extubation is often feasible
and further facilitates improvement of early graft blood flow due to
negative intrathoracic pressure during SV, reduced ICU stay and d
incidence of nosocomial infections.
• Analgesia: PCA/epidural/paravertebral blocks have all been described.
However, regional techniques are discouraged in many centres because
of coagulopathy, instead relying more on regular systemic analgesics
(opioid PCA, paracetamol) and occasionally wound catheters. Avoid
NSAIDs (interaction with calcineurin inhibitors to induce renal failure).
• Postoperative fluids: maintenance fluid/NG feed at 1.5mL/kg/h.
• Bleeding postoperatively is relatively uncommon.
• Graft 1° non-function/initial poor function due to vascular issues
(hepatic artery thrombosis, portal vein thrombosis) or the graft itself
occurs in up to 5–10% of cases,17 requiring retransplantation.
• Other postoperative problems include sepsis, AKI and acute rejection.
These are managed medically with good results.
• Immunosuppression is usually started with standard triple therapy
(steroid/mycophenolate/tacrolimus) and then tailored to the individual,
guided by unit policy. Other drugs in current use include basiliximab,
ciclosporin, azathioprine and sirolimus.
• Long-term results of liver transplantation are continually improving.
One-year survival figures in major centres now run between 85% and
97% (risk-adjusted),13 with a good long-term quality of life.
704
Hepatic resection
Procedure Resection of liver tissue
Time 2–6h
Pain As for transplantation. Epidural more common
Position Supine, arms out, reverse Trendelenburg position
Blood loss Minimal to 900mL, X-match 5–10 units
Practical techniques ETT, IPPV
References
1 Stanley AJ, Laine L (2019). Management of acute upper gastrointestinal bleeding. BMJ, 364, l536.
2 National Institute for Health and Care Excellence (2012). Acute upper gastrointes-
tinal bleeding overview. [NICE pathway] M http://pathways.nice.org.uk/pathways/
acute-upper-gastrointestinal-bleeding
3 Bennett C, Klingenberg S, Langholz E, et al. (2014). Tranexamic acid for upper gastrointes-
tinal bleeding. Cochrane Database Syst Rev, 11, CD006640. M https://www.cochrane.org/
CD006640/UPPERGI_tranexamic-acid-an-agent-that-promotes-blood-clotting-for-serious-or-
uncontrolled-upper-gastrointestinal-bleeding
4 Vadera S, Yong CWK, Gluud LL, et al. (2019). Band ligation versus no intervention for primary
prevention of upper gastrointestinal bleeding in adults with cirrhosis and oesophageal varices.
Cochrane Database Syst Rev, 6, CD012673.
5 Chana A, James M, Veale P (2016). Anaesthesia for transjugular intrahepatic porto systemic shunt
insertion. BJA Educ, 16, 405–9.
6 DeGasperi A, Corti A, Corso R, et al. (2009). Transjugular intrahepatic portosystemic shunt
(TIPS): the anesthesiological point of view after 150 procedures managed under total intravenous
anesthesia. J Clin Monit Comput, 23, 341–6.
7 Pivalizza EG, Gottschalk LI, Cohen A, et al. (1996). Anesthesia for transjugular intrahepatic
portosystemic shunt placement. Anesthesiology, 85, 946.
8 Duncan IC (2004). The transjugular intrahepatic portosystemic shunt (TIPSS) procedure—a re-
view. SA J Radiol, 8, 4–8.
9 Afdhal NH, Curry MP (2010). Early TIPS to improve survival in acute variceal bleeding. N Engl J
Med, 362, 2421–2.
10 Rajoriya N, Tripathi D (2014). Historical overview and review of current day treatment in the
management of acute variceal haemorrhage. World J Gastroenterol, 20, 6481–94.
11 García-Pagán JC, Caca K, Bureau C, et al. (2010). Early use of TIPSS in patients with cirrhosis and
variceal bleeding. N Engl J Med, 362, 2370–9.
12 NHS Blood and Transplant (2012). Guideline for referral for liver transplant assessment. M http://
odt.nhs.uk/pdf/advisory_group_papers/LAG/referral_for_transplantation.pdf
13 NHS Blood and Transplant (2019). Annual report on liver transplantation. Report for 2018/2019
(1 April 2009–31 March 2019). M https://nhsbtdbe.blob.core.windows.net/umbraco-assets-
corp/16782/nhsbt-liver-transplantation-annual-report-2018-19.pdf
14 Trotter JF (2017). Liver transplantation around the world. Curr Opin Organ Transplant, 22, 123–7.
15 Kashimutt S, Kotze A (2017). Anaesthesia for liver transplantation. BJA Educ, 17, 35–40.
16 Deshpande R, Chadha RM (2018). Anaesthesia for orthotopic liver transplantation.
Anaesthesia Tutorial of the Week 377. M https://resources.wfsahq.org/atotw/
anaesthesia-for-orthotopic-liver-transplantation/
17 Pretto EA, Biancofiore G, DeWolf A, et al. (2015). Oxford Textbook of Transplant Anaesthesia and
Critical Care. Oxford: Oxford University Press.
18 Hartog A, Mills G (2009). Anaesthesia for hepatic resection surgery. Contin Educ Anaesth Crit Care
Pain, 9, 1–5.
19 Egger ME, Gottumukkala V, Wilks JA, et al. (2017). Anesthetic and operative considerations for
laparoscopic liver resection. Surgery, 161, 1191–202.
20 Cheng F, Yang Z, Zeng CJ, et al. (2018). Anaesthetic management of modified ex vivo liver resec-
tion and autotransplantation. Ann Transplant, 23, 274–84.
21 Kelliher L, Jones C, Dickinson M, et al. (2013). Epidural anaesthesia and analgesia for liver resec-
tion. Anaesthesia, 68, 975–6.
708
Chapter 28 709
Endocrine surgery
Pete Ford and Peter Valentine
Thyroidectomy 710
Parathyroidectomy 714
Phaeochromocytoma 716
Carcinoid tumours 720
071
Thyroidectomy
Procedure Removal of all or part of the thyroid gland
Time 1–2h, depending on complexity
Pain +/++
Position Shoulder bolster and head ring. Head-up tilt
Blood loss Usually minimal. Potentially major if retro-
sternal extension
Practical techniques IPPV + reinforced ETT
General considerations
(See also % pp. 223–5.)
• Complexity can vary from removal of a thyroid nodule to removal of a
long-standing retrosternal goitre to relieve tracheal compression.
• Retrosternal goitre is usually excised through a standard incision, but
occasionally a sternotomy is required.
• Recurrent laryngeal nerves and parathyroid glands may be damaged or
removed.
• Straightforward unilateral surgery can be performed under superficial
and deep cervical plexus block, but GA is usual (see % p. 1118).
Preoperative
• Ensure that the patient is as near euthyroid as possible (see %
pp. 223–5).
• Check for complications associated with hyperthyroidism: AF,
tachycardia, proptosis.
• Acute preparation of thyrotoxic patients involves iodine and
glucocorticoid—both inhibit the conversion of T4 to T3 and narrow the
window (7–10d) for surgery, necessitating joint management with the
surgeon and endocrinologist.
• Check biopsy histology for malignancy.
• Ask about duration of goitre. Long-standing compression of the trachea
may be associated with tracheomalacia.
• Ask about positional breathlessness. Assess the airway.
• Examine the neck. How big is the goitre? Consistency: malignant goitres
are hard. Can you feel below the gland (retrosternal spread)? Is there
evidence of tracheal deviation (check the radiograph)?
• Look for signs of SVC obstruction: distended neck veins that do not
vary with the respiratory cycle.
• Listen for stridor.
• Check the range of neck movements preoperatively, and do not extend
them outside of their normal range during surgery.
• Preoperative paracetamol/NSAIDs (PO or PR) help postoperative pain
control.
Investigations
• FBC, U&E, Ca2+ and thyroid function tests are routine.
• Chest radiograph. Check for tracheal deviation and narrowing. Thoracic
inlet views may be necessary if retrosternal extension is suspected,
Thyroidectomy 711
Postoperative stridor
• Haemorrhage with tense swelling of the neck. Remove clips from the
skin, and sutures from the platysma/strap muscles to remove the clot.
In extremis, this should be done at the bedside. Otherwise return to
theatre without delay. A haematoma will affect lymphatic and venous
drainage of the upper airway, causing laryngeal and pharyngeal oedema.
Removing the haematoma will not always restore airway patency
immediately. IV dexamethasone and nebulised adrenaline may help
acutely.
• Tracheomalacia. Long-standing large goitres may cause tracheal collapse.
This is a very rare complication. Immediate reintubation, followed by
tracheostomy, may be necessary.
• Bilateral recurrent laryngeal nerve palsies. This may present with
respiratory difficulty immediately postoperatively or after a variable
period. Stridor may only occur when the patient becomes agitated.
Assess by fibreoptic nasendoscopy. May require tracheostomy.
Other postoperative complications
Hypocalcaemia
• Hypocalcaemia from parathyroid removal is rare. Serum Ca2+ should be
checked at 24h, and again daily if low.
• Presentation: may present with signs of neuromuscular excitability,
tingling around the mouth or tetany. May progress to fits or ventricular
arrhythmias.
• Diagnosis: carpopedal spasm (flexed wrists, fingers drawn together)
may be precipitated by cuff inflation (Trousseau’s sign). Tapping over the
facial nerve at the parotid may cause facial twitching (Chvostek’s sign).
Prolonged QT interval on ECG.
• Treatment: serum Ca2+ below 2mmol/L should be treated urgently with
10mL of 10% calcium gluconate over 3min plus alfacalcidol 1–5g PO
(calcium gluconate is preferable, as calcium chloride will cause tissue
necrosis if extravasation occurs). Check the level after 4h, and consider
Ca2+ infusion if still low. If hypocalcaemic, but level above 2mmol/L,
treat with PO Ca2+ supplements (see also % p. 227).
Thyroid crisis
(See % pp. 224–5.)
Pneumothorax
Pneumothorax is possible if there has been retrosternal dissection.
Further reading
Dempsey GA, Snell JA, Coathup R, et al. (2013). Anaesthesia for massive retrosternal thyroidectomy
in a tertiary referral centre. Br J Anaesth, 111, 594–9.
Cook TM, Morgan PJ, Hersch PE (2011). Equal and opposite expert opinion. Airway obstruction
caused by a retrosternal thyroid mass: management and prospective international expert opinion.
Anaesthesia, 66, 828–36.
Farling PA (2000). Thyroid disease. Br J Anaesth, 85, 15–28.
471
Parathyroidectomy
Procedure Removal of solitary adenoma or four glands for
hyperplasia
Time 1–3h
Pain +/++
Position Shoulder bolster and head ring. Head-up tilt
Blood loss Usually minimal
Practical techniques IPPV + ETT
General considerations
(See % p. 226.)
• Usual indication for operation is 1° hyperparathyroidism from
parathyroid adenoma.
• With preoperative localisation, removal of simple adenoma has been
described using sedation and LA. GA is more usual.
• Carcinoma may require en bloc dissection.
• Total parathyroidectomy may also be performed in 2°
hyperparathyroidism associated with CKD.
• Hypercalcaemia may produce significant debility, particularly in the
elderly.
Preoperative
Hypercalcaemia is usual. With moderate elevation, ensure adequate hydra-
tion with 0.9% sodium chloride. Levels over 3mmol/L should be corrected
before surgery, as follows:
• Urinary catheter
• One litre of 0.9% sodium chloride in the 1st hour, then 4–6L over 24h
• Pamidronate 60mg in 500mL of 0.9% sodium chloride over 4h
• Watch for fluid overload—CVP measurement may be necessary.
Monitor electrolytes, including Mg2+, phosphate and K+.
Severe hypercalcaemia may occasionally necessitate emergency surgery. It
may cause arrhythmias and may antagonise the effects of NDMRs.
• Preoperative imaging using ultrasound and technetium-99m sestamibi
scanning may be used to localise parathyroid adenomas, allowing a
minimal access or targeted approach with a 2cm incision over the
suspected gland.
• 2° hyperparathyroidism occurs 2° to low serum Ca2+ in CKD. In this
situation:
• Total parathyroidectomy may be required. Control afterwards is
easier if no functioning parathyroid tissue is left.
• Dialysis will be required preoperatively.
• The risk of bleeding is i.
• Alfacalcidol is usually started preoperatively.
• 1° hyperparathyroidism has been associated with an i risk of death
from CVS disease, hypertension, LVH, valvular and myocardial
calcifications, impaired vascular reactivity, alterations in cardiac
conduction, impaired glucose metabolism and dyslipidaemia. PTH has
serious consequences on cardiac function in renal failure.
Parathyroidectomy 715
Phaeochromocytoma
Procedure Removal of one or two adrenals or extra-adrenal tumour
Time 1–2h open, possibly longer if laparoscopic
Pain +/++ (depending if open or laparoscopic)
Position Lateral or supine for open, lateral for laparoscopic
Blood loss Variable
Practical IPPV + ETT, arterial and CVP lines ± CO monitor
techniques
Perioperative
• Laparoscopic or open adrenalectomy through a midline, transverse or
flank incision (introduction of gas for laparoscopic resection can result
in hypertension in normal subjects, and this may be exaggerated in
patients with phaeochromocytomas).
• Premedication PRN (e.g. temazepam 20–30mg).
• Monitoring to include direct BP and CVP (triple lumen to allow drug
infusions). Consider CO monitoring in patients with CVS disease and
catecholamine cardiomyopathy.
• Large-bore IV access.
• Monitor and maintain temperature, particularly during laparoscopic
resection which can be prolonged.
• Induction: avoid agents that release histamine, and thus catecholamines
(use propofol, alfentanil or remifentanil and vecuronium or
rocuronium).
• Hypotension is unlikely at induction and can be treated with either
ephedrine, metaraminol or phenylephrine. Due to preoperative α-
blockade, doses will likely need to be i. Rarely, dilute adrenaline may be
required.
• Maintenance: if using volatile, use isoflurane or sevoflurane. Desflurane
should be avoided, as it can cause sympathetic nervous system
activation.
• Consider epidural with opioid and LA for open procedures
(sympathetic blockade will not prevent catecholamine-induced
vasoconstriction); otherwise fentanyl/alfentanil/remifentanil until
tumour removal, when morphine (10–20mg) can be substituted.
• Nicardipine and Mg2+ are also useful (block catecholamine release,
block receptors and provide direct vasodilation and possibly myocardial
protection).
• Mg2+ is started prior to induction, given as a bolus of 2–4g, and then
continued at a rate of 1–2g/h. It is normal for the patient to feel
nauseated with the Mg2+ bolus.
• Surges in BP can occur at induction, with formation of the
pneumoperitoneum and with tumour handling. The fluctuations in
BP tend to be transient, and medication needs to respond in a similar
fashion. Hypertension can be treated in a number of ways: intermittent
2g boluses of Mg2+, boluses of remifentanil, phentolamine, sodium
nitroprusside or labetalol (if associated with tachycardia).
• Control HR at <100bpm with the β-blocker of choice.
• Once the tumour is resected, BP takes several minutes to decline.
Prevent hypotension by ensuring an adequate preload. Maintain a high
CVP of 10–15mmHg. Several litres of a crystalloid may be needed.
• Hypotension following resection can be due to low CO or a low
SVR. Treat the former with low-dose adrenaline, and the latter
with metaraminol or phenylephrine. Vasopressin has been used in
resistant hypotension. Terlipressin 1mg bolus, followed, if required, by
vasopressin, starting at 0.04 units/min, then titrated to effect.
• It is unusual to require inotropic support by the time the patient is ready
to leave theatre, unless there are coexisting medical problems.
Phaeochromocytoma 719
Postoperative
• Patient should be nursed in ICU/HDU for 12h.
• Monitor blood glucose. The withdrawal of catecholamine excess can
lead to severe hypoglycaemia.
• If both adrenals are resected, the patient will require steroid support
immediately. Hydrocortisone 100mg bolus in theatre, decreasing to
maintenance dose after surgical stress. Fludrocortisone 0.1mg daily may
be commenced with oral intake.
• Even when only one adrenal is removed, patients may occasionally be
relatively hypoadrenal and require support. If this is suspected (e.g.
unexpectedly low BP), a small dose of hydrocortisone (50mg) will do
no harm, while the result of cortisol estimation is awaited.
Special considerations
Pregnancy
• There are many reports of the combination of a newly diagnosed
phaeochromocytoma and pregnancy. Overall mortality is up to 17%.
• Phenoxybenzamine and metoprolol are safe.
• If phaeochromocytoma is diagnosed before mid trimester, it should be
resected at this stage.
• There is high mortality associated with normal delivery; consider lower-
segment Caesarean section (LSCS), with or without resection of the
phaeochromocytoma at the same procedure.
Management of an unexpected phaeochromocytoma
• Any patient who has unexplained pulmonary oedema, hypertension or
severe unexpected hypotension should prompt consideration of the
diagnosis; however, it can be very difficult. There is no quick available
test to support the diagnosis in the acute situation.
• Once the diagnosis has been considered, if possible, surgery should be
discontinued to allow acute treatment, investigation and blockade prior
to definitive surgery. Attempts to remove the tumour during a crisis
may result in significant morbidity, or even mortality.
• Treatment acutely should consist of vasodilators and IV fluid; this
may be counterintuitive in a patient with severe pulmonary oedema.
The circulating volume in patients with phaeochromocytoma may be
markedly reduced, and vasodilation will result in a profound drop in BP.
GTN can usually be successfully titrated in this situation.
• Patients who present with hypotension have an acutely failing heart due
to profound vasoconstriction. These are the most difficult patients in
whom to make the diagnosis and to treat. Additional catecholamines in
this situation merely fuel the fire but are difficult to resist. The mortality
rate is very high.
Further reading
Subramaniam R (2011). Phaeochromocytomas—current concepts in diagnosis and management.
Trends Anaesth Crit Care, 1, 104–10.
James MFM (2010). Adrenal medulla: the anaesthetic management of phaeochromocytoma. In:
James MFM (ed). Anaesthesia for Patients with Endocrine Disease. Oxford: Oxford University Press;
pp. 149–69.
Prys-Roberts C (2000). Phaeochromocytoma—recent progress in its management. Br J Anaesth,
85, 44–57.
O’Riordan JA (1997). Pheochromocytomas and anesthesia. Int Anesthesiol Clin, 35, 99–127.
720
Carcinoid tumours
Carcinoid tumours are derived from argentaffin cells and produce pep-
tides and amines. They occur in the GI tract (75%), bronchus, pancreas and
gonads. Surgery may be performed to remove the 1° tumour and debulk
liver metastases in carefully selected patients.
Conduct of anaesthesia in patient with carcinoid syndrome
Best managed by centres familiar with the difficulties. Major complications
anticipated include profound swings in BP, fluid and electrolyte shifts and
bronchospasm.
• Preoperatively treat symptomatically with antidiarrhoeal agents,
bronchodilators, correction of dehydration/electrolyte imbalance and
treatment of heart failure.
• Preoperatively, some centres will use continuous infusions of octreotide
50–100 micrograms/hour; others give 100 micrograms SC tds. Although
schedules vary from weeks (SC) to hours (IVI), both are only of benefit
even if given before surgery to suppress basal amine turnover.
• Avoid factors that may trigger carcinoid crises: anxiety and drugs that
release histamine, e.g. morphine.
• Premedication: anxiolytic (benzodiazepine) and octreotide 50–500
micrograms SC 1h preoperatively, if not already treated; otherwise
continue with preoperative regime.
• Monitoring should include invasive BP preinduction (both induction
and surgical manipulation of the tumour can cause large swings), CVP,
regular blood glucose and blood gases. CO monitoring will guide fluid
therapy and help in managing hormone-induced preload and afterload
variations, particularly if cardiac complications present.
• Right heart failure increases hepatic venous congestion which
predisposes to bleeding in liver surgery. Limiting IV fluid initially in these
patients and permitting controlled hypotension may reduce bleeding.
• Consider an epidural. Benefits include a reduced risk of a carcinoid crisis
with d stress response 2° to good analgesia; however, low doses of LA
should be used.
• Give octreotide 100 micrograms IV diluted to 10 micrograms/mL,
slowly at induction. Prevent pressor response to intubation.
• Suxamethonium has been used safely for RSI, although fasciculations
may theoretically stimulate hormone release by increasing the intra-
abdominal pressure, so consider rocuronium.
• Maintenance: both TIVA and inhalation techniques have been used
successfully.
• Octreotide (10–20 microgram boluses IV) to treat severe hypotension.
• Avoid all histamine-releasing drugs (atracurium, morphine) and
catecholamines (release serotonin and kallikrein, which activate
bradykinins).
• Labetalol, esmolol or ketanserin (5-HT2 receptor blocker) can be used
for hypertension.
• ICU or HDU is required.
Carcinoid tumours 721
Urological surgery
Mark Catolico
Cystoscopic procedures 724
Transurethral resection of the prostate 728
Transurethral resection of bladder tumour 731
Open simple prostatectomy and radical prostatectomy 732
Nephrectomy and partial nephrectomy 733
Radical cystectomy 735
Robot-assisted laparoscopic prostatectomy 737
Percutaneous stone removal 739
Extracorporeal shock wave lithotripsy 740
Testicular surgery 741
Jeremy Campbell
Renal transplant 742
See also
% Circumcision/hypospadias repair p. 941
% Orchidopexy p. 942
724
Cystoscopic procedures
• A large number of urological procedures are performed via the
cystoscope. These include cystoscopy, transurethral resection of the
prostate (TURP), bladder neck incision, transurethral resection of
bladder tumour, ureteroscopy and/or stone removal or stent insertion.
• The majority of patients are undergoing procedures for benign prostatic
hypertrophy or carcinoma of the bladder. The incidence of both these
conditions increases markedly over 60y, and bladder cancer is smoking-
related, so patients frequently have CAD and COPD.
• FBC, creatinine and electrolytes should be checked preoperatively,
because bladder cancers can bleed insidiously. Both bladder cancer and
benign prostatic hypertrophy can cause an obstructive uropathy/renal
impairment, and drugs and the technique should be chosen accordingly.
• Flexible cystoscopy is largely used for diagnostic purposes, does
not require full bladder distension and can normally be performed
under LA. Biopsies can be taken this way, with only a small amount
of discomfort, and skilled surgeons can perform retrograde ureteric
catheterisations. Occasional patients insist on sedation/GA for flexible
cystoscopy. Midazolam or propofol is ideal.
• Rigid cystoscopy requires GA, due to the scope diameter and the use
of an irrigating solution to distend the bladder and allow visualisation
of the surgical field. If large volumes of irrigant are absorbed, systemic
complications due to fluid overload can result (see % pp. 729–30).
• Spinal anaesthesia works well for rigid cystoscopic procedures and is
commonly used for TURP. Sensory supply to the urethra, prostate,
bladder neck and bladder mucosa is from S2 to S4. Pain from bladder
distension, however, is carried by T10–L2, so a higher block is required.
Many patients will request sedation. In the elderly population, 1–2mg of
midazolam is usually adequate. Higher doses may result in loss of airway
control, confusion and restlessness. A low-dose propofol infusion is an
alternative. Spinal anaesthesia is advantageous for patients with severe
COPD, as long as the patient can lie flat without coughing.
• Either hyperbaric or isobaric bupivacaine can be used. Hyperbaric
bupivacaine usually produces a higher block than the isobaric solution,
especially when the injection is performed with the patient in the lateral
position and then turned supine; 2.5–3mL of ‘heavy bupivacaine’ 0.5%
usually gives a block to T10. Do not tilt the patient head-down, unless
the block is not sufficiently high.
• Other short-acting drugs increase options for effective ambulatory
spinal anaesthesia (level T10 and below); 40–50mg (4–5mL) of plain
chloroprocaine 1% for procedures of up to 40min, or 40–60mg (2–
3mL) of hyperbaric prilocaine 2% for procedures lasting up to 90min.
These options provide more predictable spinal anaesthesia, compared
with bupivacaine, and quicker readiness for discharge (see % Fig. 18.2).
• Patients with chronic chest disease tend to cough on lying flat. During
surgery under regional block, coughing can seriously impair surgical
access. Sedation can help to reduce the cough impulse.
• Patients with spinal cord injuries (see % pp. 303–8) often require
repeated urological procedures. Bladder distension during cystoscopy is
very stimulating and prone to cause autonomic hyperreflexia, so a GA
or spinal is advisable—check previous anaesthetic charts.
Cystoscopic procedures 725
Preoperative
• Patients are frequently elderly with coexisting disease and on multiple
medications.
• Check creatinine and serum Na+; suggest postponing surgery if Na+ is
significantly low, as this is likely to fall further with absorption of irrigant.
• Heart failure or uncontrolled AF is a particular risk due to fluid
absorption. Aim for optimal medical control preoperatively.
• Assess the mental state and communication—spinal anaesthesia is
difficult if the patient is confused or deaf.
Perioperative
• Insert a large cannula, and use warmed IV fluids.
• Spinal anaesthesia: in theory, it is easier to detect changes in the mental
state and signs of fluid overload (see % pp. 729–30); shown in some,
but not all, studies to reduce blood loss; 2.5–3mL of bupivacaine (plain
or hyperbaric) or consider alternative LA solutions (see % Fig. 18.2);
frequent BP check—hypotension unusual with the above doses but can
occur suddenly; check BP at the end when the legs are down (unmasks
hypotension).
• GA: consider intubation if the patient is very obese or has a history of
reflux; intraoperative fentanyl or morphine plus multimodal analgesia
(paracetamol, NSAID and tramadol/codeine) are usually adequate;
unusual to need opioids postoperatively.
• Blood loss can be difficult to assess. In theory, can be calculated from
measuring Hb and the volume of discarded irrigation fluid. In practice,
it is more common to visually assess the volume and colour, but this
can be misleading. Checking the patient’s Hb with a bedside device (e.g.
HemoCue®) is useful. Blood loss is generally related to the size and
weight of prostatic tissue excised (normally 15–60g), the duration of
resection and the expertise of the operator.
• Antibiotic prophylaxis usually required.
• Obturator spasm (see % p. 731).
• Fluid therapy: crystalloid can be used initially. Bear in mind that a
significant volume of hypotonic irrigating fluid may be absorbed, so do
not give excessive volumes and never use glucose. Be ready to transfuse
if the Hb falls below the transfusion trigger.
Transurethral resection of the prostate 729
Postoperative
• Bladder irrigation with 0.9% sodium chloride via a three-way catheter
continues for 724h, until bleeding is reduced; inadvertent slowing of
irrigation can lead to clot retention.
• There is generally little pain, but discomfort from the catheter or
bladder spasm may be a problem (see % p. 725).
• Severe pain suggests clot retention, bladder spasm or bladder
perforation (see % p. 725).
• Clot retention can give a very distended painful bladder and vagal
symptoms. It requires washout, sometimes under anaesthetic.
• Bleeding can continue and require further surgery; resuscitation may be
necessary.
• Measure FBC, creatinine and electrolytes the day following surgery.
Special considerations
• Hypothermia may result when large volumes of irrigation fluid are used
(the fluid should be warmed to 37°C).
• If the prostate is very large (>100g), a simple open prostatectomy may
carry fewer complications.
• The risk of complications increases with resection times of >1h. If
a resection is likely to take longer than an hour, consider limiting the
resection to one lobe only, leaving the other to be done at a later date.
• Bipolar TURP has been shown to reduce the overall complication rate,
transfusion rate and TURP syndrome.
Laser TURP and transurethral vaporisation of the prostate
• Several ‘minimally invasive’ techniques using lasers and other forms
of heat have been developed which reduce the prostate size.
These generally cause less bleeding and absorption of fluid so are
sometimes chosen for patients perceived to be at higher risk from
conventional TURP.
• Laser vaporisation techniques can be done under LA on an outpatient
basis. These may be preferred in patients on anticoagulation because of
their haemostatic effect on prostate tissue.
Brachytherapy for localised prostate carcinoma
• This consists of insertion of radioactive pellets through rods positioned
in the prostate under ultrasound control. This is usually done outside of
theatre in the radiotherapy department.
• The patient may require two or more procedures in the same day.
Repeated GAs are possible, but a spinal catheter topped up before each
procedure works well. Consider risks of remote site anaesthesia.
• For a single treatment, a spinal, using 0.5% bupivacaine with fentanyl 15
micrograms, is effective and allows safe transfer to radiotherapy.
TURP syndrome
• A combination of fluid overload and hyponatraemia, which occurs when
large volumes of irrigation fluid are absorbed via open venous sinuses.
• Classic TURP uses monopolar cautery. Therefore, non-conductive
(non-electrolyte) irrigation fluid must be used to allow diathermy
current to be focused and avoid thermal burns. The most commonly
used irrigant is glycine 1.5% in water, which is hypotonic (osmolality
220mmol/L).
730
Preoperative
• Slow-growing tumours of the bladder epithelium are common in the
elderly. They are best managed by periodic resection of the tumours
within the bladder, rather than aggressive complete removal.
• Commonest in smokers; check for CAD and COPD.
• Check Hb; chronic blood loss is common.
• Check renal function.
• Refer to previous anaesthetic charts; many patients have repeated
surgery.
Perioperative
• Obturator spasm occurs when the obturator nerve, which runs
adjacent to the lateral walls of the bladder, is directly stimulated by
the diathermy current. It causes adduction of the leg and can seriously
impair surgical access and increase the risk of bladder perforation. It can
usually be controlled by reducing the diathermy current or intermittent
use of NMBAs.
• Antibiotic prophylaxis.
Postoperative
• Pain can be a problem with extensive resections; NSAIDs are useful
(check renal function) and oral opioids may be needed.
• Bladder spasm is common (see % p. 725).
Special considerations
• If using a spinal anaesthetic, ensure block to above T10 (see % pp. 724–6).
732
Preoperative
• Simple prostatectomy is usually carried out in elderly men and can be
treated as TURP.
• Radical: patients are selected if relatively young and medically fit.
• Check renal function.
• Consider COX-2 selective inhibitors, gabapentinoids and
dexamethasone as preoperative analgesic interventions.
• Consider HDU bed for radical prostatectomy, depending on local
practice and medical factors.
Perioperative
• Prepare for major blood loss with a large IV cannula, blood warmer,
forced air warming blanket, etc.
• A Pfannenstiel-type incision is used for simple, and lower midline for
radical, prostatectomy.
• Consider using an arterial line and CVP line or CO monitoring,
particularly in patients with CVS disease.
• Ensure blood is available, and reorder intraoperatively, as necessary.
• Cell salvage techniques can be useful where blood loss is expected to
be substantial (radical prostatectomy).
• Air embolism is a possible complication.
• Epidural analgesia is no longer recommended (see the European Society
of Regional Anaesthesia and Pain Therapy’s PROSPECT reference, %
Further reading, p. 744).
• Consider using remifentanil infusion intraoperatively.
Postoperative
• For open prostatectomy, LA wound infiltration administered at the end
of surgery is recommended. Lidocaine infusion is recommended for
radical prostatectomy. PCA may be a useful alternative.
Nephrectomy and partial nephrectomy 733
Preoperative
• Ascertain the pathology and surgical incision planned before deciding on
the technique and monitoring.
• Check Hb; renal tumours can cause anaemia without blood loss.
• Check BP and renal function; ‘non-functioning’ kidney or renovascular
disease is associated with renal impairment and hypertension.
• Consider cell salvage intraoperatively.
• Check serum electrolytes; renal tumours can cause inappropriate ADH
secretion.
• Check the chest radiograph if there is a tumour; there may be
metastases, pleural effusions, etc.
• Radiofrequency ablation (RFA) is an option for patients with small
cortical tumours (<3cm), and those who present a high surgical risk or
have compromised renal function.
Perioperative
• Nephrectomy and partial nephrectomy can be carried out via open,
laparoscopic or robot-assisted laparoscopic approaches.
• For large tumours and polycystic kidneys, surgical practice in the UK
is an open laparotomy via a paramedian or transverse incision for a
tumour, and a loin incision with a retroperitoneal approach for other
pathologies or donor nephrectomy.
• Loin incision requires the ‘kidney position’, i.e. lateral with the patient
extended over a break in the table. A marked fall in BP is common on
assuming this position due to reduced venous return from the legs and
possible IVC compression. Further compression during surgery may
result in a severe reduction in venous return and CO.
• Ask the surgeon about the predicted extent of surgery; a large tumour
may necessitate extensive dissection, possibly via a thoracotomy, or
opening of the IVC to resect tumour margins, in which case sudden,
torrential blood loss is possible. Occasionally, the IVC is temporarily
clamped to allow dissection and to control haemorrhage; this gives a
sudden fall in CO. Inform the surgeon if BP falls suddenly; have fluids
and blood checked and available to infuse immediately under pressure,
and have a vasoconstrictor or an inotrope, such as metaraminol or
ephedrine, prepared.
734
• Use large IV cannulae, blood warmer, central venous line and arterial
line if the procedure is anything other than an uncomplicated, non-
malignant nephrectomy or a small isolated tumour.
• If an epidural is used, a high block will be required postoperatively, but
use it cautiously intraoperatively until bleeding is under control.
Postoperative
• All approaches are painful; epidurals are useful but need to cover up to
T7/8 for a loin incision. Rectus sheath catheters may be useful for the
anterior approach. PCA or an opioid infusion is an alternative.
• Intercostal blocks will give analgesia for several hours after a loin
incision.
• Wound infiltration catheters have also proved very effective.
• NSAIDs are useful if renal function is good postoperatively and the
patient is not hypovolaemic. Use cautiously.
• Monitor hourly urine output.
Partial nephrectomy
• Recommended as the preferred option in organ-confined tumours
measuring up to 7cm.
• Blood loss can be large, as vessels are more difficult to control.
• Some surgeons suggest the administration of mannitol 12.5g,
furosemide 10mg and/or heparin 3000 units before clamping of the
renal artery in an attempt to maintain renal perfusion and minimise
ischaemia. Cooling with ice can also be used.
• If the renal function is markedly impaired preoperatively, optimisation
of fluid balance throughout the perioperative period is extremely
important. Admission to HDU postoperatively should be considered.
Radical cystectomy 735
Radical cystectomy
Procedure Excision of bladder plus urinary diversion procedure (e.g.
ileal conduit) or neobladder reconstruction (orthotopic
bladder formation)
Time 3–5h (longer with bladder reconstruction)
Pain ++++
Position Lithotomy plus head-down
Blood loss 700 to >3000mL, X-match 4 units, use cell salvage
Practical ETT, IPPV, arterial line ± oesophageal Doppler/CVP ±
techniques rectus sheath catheters/PCA/epidural
Preoperative
• Consider the use of an ‘enhanced recovery pathway’.
• Check for IHD/COPD, plus renal function and FBC.
• Book an HDU bed, depending on local practice/coexisting problems.
• Ensure thromboprophylaxis is prescribed.
Perioperative
• The commonest postoperative problem is prolonged ileus, which
contributes significantly to morbidity and mortality, and several of the
measures recommended are thought to reduce its incidence.
• Prepare for major blood loss; large IV cannulae, blood warmer, CVP or
oesophageal Doppler CO and direct arterial monitoring are routine.
Ensure blood is available, and reorder intraoperatively, as necessary.
Consider autotransfusion intraoperatively. If blood salvage is used,
discontinue it when the bowel is opened.
• If rectus sheath catheters are to be used, insert after induction. Surgical
incision is subumbilical midline and does not permit easy placement of
catheters during surgery.
• Remifentanil infusion gives stable anaesthesia and controllable BP; mild
hypotension can aid surgery by reducing blood loss.
• Epidurals are now used infrequently, but if placed, use cautiously
intraoperatively; there will be plenty of time after the main blood-losing
episode to establish an adequate block.
• Take measures to prevent heat loss, e.g. forced air warming blanket.
• Antibiotic prophylaxis as for bowel resection.
• Use of NGTs is now rare; ask the surgeon if specifically required.
• Blood loss can be insidious from pelvic venous plexuses; consider
weighing swabs.
• Air embolism is a possible complication, as in any major pelvic surgery.
Postoperative
• Rectus sheath catheters (for up to 5d), with or without a PCA,
have proven very effective. Visceral pain tends to last for 24–36h
postoperatively, requiring parenteral opioids. This technique enables
early mobilisation, return of bowel function and d postoperative ileus/
length of hospital stay. There is some evidence that anastomotic leak
is i with the use of NSAIDs, so use cautiously after checking the renal
function.
736
Robot-assisted laparoscopic
prostatectomy
(See % pp. 480–2.)
Preoperative
• The commonest use of surgical robots to date is in urology, mostly for
radical prostatectomy (robot-assisted laparoscopic prostatectomy).
• Advantages to the patient may include a reduction in blood loss, pain
and length of stay ± a reduced incidence of incontinence and erectile
dysfunction.
• Advantages to the surgeon over conventional laparoscopy include
provision of 3D vision, filtration of any hand tremor, scaling of hand
movements, greater range of movements within the patient and a
comfortable and stable position.
Perioperative
• Positioning of the patient is important. Long operative times with steep
head-down tilt have been associated with:
• Neurapraxia (especially brachial). Take care with positioning, and use
shoulder brace. Do not hyperextend the legs in lithotomy.
• Facial/airway oedema and stridor.
• Acid burns to eyes and oral ulceration due to reflux of gastric acid.
Premedicate with a PPI (omeprazole 40mg); consider an OGT (not
NGT due to epistaxis risk) and throat pack, and protect the eyes with
lubricating ophthalmic ointment/pads.
• i ICP (exacerbated by hypercapnia) and i IOP (beware patients with
glaucoma).
• Insert ETT as short as possible (risk of endobronchial intubation), and
tape in position to minimise cerebral venous obstruction.
• Access to the patient is poor, so ensure reliable, large-bore venous
access on the left side because of robot arm positioning.
• Robotic equipment is locked in position once inserted into the
abdomen, so any inadvertent patient movement can cause grave
surgical complications. A remifentanil infusion works well and allows
intermittent boluses of muscle relaxant only as required.
• Avoid using N2O.
• Communicating with the surgeon may be difficult due to the bulk and
space required for the equipment. The team needs to be familiar with
the audio equipment and also able to undock and remove the robot
quickly in case of an emergency requiring resuscitation.
• Large urine output can interfere with the surgical field; use minimal IV
fluid (<1000mL) until anastomosis is complete (may also reduce the risk
of airway oedema).
738
Postoperative
• Perform leak test prior to extubation to assess airway swelling.
• Cerebral oedema may be problematic. A short-acting volatile agent
with remifentanil allows rapid assessment of the conscious level
postoperatively. Most patients experience a degree of cerebral irritation
or agitation initially on wakening.
• Postoperative pain is considerably less than for open procedures but
can still be severe enough to require opioid analgesia for a short period,
in addition to simple analgesics. In some institutions, use of intrathecal
diamorphine up to 1mg is commonly used.
Percutaneous stone removal 739
Preoperative
• Usually healthy young and middle-aged adults, but stones may be due to
an underlying metabolic problem or due to bladder dysfunction from a
neurological disability.
• Check renal function.
Perioperative
• Patient initially in the lithotomy position to insert ureteric stents, then
turned semi-prone to place nephrostomy posterolaterally below the
12th rib, under radiographic control—be aware of the potential to
dislodge lines and for pressure area damage.
• Consider a reinforced ETT to prevent kinking, and secure well. The
head needs to be turned toward the operative side, so it is best to
position the ETT in the same side of the mouth.
• Support the chest and pelvis to allow abdominal excursion with
ventilation.
• Support and pad the head, arms and lower legs, and pad the eyes.
• Check ventilation during and after position changes.
• Ventilation may need to be temporarily interrupted for radiographs.
• Antibiotic prophylaxis may be required.
Postoperative
• Pain from nephrostomy is variable.
• Multimodal: paracetamol, NSAIDs (check renal function), PCA
morphine or PO tramadol.
Special considerations
• Hypothermia can occur if large volumes of irrigation fluid are used.
• Insertion of nephrostomy is often close to the diaphragm, with
the possibility of breaching the pleura, causing a pneumothorax or
hydrothorax—if in doubt, perform a CXR postoperatively.
• Rupture of the renal pelvis is a recognised complication, when large
volumes of irrigant may enter the retroperitoneal space.
• Postoperative Gram-negative septicaemia is a significant risk after any
urinary tract surgery for stones (see % pp. 1035–9).
740
In the early days of extracorporeal shock wave lithotripsy, patients were sus-
pended in a water bath in a semi-sitting position, which produced a number
of problems for the anaesthetist. Developments in the 1980s meant that
a water bath was no longer required, and more recent refinements of the
ultrasound beam have made it less uncomfortable, so that, with most cur-
rent lithotripters, only few patients need anaesthesia or sedation.
Preoperative
• Patients often undergo repeated lithotripsy, so refer to previous
treatment records where possible.
• Premedication with paracetamol/NSAIDs (note renal function) is
usually effective for treatment.
Perioperative
• Lateral position with arms above the head.
• Renal stones are located using ultrasound or an image intensifier, and
the shock wave focused on the stones.
• Antibiotic prophylaxis may be required.
Postoperative
Mild discomfort only; oral analgesics or NSAIDs are adequate.
Special considerations
• Shock wave can cause occasional dysrhythmias, which are usually
self-limiting. If persistent, the shock waves can be delivered in time
with the ECG (refractory period). Judicious use of anticholinergics
(glycopyrronium 200 micrograms) will increase the HR and increase the
frequency of delivered shock.
• Pacemakers can be deprogrammed by the shock wave; seek advice
from a pacemaker technician.
• Energy from shock waves is released when they meet an air/water
interface. It is advisable to use 0.9% sodium chloride, rather than air, for
‘loss of resistance’ if siting an epidural.
Testicular surgery 741
Testicular surgery
Procedure Removal/biopsy of testis, marsupialisation of hydrocele,
vasectomy, testicular torsion
Time 30min to 1h
Pain ++/+++
Position Supine
Blood loss Not significant
Practical GA, LMA, spermatic cord block. RSI/ETT if emergency
techniques (e.g. torsion). Spinal or LA infiltration
Preoperative
• Often suitable for day surgery.
Perioperative
• Beware vagal responses—have atropine ready.
Special considerations
• Innervation of testes and scrotum: somatic innervation is via the
ilioinguinal, genitofemoral, pudendal and posterior scrotal nerves
(branches of the posterior cutaneous nerve of the thigh) with nerve
root contributions from L1 to S3. Autonomic innervation is from the
sympathetic chain T10–L4 and the parasympathetic plexus S1–S3. Local
techniques therefore need to cover T10–S3.
• A spermatic cord block can be used as an adjunct to GA or as part of a
local technique for scrotal surgery. The block covers all nerves, except
the pudendal and posterior scrotal branches. If used as part of an LA
technique, supplemental infiltration of the scrotal skin is also required.
• The spermatic cord is best blocked under direct vision by the surgeon.
However, if a local technique is planned, feel for the spermatic cord as it
enters the top of the scrotum, and infiltrate 5–10mL of LA around it.
742
Renal transplant
Procedure Transplantation of cadaveric or live donor organ
Time 90–180min
Pain ++/+++
Position Supine
Blood loss Not significant to 500mL
Practical ETT and IPPV, CVP
techniques
Preoperative
• Usual problems relate to CKD and uraemia (see % pp. 193–5).
• Chronic anaemia is common (Hb usually around 80-100g/L). Do not
transfuse to normal levels.
• IHD is common and should be assessed and treated during workup for
transplantation.
• There has often been recent haemodialysis. Therefore, some degree of
hypovolaemia is common.
• Check post-dialysis bloods, including K+.
Perioperative
• Avoid A–V fistulae when placing IV cannulae and BP cuff. Avoid using
antecubital veins or veins on the radial side of the wrist, if possible (they
may be needed for future fistulae).
• Gently fluid-load prior to induction; wide swings in arterial pressure
may occur.
• Commonly used agents that are safe in renal failure include fentanyl,
remifentanil, propofol, atracurium and sevoflurane.
• Consider a central line under ultrasound guidance and monitor CVP.
Avoid the subclavian vein (risk of subclavian stenosis which precludes a
future fistula). Consider an arterial line.
• Prior to graft reperfusion, administer fluids to increase CVP to 12–
15mmHg and MAP to >80mmHg to optimise perfusion. Ephedrine
and/or metaraminol may be used cautiously to increase BP if the
patient is optimally filled.
• Maintain normothermia.
• Many centres administer diuretics (e.g. mannitol/furosemide)
and immunosuppressants (e.g. methylprednisolone) prior to graft
reperfusion. Check local protocols.
• Avoid blood transfusion if possible, although it may be needed if there
is surgical bleeding or Hb <80g/L.
Renal transplant 743
Postoperative
• Regular paracetamol and PCA is usually adequate. A fentanyl PCA
is preferable. Be cautious with morphine due to reduced clearance
and risk of respiratory depression. An epidural/spinal is not
usually necessary; there is a risk of bleeding on insertion (residual
anticoagulation from haemodialysis, poor platelet function, etc.) and
may cause hypotension. Consider a TAP block.
• Avoid NSAIDs.
• Monitor CVP and urine output hourly. Maintain mild hypervolaemia to
promote diuresis. Many units have protocols.
74
Further reading
Morkane CM, Fabes J, Banga NR, Berry PD, Kirwan CJ (2019). Perioperative management of adult
cadaveric and live donor renal transplantation in the UK: a survey of national practice. Clin Kidney
J, 12, 880–7.
Rattenberry W, Hertling A, Erskine R (2019). Spinal anaesthesia for ambulatory surgery. BJA Educ,
19, 321–8.
Dutton TJ, Daugherty MQ, Mason RG, McGrath JS (2014). Implementation of the Exeter enhanced
recovery programme for patients undergoing radical cystectomy. BJU Int, 113, 719–25.
Berger JS, Alshaeri T, Lukula D, Dangerfield P (2013). Anesthetic considerations for robot assisted
gynecologic and urology surgery. J Anesth Clin Res, 4, 1–7.
Irvine M, Patil V (2009). Anaesthesia for robot-assisted laparoscopic surgery. Contin Educ Anaesth
Crit Care Pain, 9, 125–9.
O’Donnell AM, Foo ITH (2009). Anaesthesia for transurethral resection of the prostate. Contin Educ
Anaesth Crit Care Pain, 9, 92–6.
Issa MM (2008). Technological advances in transurethral resection of the prostate: bipolar versus
monopolar TURP. J Endourol, 22, 1587.
Maffezzini M, Campodonico F, Canepa G, Gerbi G, Parodi D (2008). Current perioperative man-
agement of radical cystectomy with intestinal urinary reconstruction for muscle-invasive bladder
cancer and reduction of the incidence of postoperative ileus. Surg Oncol, 17, 41–8.
Hanson R, Zornow M, Conlin M, Brambrink A (2007). Laser resection of the prostate: implications
for anesthesia. Anesth Analg, 105, 475–9.
SarinKapoor H, Kaur R, Kaur H (2007). Anaesthesia for renal transplant surgery. Acta Anaesthesiol
Scand, 51, 1354–67.
Conacher ID, Soomro NA, Rix D (2004). Anaesthesia for laparoscopic urological surgery. Br J
Anaesth, 93, 859–64.
European Society of Regional Anaesthesia and Pain Therapy. Radical prostatectomy. Summary recom-
mendations. Notes on PROSPECT recommendations. M https://esraeurope.org/wp-content/up-
loads/2019/03/Summary-recommendations-Radical-Prostatectomy_ENG.pdf
Chapter 30 745
Gynaecological surgery
Claire Todd
General principles 746
Evacuation of retained products of conception/suction or
vacuum termination of pregnancy 749
Diagnostic laparoscopy/laparoscopic sterilisation 750
Hysterectomy 751
Ectopic pregnancy 753
746
General principles
Many gynaecological patients are fit and undergo relatively minor proced-
ures as day cases. Others are inpatients undergoing more major surgery.
Elderly patients often require operations to relieve pelvic floor prolapse.
• Many patients are apprehensive, with corresponding higher induction
doses required.
• PONV is a particular problem. With high-risk patients, use
appropriate techniques; avoid N2O, give prophylactic antiemetics and
consider TIVA.
• Pelvic surgery is associated with DVT. Ensure that adequate prophylactic
measures are taken.
• Prophylactic antibiotics reduce postoperative wound infection rates for
certain operations. Check your hospital protocol.
• Vagal stimulation may occur during cervical dilation, traction on the
pelvic organs or the mesentery or during laparoscopic procedures.
• Take care during patient positioning. Patients are often moved
up or down the table, when airway devices can be dislodged and
disconnections can occur. Pre-existing back or joint pain may be
worsened in the lithotomy position, and if the legs are supported in
stirrups, there is a potential for common peroneal nerve injury.
• It may be reasonable to ask the gynaecologist to administer analgesic
drugs rectally during anaesthesia. Ensure that you have the patient’s
permission to do so.
• Ensure patients are kept warm during longer cases.
• Major gynaecological surgery can incur considerable blood loss and may
be prolonged. Cell salvage should be available for such cases.
• Many gynaecological operations formerly done through an open
approach (e.g. hysterectomy, tubal pregnancy repair) are now done
primarily using laparoscopic techniques.
Miscellaneous gynaecological procedures
Table 30.1 presents the important information for those procedures which
are not covered in the individual topics within this chapter.
General principles 747
(Continued)
748
Preoperative
• ERPC: remaining products of conception may have to be surgically
removed after an incomplete miscarriage. This usually occurs between
6w and 12w gestation. Substantial blood loss may have occurred
preoperatively and may continue perioperatively. IV access and
crystalloid infusion are required if the haemorrhage appears anything
more than trivial.
• Suction or vacuum termination of pregnancy (STOP/VTOP) is a
procedure undertaken at up to 12w gestation.
Perioperative
• LMA or face mask. Intubate unfasted emergency patients. Avoid high
concentrations of volatile agents due to the relaxant effect on the
uterus. Propofol induction followed by intermittent boluses or propofol
TCI and an opioid (alfentanil or fentanyl) is appropriate.
• A drug to help contract the uterus and reduce bleeding may be
requested. Oxytocin 3–5 units can be given slowly.
Postoperative
Oral analgesics and antiemetics.
Special considerations
• Pregnancies beyond 12w can be terminated surgically by dilation and
evacuation. The procedure is similar to a STOP/VTOP, but there is
greater potential for blood loss.
• If there are symptoms of reflux oesophagitis, ranitidine or PPI
premedication and intubation are indicated.
• If a pregnancy has gone beyond 16w, it may be terminated medically
with prostaglandin. These patients may still require an ERPC and are
more likely to suffer significant blood loss.
750
Diagnostic laparoscopy/laparoscopic
sterilisation
Procedure Intra-abdominal examination of gynaecological
organs ± treatment ± clips to Fallopian tubes
Time 30–60min
Pain +/++
Position Lithotomy
Blood loss Nil
Practical techniques LMA/ETT, IPPV, day case
Preoperative
• Usually young and fit. Give oral analgesics preoperatively.
Perioperative
• Use a short-acting opioid (e.g. fentanyl).
• Administer antiemetics to ensure same-day discharge.
• Encourage infiltration of the skin incisions with LA.
• The traditional airway management is endotracheal intubation with
minimal doses of muscle relaxants, as cases are generally quick. Monitor
with a nerve stimulator, using reversal agents accordingly.
• An alternative technique for uncomplicated short procedures is to use
an LMA. This is only suitable for non-obese patients; the potential for
gastric regurgitation and aspiration must be assessed carefully. Surgeons
may find SV difficult and request paralysis.
Postoperative
Further opioids or antiemetics may be required.
Special considerations
• Bradycardias are common due to vagal stimulation. Atropine should be
readily available; ask surgeons to release the pneumoperitoneum.
• Shoulder pain is common postoperatively due to diaphragmatic
irritation. Although self-limiting, it can be difficult to treat and is d by
expelling as much CO2 as possible at the end of the procedure.
• If significant endometriosis is found and excised, postoperative pain can
be severe and same-day discharge is likely to be difficult.
• Very rarely, CO2 gas may be inadvertently injected intravascularly,
resulting in VAE (see % pp. 584–5). This results in V/Q mismatch,
with a fall in ETCO2, impaired CO, hypotension, arrhythmias and
tachycardia. Alert the surgeon and resuscitate the patient.
• If an LMA is used, consider premedication with PO ranitidine or a PPI,
and the use of a device with a gastric channel (e.g. ProSeal™).
Hysterectomy 751
Hysterectomy
Procedure Removal of uterus (may also include ovaries ± Fallopian
tubes as bilateral salpingo-oophorectomy)
Time 1–3h, depending on surgical approach
Pain + to +++
Position Supine, head-down or lithotomy
Blood loss 250–1500mL, G&S
Practical LMA, SV suitable for vaginal hysterectomy
techniques ETT, IPPV required for laparoscopic or open cases
Spinal diamorphine useful for analgesia
Preoperative
• Indications for hysterectomy vary from vaginal/uterine prolapse,
menorrhagia and uterine fibroids to gynaecological malignancies.
• Patients may be anaemic if they have had menorrhagia or
postmenopausal bleeding.
• Renal function may be abnormal if an abdominal mass has been
compressing the ureters.
• PONV is common.
• Those who have been treated with preoperative chemotherapy to
debulk tumours are frequently anaemic, frail and malnourished. They
should be considered high-risk patients.
• Cell salvage should be used for all open and radical hysterectomies.
• Ensure prophylaxis for DVT has been initiated.
Perioperative
• Airway management as above.
• Antibiotic prophylaxis is usually required.
• Steep, head-down positioning is required for a laparoscopic approach.
• Blood loss is variable; some hysterectomies bleed more than expected.
X-match blood early if bleeding appears to be a problem.
• Heat loss through the abdominal incision can be significant. Use a forced
air warming blanket over the upper body during the operation.
Postoperative
• Pain is usually reasonably well controlled with oral analgesics for vaginal
and laparoscopic cases. These patients are usually ready for discharge
within 48h.
• Open cases will require additional postoperative analgesia. Options
include PCAs, rectus sheath catheters and central neuraxial blockade.
Spinal anaesthesia with diamorphine is now preferred to epidurals.
Vaginal hysterectomy
• Often supplemented by an anterior ± posterior repair which reduces
bladder and bowel prolapse through the vagina. It is usually not possible
to remove the Fallopian tubes and ovaries during a vaginal hysterectomy
because of the restricted surgical field.
752
Ectopic pregnancy
Procedure Laparoscopy (less commonly laparotomy) to
stop bleeding from ruptured tubal pregnancy
Time 60min
Pain ++/+++ (depending on surgical approach)
Position Lithotomy
Blood loss Can be massive, X-match 2 units
Practical techniques ETT, IPPV
Preoperative
• The presentation is variable. A stable patient may have ill-defined
abdominal pain and amenorrhoea; others may present with life-
threatening abdominal haemorrhage. At least one large-bore IV cannula
should be inserted prior to theatre, and crystalloids or blood products
infused, according to the clinical picture.
• FBC, X-match and possibly a clotting screen should be requested on
admission.
• Seek help from a 2nd anaesthetist if the patient is unstable.
Perioperative
• RSI
• Careful IV induction as significant blood loss can be concealed.
• Continue IV fluid resuscitation and actively warm the patient.
Postoperative
• Clotting abnormalities are not uncommon if large volumes of blood
have been lost. Send a clotting screen or perform point-of-care
coagulation testing.
• Analgesia requirements will vary, depending on surgical approach. May
require a PCA.
Special considerations
• Patients are young and generally compensate for significant volumes
of blood loss, meaning the preoperative clinical picture can be falsely
reassuring.
• In most centres, the operation is performed laparoscopically and
only converted to a laparotomy if there are complications. Be aware
that the pneumoperitoneum may impede venous return, resulting in
hypotension.
754
Chapter 31 755
See also
% Cleft lip and palate pp. 943–4
756
General principles
Airway problems are the major concern in ENT surgery, related to both the
underlying clinical problem and the shared airway.
Presenting pathology may:
• Produce airway obstruction
• Make access difficult or impossible.
Surgeons working in, or close to, the airway can:
• Displace, obstruct or damage airway equipment
• Obscure the anaesthetist’s view of the patient
• Limit access for the anaesthetist during operation
• Produce bleeding into the airway (intra-and postoperatively)
• Potentiate postoperative airway swelling/obstruction.
The surgeon and anaesthetist should plan together to use techniques/equip-
ment that provide good conditions for surgery, while maintaining a safe,
secure airway. Whenever an airway problem is suspected intraoperatively,
correcting it is the first priority, stopping the surgery, if necessary. Other
structures around the head are inaccessible during surgery and need pro-
tection, especially the eyes. Ensure they are kept closed with appropriate
tape, padded as necessary, and that pressure from equipment is prevented,
especially for long cases.
Airway/ventilation management
Tracheal tube or laryngeal mask airway
• Traditionally, an ETT has been used for airway protection for the
majority of ENT work.
• Preformed RAE tubes provide excellent protection with minimal
intrusion into the surgical field.
• An oral, south-facing RAE tube is used for nasal and much oral surgery,
although a nasal tube (north-facing) allows better surgical access to the
oral cavity.
• An LMA, often of the reinforced flexible type, offers an alternative
approach. It provides adequate protection against aspiration of blood
or surgical debris and avoids complications of tracheal intubation/
extubation. It restricts surgical access to a greater degree, however,
and is more prone to displacement during surgery (with potentially
catastrophic results).
Spontaneous ventilation or intermittent positive pressure ventilation
• Continuous NMB is not required for most ENT surgery and facial nerve
monitoring is commonly utilised.
• Ventilator advances mean many ENT anaesthetists favour SV or
pressure-supported SV. This allows titration of analgesia and improves
success for deep extubation techniques.
• The use of remifentanil/opioid infusions to optimise surgical conditions
(and avoid NMBs) commonly requires IPPV through either ETTs
or LMAs.
• Spontaneously ventilating patients with an IV anaesthetic technique is
now commonplace. Multiple induction techniques are described.
General principles 757
Nasal vasoconstrictors
• Topical vasoconstrictors are routinely used to reduce bleeding in nasal
surgery, administered by spray, gel or soaked swabs. Cocaine-containing
solutions (e.g. Moffett’s solution: cocaine, sodium bicarbonate and
adrenaline) are declining in usage, largely due to concerns over drug
storage/availability and systemic toxicity (hypertension, arrhythmias,
euphoria). Maximum topical cocaine dose is 3mg/kg.
• Proprietary decongestants are a commonly used alternative such as
pseudoephedrine or phenylephrine, which are equally effective.
• Systemic absorption can result in a transient sympathomimetic
response.
• Infiltration with adrenaline-containing solutions may be used in addition,
with greater risk of systemic effects.
Remifentanil
• The intense opioid action of remifentanil, combined with its rapid
recovery profile, has led to its widespread use in ENT, particularly for
major cases.
• Normally given by infusion, clinical applications include:
• Middle ear surgery/major head and neck resections (controlled
arterial pressure reduces bleeding)
• Parotidectomy (facilitates IPPV without relaxant)
• Laryngoscopy/pharyngoscopy (attenuates hypertensive response)
• Procedures requiring nerve monitoring (NMBs contraindicated).
• Beware of bradycardia/hypotension when used at induction,
particularly in the elderly.
• Interpatient variability greatly limits the value of predetermined infusion
schemes.
• For major surgery, to prevent postoperative rebound hypertension/
agitation in recovery, continue remifentanil at a low infusion rate or give
longer-acting opioid (morphine) 15–20min before the end of surgery;
clonidine up to 2 micrograms/kg IV or dexmedetomidine may also be
of use.
Miscellaneous ear, nose and throat procedures
Table 31.1 presents the important information for those procedures which
are not covered in the individual topics within this chapter.
References
1 NHS Improvement (2018). Recommendations from National Patient Safety Agency alerts that re-
main relevant to the Never Events list 2018. M https://improvement.nhs.uk/documents/2267/
Recommendations_from_NPSA_alerts_that_remain_relevant_to_NEs_FINAL.pdf
Table 31.1 Miscellaneous ENT procedures
(Continued)
759
760
760
Table 31.1 (Contd.)
Operation Description Time Pain Position Blood loss Notes
(min)
Rhinoplasty Cosmetic alteration or 60–90 ++ Head-up tilt, head ring Small RAE tube or reinforced LMA, SV or IPPV, throat
Chapter 31
Nebulised adrenaline
• Appears to be useful in reducing stridor associated with various
obstructive aetiologies in case reports (better evidence lacking). Widely
utilised, 1–5mg of adrenaline nebulised in O2.
Helium
• Medical Heliox (mixtures may be 21/70 or 30/70 O2/helium). A similar
viscosity to air, but lower density increases tendency to laminar flow and
decreases resistance in turbulent flow. Limited by reduced O2 content
of any mixture useful for flow characteristics.
Continuous positive airway pressure
• Splints any collapsing airway segment. Variable availability in emergency
setting and high-flow nasal cannulae likely better tolerated.
Investigations
Consider potential benefit of further investigations:
• Nasendoscopy: quick and relatively low risk of airway trauma, may
offer significant information; anaesthetist should be present if not
performing.
• CT: rapid and accurate assessment, usually well tolerated, may be
performed lateral or even supine if necessary. Reconstructions allow 3D
assessment. No information on any dynamic or postural contribution to
airway patency.
• MRI: gold standard for soft tissue imaging; however, limited availability,
prolonged scan times and expected intolerance of supine position with
coil over airway render MRI largely impractical in acute setting.
Management: approach to securing airway
The main problems in securing airway access are:
• Airway obstruction likely to be worsened by lying the patient flat, GA
(all techniques) or instrumenting the airway (laryngospasm, bleeding).
• Identifying the laryngeal inlet may be difficult because of anatomical
distortion (especially supraglottic lesions), secretions or blood.
• Severe stenosis may make passage of the tube difficult (particularly
glottic or subglottic tumours).
There is little evidence to support any one particular anaesthetic technique.
Patient presentations and anaesthetic experience vary widely. However,
the use of IV induction agents and/or NMBAs carries the catastrophic risk
of CICO in a patient unable to breathe spontaneously. Advances in O2
delivery techniques and VL are transforming planned approaches to the
obstructed airway, and high-flow nasal cannulae may augment any chosen
technique and offer ongoing oxygenation and potentially provide some
airway splinting during securing of the airway.
Traditionally, the three main options for establishing secure access in an
obstructed airway are:
• Direct laryngoscopy and intubation under deep inhalational anaesthesia
(SV): increasing consideration of SV under IV anaesthesia.
• AFOI under LA
• Tracheostomy under LA (or deep inhalational GA with face mask or
LMA in less severe cases).
764
Jet ventilation
Jet ventilation describes the delivery of a jet stream of gas from a high-
pressure source, delivered into an open airway and generally relying on
passive exhalation. Jet ventilation carries significant risks, i by unfamiliarity
with the technique. Jet delivery via misplaced/misdirected cannula can have
catastrophic consequences. Inadequate gas exchange is common.
• Low-frequency jet ventilation, usually achieved using an injector system,
such as the manually driven adjustable-flow Manujet®, but also describes
rescue techniques for CICO scenarios utilising more simply constructed
systems. This may be connected via:
• Cricothyroidotomy needle/cannula placed through the cricothyroid
membrane under LA before induction and aimed towards the carina.
Commercial versions available or a Tuohy needle can be used.
• Jet catheter (rigid, non-compliant) with the tip placed midway down
the trachea. Multiple catheters available with gas sampling/pressure
monitoring port or made from laser-resistant material.
• Injector needle attached to the proximal end of the operating
laryngoscope/rigid bronchoscope, and ventilation started when
correctly aligned with larynx/trachea. Various needle sizes available
with different flow rates. Technique not suitable if good view of
larynx is unobtainable and has disadvantage of blowing debris/smoke
into trachea with ventilation.
• High-frequency jet ventilation requires specialised ventilators capable
of performing high frequencies (typically 1–10Hz) and experience
with the technique. Warmed and humidified inspiratory jets are
electronically controlled. Air is entrained along with inspiratory jet
but smaller VTs utilised. Frequency, driving pressure, inspiratory time
and gas composition are usually adjustable; however, the degree of air
entrainment means delivered FiO2 may vary.
• Most modern systems monitor airway pressures and feature cut-offs
and improved safety features. Inspiratory pauses are required for
more accurate CO2 sampling.
• Indications for jet ventilation importantly include:
• Emergency airway management via a transtracheal/cricothyroid
membrane cannula
• Airway surgery (including laser) for laryngeal/tracheal stenosis, major
conducting airway surgery
• Thoracic surgery, including non-dependent lung ventilation during lung
isolation techniques.
• Lung-protective ventilation strategies/rescue in ICU.
76
Grommet insertion
Procedure Myringotomy and grommet insertion, usually bilateral
Time 5–15min
Pain +
Position Supine, head tilted to side, head ring
Blood loss Nil
Practical Face mask or LMA, SV using T-piece or paediatric circle
techniques
Preoperative
• Usually children (1–8y), normally day case.
• Repeated ear infections; check for recent URTI.
• Paracetamol/NSAID PO.
Perioperative
• LMA commonly used.
• Face mask suitable if surgeon happy to work round it, but assistant
needed to adjust vaporiser, etc. Insert Guedel airway before draping,
and ensure reservoir bag visible throughout (T-piece ideal if face
mask used).
Postoperative
• Need for additional analgesia unlikely.
Special considerations
• If face mask airway difficult, change early to LMA.
• Reflex bradycardia occasionally seen related to partial vagal innervation
of tympanic membrane.
Tonsillectomy/adenoidectomy: child 767
Tonsillectomy/adenoidectomy: child
Procedure Excision of lymphoid tissue from oropharynx (tonsils) or
nasopharynx (adenoids)
Time 20–30min
Pain +++
Position Supine, pad under shoulders
Blood loss Usually small, can bleed postop
Practical South-facing RAE tube or reinforced LMA, placed in
techniques groove of split blade of Boyle–Davis gag; SV or IPPV
Preoperative
• Careful history to exclude/define OSA or active infection. Consider
overnight bed if history/sleep study indicates moderate/severe OSA.
• Topical LA on hands (mark sites of veins).
• Consider paracetamol/NSAID PO.
• Consent for PR analgesia if to be used.
Perioperative
• IV or inhalational induction (sevoflurane ± N2O): oropharyngeal airway
useful if nasopharynx blocked by large adenoids.
• Intubate (RAE) using relaxant or deep inhalational/IV anaesthesia, or
insert LMA using propofol/opioid or deep inhalational anaesthesia.
• Secure in midline, no pack (obscures surgical field).
• Beware surgeon displacing/obstructing tube intraoperatively,
particularly after insertion or opening of Boyle–Davis gag.
• T-piece ideal for SV, but ensure reservoir bag always visible.
• Reliable IV access essential, IV fluids routine.
• Analgesia with morphine or fentanyl titrated IV plus paracetamol/
NSAID (if not given preoperatively). Consider tramadol.
• Antiemetic: at least one recommended—dexamethasone or
ondansetron.
• Careful suction of oropharynx and nasopharynx at end under direct
vision (generally done by surgeon).
• Extubate left lateral/head-down (tonsil position), with oropharyngeal
airway. Refer to deep or light extubation discussion (see % p. 757).
Postoperative
• Keep patient in tonsil position until airway reflexes return.
• High-quality recovery care essential.
• Analgesia with IV morphine/fentanyl initially, then PO paracetamol/
NSAID/morphine. Dexmedetomidine has been used.
• Leave IV cannula (flushed) in place in case of bleeding.
Special considerations
• In small children, a pillow/roll under the shoulders can be used to
provide the necessary tilt.
• Avoid blind pharyngeal suction with a rigid sucker, as this may start
bleeding from the tonsil bed.
768
Tonsillectomy in adults
As for child, except:
• Usually more painful postoperatively in adult: give morphine/long-acting
opioid in theatre. Consider tramadol.
• IPPV with relaxant technique used more commonly. Deep extubation
may be more reliant on airway adjuvant.
• Occasionally, patients present with peritonsillar abscess (quinsy). Now
normally treated with antibiotics, and tonsillectomy performed later. If
drainage essential because of airway swelling, pus usually aspirated with
syringe and large needle under LA infiltration.
70
Myringoplasty
Procedure Reconstruction of perforated tympanic membrane
with autograft (usually temporalis fascia)
Time 60–90min
Pain ++
Position Supine, head tilted to side, head ring, head-up tilt
Blood loss Minimal
Practical South-facing RAE tube or LMA (usually reinforced); SV
techniques or IPPV
Preoperative
Usually young, fit patients.
Perioperative
• Ensure coughing avoided during surgery; LA spray to larynx; monitor
NMB if IPPV–relaxant technique used.
• Dry field improves the surgical view, though not as important as for
stapedectomy; head-up tilt and avoiding hypertension/tachycardia
normally sufficient.
• Remifentanil infusion suitable.
• Routine antiemetic useful.
Postoperative
• PRN paracetamol or NSAID PO/IV; may need morphine.
• PRN antiemetic.
Special considerations
Using N2O may produce diffusion into the middle ear and risk the graft
lifting off; either avoid or discontinue 20min before the end of the case.
Stapedectomy/tympanoplasty 771
Stapedectomy/tympanoplasty
Procedure Excision/reconstruction of damaged middle ear
structures
Time 2–4h
Pain ++/+++
Position Supine, head tilted to side, head ring, head-up tilt
Blood loss Minimal
Practical South-facing RAE tube or LMA (usually reinforced).
techniques IPPV normally. Arterial line often used
Preoperative
• Check for CVS disease, as this will limit the degree of hypotension
possible.
• Oral premedication options include benzodiazepines, β-blockers and
clonidine.
Perioperative
• If surgical use of nerve integrity monitoring, avoid NMBs.
• Bloodless field enables greater surgical accuracy. Simple measures
include: potent opioid preinduction; ensuring coughing avoided at
intubation (LA spray to larynx helpful); head-up tilt to reduce VP.
• Further benefit achieved by lowering arterial BP (mean of 50–60mmHg
in healthy patients) and HR (<60bpm).
• Remifentanil infusion ideal to achieve this. Alternatively, use IV labetalol
(combined α-/β -blocker, 5mg increments) or IV β-blocker (metoprolol
1mg increments, esmolol infusion) plus vasodilator (isoflurane,
hydralazine 5mg increments). Arterial line strongly advised with CVS
disease or if potent vasodilators used; head-up tilt further reduces
perfusion pressure to the brain.
• Give at least one antiemetic routinely. Consider prochlorperazine
(discuss vertigo risk with surgeon).
Postoperative
• Regular antiemetic for 24–48h.
• PRN paracetamol or NSAID PO/IV/PR; may need morphine.
Special considerations
• N2O diffusion into the middle ear may disrupt surgery, though less
important than in myringoplasty. Either avoid or discontinue 20min
before the end of the case.
72
Preoperative
• Obstructive airways disease often associated with nasal polyps.
• Combination of procedures mentioned in the box above frequently
performed.
Perioperative
• Face mask ventilation often needs Guedel airway due to blocked nose.
• Nasal vasoconstrictor usually applied (topical or infiltration).
• Leave eyes untaped for polypectomy (the optic nerve can be close, and
the surgeon needs to check for eye movement).
• TIVA and remifentanil ideal for improved surgical conditions; aim to
control arterial BP (mean 50–60mmHg in healthy individuals).
• Suction pharynx (particularly behind soft palate for the ‘coroner’s clot’;
see % p. 757) before extubation; less easy with LMA.
Postoperative
• Analgesia with PRN paracetamol or NSAID PO/IV/PR.
• Nose usually packed, producing obstruction of nasal airway; if
disturbing to patient, or in cases of OSA, nasopharyngeal airway(s) can
be incorporated into the pack.
• Sit patient up as soon as awake to reduce bleeding.
Special considerations
• Leave IV cannula in overnight, as can bleed postoperatively.
Microlaryngoscopy 773
Microlaryngoscopy
Procedure Examination of larynx using operating microscope (plus
excision/biopsy; may use laser)
Time 10–30min
Pain +/++
Position Supine, pad under shoulders, head extended
Blood loss Nil
Practical Microlaryngeal tube and conventional IPPV. TIVA and
techniques jet ventilation using injector system (O2 plus entrained
air) via:
• Injector needle on the operating laryngoscope
• Semi-rigid tracheal catheter
• Cricothyroidotomy needle/cannula
Jet ventilation
(See % p. 765.)
• Ventilation achieved using an injector system, and delivered usually via
rigid jet catheter.
• Induce in theatre, or use an LMA or a microlaryngeal tube initially; then
remove, place jet catheter and commence jet ventilation when surgical
team ready.
• Ensure the anaesthetic machine in theatre is situated close to enable
easy face mask ventilation at induction/recovery.
• TIVA needed for maintenance (propofol/remifentanil infusion).
• Ventilation techniques vary, depending on device and surgery. Adjust
inspiratory flow (alter injector settings, or change needle size) to
produce appropriate degree of chest expansion.
• Accurate flow/pressure measurement not easy; barotrauma a potential
risk, oxygenation often exceeds CO2 clearance.
• Stop ventilation intermittently during surgical work (clear
communication essential).
• Provides minimal obstruction to surgical view.
• At end of the case, may continue jet ventilation until SV re-established
or more commonly discontinue and ventilate by alternate airway until
SV recommences.
Preoperative
• Patients often elderly and usually smokers; CVS/respiratory system
problems common.
• Carefully assess the airway for evidence of obstruction. History,
examination, ENT clinic assessment, plain films and CT scan may
all help, but if any degree of stridor present, obstruction must be
substantial (see % pp. 384–7).
• Ensure all equipment is ready before induction, including
cricothyroidotomy kit, and surgeon is prepared for emergency
tracheostomy, if required.
Perioperative
• If airway obstruction suspected, secure airway initially, using principles
outlined (see % Emergency management of the obstructed airway,
pp. 384–7). Inserting a cricothyroid cannula under LA preinduction
provides a route for ventilation in the event of total obstruction.
Detailed airway and rescue preplanning essential.
• Give short-acting opioid (alfentanil, remifentanil) to attenuate
hypertensive response. High-dose infusion may prevent need for muscle
relaxation if surgical field immobility required.
• If muscle relaxation planned, use of rocuronium and reversal with
sugammadex may be an option.
• LA spray to larynx reduces risk of laryngospasm, though this impairs
airway protection, so recover left lateral, head-down.
Microlaryngoscopy 775
Postoperative
• Analgesia with PRN paracetamol or NSAID PO/IV/PR.
• May develop stridor postoperatively from oedema of an already
compromised airway. Dexamethasone 8–12mg IV sometimes used to
prevent this. Consider nebulised adrenaline.
Special considerations
• Careful planning required if airway laser to be utilised.
• Airway laser surgery carries significant risk of airway fire, as well as
collateral tissue damage/injury to both patient and staff. Excellent
teamwork and adherence to local health and safety policies essential.
• Microlaryngoscopy can be used to inject inert material (e.g. silicone)
into paralysed vocal cords to improve phonation, though this can lead
to airway obstruction if overdone.
References
5 Patel A, Nouraei SAR (2015). Transnasal Humidified Rapid Insufflation Ventilatory Exchange
(THRIVE): a physiological method of increasing apnoea time in patients with difficult airways.
Anaesthesia, 70, 323–9.
76
Tracheostomy
Procedure Insertion of an ETT via neck incision
Time 30min
Pain ++
Position Supine, pad under shoulders, head ring, head-up tilt
Blood loss Normally small, though can bleed from thyroid vessels
Practical IPPV, ETT with tubing going ‘north’, changed to tracheos-
techniques tomy tube during case. LMA if airway not a problem, IPPV
or SV. Can be done under LA
Preoperative
• Normally done for long-term ICU ventilation or airway obstruction.
• ICU patients almost certainly already intubated. If ventilation difficult
and oxygenation critical, set up ICU ventilator in theatre, using TIVA,
rather than inhalational agents.
• Stop NG feeds, if applicable.
• If tracheostomy is for airway obstruction, secure airway initially, using
principles outlined (see % Preoperative airway obstruction, pp. 762–4).
• Before induction, ensure all equipment prepared (including
cricothyroidotomy kit) and the surgeon ready for emergency
tracheostomy, if required.
Perioperative
• Secure ETT with tape to allow easy removal during case, with pilot cuff
readily accessible.
• Aspirate NGT (if present), and clear oropharynx of secretions before
draping.
• Drape patient to allow anaesthetist access to ETT for tube change.
• Long tubing needed for breathing circuit and gas sampling.
• Before changing to tracheostomy tube, preoxygenate for 3–4min
(increasing volatile agent as necessary), and check NMB is adequate.
• Ensure scrub nurse has correct tracheostomy tube and sterile
catheter mount.
• Deflate ETT cuff before surgeons incise trachea, so it can be reinflated
and ventilation continued if problems occur.
• Withdraw ETT slowly into upper trachea (do not remove from trachea
until tracheostomy secure and certain), and connect breathing circuit
and capnograph to new tracheostomy tube via sterile catheter mount.
• Beware false passage created during tracheostomy tube insertion,
especially in the obese; check position with fibreoptic endoscopy, if
any doubt.
• If problems occur, remove tracheostomy tube and advance ETT back
down trachea.
Postoperative
• Regular suction to new tracheostomy (blood, secretions).
• Humidify inspired gases.
• Analgesia in recovery with paracetamol or NSAID IV/PR or morphine
IV. Usually little analgesia required thereafter.
Tracheostomy 777
Laryngectomy
Procedure Excision of larynx (epiglottis and glottis) with creation of
an end-stomal tracheostomy
Time 3–4h
Pain +++
Position Supine, pad under shoulders, head ring, head-up tilt
Blood loss Moderate to substantial; X-match 2 units
Practical IPPV, ETT with tubing going ‘north’, changed to
techniques tracheostomy during case
Arterial line, urinary catheter, CVP line for long/
complicated surgery or if indicated by cardiac disease
Preoperative
• Some degree of airway obstruction likely. Patient likely to have had
recent GA (for diagnosis) to guide airway management; beware if some
time has elapsed.
• If no recent GA, assess the airway as for microlaryngoscopy (see %
pp. 773–5).
• Usually smokers; CVS/respiratory system problems and malnutrition
common.
• Discuss implications of tracheostomy preoperatively (communication,
secretions, coughing produced by tube). Speech therapist will do much
of this.
Perioperative
• Insert fine-bore NG feeding tube at induction, and fix securely (can be
sutured to nasal septum).
• Warming blanket and fluid warmer.
• Long tubing needed for breathing circuit and gas sampling tube.
• Remifentanil infusion ideal.
• Substantial blood loss can accumulate under drapes at back of neck and
may not be apparent until end of case.
• For CVP access, all neck lines hinder surgery; femoral best, though
antecubital fossa (ACF) or subclavian can be used.
• Antibiotic prophylaxis for at least 24h.
• When changing to tracheostomy tube, see precautions for
tracheostomy (see % pp. 776–7), though end-stoma makes tracheal
access safer and easier.
• During surgery, long tube (armoured or special preformed) via
tracheostomy is useful to enable surgical access round stoma, then
changed for standard tracheostomy tube at end.
Postoperative
• HDU ideal.
• Humidification and regular suction essential (blood, secretions).
• New tracheostomy produces protracted coughing—morphine,
benzodiazepines or low-dose propofol useful for control.
• Analgesia with PRN morphine IV/NG, plus PRN paracetamol or
NSAID NG/IV/PR. Analgesic requirements usually surprisingly low.
• Antiemetic, as required.
Laryngectomy 779
Special considerations
• Beware of air emboli (see % pp. 584–5) during dissection—early
detection by sudden fall in ETCO2.
• For previous laryngectomy patients presenting for surgery, to ventilate
via stoma, use paediatric face mask turned through 180°, LMA applied
to neck or intubate awake after LA spray to stoma. Tracheostomy tube
insertion is usually easy, though check stoma for stenosis or tumour
recurrence, and always preoxygenate.
• Partial laryngectomy, with laryngeal reconstruction and temporary
tracheostomy, favoured by some as alternative to radiotherapy in early
laryngeal tumours.
780
Preoperative
• Assess airway carefully, as may be an associated head and neck tumour
or previous major surgery.
• May be performed with another procedure, e.g. laryngectomy.
Perioperative
• Forced air warming blanket and fluid warmer.
• Long tubing is needed for the breathing circuit and gas sampling.
• Remifentanil infusion ideal.
• Can bleed briskly from large neck vessels, with substantial accumulation
of blood under drapes (may not be apparent until end of case).
• For CVP access, femoral is best. Must avoid remaining jugulars, as head
and neck venous drainage dependent on them.
Postoperative
• Head and neck oedema likely for several days (impaired venous
drainage). Keep head up as much as possible, and avoid excessive IV
fluids.
• To reduce chance of agitation/rebound hypertension and wound
haematoma in recovery, continue remifentanil at a low infusion rate,
or give morphine 15–20min before end of surgery; clonidine up to 2
micrograms/kg IV or dexmedetomidine also very useful. Treat any
hypertension early.
• Analgesia with PRN paracetamol or NSAID PO/IV/PR, morphine PO/
IV. Surprisingly low analgesic requirements normally.
• Antiemetic, as required.
Special considerations
• Beware of air emboli during dissection—early detection by sudden fall
in ETCO2 (see % pp. 584–5).
• Surgical manipulation of carotid sinus can produce marked bradycardia.
• If neck dissection previously done on other side, oedema is usually
worse and can raise ICP. Dexamethasone 8–12mg IV preoperatively
(then 4mg IV 6-hourly) is used by many to reduce this.
Parotidectomy 781
Parotidectomy
Procedure Excision of parotid gland, usually preserving facial nerve
Time 2–5h
Pain ++/+++
Position Supine, head ring, head tilted to side and moderately
extended, head-up tilt
Blood loss Small/moderate, G&S. Greater for malignancy
Practical South-facing RAE tube and IPPV normally used, though
techniques SV possible for suitable patients. Reinforced LMA and
IPPV or SV also possible. No NMB during dissection
around facial nerve
Preoperative
• Check if suitable for SV—not if elderly, obese or respiratory disease.
• Check mouth opening, especially if malignant.
Perioperative
• Forced air warming blanket, fluid warmer ± urinary catheter.
• Avoid NMB after initial dose (check recovery with PNS) to allow
surgical testing for facial nerve.
• Remifentanil infusion ideal to allow IPPV without NMB and also reduce
blood loss.
• Alternatively, suppress respiratory drive with other opioid, volatile
agent or propofol infusion, plus moderate hyperventilation.
• LA spray to larynx useful to prevent coughing.
• If SV used, ensure patient settled initially using high level of
volatile agent.
Postoperative
• To reduce chance of agitation/rebound hypertension and wound
haematoma in recovery, continue remifentanil at a low infusion rate or
give morphine 15–20min before end of surgery; keep head up, and treat
hypertension early; clonidine up to 2 micrograms/kg IV is very useful.
• Antiemetic, as required.
• Analgesia with PRN morphine IV/PO, paracetamol or NSAID PO/IV/PR.
Special considerations
• Surgeon normally uses nerve stimulator to identify facial nerve during
dissection and may wish to leave ipsilateral eye exposed to monitor
response.
• Large-bore IV access at start, as occasionally bleeds substantially
(especially malignant tumours).
782
Chapter 32 783
See also
% Radical neck dissection p. 780
% Parotidectomy p. 781
% Tracheostomy pp. 776–7
784
Oral/maxillofacial surgery
General principles
Anaesthesia for intraoral/maxillofacial procedures requires management of
a shared (often difficult) airway. Nasal intubation is frequently used to im-
prove surgical access to the mouth, facilitate X-rays and allow assessment
of bite alignment. At the preoperative visit, check nostril patency and ask
about epistaxis and the use of anticoagulants. Discuss the choice of airway
with the surgeon.
• Simple intraoral procedures are usually possible using a reinforced LMA.
For unilateral intraoral procedures, an oral ETT (e.g. RAE tube) placed
on the opposite side of the mouth may be acceptable. Oral airways may
be dislodged, and vigilance is required (particularly LMAs which tend to
obstruct as they migrate forwards).
• If the nasal route is chosen for intubation, use LA and/or a
vasoconstrictor mixture (lidocaine 5%/phenylephrine 0.5% or
xylometazoline). There are many varieties of nasal tube; the ‘Ivory
Preformed North-Facing Nasal’ from Portex® is ideal. These preshaped
tubes are made of soft material and cause little nasal trauma. Sizes of
6.0, 6.5 and 7.0mm should be available. Place in warm water before
use to soften the material even further. The tube should be padded
with gauze to protect the patient’s forehead. Consider fixing the ETT,
NGT and temperature probe with clear adhesive film. Avoid excessive
tension/pressure on the alar margin which risks causing necrosis. The
surgeon will need to recheck periodically.
• Patients who have had previous surgery and/or radiotherapy may have
thick, fixed (‘woody’) soft tissues and poor neck mobility. Intubation
may be harder than predicted by bedside tests. Consider VL techniques
(e.g. CMAC®/Glidescope® or fibreoptic intubation).
• Protect the eyes with tape and eye pads or surgically positioned plastic
contact lenses (e.g. the Crouch Corneal Protector®).
• Position the patient with the head at the opposite end to the anaesthetic
machine. A long breathing circuit and gas analysis/spirometry lines
are normally required. Secure the breathing circuit with a tube holder.
Ensure the pilot cuff is accessible and clear from the eyes.
• Stabilise the head with a horseshoe or head ring. For operations on
the roof of the mouth, use a bolster under the shoulders to extend
the neck further. Positioning the patient slightly head-up will reduce
bleeding.
• Routine use of throat packs is not recommended. If they are used, they
should be placed by the surgeon and a robust system should be in place
to ensure that they are not inadvertently left in situ. This should include:
• Discussion at ‘Time Out’
• A visual reminder (e.g. throat pack sticker and an entry on the swab/
sharps board)
• Confirmation of removal in the ‘Sign Out’ swab count
• Clear documentation.
Oral/maxillofacial surgery 785
Extubation
• There is a risk of aspiration of blood, pus and debris. The oropharynx
and larynx should be suctioned at the end of the case (preferably under
direct vision). Patients should be extubated sitting at 30–45° to reduce
bleeding from venous congestion (or in the left lateral position with
head-down tilt if there is a high risk of airway soiling).
• Some anaesthetists extubate the patient using a ‘deep’, spontaneous
breathing technique. Some exchange the ETT for an LMA and allow the
patient to wake slowly in recovery. Others prefer to extubate awake.
• Whichever technique is used, the aim is to avoid bleeding and swelling
caused by coughing and straining. The use of a nasotracheal tube or
LMA, which do not stimulate the gag reflex as much as an oral tube,
facilitates a smoother extubation. Consider also spraying the vocal
cords with lidocaine at intubation.
• If a nasal tube has been used, it is possible to convert it into a
nasopharyngeal airway by withdrawing it until the tip lies in the
oropharynx, inserting a safety pin (to prevent the tube from slipping
back into the nostril) and cutting at the 15cm mark.
786
Mandibular fractures
Procedure Reduction and fixation of a fractured mandible
Time 1–3h
Pain +
Position Supine, with head-up tilt, head ring
Blood loss Variable.G&S usually not required
Practical techniques Nasal tube and IPPV. Fibreoptic intubation may
be required
Maxillary/mandibular osteotomy
Procedure Surgical realignment of facial skeleton
Time 3–6h
Pain ++
Position Supine, with head-up tilt, head ring
Blood loss Variable. Occasionally can be severe. G&S
Practical techniques Nasal tube and IPPV. Consider arterial line
Preoperative
• Assess airway, paying attention to tumour site and size, relevant
imaging, obstructive symptoms, mouth opening and neck mobility,
anaesthetic records, history of radiotherapy and previous maxillofacial/
neck surgery. Discuss with the surgeon.
• Patients frequently have a history of smoking and high alcohol intake.
Look for cardiovascular and respiratory comorbidity.
• Prepare long breathing circuit.
Perioperative
• Position and drape to allow access to head, neck and donor sites.
• Apply warming blanket and insert a temperature probe. Warming may
need to be reduced after 2–3h, as patients tend to overheat.
• Fine-bore feeding NGT should be inserted before surgery begins if
likely to be needed postoperatively.
• Ensure pressure areas are padded. Check periodically—pressure
damage and tissue loss can occur with prolonged surgery (especially
heels, elbows, nose and forehead).
• Give appropriate antibiotic prophylaxis as per local protocol (e.g. co-
amoxiclav 1.2g or clindamycin 600mg).
• Give steroids (e.g. dexamethasone 6.6mg) to reduce postoperative
swelling and for analgesia.
• If the surgery involves laser resection, minimise risks to the patient and
staff by reducing FiO2, using a laser tube if possible, inflating the cuff
with 0.9% sodium chloride (± methylthioninium chloride (methylene
blue)), using smoke-filtering masks and wearing eye protection. The
surgeon should use protective 0.9% sodium chloride-soaked swabs,
non-reflective instruments and smoke extraction (see % pp. 476–9).
• Avoid hypertension (see % pp. 1068–9). Normalise BP before wound
closure to check for bleeding.
Maxillofacial tumour surgery 791
Dental extractions
Procedure Dental extractions
Time 2–30min (much longer for additional restorative
work in adults)
Pain +/++
Position Supine
Blood loss Nil
Practical techniques LMA/nasal mask (nasal ETT for prolonged re-
storative work)
Preoperative
• Usually children 3–12y, dental phobics or patients with learning
difficulties.
• Beware of undiagnosed pathology, e.g. heart murmurs.
• Obtain consent for analgesic suppositories, if required.
• Give pre-emptive oral analgesia, e.g. paracetamol and ibuprofen.
• If a sedative premedication is needed, consider buccal or nasal
midazolam (500 micrograms/kg, max 10mg). Buccal absorption is more
rapid than oral. Effects are variable, and the patient should be closely
observed. Higher doses of up to 20mg (off product licence) have been
used successfully in larger adults.
• Ketamine, dexmedetomidine and clonidine are alternatives.
• Apply a topical anaesthetic for cannulation if IV induction planned.
Perioperative
• Give propofol for IV induction, and sevoflurane for inhalational
induction.
• Tape the eyes closed.
• Maintenance with volatile agent or IV agent.
• Use LA infiltration (by dentist/oral surgeon); opioids are not usually
needed for short day cases.
• Simple extractions do not usually require antibiotic cover.
• Stabilise the head and neck manually during the procedure.
Postoperative
• Place young children in the lateral position, slightly head-down at the
end.
• Regular paracetamol and ibuprofen.
Special considerations
• The operator may apply considerable pressure during extraction, often
resulting in an airway-obstructing ‘reverse jaw thrust’. The anaesthetist
should apply counterpressure to support and stabilise the head and
airway.
• Beware of potential hypoxia. Give 100% O2 for maintenance, if
necessary.
• Children with blocked noses can be safely anaesthetised using an LMA
(provided there is no URTI).
• (See Fig. 32.1 for dentition labelling nomenclature.) X-rays should be
displayed during surgery to ensure the correct teeth are removed.
Dental extractions 795
Quadrant labelling: Full set of deciduous teeth: Full set of adult teeth:
1: central incisor
2: lateral incisor 8 8
3: cuspid/canine
4: 1st premolar
5: 2nd premolar 8 13xx 8
6: 1st molar Example documentation
7: 2nd molar
8: 3rd molar (wisdom teeth)
X: roots
$: unerupted teeth
Preoperative
• Careful assessment of the airway. Check nostrils for patency.
• If the patient has a dental abscess, there may be marked swelling of the
face and severe trismus. AFOI may be necessary (see % pp. 393–6).
Perioperative
• Consider an LMA/oral tube for simple/unilateral extractions.
• For more complex procedures, consider a preformed nasal tube.
• Protect the eyes with tape and pads.
• The surgeon should anaesthetise the appropriate terminal branches of
the maxillary division (infraorbital, greater palatine, nasopalatine) and
mandibular division (inferior alveolar, lingual, buccal, mental) of the
trigeminal nerve with LA.
• Give an opioid and NSAID/paracetamol pre-or intraoperatively.
• IV antibiotics may be administered to minimise the risk of infection
(e.g. co-amoxiclav 1.2g or clindamycin 600mg for patients with penicillin
allergy). Check your local antibiotic policy.
• Steroids (e.g. dexamethasone 6.6 mg IV) may be given for antiemesis
and to minimise swelling.
Postoperative
• Balanced analgesia with regular paracetamol and NSAIDs. Prescribe
rescue analgesia with PRN tramadol or codeine phosphate. (Codeine is
no longer advised for children.)
Special considerations
• Talk to the surgeon to ascertain the likely length of surgery. Remember
that some patients require GA only because they are ‘dental-phobic’.
The surgical extractions may be simple, and the operative time
consequently very short. A short-acting muscle relaxant may be
required.
Extraction of impacted/buried teeth 797
Further reading
Royal College of Anaesthetists (2021). Chapter 12: guidelines for the provision of anaesthesia services
for ENT, oral maxillofacial and dental surgery 2021. M https://www.rcoa.ac.uk/gpas/chapter-12
Athanassoglou V, Patel A, McGuire B, et al. (2018). Systematic review of benefits or harms of routine
anaesthetist-inserted throat packs in adults: practice recommendations for inserting and counting
throat packs: an evidence-based consensus statement by the Difficult Airway Society (DAS), the
British Association of Oral and Maxillofacial Surgery (BAOMS) and the British Association of
Otorhinolaryngology, Head and Neck Surgery (ENT-UK). Anaesthesia, 73, 612–18.
Coyle M, Tyrrell R, Godden A, et al. (2013). Replacing tracheostomy with overnight intubation to
manage the airway in head and neck oncology patients: towards an improved recovery. Br J Oral
Maxillofac Surg, 51, 493–6.
National Institute for Health and Care Excellence (2008, updated 2016). Prophylaxis against infective
endocarditis: antimicrobial prophylaxis against infective endocarditis in adults and children undergoing
interventional procedures. Clinical guideline [CG64]. M https://www.nice.org.uk/guidance/cg64/
Coulthard P (2006). Conscious sedation guidance. Evid Based Dent, 7, 90–1.
The Society for the Advancement of Anaesthesia in Dentistry (SAAD). M http://www.saad.org.uk/
798
Chapter 33 799
Ophthalmic surgery
Peter B Williamson
Relevant anatomy and physiology 800
Preoperative considerations 802
Local anaesthetic techniques 804
General anaesthesia and sedation 808
Vitreoretinal surgery 811
Cataract and anterior chamber surgery 812
Strabismus surgery 813
Dacryocystorhinostomy 814
Penetrating globe injury 815
80
Tendon of
superior oblique
Central compartment
RETROBULBAR
Orbital
Levator palpebrae septum
superioris
Superior rectus
Optic
nerve
Superior
tarsus
Inferior
Inferior rectus
tarsus
Maxillary sinus
Orbital
Fascial sheath septum
of eyeball
Inferior
Peripheral
oblique
compartment
PERIBULBAR
Fig. 33.1 Vertical section through the orbit. Reproduced with permission of Oxford
Publishing Limited through PLSclear from McLeod G, et al. (2012) Principles and Practice of Regional
Anaesthesia, with permission from Oxford University Press. Copyright © Oxford University Press,
2012.
Relevant anatomy and physiology 801
Preoperative considerations
Preoperative assessment
Although classically described as the ‘extremes of age’, all age groups can
present for ophthalmic surgery:
• Paediatric: treatment of congenital pathology and strabismus
• Adult: treatment of refractive errors, floaters, penetrating eye injury
and ptosis
• Elderly: treatment of cataracts, retinal detachment and glaucoma.
The patient population tends to share some common features:
• DM or hypertension: predisposition to retinal pathology and
detachment; relevant as risk factors for cerebrovascular disease
and IHD
• COPD: predisposition to retinal vascular disease, more likely to cough
during surgery
• Thyroid disease: predisposition to ocular pathology; relevant as risk
factors for OSA and difficult airway
• Systemic diseases with ophthalmic presentations such as multiple
sclerosis, inflammatory bowel disease, sarcoidosis and connective tissue
disease
• Anxiety: very few people are relaxed about the notion of a surgeon
performing microsurgery on one of their most valued organs, let alone
awake with a drape over their head.
In addition to standard preoperative assessment and in-depth questioning
regarding the issues above, make special note of:
• The patient’s ability to lie flat and still
• Axial length (if available) on cataract biometry—if >26mm, it may
preclude peribulbar block
• INR/APTT/anticoagulant usage—peribulbar blocks may be
contraindicated with a certain degree of coagulopathy (exact cut-offs
may be dictated by local protocols)
• Tamsulosin—predisposes to ‘floppy iris syndrome’ which can make a
routine cataract more difficult.
Anaesthetic strategy
Determining conduct of anaesthesia (LA, sedation or GA) is one of the
most crucial strategic decisions to be made preoperatively.
LA techniques can be used in conjunction with sedation or GA as appro-
priate and each combination will present a different risk/benefit analysis. LA
techniques are usually preferred due to minimising cardiovascular instability
and drug load, providing good operating conditions and maintaining high
list turnover. They can also be performed by most ophthalmic surgeons.
Patient cooperation during block insertion is highly indicative of their likely
behaviour on the operating table.
Consider:
• Patient factors: level of cooperation/hearing/comprehension, degree
of anxiety and claustrophobia, movement disorders precluding
remaining still and flat, predilection for coughing, ASA grade and factors
which increase the risk of GA
• Anaesthetic factors for converting to GA: ease of IV access, degree of
shared airway
Preoperative considerations 803
(a) (b)
Orbit
M
M
ON
M
M
Fig. 33.2 Sub-Tenon’s block. (a) Making the incision in the inferior nasal quadrant of
the conjunctiva for a sub-Tenon’s block. (b) Cross-section through the orbit showing
the position of the needle during a sub-Tenon’s block. M, extraocular muscles; ON,
optic nerve. Black triangles, Tenon’s fascia; black arrow, sub-Tenon’s space; white
arrow, conjunctiva .Reproduced with permission of Oxford Publishing Limited through PLSclear
from Warman P. et al. (2014) Oxford Specialist Handbook of Regional Anaesthesia, Stimulation and
Ultrasound Techniques. Copyright © Oxford University Press, 2014.
• Clean the lids, eyelashes and eyebrows with iodine prep solution, then
retract the lower lid with a speculum.
• Ask the patient to look ‘up and out’ or to follow your fingers to the
correct position.
• Identify an avascular area about 5mm away from the limbus in the
inferonasal quadrant.
• Use Moorfields forceps to lift the conjunctiva.
• Make a small incision with blunt-ended Westcott’s scissors; you should
see the plain white, relatively avascular Tenon’s capsule.
• In some cases, you can proceed straight to insertion of a blunt sub-
Tenon’s cannula in an inferonasal direction and then injection; in others,
further blunt dissection of the plane with the scissors is required.
• Once the cannula is past the equator of the globe (syringe almost
vertical, perpendicular to the patient), you can administer LA
injectate—warn the patient they will experience some pressure behind
the eye at this point.
• Usual volume of injectate is 3.0–5.0mL of LA; then tape the blocked
eye closed.
• Complications: if you see considerable chemosis, you might be in
the wrong plane (subconjunctival); more serious complications are
extremely rare.
Peribulbar block
(See Fig. 33.3.) An extraconal injection of LA; quick to perform either via
the conjunctiva (cleaner and easier to anaesthetise) or transcutaneously
(if the patient cannot keep eye open) without requiring a speculum; pro-
vides good akinesia and analgesia with minimal disruption of conjunctiva.
However, as a sharp needle technique, it introduces the risk of globe per-
foration (<0.1%) and retrobulbar haemorrhage (0.07%). It is more dan-
gerous in the long eye (axial length >26mm increases the risk of globe
806
(a) (b)
• Establish needle entry point: at the medial canthus, clear of the lacrimal
apparatus and medial to the caruncle at the very edge of the skinfold.
• Insert 25G 25mm hypodermic needle perpendicular to the patient’s
face, parallel to the medial wall of the orbit, to a depth of 10–20mm
and administer a further 2.0–4.0mL of LA injectate, then tape the
blocked eye closed.
• Look for: akinesia of the eye, ptosis and block of orbicularis oculi.
• Complications: local complications include lower lid filling (which can
be remedied with firm digital massage), patient complaining of numb
teeth, globe perforation (if you see involuntary movement of the globe,
stop the block immediately and inform your surgeons) and retrobulbar
haemorrhage (rapidly proptosing eye); systemic side effects include
bradycardia and vasovagal syncope, or seizures in very rare cases.
Retrobulbar block
(See Fig. 33.4.) Retrobulbar block (intraconal injection of LA) is no longer
routinely performed due to the higher incidence of retrobulbar haemor-
rhage, globe perforation, LA toxicity and total spinal. It is still of clinical
relevance as rapid ptosis and block onset with only a few mL of LA during a
peribulbar block could indicate inadvertent retrobulbar block—either stop
injecting or adjust the dose to 2.0–4.0mL. Inform your surgeon of likely
retrobulbar injection.
Tendon of
Central compartment superior oblique
RETROBULBAR
Orbital
Levator palpebrae septum
superioris
Superior rectus
Optic
nerve Superior
tarsus
Orbital
Inferior rectus septum
Maxillary sinus
Fascial sheath
of eyeball
Peripheral
compartment
PERIBULBAR Inferior
tarsus
Emergence
The key objective at emergence is to prevent coughing, which raises IOP
and strains ophthalmic sutures.
• Optimising the conditions and timing for the removal of the airway are
both important.
• Additional techniques sometimes employed to remove the airway
include: deep extubation and/or exchange to an SGA/oropharyngeal
airway, spraying the cords with lidocaine and IV injection of lidocaine
(1mg/kg).
Sedation
• If surgery is proceeding under topical or block, it is not uncommon for
the patient and/or surgeon to request sedation.
• There is still a widespread belief that sedation is universally ‘safer than
GA’ when, in fact, the patient can be disinhibited, uncooperative and
free to move and/or hypoventilate intraoperatively.
• Careful patient selection is vital.
• IV access, supplementary O2 and standard monitoring are required—
capnometry attached to either nasal cannulae or a face mask modified
to avoid impinging on the surgical field is ideal.
• Midazolam 0.5–2.0mg has a role despite the risk of POND, given the
need for both cooperation and anxiolysis.
• Very low doses of propofol (10–30mg) can also provide anxiolysis and
gentle suppression of consciousness during block insertion.
• Boluses of opioids such as alfentanil (100–200 micrograms) or fentanyl
(25–50 micrograms) can be titrated to effect if the patient experiences
pain, but must be offset against the risk of inducing nausea and vomiting.
• Allow the patient to wake after block insertion, but before surgery
begins—patients who regain consciousness after this are likely to be
distressed by their change in situation (different room, drapes, light
shining in their eye, etc.) and reach for their eye almost as a reflex.
• Reassure patients verbally; hold their hand, and regain their full
cooperation before surgery.
• Have a plan to convert to GA if required.
Vitreoretinal surgery 811
Vitreoretinal surgery
Procedures Intraocular posterior chamber retinal surgery, including
vitrectomy, cryo/laser therapy, removal/insertion of oil/
gas, scleral banding and retinopexy
Time 90–180min
Pain ++/+++
Position Supine
Blood loss None
Practical Reinforced LMA + IPPV + LA block
techniques ETT (RAE or reinforced) + IPPV + LA block
LA block ± sedation
Preoperative
• Past medical history often includes COPD, hypertension, DM and IHD
as these are also risk factors for retinal disease.
• Check axial length if possible—patients may have long eyes (hence the
retinal detachment) which may preclude peribulbar block.
• Patients sometimes come for repeat admissions and are used to having
ophthalmic procedures (it can be difficult to site a sub-Tenon’s because
of scarring of the tissue planes).
• ‘Mac-on’ retinal detachments (where the macula remains undetached)
are urgent sight-saving procedures.
Perioperative
• Surgery is long, stimulating and performed in the dark.
• Many require a GA due to length and complexity of the procedure.
• Additional LA block is highly advised to smoothe out the intense
stimulation, and is often inserted by the surgeon following port insertion
(either a sub-Tenon’s or careful medial peribulbar).
• Ensure adequate opioids on board to cover the extremely stimulating
port insertion (alfentanil bolus or remifentanil infusion).
• IPPV via an SGA with either TIVA or a volatile is ideal.
• Avoid N2O as the surgeons use gases of specific densities and
postoperative posturing to hold retinal detachments in place.
• Modest doses of fentanyl, morphine or diamorphine may be required
for postoperative analgesia in very painful cases, e.g. cryotherapy.
• Ensure adequate depth of anaesthesia during the final phases of
surgery—the ports are removed last, so the globe is ‘open’ right to the
end.
Postoperative
• The LA block is usually sufficient.
• Some patients might require simple analgesics, e.g. paracetamol and
tramadol, especially if cryotherapy was part of surgery.
281
Preoperative
• Ensure the patient can be still and flat for cataract extraction.
• Highlight any manual handling issues which might disrupt a high-turnover
list.
Perioperative
• Cataract extractions are almost always performed under topical LA or
sub-Tenon’s block.
• Requests for sedation are not uncommon (see % p. 810).
• Tape a swab over the ear on the operative side to catch irrigation fluid.
• GA cataracts can usually be undertaken with the patient spontaneously
breathing through an SGA—opioids at induction are to be used
cautiously, given the 10–15min procedure time.
• Patients with active inflammation, e.g. due to glaucoma, often need a
block as topical LA is less effective.
• Shunt insertion and trabeculectomy are longer procedures, which
usually require a GA and can be blocked by the surgeons towards the
end (owing to the operation being on the conjunctiva itself ).
• For longer procedures, IPPV is recommended; using an LMA to facilitate
coughless emergence must be balanced against the risk of aspiration.
Postoperative
• Postoperative analgesic requirements are negligible as topical LA is very
effective.
Strabismus surgery 813
Strabismus surgery
Procedures Extraocular squint correction
Time 60min
Pain ++
Position Supine
Blood loss None
Practical techniques Reinforced LMA + IPPV/SV
ETT (RAE or reinforced) + IPPV
Preoperative
• Common paediatric day case.
• Patients are usually otherwise well. Strabismus can occasionally be part
of a syndrome.
• Consider a sedative premedication if the child is distressed (they may
have visual impairment).
Perioperative
• Requires a GA (IV or inhalational induction as indicated).
• Avoid suxamethonium as it alters extraocular muscle tone and there
may be some association between squints and MH.
• Depth of anaesthesia should facilitate neutral gaze; TIVA with propofol
is useful as it also reduces PONV.
• Be vigilant for the oculocardiac reflex—avoid hypercapnia and be
prepared to treat with vagolytics.
• SV via an LMA is usually sufficient; IPPV may be required if ETCO2 is
high; intubate if indicated.
• Multimodal PONV prophylaxis (ondansetron 0.1 mg/kg,
dexamethasone 0.1 mg/kg).
• Sub-Tenon’s block performed by the surgeon, paracetamol 15mg/kg
and diclofenac 1mg/kg for postoperative analgesia (avoid opioids if
possible).
Postoperative
• There is a high incidence of PONV, especially with opioids.
• Moderate analgesic requirements, e.g. PO morphine or tramadol.
• Standard paediatric day case concerns.
481
Dacryocystorhinostomy
Procedures EUA tear duct, insertion of drainage tube,
dacryocystorhinostomy
Time 45min
Pain +/++
Position Supine + head-up
Blood loss Low, but near airway
Practical techniques ETT (RAE or reinforced) + IPPV
Reinforced LMA + IPPV
Preoperative
• Usual concerns for eye and ENT surgery apply.
• Establish if the patient is likely to tolerate hypotension.
Perioperative
• Standard anaesthetic induction of choice as indicated.
• Using an SGA avoids complications of intubation, but blood may soil
the airway in some difficult procedures.
• Multimodal approach to minimising blood loss: Moffett’s solution/
co-phenylcaine to the nose after induction, IPPV desirable as moderate
hypocapnia reduces blood loss, head-up tilt to improve venous
drainage, moderate induced hypotension (remifentanil can be useful).
• Traditionally, a throat pack was used for all cases, but this is falling out
of favour based on risk/benefit.
• Analgesia usually consists of paracetamol, an NSAID and remifentanil
infusion plus a bolus of longer-acting opioid.
• Magnesium can also be useful both to reduce BP and as an analgesic.
• Ask your surgeon to give LA to the ducts if possible.
Postoperative
• Postoperative analgesia can be provided by paracetamol, an NSAID and
an oral opioid such as tramadol or codeine.
Penetrating globe injury 815
Preoperative
• In addition to standard anaesthetic concerns, adults with penetrating
eye injury are often extremely anxious, in pain and unfasted.
• Children represent a particular problem as they are usually also
uncooperative, crying and rubbing their eye.
• Surgery is an emergency, as coughing or straining can result in expulsive
haemorrhage of globe contents, but must be balanced against fasting
and optimising for GA.
• Use preoperative opioid analgesia with extreme caution (as vomiting is
catastrophic) and give pre-emptive antiemetics.
Perioperative
• Patients should generally be treated as being at risk of aspiration,
rendering SGAs less useful.
• Depending on the clinical scenario, induction can be ‘ophthalmic’ or an
RSI for rapid airway control in the unfasted patient, or have elements
of both.
• RSI dose of rocuronium (1.0–1.2mg/kg) with rescue dose of
sugammadex (16mg/kg) on standby in case of difficult airway is ideal.
• Suxamethonium raises IOP (vs induction agents which lower it) and
familiarity with its use is falling; however, it may still be used.
• Intubating with VL as 1st-line reduces the pressor response and
removes the need for multiple laryngoscopies with difficult airways.
• LA techniques are not effective (or even possible) with these cases;
long-acting IV opioids are commonly required.
Postoperative
• Recovery analgesia can be provided with topical LA drops and boluses
of fentanyl, morphine or diamorphine as required.
• Regular ward analgesia can be paracetamol, an NSAID of choice and a
PRN weak opioid given PO.
Further reading
Anker R, Kaur N (2017). Regional anaesthesia for ophthalmic surgery. BJA Educ, 17, 221–7. M
https://doi.org/10.1093/bjaed/mkw078
681
Chapter 34 817
See also
% Endovascular treatment of intracranial aneurysms p. 580
% Endovascular thrombectomy p. 582
% Endovascular stenting of elective or emergency abdominal
aortic aneurysm p. 597
% Resuscitative endovascular balloon occlusion of the aorta
p. 1000
81
Anaesthesia for CT
• CT scanning does not restrict the type of equipment used, but space
can be limited, so compact machines and monitors are ideal.
• The patient, anaesthetic machine and monitors must all be visible from
the control room.
• The patient’s head is usually accessible during CT scanning, so an SGA
may be used if airway protection is not required.
• Anaesthesia or sedation sufficient to produce immobility and lack of
awareness is all that is required for diagnostic procedures.
Hazards
• CT scanning uses ionising radiation, so it is preferable for the
anaesthetist to monitor the patient from outside the scan room. If it
is necessary to remain near the patient, wear appropriate radiation
protection and use barriers if available.
• Cannulae, catheters, drains and ETTs can pull out during movement of
the patient through the scanner—check nothing snags beforehand.
Contrast media
• IV contrast media for X-ray imaging are usually iodine-based, non-ionic,
water-soluble compounds. Agents may trigger allergic reactions (ask
about iodine sensitivity).
• Radiographers will usually give IV contrast, but you may be asked to
administer it in anaesthetised/paediatric patients. The radiographers
should ensure the correct volume (dependent on preparation,
investigation, age and weight) is provided according to local policy.
• Some ‘dynamic’ investigations (e.g. aortography) require contrast to be
administered while the scan is occurring.
• Contrast is viscous and can be difficult to inject through small cannulae
or injection ports.
• Automated contrast injectors should not be connected to standard
central venous lines. The high pressure developed by the rapid injection
of viscous medium down a long, narrow lumen can burst the line.
PowerLine® catheters allow power-injection of contrast media.
• Contrast media may cause kidney injury in patients with dehydration
or impaired renal function, so ensure patients are adequately hydrated.
Lactic acidosis can be precipitated in patients taking biguanides
(metformin)—ideally avoid for 48h before and after the scan.
Practical considerations
• Move metal-containing objects (e.g. ECG leads, pressure transducer
cables) away from the area being scanned to prevent X-ray artefact.
• Thoracic and abdominal scans may require ‘breath-holds’ of a few
seconds to reduce respiratory movement artefact. Both paralysed and
spontaneously breathing patients can be ventilated manually, and their
lungs held in inspiration for each individual scan.
• The patient’s arms ideally need to be positioned above the head during
thoracic and abdominal scans. Soft Velcro straps attached to the gantry
or wide adhesive tape are useful for securing the limbs.
820
Equipment safety
All equipment and implants are classified into one of three categories:
• MRI Safe: contains no material that would cause a hazard. Can be taken
right into the scanner.
• MRI Conditional: safe for use under conditions specified by the
manufacturer. Do not place MRI conditional kit on the moving table as it
might move beyond the 5mT line.
• MRI Unsafe: must not be taken into the MRI scanner.
The scan room is usually shielded to stop external electrical interference
swamping the MRI signals. All electrical equipment in the scan room must
also be fully shielded. Electrical conductors entering the room (e.g. moni-
toring cables) require special radiofrequency filters.
Two alternative approaches are feasible
• Specialised ‘MRI Conditional’ equipment within the scan room
• Conventional kit outside the magnetic field in the control room.
Departments should standardise on one approach, depending on space,
funds and frequency of use. Each approach has its pros and cons.
Typical setup
• Induction and recovery area adjacent to, but outside the scan room,
equipped with conventional anaesthetic machine and monitoring.
• Non-magnetic tipping trolley for patient transfer into the scanner.
• Piped gases, scavenging and suction in induction and scan areas.
• Either a compact anaesthetic machine and ventilator in the control
room with a 10m coaxial (Bain) breathing system and a gas/agent
side-stream analyser with capnograph display fitted with an extended
sampling tube (increases the response time by 5–10s).
• Or an ‘MRI Conditional’ anaesthetic machine in the scan room with
circle circuit.
• ‘MRI Conditional’ monitoring devices: fibreoptic pulse oximeter probe
with shielded cable; ECG with carbon fibre leads and electrodes; NIBP
cuffs with an extended hose and non-metallic connectors.
• Multiple manufacturers produce ‘MRI Conditional’ monitor units within
the scan room, with a slave unit in the control room.
Practical considerations and techniques
Airway
• Patient access is restricted physically and ‘magnetically’. Ensure the
airway and vascular access are well secured.
• Intubate and ventilate: babies and small children (<10kg), patients with
raised ICP (or suspected raised ICP) or patients needing a protected
airway. A RAE tube keeps the breathing circuit clear of the coil in
patients having head scans.
• SV via an SGA can be considered in larger children and adults with no
risk of raised ICP. Do not use a flexible LMA containing a metal wire
spiral. i-gels have no metallic components.
• Tape the pilot balloon of a cuffed ETT or LMA outside the coil to avoid
image distortion by the metal spring.
82
Sedation
• Benzodiazepine sedation (PO or IV) may be used for healthy, but
claustrophobic adults. Strong analgesia may be required for patients
with severe back or root compression pain to tolerate positioning.
• The role of sedation for MRI scanning in children is unclear. Some
children’s centres have reported successes with structured sedation
programmes, e.g. using dexmedetomidine. However, the safety of
having heavily sedated children in the medical imaging department
without direct anaesthetic supervision has been questioned.
Tips for IPPV through a 10m breathing system
• Use a system that functions as a ‘T-piece’ (Mapleson D or E), so dead
space is unaffected by the length. Ayre’s T-piece and Bain systems work
well. Both can be used for babies and small children.
• Airway pressures measured near the ventilator may not accurately
represent distal pressures at the ETT.
• VT delivered to the lungs will be reduced by ‘compression losses’ of the
gas within the system and by expansion of the tubing during inspiration,
making it difficult to compensate for significant leaks around uncuffed
ETTs—use a slightly larger tube to minimise leaks.
• As a result of these effects, IPPV using a simple pressure generator
(e.g. Penlon Nuffield 200 with a Newton valve) may not be effective in
children weighing >15kg.
• i expiratory resistance of some long systems (e.g. Ayre’s T-piece)
generates a PEEP which increases with FGF.
Intensive care patients
• MRI scans in ICU patients confer greater risk and require detailed
planning. The risk/benefit balance should be assessed by senior
clinicians. Avoid scanning patients who are haemodynamically or
otherwise unstable unless this will have a substantial impact on
outcome.
• As the patient may lack capacity, full checks (including, if necessary, plain
radiographs) must be performed to confirm there are no hazardous
metallic implants or foreign bodies present.
• Conventional monitoring (including ICP transducers and temporary
pacing wires) should be removed or replaced with ‘MRI Safe’ equipment
before the patient enters the scan room.
• Infusion lines must be long enough to allow pumps to be located at a
safe distance from the magnet—ideally outside the scan room. Prepare
duplicate pumps in the control room, with extended infusion lines
threaded with the breathing system into the scan room. Connect the
patient to the running infusions while outside the room. Be especially
cautious with infusions such as noradrenaline—check the patient is
stable, then move into the scanner.
Cardiac arrest
• Start basic life support (BLS) with a non-metallic self-inflating bag.
Rapidly remove the patient from the scan room on a non-magnetic
trolley and continue ALS outside the 0.5mT boundary.
• Do not attempt ALS in the scan room and do not allow the cardiac
arrest team into the scan room.
Anaesthesia for interventional radiology 823
Embolisations
• Blood vessels are selectively occluded to treat or prevent bleeding and
stop tumour growth. A variety of agents, including metal coils, special
foams, plugs and microbeads, are used to induce the embolus.
• Superficial procedures, the use of alcohol for embolisation or procedures
involving AVMs can be very painful and require sedation or GA.
• Interventional radiology treatment of intracranial aneurysms requires
GA because the patient must be completely still. Similar anaesthetic
techniques as for craniotomy (see % pp. 561–2; % pp. 580–1), with an
ETT, invasive monitoring, avoidance of changes in CPP and maintenance
of normocapnia and normothermia, should be used.
• Uterine artery embolisation is included in NICE guidance [IPG367] for
fibroid disease. Balloon occlusion of uterine arteries can be considered
prior to CS in a patient anticipated to bleed, or can be inserted
emergently in the management of 1° postpartum haemorrhage (though
the logistical challenges to facilitate this transfer are often considerable).
• Chemoembolisation: combination of delivering cancer treatment
directly to a tumour and then blocking its blood supply.
• Patients who require emergency embolisation for trauma-related
haemorrhage (e.g. spleen, kidney, liver, intercostal arteries) require
the presence of an anaesthetist, even if not having sedation or GA, to
manage the transfusion and all other aspects of their care.
Radiofrequency ablation
• RFA destroys tissue by heating, e.g. a tumour. Although the ablation
of the tumour is fairly quick, the localisation can take time and the
procedure is painful and stimulating, so requires a GA.
• RFA is commonly used to treat hepatic and renal tumours—either
metastases, difficult-to-reach tumours, or tumours in those patients
who are too frail for an open procedure.
Thrombolysis and thrombectomy
• Minimally invasive dissolution, or removal, of blood clots to improve
blood supply. Contrast media is used to help define the clot, which is then
dissolved by medication or removed by a mechanical device. This can
be used in the acute management of CVE, to treat arteries in diseased
vascular beds, DVT, coronary emboli, PEs and thromboses in fistulae.
• Anaesthetic technique for acute CVE thrombectomy should be
determined on an individual patient basis. Whether LA only, sedation
or GA is chosen, adherence to standard physiological targets (see
% pp. 558–60; % pp. 578–9) is required.
Transjugular intrahepatic portosystemic shunt
(See % p. 698.)
• A stent, inserted via the jugular vein, is used to connect the portal vein
and hepatic vein, thereby reducing portal hypertension and bleeding risk
in patients with end-stage liver disease.
• GA with ETT and invasive monitoring is the preferred technique due
to procedure duration and the patient’s physiological condition and
comorbid disease. Coagulopathy is common, may be profound, and
should be corrected.
• Peri-procedural risks include haemorrhage, heart failure and
encephalopathy. Postoperative care may require HDU.
Anaesthesia for interventional radiology 825
Other procedures
• Vertebroplasty/cementoplasty: injection of cement into bone to reduce
pain in tumours and fractures. Can be painful and requires sedation or
GA.
• Cryoablation: destruction of tissue by freezing. Typically not painful, and
often sedation is all that is required.
• Vascular catheter placement: sedation and LA are suitable for most
patients; GA will be required for children.
• GI viscera can be dilated and stented. Oesophageal dilation can be
painful and requires analgesia and consideration of requirement for
airway protection in case of regurgitation.
• IVC filter insertion: not painful.
Fluid aspiration, biopsies and percutaneous drain
placements
• Usually performed under ultrasound guidance, but may require CT for
deeper structures. Typically not painful.
• Discuss positioning and apnoeic periods with the radiologist
pre-procedure.
826
• Induction of the patient is most easily performed in the lab itself, but
this comes with noise and distraction—be prepared to manage this.
Make sure there is good access to the patient’s airway, your drug and
airway trolleys and anaesthetic machine when inducing anaesthesia on
the procedure table. Move the C-arm out of the way, if possible.
• In some situations (difficult airway, risk of regurgitation, morbid
obesity), it may be better to induce the patient on a trolley or bed to
allow for a more head-up position or the ability to tilt the trolley.
• Maintaining normothermia can be challenging—use a fluid warmer and
an underbody forced air warming device.
• Many patients are anticoagulated. For those who are not (or have
had their anticoagulation reversed for the procedure), remember to
consider VTE prophylaxis such as calf pumps.
• Ensure recovery facilities are available with an appropriately equipped
recovery bay and experienced recovery nurses. In some situations, it
may be necessary to transfer the patient to a theatre recovery area.
• Some patients will need to remain monitored on the cardiology ward
overnight. The need to apply compression to groin access sites may
limit the degree of head-up positioning in the early postoperative
period.
• In the event of unexpectedly prolonged and complicated procedures,
maintain contact with colleagues in theatres such as the duty
anaesthetist or the on-call anaesthetic team. Breaks, advice and/or
immediate help may be required. Anaesthetic activities running over
time in remote sites can be easily overlooked.
82
Other considerations
• The procedure table is narrow and does not tip or go head up. Table
controls may be distant and unfamiliar—the radiographer can assist.
Patients with a difficult airway or obesity may be better anaesthetised
on a trolley and transferred once asleep.
• Use an ‘underbody’ forced air warmer with temperature monitoring.
• Femoral venous access is used to access the heart; remifentanil infusion
as part of the anaesthetic technique can reduce coughing at extubation
and subsequent groin haematoma.
• Sodium chloride 0.9% irrigation around the ablation catheter tip
results in a significant fluid load (1.5L). Balance with restricted fluids
± vasopressors if needed, as urinary catheterisation is not usually
performed.
• In the cath lab, the WHO sign-in is performed with the whole team.
• Once the patient is asleep, wires, monitors, drip stands and the
anaesthetic machine need to be positioned to avoid the C-arm and
allow visualisation of the monitor and patient access as required.
During the procedure
• Relatively unstimulating procedure—BP support may be required.
• TOE can be needed to visualise trans-septal left atrial access when
challenging with fluoroscopy alone.
• Heparin is always given for left-sided procedures, even when the patient
is anticoagulated. ACT target usually >300s and reversed by protamine
at the end; this is usually managed by the cardiologist.
• Induced arrhythmias may cause haemodynamic instability and it can be
necessary to cardiovert the patient during the procedure.
• Isoprenaline and adenosine may be given at the discretion of the
cardiologist towards the end of the procedure and will cause
tachyarrhythmias and brief asystole, respectively.
• Analgesia requirements are minimal—LA at access sites, IV paracetamol
and antiemetics are sufficient.
• An in–out catheter can improve comfort in recovery.
Complications
• Include vascular injury/pseudoaneurysms/haematomas/A–V fistulae
(1:100).
• The cardiologist will routinely perform a TOE at the end of the
procedure to check for tamponade; a sudden unexplained drop in
BP during the procedure could indicate tamponade and should be
communicated (1:100–1:200 risk).
• Oesophageal injuries such as perforation or atrio-oesophageal fistula
are serious complications but typically present 7–10d post-AF ablation.
• Phrenic nerve injury is usually transient and is particularly common
during cryoballoon ablation of AF.
• Pericardial effusion (1:100–1:200).
• CVE (1:250).
834
Further reading
Wilson SR, Shinde S, Appleby I, et al. (2019). Guidelines for the safe provision of anaesthesia in
magnetic resonance units 2019. Guidelines from the Association of Anaesthetists and the Neuro
Anaesthesia and Critical Care Society of Great Britain and Ireland. Anaesthesia, 74, 638–50.
Dooley N, Lowe M, Ashley EMC (2018). Advances in management of electrophysiology and atrial
fibrillation in the cardiac catheter laboratory: implications for anaesthesia. BJA Educ, 18, 349–56.
Levy D, Bigham C, Tomlinson D (2018). Anaesthesia for patients with hereditary arrhythmias part I:
Brugada syndrome. BJA Educ, 18, 159–65.
Royal College of Radiologists (2018). Sedation, Analgesia and Anaesthesia in Radiology Department,
2nd edn. London: Royal College of Radiologists.
Harris P, Lysitsas D (2016). Ventricular arrhythmias and sudden cardiac death. BJA Educ, 16, 221–9.
Mavrides E, Allard S, Chandraharan E, et al.; Royal College of Obstetricians and Gynaecologists
(2016). Prevention and management of postpartum haemorrhage. BJOG, 124, e106–49.
Landrigan-Ossar M (2015). Common procedures and strategies for anaesthesia in interventional
radiology. Curr Opin Anesthesiol, 28, 458–63.
Barnard M, Martin B (2010). Cardiac Anaesthesia (Oxford Specialist Handbooks). Oxford: Oxford
University Press.
National Institute for Health and Care Excellence (2010). Uterine artery embolisation for fibroids.
Interventional procedures guidance [IPG367]. M https://www.nice.org.uk/guidance/IPG367
Sweeting CJ, Thomas PW, Sanders DJ (2002). The long Bain breathing system: an investigation into
the implications of remote ventilation. Anaesthesia, 57, 1183–6.
836
Chapter 35 837
See also
% Obstetric anaesthesia in the patient with a spinal cord injury
pp. 307–8
% Pregnancy and trauma p. 988
83
• Renal blood flow increases by 75% at term and GFR by 50%. Both urea
and creatinine plasma concentrations fall.
• Neurological tissue has a greater susceptibility to the action of LA
during pregnancy and ‘MAC’ is also reduced.
• The volume of distribution increases by 5L, affecting predominantly
polar (water-soluble) agents. Lipid-soluble drugs are more affected by
changes in protein binding. The fall in albumin concentration increases
the free active portion of acidic agents, while basic drugs are more
dominantly bound to α-1 glycoprotein. Some specific binding proteins,
such as thyroxine-binding protein, increase in pregnancy.
• Plasma cholinesterase concentration falls by about 25%, but due
to the increased volume of distribution, the duration of action of
suxamethonium is little changed.
840
Neurological damage
• Neurological sequelae following delivery under GA is as common as
delivery under CNB anaesthesia, suggesting that obstetric causes from
nerve compression (e.g. pressure from fetal head, prolonged labour or
poor maternal positioning) are probably more common than any effects
from the CNB technique.
• Direct nerve root damage may be associated with pain on insertion
of a CNB. Temporary neurological deficits occur in roughly 1:3000
procedures. Prolonged neurological deficit is much rarer (71:15 000)
and permanent major neurological damage probably occurs in
<1:80 000 CNBs in the obstetric population.
• Neurological damage from potentially reversible causes, such as
infection (e.g. vertebral canal abscess), ischaemia or haemorrhage (e.g.
subdural haematoma), may be immediate or delayed.
• It is unusual to have a dense motor block (an inability to straight leg
raise) in the context of low-concentration LA epidural infusions or
if >4h have passed since the last high dose of spinal or epidural LA.
Immediate anaesthetic review is indicated.
• If an epidural haematoma is suspected and an epidural catheter is in situ,
this should remain until the diagnosis has been excluded as removal may
worsen potential bleeding. Removal of epidural catheters in any patient
should be done with consideration of coagulation status.
• Symptoms from a vertebral canal abscess can occur anytime between a
few days to several months after the CNB procedure. Diagnosis can be
difficult, with fever, back pain, neurological deficit and signs of localised
infection variably present. A high index of suspicion is required.
• Reversibility is time-critical. Depending on the context, urgent MRI with
neurosurgical review and/or nerve conduction studies may be required.
Dural puncture and postdural puncture headache
(See % pp. 848–51.)
84
Symptomatic treatment
• Bed rest alleviates symptoms, but the effect is usually transient
and increases the risk of VTE. If immobile for ≥24h, consider VTE
prophylaxis (time LMWH doses to avoid delaying blood patch if
needed).
• Adequate fluid intake (usually oral) should be encouraged, although
there is no evidence that hydration reduces the incidence of PDPH.
Excessive fluid intake may be harmful.
• Simple analgesics are the mainstays of symptomatic treatment. They
should always be offered, even though they are unlikely to completely
relieve a PDPH.
• Caffeine reduces intracranial vasodilation which is partially responsible
for the headache. There is limited evidence that the severity of PDPH
is reduced and some concern that seizures may be increased with high-
dose caffeine. A maximum of 900mg of caffeine is recommended per
day, reduced to 200mg if breastfeeding. A high-energy drink or coffee
contains 7150mg of caffeine.
• There is insufficient evidence currently to recommend routine use of
any of the following: sphenopalatine ganglion block, greater occipital
nerve blocks, theophylline, ACTH analogues, steroids, triptans,
gabapentin, acupuncture, epidural opioid or fluid.4
• Definitive treatment is with epidural blood patching.
Epidural blood patch
Only a third of postpartum women with PDPH will have complete reso-
lution of symptoms after an epidural blood patch, although 50–80% will re-
port some benefit. Relapse can occur and the need for a 2nd blood patch is
common.5 Lower success rates occur if blood patches are performed <48h
after the dural puncture.
The proposed mechanism of action of blood patch is twofold—blood
injected into the epidural space compresses the dural sac and raises the ICP,
which can produce almost instant improvement in pain. Secondly, blood
forming a clot over the dural tear seals the CSF leak and the dural sac grad-
ually refills.
Although serious complications after blood patching are rare, backache
is common—35% of women experience some discomfort 48h post-patch
and 16% have prolonged backache (mean duration 27d). Repeated dural
puncture is possible, and neurological deficits, arachnoiditis, infection,
epileptiform fits and cranial nerve damage have all been reported.
Technique
• Written information should be offered to the patient and written
consent obtained. Consent should include reference to the success
rate (as above), and that repeat dural puncture is possible, that back
pain during and for several days after epidural blood patch is common
and that there can be significant and rare complications, including nerve
damage, bleeding and infection.
• The patient should be apyrexial with a normal WCC.
• Two operators are required. One should be an experienced
‘epiduralist’, and the other is required to take blood in a sterile manner.
• The patient may benefit from a period of bed rest before performing
the patch to reduce the CSF volume in the epidural space.
Dural puncture and postdural puncture headache 851
• Aseptic technique must be meticulous at both the epidural site and the
site of venepuncture.
• Blood injected into the epidural space predominantly spreads cephalad,
so blood patches should be performed at the same or lower interspace
as the dural puncture, with the woman in the lateral position to
minimise CSF pressure in the lumbar dural sac.
• When the epidural space has been identified, 20mL of blood is
obtained.
• Inject the blood slowly through the epidural needle until either a
maximum of 20mL has been given or pain develops (commonly in
the back or legs). If pain occurs, pause and if the pain resolves, try
continuing a slow injection. If the pain recurs, then stop.
• Maintain bed rest for 2h to allow a clot to form.
• As far as possible, the patient should avoid straining, lifting or excessive
bending for 48h.
• Follow-up is still required and every woman should have clear
instructions to contact the anaesthetists again if symptoms recur.
852
Caesarean section
With all CS, it is vital that the obstetrician clearly communicates the degree
of urgency to all staff. The classification in Table 35.2 is a modification of
that originally proposed by Lucas.
There are three principal techniques for CNB: epidural, spinal and CSE.
Epidural anaesthesia is mostly used for women who already have labour
epidural analgesia. Spinal anaesthesia is the most popular technique for
elective CS, although in some centres, CSE is preferred.
The speed of onset of sympathectomy that occurs with spinal anaes-
thesia (as opposed to epidural) results in a greater fall in maternal CO and
BP (see % p. 861) and may be associated with a more acidotic neonate at
delivery. When there is particular concern about the speed of onset of a
block, a CSE approach can be used, injecting only a small dose of intrathecal
LA and extending the block if required using the epidural catheter. Spinal
anaesthesia generally provides a better quality of analgesia than epidural
anaesthesia.
Preparation for CS
Whatever anaesthetic technique is chosen, careful history should be taken
and appropriate examination performed. This should include checking:
• Blood group and antibody screen. Routine X-matching of blood is not
required, unless haemorrhage is expected or antibodies that interfere
with X-matching are present.
• Ultrasound reports to establish the position of the placenta. A low-
lying anterior placenta puts a woman at risk of major haemorrhage,
particularly if associated with a scar from a previous CS (see %
pp. 884–5).
An explanation of the technique should be offered. Although CS under
CNB becomes routine for the anaesthetist, it can be intimidating for the
mother. Reassurance and support are important. The possibility of compli-
cations must be mentioned, including the risk of intraoperative discomfort
and its management. Pain during CNB remains a leading obstetric anaes-
thetic cause of maternal litigation. Document all complications that are
discussed.
Caesarean section: epidural 855
Spinal anaesthesia is the most commonly used technique for elective CS.
Technique
• Preparation as per CS under epidural (see % pp. 855–6).
• A sitting position usually makes finding the midline easier, which may
be helpful with obese patients and may be associated with a faster
onset, although the height of block is less predictable. A lateral position
is associated with a slower onset of block, particularly if a full lateral
position is maintained until the block has fully developed. The block
height may be slightly more consistent, and women sometimes find it
more comfortable than sitting.
• Perform spinal anaesthetic at L3/4 interspace or lower using a 25G
or smaller pencil-point needle. The level of the iliac crests usually
corresponds to the spinous process of L4 (Tuffier’s line), although there
is variation between individuals.
• With the orifice pointing cephalad, inject the anaesthetic solution,
e.g. 2.5mL of 0.5% hyperbaric bupivacaine with 300 micrograms
diamorphine or 15 micrograms fentanyl. Intrathecal diamorphine
improves postoperative analgesia, while intrathecal fentanyl has little
postoperative analgesic benefit.
• After injection of the solution, move the woman to a supine position
with left lateral tilt or wedge. When hyperbaric LA solutions are used, it
is important that the cervical spine is kept elevated (pillow) to prevent
LA spreading to the cervical dermatomes.
• Hypotension is more common with spinal anaesthesia than with
epidural anaesthesia. Try to prevent hypotension, rather than treating it
after it has occurred. When possible, a continuous infusion of pressor
agent should be started at the time of the injection of spinal LA (see
% p. 861).
• Continue as for epidural anaesthesia for CS (see % pp. 855–6).
85
Special considerations
• Although the incidence of major complications of CNB, as identified by
the Third National Audit Project of the RCoA, was higher when a CSE
technique was used, the numbers were very small (two or four patients,
depending on whether an optimistic or a pessimistic analysis was used)
and the study cautions against overinterpretation of these results.
860
Inadequate anaesthesia
Every patient should be warned of the possibility of intraoperative discom-
fort and this should be documented. Of attempted CNB anaesthetics for
CS 1-5% are inadequate for surgery. The majority should be identified be-
fore the operation commences.
Inadequate block identified before surgery has started
Epidural
• If no block develops, then the catheter is incorrectly positioned. It may
be reinserted or a spinal performed.
• If a partial but inadequate block has developed, the epidural may be resited
or withdrawn slightly. If the toxic limit for the LA agent has been reached,
elective procedures can be abandoned, but for urgent procedures, a GA
or a spinal anaesthetic will be required. Be very cautious about converting a
partially functioning epidural anaesthetic to a spinal anaesthetic. Although a
normal spinal dose of hyperbaric LA is commonly used, aggressive control
of the spread of LA is needed to prevent a high or total spinal occurring.
This is done by positioning the head up initially and then slowly lowering the
head to achieve the required level of block.
Spinal
• If no block develops, a repeat spinal may be performed.
• If a partial but inadequate block develops, an epidural may be inserted
and slowly topped up.
• Use a GA if required.
Intraoperative inadequate block
In this situation, good communication with the mother and surgeon is es-
sential. If possible, stop surgery. Identify the likely cause of pain (e.g. in-
adequately blocked sacral nerve roots, peritoneal pain). Try to give the
mother a realistic expectation of continued duration and severity of pain.
If the pain has occurred before the delivery of the fetus, it is very likely that
a GA will be required.
• If the patient requests GA, in all but exceptional circumstances, comply.
• If the anaesthetist feels that the severity of pain is not acceptable,
persuade the patient that GA is required.
Spinal
Reassure and treat with:
• Inhaled N2O
• IV opioid (e.g. 25–50 micrograms fentanyl, repeated as necessary)—
inform the neonatologists that opioid has been given
• Surgical infiltration of LA (care with total dose)
• GA.
Epidural/CSE
• Treat as per spinal anaesthesia, but in addition, epidural opioid (e.g. 100
micrograms fentanyl) and/or more epidural LA can be given.
Hypotension 861
Hypotension
Hypotension is common with CNB anaesthesia, especially spinal anaes-
thesia.7 Preventing hypotension, rather than treating it after it has occurred,
is associated with better fetal and maternal outcomes. Aim to maintain the
systolic BP at ≥90% of baseline.
Prophylactic pressor agents are key, but it is also important to minimise
aortocaval occlusion (i.e. lateral tilt) and a fluid co-load should be routine
unless fluid is being restricted.
Pressor agents
Using prophylactic pressor agents is beneficial for both mother and fetus.
α-agonists (phenylephrine and metaraminol) should be considered as the 1°
agents. Ephedrine (6mg bolus) is an acceptable alternative, despite possibly
causing marginally more fetal acidosis than phenylephrine. Noradrenaline,
which has both α and β action, has been shown to have marginal advantage
over phenylephrine, but currently its use as a peripheral infusion remains
controversial. Phenylephrine bolus doses of 50–100 micrograms can cause
reflex bradycardias, so if possible, use a phenylephrine or metaraminol in-
fusion instead. A reduction in HR is associated with a reduced CO, so treat
bradycardia with either ephedrine or an anticholinergic agent. A simple re-
gime for phenylephrine infusion is outlined below.
• Put 20mL of 100 micrograms/mL of phenylephrine in a syringe driver.
• Start infusion of 30mL/h as the spinal solution is injected.
• Titrate to response in increments of 10mL/h.
• Expect the HR to slow—give anticholinergic agents as required.
• Reduce and stop the infusion post-delivery.
• In pre-eclamptic and hypertensive individuals, start at a lower
infusion rate.
Fluid
Crystalloid preloading is ineffective at preventing hypotension, and in
women with severe pre-eclampsia, large preloads are harmful, predisposing
to pulmonary oedema. Using colloids as a preload is more effective, but
colloids are associated with a variety of problems, including anaphylaxis and
clotting abnormalities.
While preloading with crystalloid is ineffective, co-loading crystalloid
(giving fluid as the block is establishing) is more effective.
A co-load should:
• Be given immediately before or during the onset of the CNB technique
to minimise redistribution
• Be limited to 10–15mL/kg of crystalloid. Larger volumes should be
avoided as they offer little advantage and may be harmful. (More fluid
may be given intraoperatively if clinically indicated.)
Do not delay an emergency CS to allow a fluid preload to be administered.
862
Antacid prophylaxis
Aspiration of particulate matter, blood or bile is associated with worse
outcomes than aspiration of gastric fluid. Fluid aspiration is commonly as-
sociated with chemical pneumonitis and the severity of this is, in turn, de-
pendent on the volume and acidity of the aspirated fluid. Use of antacids
and prokinetic agents can elevate the gastric pH and reduce the intragastric
volume. A suggested regime is the following.
Elective surgery
• Ranitidine 150mg or omeprazole 40mg PO 12h and 2h before surgery.
• Metoclopramide 10mg PO 2h before surgery.
• 30mL of 0.3M sodium citrate immediately before induction of GA.
(Gastric pH >2.5 is maintained for only 30min after 30mL of 0.3M
sodium citrate. If a GA is required after this, a further dose of citrate is
required.)
Emergency surgery
If prophylaxis has not already been given:
• Ranitidine 50mg by slow IV injection immediately before surgery.
Remember this will not alter the risk if aspiration occurs during
induction but may offer benefit by the time of extubation.
• Metoclopramide 10mg IV injection immediately before surgery.
• 30mL of 0.3M sodium citrate PO immediately before induction of GA.
Effect of general anaesthesia on the fetus
Lower fetal Apgar scores at 1 and 5min are more common when GA is used
for CS. Most anaesthetic agents, except for muscle relaxants, rapidly cross
the placenta. Thiopental can be detected in the fetus within 30s of admin-
istration, with peak umbilical vein concentration occurring at around 1min.
Umbilical artery to umbilical vein concentrations approach unity at 8min.
Opioids administered before delivery may cause fetal depression. If there is
a specific indication for opioids before delivery, they should be given and the
neonatologist informed. Hypotension, hypoxia, hypocapnia and excessive
maternal catecholamine secretion may all be harmful to the fetus.
864
Failed intubation
(See also % pp. 368–72.)
Failed intubation occurs much more commonly in the obstetric popula-
tion (71:400).8 If a failed intubation occurs, the mortality is 71:90. Causes of
failed intubation include obesity, increased fatty tissue, pharyngeal/laryngeal
oedema, large tongue, large breasts, incorrect cricoid pressure, complete
dentition and the experience and training of anaesthetic staff.
The Obstetric Anaesthetists’ Association and the DAS produced three
algorithms in 2015: (1) for safe obstetric GA, (2) for obstetric failed in-
tubation and (3) for CICO scenarios (M https://www.oaa-anaes.ac.uk/as-
sets/_managed/cms/files/Clinical%20Guidelines/Guideline_Algorithms_
2015.pdf ).
Before embarking on a GA, it is important to have thought about alterna-
tive plans if intubation is difficult or if intubation fails, and to have discussed
these plans with the anaesthetic assistant. GA checklists can greatly assist
with this.
In the event of a failed intubation, deciding on whether to continue sur-
gery or to wake the mother can be difficult. Factors to consider include the
mother’s condition, the fetal condition (while waiting for the muscle re-
laxant to wear off, fetal monitoring can be reapplied and this may give useful
additional information), the experience of the anaesthetist, the anticipated
difficulty of the surgery, patient factors, including obesity and starvation
status, and the difficulty of alternative methods of anaesthesia. Additional
factors that can only be established after the airway has been rescued after
a failed intubation include the method by which the airway is rescued (i.e.
2nd-generation SGA device or difficult mask ventilation) and whether any
airway trauma has occurred. Remember that when a failed intubation oc-
curs, the priority is oxygenation.
If the decision is to continue surgery, ideally a 2nd-generation SGA device
would be inserted (release cricoid pressure before insertion), and empty
the stomach with an OGT. The anaesthetist will have to decide on whether
to opt for spontaneous respiration or paralyse (ideally with rocuronium if
sugammadex is readily available) and ventilate. Remember to ask the ob-
stetricians to avoid fundal pressure at delivery if possible, because fundal
pressure can increase intragastric pressure to >70mmHg. Try to avoid fur-
ther instrumentation of the airway, but be prepared for front of neck ac-
cess, and if familiar, have a fibreoptic scope immediately to hand.
Postoperative analgesia 865
Postoperative analgesia
Most postpartum women are very well motivated and mobilise quickly.
However, effective analgesia does allow earlier mobilisation. The main-
stays of postoperative analgesia are opioids, NSAIDs and paracetamol. The
route that these are given is dependent on the intraoperative anaesthetic
technique.
Opioids
Intrathecal/epidural opioid
• CNB fentanyl lasts little longer than CNB LA and has little postoperative
analgesic benefit. If an epidural catheter is left in situ, epidural fentanyl
may be given as an infusion or as intermittent postoperative boluses
(50–100 micrograms up to 2-hourly for two or three doses). However,
this is rarely done.
• Intrathecal diamorphine (300–400 micrograms) can be expected to
provide 6–18h of analgesia. More than 40% of women will require no
other postoperative opioid. Higher doses have been recommended
but are associated with an increased incidence of side effects. Pruritus
is very common (60–80% of cases), although only 1–2% have severe
pruritus. The evidence that antihistamines reduce pruritus caused by
CNB opioids is poor.
• Epidural diamorphine (2.5mg in 10mL of 0.9% sodium chloride)
provides 6–10h of analgesia after a single dose. Intermittent doses may
be given if the epidural catheter is left in situ.
• Intrathecal preservative-free morphine (100 micrograms) provides long-
lasting analgesia (12–18h). However, pruritus and nausea are common.
Doses above 150 micrograms are associated with increased side effects
without improved analgesia. The low lipophilicity of morphine may
increase the risk of late respiratory depression. Epidural morphine
(2–3mg) provides analgesia for 6–24h, but pruritus is again common and
nausea occurs in 20–40% of cases. Diamorphine is used much more
commonly in the UK than morphine.
IV patient-controlled analgesia or oral opioids
• IV PCA or PO opioids can be used, although these are not as effective
as CNB analgesia.
Neonatal effects of maternal opioids
• A small quantity of opioid may be transferred to the neonate through
breast milk (see % pp. 867–8). Rarely, this can be associated with
neonatal respiratory depression.
NSAIDs
• NSAIDs are very effective postoperative analgesics, reducing opioid
requirements. They should be administered regularly whenever
possible, but beware renal impairment in severe pre-eclampsia, and
care with significant haemorrhage.
86
Drug Comment
Opioids Small amount delivered to neonatal serum. Minor concern
about the long duration of action of pethidine’s metabolite
norpethidine. Avoid codeine, and care with other oral opioids
if mother or neonate excessively drowsy (see % p. 868)
NSAIDs Most NSAIDs are considered safe in breastfeeding. Some
would advise caution with aspirin because of unsubstantiated
concerns about causing Reye’s syndrome in the neonate
Antibiotics Penicillins and cephalosporins are safe, although trace
amounts may be passed to the neonate
Tetracycline should be avoided (although absorption
is probably minimal because of chelation with calcium
in milk)
Chloramphenicol may cause bone marrow suppression in
the neonate and should be avoided
Ciprofloxacin is present in high concentrations in breast
milk and should be avoided
Antipsychotics Generally suggested that these are avoided, although the
amount excreted in milk is probably too small to be harmful.
Chlorpromazine and clozapine cause neonate drowsiness
Cardiac drugs Amiodarone is present in milk in significant amounts and
breastfeeding should be discontinued
Most β-blockers are secreted in minimal amounts. Sotalol
is present in larger amounts
While enalapril and captopril have no known adverse
effects, other ACE inhibitors, ARBs and amlodipine should
be avoided
Anticonvulsants While carbamazepine does not accumulate in the neonate,
phenobarbital and diazepam may. Neonates should be
observed for evidence of sedation
86
Retained placenta
• IV access with 16G or larger cannula.
• Assess total amount and rate of blood loss and cardiovascular stability.
Blood loss may be difficult to accurately assess. If rapid blood loss is
continuing, then urgent X-match and evacuation of placenta under GA
is required.
• CNB anaesthesia is safe, provided estimated blood loss is <1000mL,
but if there are signs suggesting hypovolaemia, GA may be required.
• Remember antacid prophylaxis.
• For GA, use an RSI technique with a cuffed ETT.
• CNB anaesthesia can be performed either by topping up an existing
epidural or with a spinal (e.g. 2–2.5mL of 0.5% hyperbaric bupivacaine
plus 15 micrograms fentanyl or 300 micrograms diamorphine
intrathecally). A T7 block reliably ensures analgesia.
• Occasionally, uterine relaxation is required. Under GA, this can be
produced by increasing the halogenated vapour concentration. Under
CNB anaesthesia, a sublingual GTN spray is usually effective, although
expect transient hypotension.
• On delivery of the placenta, give 5 units of oxytocin ± an infusion of
oxytocin (e.g. 40 units in 500mL of crystalloid over 4h).
• At the end of the procedure, give an NSAID unless contraindicated.
870
Fetal neuroprotection
Magnesium
• Magnesium should be considered for all women expected to deliver
before 34w gestation to reduce the incidence of cerebral palsy in
the baby.9
• Dose of magnesium for neuroprotection is 4g IV bolus of magnesium
sulfate over 15min, followed by an IVI of 1g/h until birth or for 24h,
whichever is sooner.
• Patients receiving magnesium should be monitored every 4h for signs of
toxicity, including recording pulse, BP, RR and deep tendon reflexes.
• If the patient develops oliguria or renal failure, monitoring for
magnesium toxicity should be performed more frequently and a
reduction in the dose of magnesium should be considered.
IN UTERO FETAL DEATH 871
Pathophysiology
Cardiorespiratory
• Hypertension and i sensitivity to catecholamine and exogenous
vasopressors
• Reduced circulating volume, but i TBW
• SVR is usually i and CO reduced
• i capillary permeability which may result in:
• Pulmonary oedema—be very careful to avoid fluid overload
• Laryngeal and pharyngeal oedema. Voice change may give an
indication of this. Stridor is a very worrying sign.
Haematological
• Reduced platelet count with i platelet consumption and
hypercoagulability with i fibrin activation and breakdown—DIC
may result
• i Hct due to reduced circulating volume.
Renal function
• Reduced GFR
• i permeability to large molecules resulting in proteinuria
• Oliguria in severe disease.
Cerebral function
• Headache, visual disturbance and generalised hyperreflexia
• Cerebrovascular haemorrhage
• Eclampsia (resulting from cerebral oedema or cerebrovascular
vasoconstriction). Clonus indicates a high risk of imminent eclampsia.
Fetoplacental unit
• Reduced fetal growth with associated oligohydramnios
• Poor placental perfusion and i sensitivity to changes in maternal BP.
• Non-reassuring CTGs.
• Changes in umbilical arterial blood flow. A reduction of umbilical arterial
diastolic blood flow, and particularly reverse diastolic flow, is indicative
of poor fetal outcome and an indication for early intervention.
Management of pre-eclampsia
Prevention
• Antiplatelet agents (aspirin 75–150mg) should be prescribed for patients
at high risk (such as chronic hypertension, type 1 or type 2 diabetes
or previous hypertensive disease) or with two or more moderate risk
factors (such as booking BMI >36kg/m2 and age >40y).
Early detection
• There are a variety of cardiovascular and biochemical markers that can
predict pre-eclampsia, including placental growth factor (the Triage PlGF
test) and the sFlt-1/PlGF ratio.11 These tests can help to exclude pre-
eclampsia in women between 20w and 35w of gestation.
874
Symptom control
• Further management is aimed at controlling the symptoms of pre-
eclampsia and preventing major harm to mother or fetus, until the
placenta is delivered. After delivery of the placenta, severe symptoms
will usually start to resolve within 24–48h.
• In general, delivery is not indicated before 37w gestational age, unless
BP cannot be controlled to below 160/90mmHg or there are other
medical indications.
• If the fetus is preterm at the time of delivery, when possible, delivery
should be delayed for administration of steroids to promote fetal lung
maturation. Magnesium may also be administered, not only to reduce
the risk of eclampsia, but also for fetal neuroprotection.
• After 37w gestational age, timing of the delivery should be agreed
between a senior obstetrician and the mother.
Antihypertensive therapy
• BP should be controlled to below 135/85mmHg to reduce maternal
morbidity, particularly from intracranial haemorrhage, encephalopathy
and myocardial ischaemia/failure. If the BP is above 160/110mmHg,
urgent treatment is required. BP should be measured every 15–30min
until it is below 160/110mmHg. Once below 160/110mmHg, the aim is
to control BP to <135/85mmHg.
• In the UK, the 1° antihypertensive agent is the combined α- and β-
blocker labetalol. If contraindicated or additional agents are required,
nifedipine or methyldopa can be used. In severe or resistant cases, IV
agents may be required (as below).
• ACE inhibitors should be avoided as they are associated with
oligohydramnios, stillbirth and neonatal renal failure.
• Rapid control of severe hypertension can be achieved with:
• Labetalol (5–10mg IV every 10min)
• Hydralazine (5mg IV aliquots to a maximum of 20mg). The 1st IV
dose of hydralazine is sometimes given with a 500mL crystalloid
fluid bolus.
• PO nifedipine (10mg). Sublingual nifedipine should be avoided
because of rapid changes in placental circulation, which may
compromise fetal condition.
Protection from eclampsia
• Magnesium sulfate reduces the incidence of eclampsia. Magnesium
treatment should be considered if any of the following are present:
clonus, persistent or recurrent headaches, visual scotoma, nausea and
vomiting, epigastric pain, oliguria, severe hypertension or progressive
deterioration in renal or liver function tests.
• For magnesium dosing, see % p. 877.
Fluid management
Fluid management in severe pre-eclampsia is critical. Intravascular volume
is depleted, but TBW is increased. Excessive fluid load may result in pul-
monary oedema, but underfilling may compromise fetal circulation and
renal function. General principles are:
• Fluid management protocols should be followed, and a named individual
should have overall responsibility for fluid therapy.
• Measure hourly urine output.
Pregnancy-induced hypertension and pre-eclampsia 875
CNB anaesthesia
Despite the depleted intravascular volume that occurs with severe pre-
eclampsia, pre-eclamptic patients are less prone to the hypotensive con-
sequences of CNB anaesthesia than normal individuals. Spinal anaesthesia
consistently produces better analgesia than epidural anaesthesia and should
not be avoided.
• Platelet count and, if necessary, a clotting screen should be assessed.
• A reduced volume of fluid co-load should be used. By the end of
the procedure, aim to have given no more crystalloid than measured
blood loss.
• Use ephedrine or phenylephrine as indicated. However, be cautious
because they may have an increased effect.
Effective postoperative analgesia is required, but avoid NSAIDs as these pa-
tients are prone to renal impairment and may have impaired platelet count
or function. When the proteinuria has resolved, which is often within 48h,
NSAIDs may be introduced.
Continue care in HDU or ICU.
Eclampsia 877
Eclampsia
Incidence
Around 2:10 000 pregnancies in the developed world,12 but there are wide
international variations. Remember most seizures in pregnancy are not due
to eclampsia. Always be alert to the differential diagnosis.
• Eclamptic fits occur most commonly in the 3rd trimester or within 12h
of delivery.
• Eclampsia is a life-threatening event.
• Management is aimed at immediate control of the fit and 2° prevention
of further fits.
Management
• Airway (left lateral position with jaw thrust), breathing (bag and mask
ventilation and measure O2 saturation), circulation (obtain IV access and
measure BP when possible; avoid aortocaval compression).
• Control fits with magnesium:
• Load with 4g IV over 5min, followed by 1g/h for 24h.
• Recurrent seizures should be treated with 2–4g IV bolus over 5min.
• The therapeutic magnesium plasma concentration is 2–4mmol/L.
Magnesium levels may be monitored clinically or with laboratory
monitoring. Loss of reflexes occurs at concentrations of >5.0mmol/L,
reduced RR at concentrations of 6.0-7.0mmol/L and cardiac arrest at
concentrations of >12.0mmol/L. Reduce infusion rate with oliguria.
• Patients on calcium channel antagonists are at particular risk of toxicity.
• Toxicity can be treated with IV calcium (e.g. 10mL of 10% calcium
chloride or calcium gluconate).
• If eclampsia occurs before delivery, once the fit has been controlled,
think about the urgency of the delivery. In general, providing the fetus
is not distressed, eclampsia is not an indication for emergency CS. The
patient should be stabilised on magnesium and then consideration given
to vaginal or operative delivery. Care should be continued on HDU
or ICU.
87
HELLP syndrome
Haemolysis, elevated liver enzymes and low platelets comprise the HELLP
syndrome. It is usually associated with pre-eclampsia or eclampsia, but
these are not a prerequisite for diagnosis. Severe HELLP syndrome has a
5% maternal mortality. HELLP rarely presents before the 20th week of ges-
tation, but one-sixth of cases present before the 3rd trimester and a further
third present postnatally (usually within 48h of delivery). Symptoms are
sometimes of a vague flu-like illness, which may delay diagnosis. Maintain a
high index of suspicion.
Features of HELLP
• Evidence of haemolysis (a falling Hb concentration without evidence
of overt bleeding, haemoglobinuria, elevated bilirubin in serum and
urine, elevated lactate dehydrogenase (LDH)). Haemolysis is the least
common element of HELLP and is an indication of severe disease.
• Elevated LFTs: AST or ALT. Epigastric or RUQ abdominal pain is present
in 90% of women with HELLP. Liver failure and hepatic rupture may
occur. Elevation of AST to >150 units/L is associated with a poorer
maternal outcome. Consider the differential diagnosis of acute fatty
liver of pregnancy. Remember the potential for hypoglycaemia. Most
women with RUQ pain and a platelet count of <20 × 109/L have had
an intrahepatic or subcapsular bleed.
• A falling platelet count: platelets <100 × 109/L are of concern, while a
count <50 × 109/L is indicative of severe disease.
• Hypertension and proteinuria are present in 80% of women with
HELLP and 50% suffer nausea and vomiting. Convulsions and GI
haemorrhage are occasional presenting features.
The only definitive treatment is delivery of the placenta. Steroids do not
alter disease progression, but if maternal condition allows, delivery may be
delayed, allowing administration of steroids to promote fetal lung maturity
if needed.
• The method of delivery depends on maternal condition and the
likelihood of successfully inducing labour. Severe HELLP syndrome may
require an urgent CS.
• Coagulation abnormalities may preclude the use of CNB. Consideration
must be given to both the absolute platelet number as well as its rate of
fall. All patients require a clotting screen.
• Be prepared for major haemorrhage.
Further management is supportive, with appropriate replacement of blood
products as required.
• Invasive monitoring is dictated by clinical condition of the patient.
• ARDS, renal failure and DIC may develop.
• After delivery of the placenta, recovery starts within 24–48h.
Massive obstetric haemorrhage 879
Diagnosis
Diagnosis of haemorrhage is usually self- evident, although concealed
bleeding can occur, especially with placental abruptions. In addition, signs
of cardiovascular decompensation may be delayed, as women are usu-
ally young and fit and start with a pregnancy-induced expansion of their
intravascular volume. Beware the woman with cold peripheries—this is ab-
normal in pregnancy. Hypotension is a late and worrying sign.
Management
• In the event of a major haemorrhage requiring surgery, do not delay
operation until X-matched blood is available.
• Clear communication with the patient, relatives and other members of
the health care team is vital.
• Ongoing blood loss calculation should be contemporaneously
communicated between team members and recorded.
• Call for help. Senior anaesthetic and surgical staff should be present.
Blood transfusion services should be alerted.
• Follow ABC principles.
• Give supplemental O2. If laryngeal reflexes are obtunded, intubate and
ventilate.
• In antenatal patients, avoid aortocaval compression.
• Insert two 14G cannulae and take blood for X-matching, FBC and
clotting screen, including fibrinogen. Bedside measurements of Hb,
lactate and clotting, when available, are very useful, but a single normal
bedside Hb estimate in the face of acute massive bleeding should not
delay giving of blood.
• Fluid resuscitate initially with crystalloid (ideally warmed).
• If required, give Group O rhesus-negative blood (i.e. ongoing blood loss
of 2–3L and/or the presence of ECG abnormalities).
• Start appropriate monitoring. Urine output and invasive monitoring of
central venous and arterial pressures may be indicated, depending on
rate of blood loss and maternal condition. However, early monitoring
of CVP is not essential, as hypotension is almost always due to
hypovolaemia.
• Treat the cause of haemorrhage (see below).
• If surgery is required:
• Do not perform CNB if the patient is hypovolaemic.
• Beware coagulopathies in the presence of concealed abruption.
• With continuing haemorrhage, further equipment, including warming
devices and rapid transfusion devices and lines, should be available.
Temperature should be monitored and optimised to aid coagulation.
• Fibrinogen is important and levels of <2.0g/dL after 1L of blood
loss are associated with major haemorrhage. Aim to maintain
fibrinogen >2.0g/dL. This can be done with fibrinogen concentrate or
cryoprecipitate. Two pools of cryoprecipitate will increase fibrinogen
concentration by 71.0g/dL, depending on the rate of consumption.
FFP, although containing some fibrinogen, may not be able to elevate
fibrinogen concentration above 2.0g/dL, as plasma from non-pregnant
donors generally have fibrinogen concentrations below this level and so
may conversely contribute to dilution.13
Massive obstetric haemorrhage 881
Maternal sepsis
Maternal sepsis is a life-threatening condition defined as organ dysfunction
resulting from infection during pregnancy, childbirth, post-abortion or the
postpartum period and accounts for 15% of maternal deaths worldwide.
The pathophysiology remains incompletely understood, but sepsis is asso-
ciated with a dysregulated host response to infection. Organ dysfunction
can be considered to be an acute increase in the Sequential Organ Failure
Assessment (SOFA) score by ≥2 points and reflects an overall mortality risk
of 710% in a general hospital population with suspected infection.22 Patients
with suspected sepsis can be stratified as high risk using the qSOFA (a quick
SOFA or ‘HAT’) which is two or more of:
• Hypotension
• Arterial hypoxaemia
• Raised lactate
• Acute oliguria (urinary output <0.5mL/kg/h)
• Deranged renal function
• Deranged liver function
• Altered mental status
• Coagulation abnormalities
• Hyperglycaemia in the absence of DM.
Management of patients with suspected/confirmed sepsis
• Management of sepsis is aimed at stabilising the patient while diagnosing
and treating the underlying cause. Treatment is more likely to be
effective if appropriate therapy is started early.
• A multidisciplinary team approach is required and should include
obstetricians, midwives, anaesthetists, microbiologists and critical
care staff. Critically ill patients should be cared for in level 2 or 3
facilities with the capability for invasive techniques of monitoring and
experienced nursing/midwifery staff.
• A protocoled approach is recommended for early resuscitation with
goal-directed treatment.
• While the ‘sepsis six’ is no longer the sole goal, following its principles
remains useful for early treatment. Within 1h, aim to achieve:
• O2 therapy (maintain saturations >94%)
• Bloods, blood cultures and septic screen
• IV antibiotics
• Fluid therapy
• ABG (monitoring pH and lactate)
• Continuous monitoring, including urine output.
• Reassess the patient regularly; involve critical care as necessary and
ensure the consultant obstetrician and anaesthetists are informed and
updated. Source control should also be considered a priority.
Cardiac disease and pregnancy 891
Teratogenicity
The fetus is at greatest risk of major teratogenesis during the period of or-
ganogenesis, predominantly in the first 12w of gestation. However, minor
abnormalities may occur after this. Causes of teratogenicity are diverse,
including infection, pyrexia, hypoxia and acidosis, as well as the better rec-
ognised hazards of drugs and radiation. Establishing whether drugs are ter-
atogens can be difficult. Current information on the risk of exposure to
many medications (but excluding most anaesthetic agents) can be found
at the UK Teratology Information Service (M http://www.uktis.org) or
the European Network of Teratology Information Services (ENTIS) (M
https://www.entis-org.eu).
Premedication
• Benzodiazepine exposure just before delivery may cause neonatal
drowsiness and hypotonia. Case reports associating benzodiazepines
with cleft lip formation have not been substantiated and a single dose
has never been associated with teratogenicity. Chronic administration
may cause neonatal withdrawal symptoms post-delivery.
• Ranitidine and omeprazole are not known to be harmful.
Induction agents
• Thiopental. Clinical experience with thiopental suggests that this is a
very safe drug to use.
• Propofol is safe to use during CS at term, but use in early pregnancy has
not been formally investigated, although it is not teratogenic in animal
studies.
• Etomidate is an inhibitor of cortisol synthesis, and if used for CS,
neonates have reduced cortisol concentrations. It is not teratogenic in
animal studies.
• Ketamine should be avoided in early pregnancy as it increases
intrauterine pressure, resulting in fetal asphyxia. This increase in
intrauterine pressure is not apparent in the 3rd trimester.
Inhalational agents
• Halogenated inhalational agents have been used extensively in
pregnancy and are safe. While theoretical concern has been expressed
about an increase in neuroapoptosis with these agents, a single
relatively short exposure is unlikely to have negative effects.27 At
high concentrations, maternal BP and CO fall, resulting in a significant
reduction in uterine blood flow. These agents also cause uterine
relaxation, which may be beneficial.
• Despite early concerns, epidemiological studies suggest that N2O is
safe. However, given that anaesthesia can be easily delivered without
N2O, it is sensible to avoid this agent.
• Muscle relaxants: because these agents are not lipophilic, only very small
quantities cross the placenta and so fetal exposure is limited. These
agents are safe to use.
• Anticholinesterase inhibitors: these agents are highly ionised and so, like
muscle relaxants, do not readily cross the placenta and are safe to use.
Chronic use of pyridostigmine to treat myasthenia gravis may cause
premature labour.
Surgery during pregnancy 895
Analgesics
• Opioids readily cross the placenta, but brief exposure is safe. Long-
term exposure will cause symptoms of withdrawal when the fetus
is delivered. Animal studies suggest possible fetal teratogenicity if
prolonged hypercapnia or impaired feeding develop as side effects of
opioid exposure.
• Chronic exposure to NSAIDs in early pregnancy may be associated
with increased fetal loss and in the 3rd trimester may cause premature
closure of the ductus arteriosus and persistent pulmonary hypertension
of the newborn. Single doses are unlikely to be harmful.
• Bupivacaine and lidocaine are safe. When used near delivery,
bupivacaine has no significant neonatal neurobehavioural effects, while
lidocaine may have a mild effect. Cocaine abuse during pregnancy
increases fetal loss and may increase the incidence of abnormalities in
the genitourinary tract.
Antiemetics
• Concern has been expressed about an association between chronic
exposure to ondansetron during the 1st trimester and cleft lip. Where
possible, ondansetron should be avoided in the 1st trimester; however,
single doses are unlikely to increase risk significantly.
896
Maternal resuscitation
Maternal cardiac arrest is fortunately rare. All the normal resuscitation drugs
should be used as indicated and defibrillation is safe for the fetus. Adrenaline
is also the drug of choice in major anaphylactic reactions. Severe hypoten-
sion associated with anaphylaxis results in very poor fetal outcomes.
The basic algorithms for adult resuscitation (see % pp. 1052–7) are ap-
propriate for maternal resuscitation, with several important differences:
• After 20w gestation, attempts must be made to minimise aortocaval
obstruction while performing effective cardiac compressions. The
fetus can be displaced with firm lateral pressure (manual uterine
displacement).
• After 4min, if CO has not been re-established, the fetus should be
delivered. This improves the chance of maternal, as well as fetal,
survival.
• Pregnant women have reduced oesophageal sphincter tone and both
cricoid pressure and intubation should be performed as early as
possible.
Consideration should be given to the diagnosis and treatment of obstetric
causes of maternal arrest, including:
• Cardiac events
• Intracranial events
• Sepsis
• Haemorrhage
• PE
• AFE
• Iatrogenic events:
• Hypermagnesaemia: treat with 10mL of 10% calcium chloride or
gluconate
• High or total spinal (which is the commonest cause of maternal
cardiac arrest on delivery suites in the UK)28—supportive treatment
• LA-induced arrhythmia—treat with 20% lipid emulsion (see %
pp. 1092–3).
References
1 Association of Anaesthetists (2013>). Regional anaesthesia and patients with abnormalities
of coagulation. M https://anaesthetists.org/Home/Resources-publications/Guidelines/
Regional-anaesthesia-and-patients-with-abnormalities-of-coagulation
2 Chau A, Bibbo C, Huang CC, et al. (2017). Dural puncture epidural technique improves labor
analgesia quality with fewer side effects compared with epidural and combined spinal epidural
techniques: a randomized clinical trial. Anesth Analg, 124, 560–9.
3 Cook TM, Counsell D, Wildsmith JAW (2009). Major complications of central neuraxial block:
report on the Third National Audit Project of the Royal College of Anaesthetists. Br J Anaesth,
102, 179–90.
4 Russell R, Laxton C, Lucas DN, et al. (2019). Treatment of obstetric post-dural puncture head-
ache. Part 1: conservative and pharmacological management. Int J Obstet Anesth, 38, 93–103.
5 Russell R, Laxton C, Lucas DN, et al. (2019). Treatment of obstetric post-dural puncture head-
ache. Part 2: epidural blood patch. Int J Obstet Anesth, 38, 104–18.
6 Ronel I, Weiniger CF (2019). Non-regional anaesthesia for labour: remifentanil in obstetrics. BJA
Educ, 19, 357–61.
7 Kinsella SM, Carvalho B, Dyer RA, et al. (2018). International consensus statement on the man-
agement of hypotension with vasopressors during caesarean section under spinal anaesthesia.
Anaesthesia, 73, 71–92.
8 Kinsella SM, Winton AL, Mushambi MC, et al. (2015). Failed tracheal intubation during obstetric
general anaesthesia: a literature review. Int J Obstet Anesth, 24, 356–74.
9 National Institute for Health and Care Excellence (2015, updated 2019). Preterm labour and birth.
NICE guideline [NG25]. M https://www.nice.org.uk/guidance/ng25
89
10 National Institute for Health and Care Excellence (2019). Hypertension in pregnancy: diagnosis and
management. NICE guideline [NG133]. M https://www.nice.org.uk/guidance/ng133
11 National Institute for Health and Care Excellence (2016). PIGF-based testing to help diagnose
suspected pre-eclampsia. Diagnostics guidance [DG23]. M https://www.nice.org.uk/guidance/
dg23
12 Pollock W, Peek MJ, Wang A, et al. (2020). Eclampsia in Australia and New Zealand: a pro-
spective population-based study. Aust N Z J Obstet Gynaecol, 60, 533–40. M https://obgyn.
onlinelibrary.wiley.com/doi/abs/10.1111/ajo.13100
13 Collis R, Collins PW (2015). Haemostatic management of obstetric haemorrhage. Anaesthesia,
70 (suppl 1), 78–86.
14 Shakur H, Roberts I, Fawole B, et al.; WOMAN Trial Collaborators (2017). Effect of early tran-
examic acid administration on mortality, hysterectomy, and other morbidities in women with
post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-
controlled trial. Lancet, 389, 2105–16.
15 Khan KS, Moore PAS, Wilson MJ, et al. (2017). Cell salvage and donor blood transfusion during
cesarean section: A pragmatic, multicentre randomised controlled trial (SALVO). PLoS Med,
14:e1002471. M https://doi.org/10.1371/journal.pmed.1002471
16 Heesen M, Carvalho B, Carvalho JCA, et al. (2019). International consensus statement on the use
of uterotonic agents during Caesarean section. Anaesthesia, 74, 1305–19.
17 Goh W, Zalud I (2016). Placenta accreta: diagnosis, management and the molecular biology of
the morbidly adherent placenta. J Matern Fetal Neonatal Med, 29, 1795–800.
18 Benson MD (2017). Amniotic fluid embolism mortality rate. J Obstet Gynaecol Res, 43, 1714–18.
19 Shamshirsaz AA, Clark SL (2016). Amniotic fluid embolism. Obstet Gynecol Clin North Am, 43,
779–90.
20 Baker C (2021). Obesity statistics. House of Commons Library. Briefing Paper Number 3336,
January 2021. M https://commonslibrary.parliament.uk/research-briefings/sn03336/
21. Denison FC, Aedla NR, Keag O, et al.; Royal College of Obstetricians and Gynaecologists.
(2018). Care of women with obesity in pregnancy: green-top guideline No. 72. BJOG, 126,
e62–106.
22 Singer M, Deutschman CS, Seymour CW (2016). The Third International Consensus Definitions
for Sepsis and Septic Shock (Sepsis-3). JAMA, 315, 801–10.
23 Shankar-Hari M, Phillips GS, Levy ML, et al. (2016). Developing a new definition and assessing
new clinical criteria for septic shock: for the Third International Consensus Definitions for Sepsis
and Septic Shock (Sepsis-3). JAMA, 315, 775–87.
24 Knight M, Clarke B, Head C, et al. (2019). Lessons on cardiovascular care. In: Knight M, Bunch K,
Tuffnell D, et al. (eds) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care—Lessons
learned to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths
and Morbidity 2015–17. Oxford: National Perinatal Epidemiology Unit, University of Oxford;
pp. 20–44.
25 Tuffnell D, Knight M, Mackillop L; MBRRACE-UK VTE Chapter-Writing Group. Lessons for pre-
vention and treatment of thrombosis and thromboembolism. In: Knight M, Bunch K, Tuffnell D,
et al. (eds) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care—Lessons learned
to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths and
Morbidity 2014–16. Oxford: National Perinatal Epidemiology Unit, University of Oxford;
pp. 34–41.
26 Royal College of Obstetricians and Gynaecologists (2015). Reducing the risk of venous thrombo-
embolism during pregnancy and the puerperium. Green-top guideline No 37a. M https://www.
rcog.org.uk/globalassets/documents/guidelines/gtg-37a.pdf
27 Sun LS, Li G, Miller TLK, et al. (2016). Association between a single general anesthesia exposure
before age 36 months and neurocognitive outcomes in later childhood. JAMA, 315, 2312–20.
28 Beckett VA, Knight M, Sharpe P (2017). The CAPS Study: incidence, management and outcomes
of cardiac arrest in pregnancy in the UK: a prospective, descriptive study. BJOG, 124, 1374–81.
Chapter 36 899
Paediatric emergencies
Paediatric advanced life Neonatal resuscitation 956
support 951 The collapsed, septic child 959
Asystole and pulseless electrical Stabilisation of the sick child
activity 954 (prior to PICU transfer) 961
Ventricular fibrillation or Paediatric doses and
pulseless ventricular equipment 963
tachycardia 955
See also
% Tonsillectomy/adenoidectomy: child pp. 767–8
% Severe bronchospasm pp. 1078–9
% Anaphylaxis pp. 1081–5
% Management of trauma pp. 1019–24
90
Neonatal/infant physiology
Paediatric anaesthesia embraces patients from the premature neonate to
the adolescent. Major differences exist between the anatomy, physiology
and pharmacological response of children and adults (Tables 36.1, 36.2 and
36.3). In anaesthetic terms, special considerations apply to the neonate.
Definitions
• Neonate: first 44w of post-conceptual age
• Infant: 1mo to 1y
• Child: 1–16y
• Young person: 16–18y
• Premature infant: <37w gestational age
• SGA: small for gestational age
• Low birthweight (LBW): <2500g
• Very low birthweight (VLBW): <1500g
• Extremely low birthweight (ELBW): <1000g.
Respiratory considerations
• At birth, each terminal bronchiole opens into a single alveolus instead of
fully developed alveolar clustering. The 20–50 million alveoli are thick-
walled and alveolar growth continues by multiplication to reach 300
million by adolescence.
• Cartilaginous ribs are horizontally aligned, so that the ‘bucket handle’
action of the adult thorax is not possible. Intercostal muscles are poorly
developed, with a lower proportion of type 1 muscle fibres and fatigue
more easily. The diaphragm has a more horizontal attachment, reducing
mechanical advantage.
• Ventilation is essentially diaphragmatic and rate-dependent. Abdominal
distension may cause splinting of the diaphragm, leading to respiratory
failure.
• Chest wall compliance is high because of the cartilaginous thorax;
intercostal or sternal recession is common with i work of breathing or
airway obstruction.
• Closing volume occurs within tidal breathing in the neonate. Minor
decreases in FRC increase the pulmonary shunt and lead to lung
collapse. The application of CPAP improves oxygenation and reduces
the work of breathing.
• Narrow airways result in i resistance, up to the age of 8y. Nasal
resistance represents almost 50% of total airway resistance, accentuating
the problem of children with nasal congestion who are obligate nasal
breathers. An NGT can increase resistance by 50% in neonates.
• Apnoea is a common postoperative problem in preterm neonates.
It is significant if the episode exceeds 20s or induces cyanosis or
bradycardia. CPAP may be helpful, with the distending pressure
triggering stretch receptors in the chest wall.
• Due to the higher metabolic rate and alveolar minute volume, volatile
agents achieve a more rapid induction and emergence than with
adults. They are profound respiratory depressants; most anaesthetised
neonates require intubation and controlled ventilation.
• Respiratory parameters of the neonate are summarised in Table 36.1.
Neonatal/infant physiology 901
Cardiovascular considerations
• PVR falls at birth, in response to a rise in PaO2/pH and a fall in PaCO2.
Subsequent closure of the foramen ovale and ductus arteriosus may
reverse with hypoxia and acidosis, leading to pulmonary hypertension
and right-to-left shunt (transitional circulation).
• The neonate has small ventricles with reduced contractile mass and
poor ventricular compliance. CO is higher than in adults (200mL/kg/
min) and rate-dependent. Normal systolic pressure is 70–90mmHg with
low SVR.
• HR of up to 200 bpm can be tolerated. Bradycardia occurs in response
to hypoxia and should be treated with O2, rather than atropine.
Neonatal and infant HR <60 bpm require external cardiac compression.
• Autonomic and baroreceptor control is fully functional at term, but
vagally mediated parasympathetic tone predominates.
• Incidence of CHD is 7–8 per 1000 live births; 10–15% have associated
non-cardiac pathology. All neonates with midline defects should be
assessed for related cardiac lesions.
• CVS parameters in children are summarised in Table 36.2.
Gastrointestinal considerations
• The liver is immature. Enzyme systems have matured by 12w, but some
drugs are metabolised more slowly and others by different enzyme
pathways from adults. The action of barbiturates and opioids in the
neonate is prolonged and enhanced.
• Bilirubin metabolism is affected by a poorly developed glucuronyl
transferase system. Rises in unconjugated bilirubin may lead to neonatal
jaundice and kernicterus by crossing the blood–brain barrier. Some
drugs (e.g. diazepam, vitamin K) displace bilirubin from plasma proteins
and can exacerbate jaundice.
• Glycogen stores are reduced in neonates. The premature baby and
stressed neonate are vulnerable to hypoglycaemia.
902
Neonate 90mL/kg
Infant 85mL/kg
Child 80mL/kg
Birth 3–3.5kg
0–1y Weight = [age (mo)/2] + 4
1–5y Weight = [age (y) × 2] + 8
6–12y Weight = [age (y) × 3] + 7
Thermoregulation
• Poorly developed thermoregulatory mechanism. High surface area to
volume ratio with minimal SC fat and poor insulation. Vasoconstrictor
response is limited, and the neonate is unable to shiver.
• Non-shivering thermogenesis is achieved by metabolism in brown fat
found in the back, shoulders and legs, and around the thoracic vessels.
This considerably increases O2 consumption and may worsen pre-
existing hypoxia. Brown fat is deficient in premature infants.
904
Fluid management
Eighty per cent of neonatal total body weight is water; the value is higher
in the preterm infant and reaches an adult level of 60% by 2y. Extracellular
water constitutes 45% of TBW at term (over 50% in the preterm) but at-
tains an adult value of 35% by early childhood. Plasma volume tends to stay
constant at 5% of total body weight, independent of age.
• Turnover of water is over double that of the adult; 40% of extracellular
water is lost daily in infants as urine, faeces, sweat and insensible
losses. A small increase in loss or reduction in intake can rapidly lead to
dehydration.
• Daily fluid maintenance is calculated from the calorie requirement:
100kcal/kg for the infant, with older children requiring 75kcal/kg, and
adults 35kcal/kg. Each kcal requires 1mL of water for metabolism.
Neonatal fluid requirements
• Fluid is initially given cautiously, as the kidneys cannot easily excrete a
water or Na+ load. Newer ‘cold-light’ phototherapy does not require i
fluid intake.
• The fluid of choice is 10% glucose. This is adjusted in increments of
2.5% to achieve normoglycaemia. A blood sugar below 2.6mmol/L is
treated with 2mL/kg of 10% glucose.
• Routinely added electrolytes are Na+ 3mmol/kg/d and K+ 2mmol/kg/d.
Other electrolytes, including Ca2+, are added as indicated.
• The first 5d of neonatal fluid requirements are given in Table 36.5.1
Preterm requirements are dependent on birthweight and may be
proportionally higher.
Postoperative hyponatraemia
• Postoperative hyponatraemia (serum Na+ <135mmol/L) is uncommon,
but more likely with the administration of hypotonic solutions, e.g.
0.18% sodium chloride/4% glucose.
• Symptoms are often non-specific, including nausea, vomiting and
headache (a common early sign). It may also present as seizure or
respiratory arrest.
• Hyponatraemic seizures respond poorly to anticonvulsants, and initial
management should be to administer an infusion of 3% sodium chloride.
Plan to increase serum Na+ to >125mmol/L or until symptoms improve
(1mL/kg of 3% sodium chloride should raise serum Na+ by 1mmol/L).
• Asymptomatic hyponatraemia can be managed with 0.9% sodium
chloride. If hypervolaemic, restrict fluids to 50% of maintenance.
Fluid resuscitation
Shock is the clinical state in which delivery of O2 and metabolic substrates
is inadequate for cellular demand.
• In compensated shock, oxygenation of the vital structures (brain and
heart) is maintained by sympathetic reflexes at the expense of non-
essential tissues. BP remains normal, with an increase in SVR.
• In decompensated shock, hypotension develops and vital organ
perfusion is compromised.
• With irreversible shock, there is cyanosis, bradycardia and gasping
respiration. This is a preterminal event.
• Hypovolaemia is the commonest cause of circulatory failure in children.
Other causes of shock include pump failure (cardiogenic), distributive
(sepsis, anaphylaxis, neurogenic) and obstructive (cardiac tamponade,
tension pneumothorax).
Fluid management 907
Anaesthetic equipment
See also % Breathing systems, pp. 350–2; % Airway equipment, pp. 355–8.
Oropharyngeal airway
• Range in size from 000 to 4 (4–10cm in length).
• Rarely useful in neonates who are obligate nasal breathers but may be
advantageous in older children or in mask ventilation to prevent gastric
distension.
• Estimating the size of the airway is crucial. Incorrect size will worsen
the airway obstruction. Correct length is equal to the distance from the
incisors to the angle of the jaw.
• The airway should not be inverted during insertion in infants, as this may
damage the palate.
Nasopharyngeal airway
• Limited application in paediatric practice. Tolerated at lighter levels of
anaesthesia than an OPA and may be of use during induction/recovery
of some congenital airway problems or OSA.
• Well lubricated prior to insertion; bleeding is possible from mucosal or
adenoidal trauma, especially in younger children.
• Appropriate length is equal to the distance from the tip of the nostril to
the tragus of the ear.
• If an ETT is used as a modified nasopharyngeal airway, the size is
calculated by: (age/4 + 3.5).
Face masks
• Clear plastic masks with an inflatable rim provide an excellent seal for
SV and assisted ventilation.
• Manufactured in a round or teardrop shape; the round shape is suitable
for neonates and infants. Also available as ‘flavoured’ masks.
• Transparent design allows for observation of cyanosis/regurgitation and
the presence of breathing.
• Size is estimated to fit an area from the bridge of the nose to the cleft
of the chin.
Supraglottic airway devices
• Tables 36.8 and 36.9 describes how to choose the appropriate size of
SGA.
• Indications and insertion techniques are similar to adult use. An
alternative method of insertion is to advance it partially inflated and
upside down behind the tongue before rotating through 180°.
• Smaller sizes have i complication rates. The effectiveness of these
smaller masks is not established for resuscitation.
• Intubating LMA (iLMA) available in size 3 which is potentially useful for
older children.
• Both the LMA ProSeal™ and i-gel® are available in a full range of
paediatric sizes.3
• LMA is best secured in slight flexion, and i-gel® in slight extension.
Anaesthetic equipment 909
Laryngoscopes
• Laryngoscope blades available in different lengths from size 0 to 3.
• Straight-blade preferable for infants ≤6mo due to high anterior larynx
(see % p. 909 for paediatric intubation).
• Polio and McCoy blades are also available.
• Many video laryngoscopes are available in paediatric sizes.
Endotracheal tubes
• Traditionally uncuffed paediatric ETTs have been used and are available
from 2.0mm to 7.0mm ID. Table 36.10 describes how to choose an
appropriate size of uncuffed tube.
• Uncuffed ETT ID (mm) may also approximate to the length of the
child’s middle finger (cm).4
• Standard cuffed tubes are available from 3.0mm ID. Microcuff® tubes
have a more distal, high-volume, low-pressure cuff. Use of a cuffed
ETT reduces intubation attempts to correctly size a tube and improves
ventilation characteristics without increasing the incidence of post-
extubation stridor.5
• Specific indications include children at high risk of aspiration, poor
lung compliance and facial burns. Cuff pressure should be limited to
20cmH2O and continuously monitored. Tube sizes are a half size lower
than uncuffed tube.
• Paediatric versions of the RAE, armoured, and laser tubes all exist. A
north-facing uncuffed preformed tube has been developed for routine
paediatric surgery.
091
Conduct of anaesthesia
See % Chapter 16 for general information on conduct of anaesthesia.
Preoperative assessment
(See % Chapter 2 for general information on preoperative considerations.)
The preoperative visit is essential in establishing a rapport with both
parents and children and in helping to dissipate anxiety. Communication
should be simple, informative and truthful.
• Involve the parents, but try to question the child directly when
appropriate and stay at eye level if possible.
• A preadmission visit reduces parental anxiety and is beneficial to
children over 6y. Play therapists can help provide an informal setting and
prepare the child by describing the course of events from the ward to
induction of anaesthesia. A collection of photographs, video or virtual-
reality tools may be helpful.6
Preoperative investigations
Routine preoperative Hb is indicated for:
• Neonates and ex-premature infants under 1y
• Children at risk of SCD (see % pp. 257–9)
• Children for whom intraoperative transfusion may be necessary
• Children with systemic disease.
A preoperative Hb of <100g/L is abnormal and needs to be investigated.
It does not necessarily entail cancellation if the child is haemodynamically
stable and otherwise well.
Routine biochemistry is required for:
• Children with metabolic, endocrine or renal disease
• Children receiving IV fluids.
The child with an upper respiratory tract infection
The preschool child develops 6–8 URTIs per year. Almost 25% of children
have a chronic runny nose due to seasonal rhinitis or adenoidal infection.
• Anaesthesia in the presence of an intercurrent URTI is associated with a
higher risk of complications in younger children, particularly <1y. There
is an i incidence of coughing, breath-holding, desaturation, excess
secretions, airway obstruction, laryngospasm and bronchospasm. This
risk is i if the child is intubated.
• Children with moderate to severe chest infections should be
postponed. This will include those with productive cough, purulent nasal
discharge, pyrexia, abnormal chest auscultation and signs of viraemia or
constitutional illness, including diarrhoea and vomiting.
• The child with a mild URTI is a difficult problem. The history in these
cases is crucial. It is important to decide whether the child is at the
beginning or at the end of the URTI. Other members of the family or
children at school may have already experienced the same infection, and
this can provide useful information.
• A child deemed to be post-viral, apyrexial, with no chest signs and constitu-
tionally well is probably fit for surgery, even if they have a runny nose.
• The decision to proceed is not always clear and requires careful
discussion with the parents. Level of urgency, complexity of surgery,
informed consent, good clinical judgement and experience are key
factors in these decisions.
491
Child protection
• Child protection training is mandatory for all hospital staff who work
with children.9
• Anaesthetists may become suspicious of child abuse during
resuscitation, on PICU, in the anaesthetic room, during the course of a
surgical procedure or rarely by direct disclosure.10
• In these situations, it is essential to act in the best interests of the child.
• If there is concern about suspected abuse, the first point of contact
should be the named clinical lead for safeguarding children or the
consultant paediatrician on call.
Consent
(See also % p. 42.)
Allow time at the end of the preoperative assessment for parents and
children to ask questions. Adopt the principle of shared decision-making
and discuss the risks associated with GA. Discuss the options of IV or
inhalational induction and plans for postoperative pain relief.
• Obtain consent for suppository, neuraxial blockade or regional/
peripheral nerve block, if indicated.
• A young person is deemed competent to consent from 16y.
• Children under 16y may have the capacity to decide, depending on their
ability to understand what is involved (Gillick competence). A Gillick-
competent child can consent to treatment against parental wishes but
cannot refuse it.
Anaesthetic neurotoxicity
• There is evidence from infant animal models that neuronal apoptosis
and neurodegeneration may be caused by prolonged or multiple
anaesthetics.
• To date, results from studies in the human infant have failed to show
adverse effects on cognitive development from a single anaesthetic
episode of short duration <1h.
• Parents/carers can be advised that surgery is carried out in infants only
when necessary and that currently there is no indication of a long-term
neurological effect from a single anaesthetic exposure.11
Preoperative fasting
(See % pp. 57–8.)
Fasting instructions (Table 36.11) are designed to minimise the risk of re-
gurgitation of gastric contents with consequent pulmonary aspiration.
• Fasting reduces the gastric volume but does not guarantee an empty
stomach. Prolonged fasting does not further reduce the risk of
aspiration and, in infants, can lead to dehydration and hypoglycaemia.
• Infants may be at greater risk of regurgitation due to reduced lower
oesophageal sphincter tone and a tendency for stomach distension
during mask ventilation. However, the incidence of pneumonitis
following aspiration in children is much lower than in adults.12
• One-hour fluid fasting for clear fluids does not significantly alter gastric
pH or residual volume, compared with 2h.13
• Clear fluids can be given safely up to 1h preoperatively,14 and the intake of
fluids (either water or a fruit squash drink) should be encouraged. Children
are less irritable at induction, and there may be a reduction in PONV.
691
Premedication
(See % Premedicants, pp. 66–8; % Sedation, p. 419.)
Routine sedative premedication is not necessary (‘parents are often the
best premedication’).
• Sedative premedication is used to reduce anxiety and facilitate
compliance at induction (Table 36.12).15
• It may also reduce PONV and postoperative delirium. Postoperative
amnesia with midazolam may reduce postoperative behavioural
changes, including nightmares, bedwetting and eating disorders,
especially in the preschool child.
• Recovery time may be prolonged.
• Indications for premedication include excessive anxiety or non-
compliance, previous distress, learning disability and behavioural issues.
• Contraindications include an anticipated difficult airway, OSA, reduced
conscious level, raised ICP and i risk of aspiration.
• Infants have not yet developed a fear of strangers and appear relatively
undisturbed when separated from their mothers. The preschool child
is vulnerable to separation anxiety in a strange environment, but
without the ability to reason. Children from 3 to 6y may require a
simple explanation and children from 6 to 12y will need a more detailed
explanation and a sense of control. Older children or adolescents may
request premedication.
• PO midazolam is commonly used. It acts within 20–30min to reduce
anxiety, leading to a more cooperative child, but with minimal delay
in recovery. The IV formulation is often used but is extremely bitter
and should be diluted in fruit juice or paracetamol syrup. The newer
preparation of buccal midazolam (Buccolam®) is tasteless and requires
little cooperation from the child. It does not affect fasting and has a
quicker onset of 10–15min. Midazolam can also be given intranasally
where it has a rapid onset of action within 5–15min but is poorly
tolerated because of the burning sensation in the nasal mucosa. Use a
mucosal atomiser device and divide the dose between each nostril.
• Ketamine causes excessive salivation and postoperative emergence
delirium (although these may be less frequent in children). It should be
given PO in combination with midazolam or IM as a last resort (use
the 50mg/mL preparation). The latter option would require careful
discussion with the parents.
• Clonidine is tasteless. It may reduce the postoperative analgesic
requirement. It has a slow onset and recovery time and may cause
bradycardia and hypotension; there is no amnesic effect.
• Dexmedetomidine may be useful intranasally as a 3rd-line drug if other
options have failed.
• An antisialogogue may be required for children with excessive
secretions, e.g. Down’s syndrome and cerebral palsy, and for the
suspected difficult airway in younger children and co-administration
with ketamine. Absorption of oral atropine is variable. To be
certain of efficacy, administer atropine 10 micrograms/kg IM 30min
preoperatively or glycopyrronium bromide (5 micrograms/kg) IM or IV.
891
Induction of anaesthesia
(See also % pp. 406–9.)
• Induction should occur in a child-friendly environment. A dedicated
paediatric theatre is not always an option. In these circumstances, a
customised paediatric anaesthetic trolley incorporating a comprehensive
range of airway and vascular equipment is important.
• Prepare drugs and equipment before the child arrives. Recheck the
weight (Table 36.4).
• Online calculators or smartphone apps can be useful to check doses.
• Precalculate the dose (and volume) of atropine and suxamethonium in
prepared syringes, as it may be given by your assistant in an emergency
(see Table 36.15). A 10mL syringe of propofol is useful as a 1st-line
treatment for laryngospasm.
• SpO2 is the minimum monitoring acceptable in the anaesthetic room,
although it will not read accurately on the agitated child. Many children
will tolerate an ECG and a BP cuff prior to induction.
Inhalational induction
(See also % pp. 391–2.)
• It is important to learn more than one method. Not all children are
susceptible to the same technique.
• Sevoflurane is rapidly acting, enabling a smooth induction. It is not
odourless but is relatively non-irritant. For the suspected difficult airway,
use sevoflurane in 100% O2; otherwise 50% N2O/O2 is satisfactory, and
anecdotally N2O may obtund the child’s sense of smell, facilitating induction.
• Emergence delirium has a reported incidence of 20% with sevoflurane.
There is a strong association with ENT surgery, preschool ♂ , parental
and patient anxiety, rapid awakening and inadequate analgesia. A single
dose of propofol 1mg/kg at the end of surgery may be of benefit.
• Involve the parent as much as possible. This may involve holding the
child or even helping with the induction.
• Position the child either supine on the trolley or across the lap of the
parent, so that the parent or anaesthetic assistant can gently restrain the
arms, if necessary. Warn the parent that the child’s head will become
floppy and need support.
• For smaller children, a cupped hand method is useful. Occlude the end
of the bag to direct all the FGF towards the patient’s mouth and nose.
• A face mask is often tolerated by older children. This can be held by the
parent, child or anaesthetist, and the child can be encouraged to blow
up the bag ‘like a balloon’. A flavoured face mask may be useful initially,
but the volatile agent rapidly becomes the dominant smell.
• The parent should be warned of abnormal movements when the child
is nearly anaesthetised.
• Once anaesthesia is achieved and the eyelash reflex is absent,
anaesthesia can be maintained with another volatile agent, if desired.
Intravenous induction
• The smaller child sits across the parent’s lap, and the arm is placed
under the parent’s axilla, thereby obstructing the child’s view. The older
child will usually lie on the trolley, with the parent on one side holding
the child’s hand, while the other is cannulated.
• The induction agent of choice is propofol 3–5mg/kg, with 1% lidocaine
(1mL/10mL propofol) added to reduce pain on injection.
920
Regional anaesthesia
Successful regional blockade provides conditions for light and haemo-
dynamically stable GA. The stress response is attenuated and early, pain-
free emergence is possible, leading to a smooth postoperative recovery.
• Few children tolerate these techniques awake, and the majority of
regional blocks are performed on anaesthetised patients.
• Motor blockade is unnecessary and low concentrations of LA can
be used. The most widely used solutions are 0.25% bupivacaine/
levobupivacaine and 0.2% ropivacaine.
Morphine
100micrograms/kg PO 6-hourly
Caudal block
Caudal extradural analgesia has a wide application in children. It is suitable
for all surgery below the umbilicus, including general surgery, urology and
orthopaedics. The technique is easier than with adults, with a higher suc-
cess rate of 795%. Epidural fat is less dense and less tightly packed in chil-
dren, with the result that LA can spread more easily and quickly. Therefore,
caudals can achieve a higher dermatomal block.24
Technique
• Position the patient in the left lateral position, with the legs flexed at the
hip. Aseptic technique is a prerequisite.
• Identify the sacral hiatus as the apex of an equilateral triangle with
the base formed by a line joining the posterior superior iliac spines
(Fig. 36.1).
• Alternatively, with the hips flexed at 90°, a line extended along the
midline of the right femur will intersect with the sacral hiatus. The natal
cleft does not always correspond to bony midline structures.
• Define the boundaries of the sacral hiatus. This is again a triangle
with the base formed by a line joining the sacral cornua and the apex
representing the lower part of the 4th sacral vertebra. The sacral hiatus
is covered by the sacrococcygeal membrane.
• Direct a short-bevelled 22G or 20G cannula at 60° to the skin from the
midpoint of the line joining the sacral cornua. A small ‘give’ indicates
penetration of the sacrococcygeal membrane. Flatten the cannula or
needle slightly, then advance. If using a cannula, withdraw the stylet
to just behind the cannula before advancing the cannula into the
caudal space. Do not advance the needle or cannula any more than
is necessary. Advancement of a cannula, rather than a needle, may
reduce the incidence of inadvertent dural or vascular puncture. Easy
progression of the cannula is a good prognostic indicator of success.
• Draw up your medications now—this ensures patience to observe any
blood or CSF flow passively up the cannula.
• Use a double-aspiration technique; if the cannula is in a small vein, the
vein may simply collapse with the 1st aspiration. Aspiration should be
repeated during injection of the LA. The commonest reason for a failed
attempt is positioning the needle too caudally.
• Ultrasound can be used to assess the caudal anatomy and to confirm
the spread of the injectate in the caudal extradural space.25
• Levobupivacaine 0.25% is commonly administered. Current guidelines
recommend that doses should not exceed 2.5mg/kg for caudal
bupivacaine, and the recommended volumes are 0.5mL/kg for blockade
of sacral dermatomes, 1.0mL/kg for lumbar dermatomes or 1.25mL/kg
for lower thoracic dermatomes.24 Duration of the block averages 4–8h.
• Caudal blockade can be extended with clonidine 1–2 micrograms/kg
but can cause intraoperative hypotension and postoperative sedation.
• Adrenaline has been implicated in cases of spinal ischaemia and should
be avoided.
• Morphine and diamorphine increase the incidence of urinary retention
and should be reserved for surgery in which catheterisation is required.
• Ketamine is no longer recommended, especially in younger children,
because of the potential risk of neuronal apoptosis.
930
Posterior
superior
iliac
spine
Sacral
cornu
Sacral
hiatus
Epidural/subarachnoid block
(See also % pp. 1114–17.)
Epidural block
(See also % pp. 1164–6.)
Epidural blockade is technically more difficult in children and requires ex-
perience. The ligamentum flavum is less well developed, and the interver-
tebral spaces are narrower. In infants, the epidural space is rarely located
at a depth >15mm and often as superficially as 10mm from the skin. The
technique is similar to that used in adults. Either a midline or a paramedian
approach is acceptable. The NAP3 study demonstrated that paediatric epi-
durals resulted in fewer complications than adults.26 Severe neurological
complications, including fatalities, have been reported in association with
using air to find the epidural space in neonates. The caudal route may rep-
resent a safer alternative with this group.
• Epidural needle: 18G for infants/children, 19G for neonates/infants
(catheter ‘end-hole’ only).
• For suitable doses, see Table 36.15.
Subarachnoid block
Paediatric spinal anaesthesia can be useful for herniotomy in neonates. The
procedure requires training specific to paediatrics and an experienced assistant.
• The infant needs to be firmly gripped in the lateral or sitting position.
The needle should be directed at right angles to the skin in the midline
below L3, with L5–S1 reported as the safest approach. Prior infiltration
of LA into the skin will help prevent patient movement.
• The block has a rapid onset, but duration is rarely >40min. If sedation
is required during the surgery, the incidence of postoperative apnoea is
comparable with a GA technique.
• Spinal needle: 5cm, 22G.
• For suitable doses, see Table 36.15.
Down’s syndrome/trisomy 21
Down’s syndrome is the commonest congenital abnormality (1.6 per 1000
deliveries). It is associated with a higher morbidity and mortality and char-
acteristic dysmorphic features, including:
• Impaired global development
• Congenital cardiac defects (40%; predominantly endocardial cushion
defects/VSD)
• Eisenmenger’s syndrome (especially if there is associated OSA)
• Recurrent respiratory tract infection (relative immune deficiency
and a degree of upper airway obstruction from tonsillar/adenoidal
hypertrophy)
• Atlantoaxial instability (30%, but frequently asymptomatic; routine X-ray
not indicated; avoid excessive neck movement)
• Epilepsy (10%)
• Obesity and potentially difficult venous access
• Hypothyroidism (40%)
• i incidence of gastro-oesophageal reflux
• Prone to hypoventilation (consider IPPV).
Assessment
• Perform careful airway assessment: relatively large tongue, crowding of
mid-facial structures, high arched narrow palate, micrognathia and short,
broad neck.
• Perform careful cardiorespiratory assessment (including investigation).
• Beware asymptomatic disease; optimise where possible, and have a
reduced threshold for postoperative HDU/ICU.
• Hypotonia (up to 75%) may compromise the airway.
• These patients are prone to atelectasis and respiratory tract infections;
consider humidified O2 ± physiotherapy.
Preoperative
• Often uncooperative (sedative premedications are often helpful; caution
if airway obstructed).
• Drying agents may be useful if hypersalivation (H caution: may have
exaggerated sensitivity to mydriatic/cardiac effects of atropine).
Postoperative
• Pain management may be problematic; consider regional blocks/LA.
PCA possible in selected patients.
• Parents/carers often indispensable in managing postoperative agitation.
934
Diaphragmatic hernia
Procedure Repair of defect in diaphragm either by suturing to
abdominal wall or with a synthetic graft
Time 1–2h
Pain +++
Position Supine
Blood loss Usually minimal to moderate
Practical techniques GA plus IPPV, arterial line
Preoperative
• 1:3000–4000 deliveries; 85% left-sided; cardiac anomalies in 20%.
• Diagnosis usually made antenatally on ultrasound. Present in respiratory
distress: i RR, cyanosis, with a scaphoid abdomen. CXR diagnostic.
• Overall mortality of 30% from lung hypoplasia, abnormal pulmonary
vasculature and pulmonary hypertension.
• Usually already intubated and ventilated. Ventilatory support can include
high-frequency oscillation (HFO) and NO.
• For high-risk cases, surgery may need to take place on the special care
baby unit if conventional ventilation is not possible.
• An NGT is essential preoperatively to prevent the stomach and small
bowel in the chest cavity from compressing the lung.
Perioperative
• Cautious ventilation via a face mask; avoid N2O.
• NGT, 2 × IV cannulae, right radial arterial line (preductal sampling).
• Keep airway pressures <25cmH2O (pulmonary hypoplasia and
consequent risk of pneumothorax). Use RR to improve ventilation.
• High-dose fentanyl (25 micrograms/kg) to reduce pulmonary
vasoconstriction response to surgical stress.
Postoperative
• Postoperative ventilation for at least 24h, then attempt to wean.
• Infant may deteriorate within 12h due to pulmonary hypertensive
crises. Pulmonary vasculature is reduced and abnormal l exaggerated
vasoconstrictive response to hypoxaemia and acidosis.
• Rarely, if minimal defect, extubate immediately.
Special considerations
• Pulmonary hypertension may be significant. Initial management includes
assisted hyperventilation with 100% O2 and fluid boluses. Other
therapies include epoprostenol, sildenafil and N2O.
• ECMO is a last resort but has been used.
• To assist weaning, a thoracic epidural may be of benefit, inserted either
conventionally or via the caudal route.
Gastroschisis/exomphalos 935
Gastroschisis/exomphalos
Procedure Replacement of abdominal contents into the
abdominal cavity
Time 2h
Pain ++/+++
Position Supine
Blood loss Moderate
Practical techniques GA + IPPV; NGT; arterial line
Preoperative
• Usually diagnosed in utero. Incidence of 1:3000–4000.
• Gastroschisis: defect in the anterior abdominal wall, usually on the
right, causing herniation of abdominal contents without a covering
sac; associated with LBW and thickened bowel wall due to exposure
to amniotic fluid; associated with younger maternal age and lower
socioeconomic status. Repair is an urgent procedure.
• Exomphalos: failure of the gut to return to the abdominal cavity during
fetal development l persistent herniation through the umbilical cord
which covers it. May include other abdominal organs. i incidence of
associated anomalies, including cardiac disease.
• Exposed abdominal contents result in large evaporative heat and water
losses and predispose to infection. They should initially be covered with
cling film or equivalent.
Perioperative
• May already be intubated. Otherwise intubate conventionally.
• Intraoperative analgesia: fentanyl 1.5–10 micrograms/kg or epidural if
extubation within 48h is contemplated.
Postoperative
• Ventilate in the head-up position, especially if the abdomen is tense.
• Assiduous attention to fluid balance. There may be large abdominal
losses of crystalloid and protein.
Special considerations
• Lines should be sited in the arms, as abdominal distension may impair
venous return from the lower body.
• Consider inserting a percutaneous long line or central line for parenteral
feeding—postoperative oedema makes cannulation difficult.
• Manual ventilation is useful to assess the effect of replacement of
abdominal contents on lung compliance to determine the correct
degree of abdominal reduction before closure.
• Complete reduction is not always possible. A silo is then created
around the extra-abdominal contents to be gradually reduced on the
ICU. Fluid loss and infection are major issues in these cases.
936
Tracheoesophageal fistula
Procedure Ligation of fistula plus anastomotic repair of
oesophageal atresia
Time 2h
Pain +++
Position Left lateral for right thoracotomy
Blood loss Moderate
Practical techniques GA + IPPV; arterial line
Preoperative
• Incidence of 1:3500; 85% comprise oesophageal atresia with distal
fistula. Majority diagnosed in utero; always exclude in cases of
polyhydramnios.
• High incidence of prematurity (30%) and cardiac disease (25%).
• Presents with choking, cyanosis on feeding and inability to pass NGT.
• Constant risk of pulmonary aspiration. A double-lumen Replogle tube
in the oesophagus allows irrigation and suction.
Perioperative
• Inhalational or IV induction. Gentle mask ventilation to minimise gastric
distension via a fistula.
• Careful ETT placement. Confirm symmetrical ventilation with the
tube distal to the fistula. Manual ventilation may be necessary to assess
lung compliance after ligation of the fistula, to assist in repair of the
oesophagus and to periodically reinflate the left lung. Surgical retraction
may impede ventilation.
• Intraoperative access will be needed to pass the transanastomotic tube
nasally to facilitate oesophageal repair.
• Intraoperative analgesia: fentanyl (5–10 micrograms/kg) or epidural by
either the thoracic or caudal route, if early weaning is anticipated.
• The operation is performed via thoracoscopic repair or via a right
thoracotomy extrapleural approach (unless right-sided aortic arch
present; 5% of cases; necessitates left thoracotomy).
• Thoracoscopic compression of the ipsilateral lung makes desaturation
common; direct compression of vascular structures (IVC and the right
atrium) reduces venous return. CO2 absorption l hypercarbia and
acidosis which may be poorly tolerated by these neonates.28
Postoperative
• Majority are ventilated postoperatively, especially if oesophageal repair
is under tension. Critical to secure the NGT or transanastomotic tube.
Special considerations
• The fistula is normally situated on the posterior aspect of the trachea,
just proximal to the carina. An FOB can be used to confirm ETT
position.
Patent ductus arteriosus 937
Preoperative
• Small premature babies: 25% of premature infants <1.5kg recovering
from hyaline membrane disease have a patent ductus arteriosus.
Associated with other cardiac anomalies.
• Indications are for failure of medical treatment which include ibuprofen,
indometacin or paracetamol, ventilator dependence and risk of
developing bronchopulmonary dysplasia.
Perioperative
• High-risk group. Operation may be undertaken on the special care baby
unit.
• Patient is usually already ventilated with full monitoring.
• Adequate IV access for transfusion. Arterial monitoring.
• IPPV with O2/air and fentanyl up to 10 micrograms/kg with a low dose
of volatile agent.
• Active heat conservation.
• Keep saturations < 96% to avoid retinopathy of prematurity.
• Local infiltration for analgesia, interpleural block by surgeon or thoracic
epidural if early weaning considered.
Postoperative
• Postoperative ventilation until stable, then attempt to wean.
Special considerations
• Sudden ligation of the ductus may precipitate an acute rise in systemic
BP and increase the risk of intraventricular haemorrhage. The duct
should be clamped gently, or alternatively the concentration of the
volatile agent can be temporarily i.
• Older children requiring patent ductus arteriosus occlusion tend to be
fit, although some present with cardiac failure. The procedure can be
performed percutaneously as a day case using a coil device.
938
Pyloric stenosis
Procedure Splitting the pylorus muscle longitudinally down
to the mucosa
Time 30min
Pain +
Position Supine
Blood loss Minimal
Practical techniques GA + IPPV, ? RSI
Preoperative
• Incidence of 1:350 births; more common in first-born ♂ ; 80% are ♂ ;
10% are premature.
• Present with biochemical abnormalities, notably hypochloraemic
alkalosis. May be dehydrated. Operation is never urgent, and full
resuscitation should occur.
• Electrolytes, particularly chloride and HCO3–, and pH should be within
normal limits, with chloride ≥100mmol/L.
Perioperative
• No complete agreement, but there is a risk of pulmonary aspiration
from gastric outflow obstruction.
• An NGT is mandatory and will be in situ. Aspirate, and do not remove.
It does not reduce the effect of cricoid pressure and may act as an
escape valve if mask ventilation increases intragastric pressure.
• IV access is usually in place. Consider RSI ± cricoid pressure if there is
excessive NG loss (>2mL/kg/h).
• Fentanyl (1 microgram/kg) plus paracetamol IV. Local infiltration (up to
1mL/kg of 0.25% bupivacaine ± adrenaline) pre-incision.
• Can be performed laparoscopically, in which case a rectus sheath block
may be useful.
• Extubate awake in the left lateral position.
Postoperative
• Remove the NGT at the end of the procedure unless mucosa breached.
• Give paracetamol regularly and PO morphine PRN.
• Feed within 6h, but maintain IV fluids until feeding is established.
• Apnoea alarm overnight.
Special considerations
• Resuscitate with 5% glucose/0.45% sodium chloride plus 20mmol/L
potassium chloride (HCO3– <32mmol/L). More severe cases will
require 0.9% sodium chloride. Replace NG loss with 0.9% sodium
chloride.
Intussusception 939
Intussusception
Procedure Reduction of invaginated bowel
Time 1–3h
Pain +++
Position Supine
Blood loss Moderate, may be large
Practical techniques RSI + IPPV
Preoperative
• Intussusception is the commonest cause of obstruction in infants over
2mo of age; incidence of 2:1000 births.
• Invagination of the bowel into an adjacent lower segment, usually at the
terminal ileum or ileocaecal valve. Rarely caused by a polyp or Meckel’s
diverticulum (5% of cases).
• Presents with paroxysmal pain, blood and mucus in stool (redcurrant
jelly stool), and a sausage-shaped mass in the right abdomen.
• 70% of cases are reduced by air or barium enema.
• Child may be profoundly shocked. Urgent fluid resuscitation with gastric
decompression and electrolyte correction will be needed and blood
may be required. Delay can result in perforated or necrotic bowel. Fluid
loss may be greater than expected.
Perioperative
• RSI. Retain the NGT in situ.
• Fentanyl 2–5 micrograms/kg plus volatile agent.
• Two cannulae of adequate size. CVP line in severe cases.
• Routine monitoring, temperature measurement and urinary catheter.
• Prolonged intussusception with ischaemic gut requiring resection often
leads to metabolic acidosis and septic shock. Admission to a paediatric
ICU will be required.
Postoperative
• TAP block, wound catheter or local wound infiltration, and morphine
NCA.
Special considerations
These children can be very challenging. They will have had unsuccessful
barium enema in the district general hospital and air enema in the regional
centre, both with sedation. They may be inadequately resuscitated. Venous
access is often challenging and a significant resuscitation is often necessary.
940
Herniotomy
Procedure Excision of patent processus vaginalis
Time 30min
Pain ++
Position Supine
Blood loss Minimal
Practical techniques LMA/SV or ETT/IPPV; spinal, caudal or local
infiltration
Preoperative
• Majority are fit ASA 1 children. More common in boys.
• 20% of preterm babies present for surgery at 740w post-conceptual age
or when ready to leave the special care baby unit.
Perioperative
• Children: inhalational or IV induction with LMA, then caudal or
ilioinguinal block and intraoperative opioids if necessary.
• Infants: intubate with controlled ventilation. With neonates, avoid
ilioinguinal block, as spread of LA may obscure the surgical field. Use
either caudal or postoperative infiltration.
• Paracetamol IV or diclofenac suppository.
Postoperative
• Day case: regular paracetamol and ibuprofen.
• Admit term babies <4w and ex-premature infants <60w post-
conceptual age overnight for SpO2 and apnoea alarm monitoring.
Special considerations
• No consensus on the most appropriate regional block. Caudal blockade
is indicated for bilateral herniotomy repair and children <20kg.
Ilioinguinal block is effective in children >5kg.
• Laparoscopic repair becoming common. Local infiltration adequate.
• The ex-premature baby may be small and O2-dependent with chronic
lung disease. Postoperative apnoea and bradycardia are documented
risks associated with GA for this group. Avoid hypocarbia and
hypothermia; O2 saturations of 90–95% are acceptable. Caffeine
(10mg/kg IV) given at induction reduces the risk of apnoea by 70%.
• To avoid a GA in the high-risk premature infant, a spinal technique may
be used. This may be technically difficult and complicated by a bloody
or dry tap. It is too short-acting for bilateral repair. Single-shot caudal is
an alternative method. Supplementary sedation results in the same risk
of postoperative apnoea as with GA.
• A strangulated hernia that does not reduce is an emergency and
requires fluid resuscitation and an NGT. Precautions should be taken
against regurgitation and aspiration.
Circumcision/hypospadias repair 941
Circumcision/hypospadias repair
Procedure Removal of prepuce (foreskin)/restoration of ur-
ethral opening to the tip of the penis
Time Circumcision: 20min; hypospadias: 1–3h
Pain ++
Position Supine
Blood loss Minimal
Practical techniques LMA + SV/IPPV, caudal/penile block/ring block
Preoperative
• Circumcision: common day case procedure; move towards conservative
management, including simple stretch or preputioplasty.
• Hypospadias is usually an isolated problem, but there may be an
association with certain rare dysmorphic syndromes.
• Obtain consent for a regional block and suppository.
Perioperative
• Inhalational or IV induction.
• If procedure <1h, LMA plus SV.
• If procedure >1h, LMA or ETT plus IPPV.
• Regional block: caudal or penile block (if hypospadias is distal) (see
% pp. 929–30; % p. 931; % p. 1132).
• Paracetamol IV and diclofenac PR.
Postoperative
• Regular paracetamol and NSAIDs. Hypospadias: consider morphine
NCA (not always necessary).
• Topical lidocaine gel can be applied frequently, without exceeding the
toxic dose.
Special considerations
• Hypospadias repair: may be a simple procedure, e.g. meatal
advancement and glanduloplasty, or extensive involving a buccal mucosa
graft. Adjust anaesthetic technique accordingly.
• A regional block should be performed prior to the surgery. Avoid
erection with a regional block plus an adequate depth of anaesthesia.
• There is no consensus as to the optimal strategy for pain relief. Caudal
is technically easier in infants, and penile block may be more suitable in
children over 10kg. Ring block is easier in boys >5kg. All methods are
effective.
• Circumcision is one of the most painful day case procedures; parents
should be warned and advised to apply topical gel regularly and
continue paracetamol for several days.
942
Orchidopexy
Procedure Release of undescended testis into scrotum
Time 45min
Pain ++
Position Supine
Blood loss Minimal
Practical techniques SV, LMA + regional block
Preoperative
• Boys, usually over 2y (2% of population).
• Common day case procedure.
• Obtain consent for a suppository and regional block.
Perioperative
• Inhalational or IV induction. LMA.
• Regional technique: caudal, ilioinguinal block or local infiltration.
• Paracetamol IV or diclofenac PR.
• Give supplementary opioids, if indicated.
Postoperative
• Regular paracetamol and ibuprofen. PO morphine if necessary.
Special considerations
• Adequate analgesia is difficult if the testis is high. In this case, aim for
a high-volume, low-concentration mid-thoracic caudal block. Use
1.25mL/kg volume of 0.25% bupivacaine with 0.9% sodium chloride
(observing maximum bupivacaine dose) (see % pp. 929–30; % p. 931).
• If an ilioinguinal block is used, only the anterior part of the scrotum is
anaesthetised; use local infiltration for the scrotal incision (see %
p. 932; % pp. 1131–2).
• Testicular traction, even with a seemingly adequate blockade, may
lead to intraoperative bradycardia or laryngospasm, especially with
an ilioinguinal block. Surgery should be stopped, and anaesthesia
deepened; supplementary opioids may be required.
• Suspected torsion of the testis is a surgical emergency, and the need for
an RSI will have to be considered. Local infiltration is adequate.
• A high testis may need surgery in two stages. The 1st procedure is to
identify the testis and, if possible, bring it down to the inguinal ring.
This is usually performed laparoscopically and will require intubation,
controlled ventilation with intraoperative opioids, IV paracetamol and
diclofenac PR.
Cleft lip and palate 943
Preoperative
• Incidence of 1:300–600 births but can be 1:25 with a family history.
• Both the lip and palate are involved together in 50% of cases.
• Isolated cleft palate incidence of 1:2000 live births. i incidence of
congenital abnormalities.
• Associated syndromes often involve a difficult airway, e.g. Pierre–Robin,
Treacher Collins and Goldenhar syndromes. Therefore, make a careful
assessment of the airway.
• Discuss risks and complications.
• Administer IM atropine 20 micrograms/kg 30min preoperatively if a
difficult airway is suspected.
Perioperative
• Inhalational or IV induction. If difficult airway is suspected, consider
inhalational induction with CPAP if necessary. Intubate deep with
the child breathing spontaneously or following muscle relaxant.
Videolaryngoscopy may be necessary.
• Caution when surgeon inserts gag. A preformed RAE tube may become
obstructed or kinked, especially the smaller sizes.
• Use a throat pack, and make sure the eyes are protected.
• Encourage LA infiltration to improve analgesia and d blood loss.
• Fentanyl (2–4 micrograms/kg) before LA, then morphine 50–150
micrograms/kg plus paracetamol IV.
• Dexamethasone 0.25mg/kg + three postoperative doses to prevent
postoperative swelling.
• Consider an infraorbital nerve block for cleft lip repair.
Postoperative
• Extubate awake. Suction the pharynx early and carefully to prevent
damage to the repair.
• Nasal stents may be inserted to maintain patency of the airway. A
tongue stitch is rarely used.
• Regular paracetamol and ibuprofen. IV morphine may be required
initially.
94
Special considerations
• Intubation is usually uncomplicated.
• The laryngoscope blade rarely lodges in the cleft. If there is a problem,
a roll of gauze can fill the gap.
• Prolonged surgery may cause a swollen tongue from pressure of the
mouth gag.
• Cleft palate repair can produce upper airway obstruction, and extreme
care is needed for extubation.
• With airway problems, opioids should be given cautiously.
Postoperative monitoring should include SpO2 and apnoea alarm.
• Cleft lip is usually repaired at 3mo, and cleft palate at 6–9mo. The lip
may be repaired at the neonatal stage to improve the scar and assist
maternal bonding. There is little evidence to support this.
Congenital talipes equinovarus 945
Preoperative
• Occurs in 1:1000 births.
• Usually an isolated anomaly but may occur in association with some
myopathic diseases, hence i theoretical risk of MH.
• Obtain consent for a suppository and regional block.
Perioperative
• Inhalational or IV induction. If prone, intubate and ventilate. Give
additional opioids, if indicated.
• Extended caudal blockade: 1mL/kg of 0.25% levobupivacaine +
clonidine (see % pp. 929–30; % p. 931).
• Paracetamol IV and diclofenac PR.
Postoperative
Regular paracetamol and ibuprofen plus PO morphine PRN.
Special considerations
For prolonged pain relief, either top up the caudal at the end of the pro-
cedure by using an indwelling epidural catheter or extend the duration of
the block by adding clonidine (1–2 micrograms/kg) to the initial dose of
bupivacaine.
946
Femoral osteotomy
Procedure Stabilising the hip in congenital dislocation by re-
aligning the proximal femur
Time 2h
Pain +++
Position Supine
Blood loss Moderate/potentially large
Practical techniques SV + LMA or ETT + IPPV, caudal/epidural
Preoperative
• Usually an isolated defect. More common in girls or where there is a
family history.
• Obtain consent for a regional block and suppository.
Perioperative
• Inhalational or IV induction. Adequate IV access.
• Caudal block plus clonidine (see % pp. 929–30; % p. 931) if hip spica to
be applied.
• Alternatively, femoral nerve block + LA to skin incision.
• Lumbar epidural if high osteotomy (see % p. 931).
• Intraoperative opioids if regional block not possible (% pp. 926–8).
• Paracetamol IV and diclofenac PR.
• Employ heat conservation measures.
• Attention to blood loss.
Postoperative
• A hip spica provides support and helps with pain relief.
• Extended caudal or morphine NCA, with regular NSAIDs and
paracetamol.
• Epidural infusion (Table 36.15) with regular paracetamol, NSAIDs + PO
morphine PRN.
Special considerations
• Blood loss may be extensive if revision surgery. Consider cell saver.
• A hip spica complicates urinary retention in girls.
Inhaled foreign body 947
Preoperative
• Commonest reason for bronchoscopy in the 1–3y age group.
• May present as an emergency acute airway obstruction.
• Presentation of lower airway obstruction may occur several days
after a history of coughing. Peanut oil is an irritant and leads to
mucosal oedema and chemical pneumonitis. CXR shows characteristic
hyperinflation of affected side during expiration, but a foreign body is
not always visible.
• Treat symptoms as indicated, e.g. dehydration, pneumonia, wheeze.
Perioperative
• Inhalational induction is usual to avoid displacing the object further. Use
100% O2 with sevoflurane.
• TIVA is becoming a more popular maintenance technique.
• Apply topical anaesthesia to the vocal cords (4% lidocaine, up to 3mg/
kg), and consider a drying agent (atropine 20 micrograms/kg IM 30min
preoperatively or 10 micrograms/kg IV at induction, or glycopyrronium
5 micrograms/kg IM or IV).
• Prior to bronchoscopy, maintain airway with a face mask or LMA.
• Rigid bronchoscopy: the Storz bronchoscope has an attachment for a
T-piece. Check compatibility before the procedure.
• For foreign objects in the upper airways, maintain SV. If tracheal/ball–
valve obstruction suspected, IPPV is contraindicated.
• If the foreign body is in the lower airway, then IPPV with a muscle
relaxant is acceptable, since the object will be pushed distally by
the bronchoscope until it can be grasped by forceps. Give assisted
ventilation via a T-piece or high-frequency jet ventilation.
• This may be a difficult surgical procedure.
Postoperative
• If bronchoscopy is traumatic, give dexamethasone 0.25mg/kg IV, then
two doses 8-hourly of 0.125mg/kg.
• Consider physiotherapy, bronchodilators and antibiotics as indicated.
948
Sedation
• The expansion of imaging techniques and diagnostic and therapeutic
interventions has led to a rise in demand for sedation services.29
• The safe sedation of children for procedures requires a systematic
approach. Compared with GA, sedation is neither cheaper nor safer.
• Anaesthetists are not always available to administer sedation, and other
medical or nursing personnel may be involved. Sedation guidelines are
essential29 and monitoring of SpO2 is mandatory. With appropriate
planning, nurse-led sedation services have been developed at several
centres following strict protocols. The children are fasted conventionally
but allowed unrestricted clear fluids.
• Safety is paramount—facilities must include an airway trolley and
monitoring and resuscitation equipment, together with all personnel
necessary to sedate the child and carry out the specific procedure. All
standard anaesthetic equipment should be available for resuscitation.
• Each sedated child must be supervised by an appropriate nurse or
doctor trained in paediatric resuscitation. Experienced medical staff
must be immediately available to assist with sedation problems or
resuscitation. There must be a contingency for overnight admission if
recovery is prolonged.
• The adult concept of sedation with verbal contact maintained is not
practical in children. There may be little difference between deep
sedation, as defined by the American Academy of Pediatrics, and
uncontrolled anaesthesia. Ideal conditions achieve depression of the
nervous system, allowing the procedures to occur, with preservation of
airway reflexes. In practice, this is difficult to achieve.
• It is important not to confuse sedation with analgesia. Painful
procedures may require a topical anaesthetic cream, infiltration with
LAs and occasionally systemic opioids.
• Contraindications include children with potential airway issues, apnoeic
episodes, respiratory disease, raised ICP, risk of pulmonary aspiration
and epilepsy.
• Medications used:
• Chloral hydrate 50–100 micrograms/kg for younger children.
• Midazolam (0.5mg/kg PO or incremental bolus doses of 0.05–
0.1mg/kg IV, up to a maximum of 0.4mg/kg) can produce good
conditions for sedation; additional property of amnesia.
• Ketamine (6–10mg/kg PO or 0.5–1mg/kg IV boluses every 10–
15min) is indicated for short, painful procedures and may be used in
combination with midazolam. Emergence delirium is less of a problem
with children, but a drying agent is often required.
• Propofol can be used alone or in combination with remifentanil for
endoscopy sedation, but the use of these drugs should be reserved
for anaesthetists.29
• Dexmedetomidine 1 microgram/kg and/or infusion 0.2–1
micrograms/kg/h. Can cause bradycardia.
• Surprisingly young children can tolerate scans awake with
encouragement, careful explanation and parental presence.
Medical problems 949
Medical problems
Acute laryngotracheobronchitis (croup)
• Croup occurs predominantly in epidemics in autumn and early spring.
The peak age of incidence is 6mo to 2y. It is viral in aetiology. The
majority of cases are due to parainfluenza, but influenza and respiratory
syncytial virus are possible.
• Symptoms are coryzal for the first few days but then progress to a
characteristic barking cough/hoarseness with profuse secretions and
occasional dysphagia. Pyrexia is mild or absent.
• The larynx, trachea and bronchi are all involved and become
oedematous, leading to the onset of stridor. An anxious child will
exacerbate the condition, as the trachea will tend to collapse on
inspiration.
• The majority of children respond to conservative measures and
reassurance. In severe cases, steroids (dexamethasone 0.25mg/kg IV
followed by two further doses 8-hourly of 0.125mg/kg) and nebulised
adrenaline (0.5mg/kg, up to a maximum of 5mg) are required.
• 10% of children are admitted, and 1% will require intubation.
• The majority of children have a single isolated episode.
Acute epiglottitis
• This is an acute life-threatening infection caused by Hib. It most
commonly presents at 2–3y.
• There is a rapid onset of oedema of the epiglottis and aryepiglottic
folds. The child has a high temperature, usually >39.5°C, and presents
sitting or leaning forwards, with drooling saliva, and unable to swallow,
with the tongue pushed forwards. Inspiratory and expiratory stridor is
rapidly progressive and is a late sign.
• Acute epiglottitis is a medical emergency. The antibiotic of choice is
ceftriaxone (50mg/kg IV once daily). Intubation is indicated in 60% of
cases. In some centres, all children are routinely intubated.
• Following the introduction of the Hib vaccine, this condition is now
rare.
Anaesthetic management of croup and acute epiglottitis
• The differential diagnosis between croup and epiglottitis is not always
obvious. If epiglottitis is even remotely suspected, there must be liaison
with an ENT surgeon at consultant level.
• Induction occurs in the anaesthetic room or operating theatre, with the
full range of appropriate equipment and monitoring available.
• During anaesthesia, the ENT surgeon should be scrubbed in theatre,
with the tracheostomy set open.
• Traditionally, IV access has been contraindicated prior to induction
because of the risk of acute glottic closure. However, the use of a
topical cream facilitates an atraumatic venepuncture. Unless access is
obviously difficult, cannulation should proceed before anaesthesia.
• Inhalational induction is performed in the sitting position, with
sevoflurane in 100% O2. Once anaesthetised, the child can be moved
to a more recumbent position and maintained with sevoflurane, up to
concentrations of 8%, if needed. CPAP should be routinely applied, but
the airway is not usually difficult to maintain.
950
Unresponsive
Open airway
5 Rescue breaths
No signs of life
15 Chest compressions
2 Rescue breaths
15 Chest compressions
Fig. 36.2 Paediatric basic life support. Reproduced with the kind permission of
Resuscitation Council UK.
Paediatric advanced life support 953
Fig. 36.3 Paediatric advanced life support. Reproduced with the kind permission of
Resuscitation Council UK.
954 Chapter 36 Paediatric and neonatal anaesthesia
Adrenaline
10 micrograms/kg every 3–5min
Post-resuscitation care
• Titrate O2 for O2 saturations of 94–98%.
• Maintain CO2 4.5–5.0kPa.
• Avoid hypotension. Consider fluids and/or inotropes.
• Suggested, but no statistical evidence for, mild hypothermia 32–34°C.30
• Moderate glucose control.
PULSELESS VENTRICULAR TACHYCARDIA 955
Rhythm check
Rhythm check
Notes
• Continue shocks 4J/kg every 2min. Resume CPR immediately after
defibrillation without checking output.
• Standard automated external defibrillators (AEDs) may be used in
children over 8y. Purpose-made paediatric pads are recommended for
children aged 1–8y, if available. Below 1y, a manual defibrillator should
be used if available, but an adult AED can be used.
• Give adrenaline 10 micrograms/kg (= 0.1mL/kg of 1:10 000 solution)
and amiodarone 5mg/kg after a 3rd shock, once compressions have
been resumed.
• Repeat adrenaline every alternate cycle (3–5min).
• Further antiarrhythmic agents:
• Repeat amiodarone 5mg/kg IV after 5th shock.
• Torsade de pointes/h ypomagnesaemia: magnesium sulfate
25–50mg/kg.
• There is no evidence that atropine confers any benefit in asphyxial
bradycardia or asystole.
• Calcium: routine use associated with i mortality. Indicated for
hyperkalaemia, hypocalcaemia and calcium channel blocker overdose.
• Sodium bicarbonate 1mmol/kg: routine use not recommended.
Indicated for hyperkalaemia and tricyclic overdose.
956 Chapter 36 Paediatric and neonatal anaesthesia
Neonatal resuscitation
Condition Acute neonatal asphyxia during the birth process
Presentation Floppy, blue or pale, HR <60bpm, diminished re-
spiratory effort
Immediate action Delay cord clamping for at least 1min. Dry, wrap
and warm the baby. Open and clear airway, five
inflation breaths with air (2–3s at 30cmH2O)
Follow-up action Cardiac compressions (3:1) at 120/min if <60bpm,
review ventilation
Investigations Record Apgar scores (Table 36.16), take cord gases
Also consider Hypovolaemia, diaphragmatic hernia, pneumo-
thorax. Consider therapeutic hypothermia
Risk factors
• Known fetal distress; Category 1 emergency CS; meconium-stained
liquor; <35w gestation.
• Prolonged delivery; vaginal breech; instrumental delivery; shoulder
dystocia; multiple births.
• Maternal drugs: opioids, GA for CS.
• Preterm delivery (prognosis is very poor if gestation <23w).
Diagnosis
• A normal newly delivered baby is pink, breathes spontaneously within
15s, has a HR >100bpm and good muscle tone and is vocal.
• A baby requiring resuscitation is floppy, silent, blue or pale, has a HR
<100bpm and gasping, diminished or absent respiratory effort (see
Apgar scores in Table 36.16).
0 1 2
Colour Pale/blue Blue extremities Pink
HR (bpm) Absent <100 >100
Response to stimulation Nil Movement Cry
Muscle tone Limp Some flexion Well flexed
Respiratory effort Absent Poor effort/weak cry Good
Source: data from Apgar A (1953) A proposal for a new method of evaluation of the newborn
infant. Anesth Analg, 32; 250–9.
Immediate management
• Keep the theatre warm. Dry and wrap the baby. Actively maintain
temperature between 36.5°C and 37.7°C. Keep warm under a radiant
heater. Use polythene wrapping for preterm babies <30w.
• Consider ECG and preductal SpO2 (right hand). Maintain
saturations <95%.
Neonatal resuscitation 957
• Open and clear the airway, but keep the neck in a neutral position.
• Routine suctioning is not recommended.
• Give five effective inflation breaths (2–3s at 30cmH2O) initially with air.
• HR should increase; continue ventilating at 30–40 breaths/min, until
spontaneous effort is adequate.
• If HR remains <60bpm, commence chest compressions with thumbs
around the chest, at a compression rate of 120/min and a ratio of 3:1
breaths. Compress the chest diameter by one-third.
• Reassess HR every 30s.
(See Fig. 36.6.)
Subsequent management
• In the neonate that remains unresponsive despite oxygenation, consider
intubation and drugs (Table 36.17). This is seldom required.
Other considerations
• If response to resuscitation is prompt (required support breaths only
and now making good, spontaneous respiratory effort), return the baby
to the parents.
• For ventilatory depression thought to be due to maternal opioids, give
naloxone 200 micrograms IM.
• Therapeutic hypothermia is indicated for term or near-term infants with
moderate to severe hypoxia.
Further reading
Resuscitation Council (UK) (2015). Guidelines: Resuscitation and support of transition of babies at
birth. M https://www.resus.org.uk/library/2015-resuscitation-guidelines/resuscitation-
and-support-transition-babies-birth
958 Chapter 36 Paediatric and neonatal anaesthesia
Fig. 36.6 Neonatal life support. Reproduced with the kind permission of Resuscitation
Council UK.
The collapsed, septic child 959
Risk factors
• Prematurity, immune deficiency, chronic cardiorespiratory disease,
endocarditis, CNS infections.
• Exposure to MRSA, Gram-negative bacteria, nosocomial infection and
fungi.
Recognition of at-risk child
• Suspected or proven infection plus two out of: temperature <36.5°C
or >38.5°C, tachycardia, altered mental state, prolonged capillary refill
time (>2s), immunocompromise and hypotension.
• Look for signs of warm or cold shock:
• Warm shock: vasodilation, bounding peripheral pulses, wide pulse
pressure
• Cold shock: cool peripheries, capillary refill time >2s, narrow pulse
pressure.
Red flag signs
• Any one sign of the following: lactate >2mmol/L; extreme tachycardia
or tachypnoea; SpO2 <90%, grunting, cyanosis, apnoea; reduced level
of consciousness, persistent hypotension and non-blanching rash/
mottled skin.
Immediate management
• Aggressive early management improves prognosis. Hypovolaemia is
severe and often under-resuscitated.
• ABC: maintain/support airway; high-flow O2 via a non-rebreathing
mask; consider ventilatory support ± intubation.
• Rapid fluid boluses of 20mL/kg of crystalloid/albumin: 80–100mL/kg
may be required to restore normovolaemia.
• Correct hypoglycaemia: 2mL/kg 10% glucose.
• Inotropic support: if no significant response to fluid, start adrenaline
0.1–0.5 micrograms/kg/min.
• Antibiotics: cefotaxime 50mg/kg IV 1st line; for 2nd line, discuss with
local microbiology team.
• Early referral to specialist centre.
960 Chapter 36 Paediatric and neonatal anaesthesia
Subsequent management
• Ventilation under sedation and paralysis: target VT 4–7mL/kg, initial
PEEP 5cmH2O. Saturation >95%.
• Inotropes:
• Cold shock: adrenaline 0.1–0.5 micrograms/kg/min IV
• Warm shock: noradrenaline 0.1–0.5 micrograms/kg/min IV.
• Risk of adrenal failure: hydrocortisone 1mg/kg qds IV.
• Consider the possibility of meningitis/encephalitis and raised ICP.
• Stabilise for transfer and prepare handover documentation. A retrieval
service may be provided by the receiving unit.
Other considerations
• Significant fluid shift from capillary leakage may result in pulmonary
oedema 2° to fluid resuscitation. If drugs are required to intubate
the child, anticipate an exaggerated fall in BP and adjust the dose
accordingly. Use ketamine, fentanyl, rocuronium and cuffed ETT. It is
wise to start inotropes and fluid resuscitation before induction.
Further reading
NHS Children’s Acute Transport Service (CATS) (2020). Clinical guidelines: septic shock. M https://
cats.nhs.uk/wp-content/uploads/guideline-sepsis.pdf
Randolph AG, McCulloh RJ (2014). Paediatric sepsis: important considerations for diagnosing and
managing severe infections in infants, children and adolescents. Virulence, 5, 179–89.
Stabilisation of the sick child (prior to PICU transfer) 961
Further reading
Many local retrieval service websites include guidelines and drug calculators. For example: Wales
& West Acute Transport for Children service (WATCh). M https://www.watch.nhs.uk/about
Managing Emergencies in Paediatric Anaesthesia (MEPA). [Simulation-based training] M https://
mepa.org.uk
Spotting the Sick Child. [Education and case studies] M http://www.spottingthesickchild.com
Roberts S, ed. (2019). Paediatric Anaesthesia, 2nd edn. Oxford: Oxford University Press.
Paediatric doses and equipment 963
Age Approx- Body Percentage ETT size ETT LMA Suxa- Atropine
imate surface of adult drug (mm) length size meth- dose
weight area dose (cm) onium (micro-
(kg) (m ) (approximate)
2
dose grams) IV
(mg) IV
Term 3.5 0.23 12.5(1/8th) 3.5 9 1 7 35
1mo 4.2 0.26 14.5 3.5 10 1 8 40
3mo 6 0.33 15 3.5 10 1.5 12 60
6mo 7.5 0.38 22 3.5/4.0 11 1.5 15 75
1y 10 0.47 25(1/4) 4.0 12 1.5/ 20 100
2
2y 12 0.53 30 4.5 13 2 24 120
3y 14 0.61 33 4.5/5 13/ 2 28 140
14
5y 18 0.73 40 5.0/5.5 14.5 2.5 36 180
7y 22 0.86 50(1/2) 6.0 15.5 2.5 44 220
10y 30 1.10 60 6.5cuffed 17 3 60 300
12y 38 1.30 75(3/4) 7.0cuffed 18 3/4 75 380
Note: weights are approximations only. Patients should be weighed accurately.
• Cefotaxime 50mg/kg
• Diazepam 0.1mg/kg IV; 0.5mg/kg PR
• Glucose (10%) 2mL/kg
• Ketamine 2mg/kg
• Lorazepam 0.1mg/kg for status epilepticus (repeatable after 10min)
• Magnesium 25–50mg/kg
• Naloxone 0.1mg/kg
• Neostigmine 50 micrograms/kg
• Paraldehyde 0.1mg/kg
• Phenytoin 10–20mg/kg
• Salbutamol 2.5mg nebuliser.
Circulation
• Blood volume: 75mL/kg (1–10y), 70mL/kg (>10y)
• Fluid bolus: 20mL/kg.
These estimations are not valid for premature infants and are intended as
rough guides only.31
Paediatric doses and equipment 965
Further reading
Roberts S, ed. (2019). Paediatric Anaesthesia, 2nd edn. Oxford: Oxford University Press.
James I, Walker I, eds. (2013). Core Topics In Paediatric Anaesthesia. Cambridge: Cambridge
University Press.
Bingham R, Lloyd Thomas A, Sury M, eds. (2007). Hatch and Sumner’s Textbook of Paediatric
Anaesthesia, 3rd edn. London: Hodder Arnold.
Baum VC, O’Flaherty JE (2006). Anaesthesia for Genetic, Metabolic and Dysmorphic Syndromes of
Childhood, 2nd edn. Philadelphia, PA: Lippincott, Williams & Wilkins.
Black A, McEwan A (2004). Paediatric and Neonatal Anaesthesia: Anaesthesia in a Nutshell. Edinburgh:
Butterworth-Heinemann.
References
1 National Institute for Health and Care Excellence (2015). Intravenous fluid therapy in children and
young people in hospital. M https://www.nice.org.uk/guidance/ng29
2 Resuscitation Council (2015). Fluid administration for volume resuscitation. In: European
Paediatric Life Support Manual, 4th edn; pp. 52–3.
3 Mihara T, Asakura A, Owada G, et al. (2017). A network meta-analysis of the clinical properties
of various types of supraglottic airway device in children. Anaesthesia, 72, 1251–64.
4 Ritchie-McLean, Ferrier V, Clevenger B, et al. (2018). Using middle finger to determine the in-
ternal diameter of uncuffed tracheal tubes in paediatrics. Anaesthesia, 73, 1207–13.
5 Chambers NA, Ramgolam A, Sommerfield D, et al. (2018). Cuffed vs. uncuffed tracheal tubes
in children: a randomised controlled trial comparing leak, tidal volume and complications.
Anaesthesia, 73, 160–8.
6 Royal Berkshire NHS Foundation Trust (2014). Your child’s general anaesthetic –magic milk and
squidgy masks. M https://www.youtube.com/watch?v=0QfFL2CGkU0
7 O’Sullivan M, Wong G (2013). Preinduction techniques to relieve anxiety in children undergoing
general anaesthesia. Contin Educ Anaesth Crit Care Pain, 13, 196–9.
8 Elliott AB, Holley AL, Ross AC, et al. (2018). A prospective study comparing perioperative anx-
iety and posthospital behavior in children with autism spectrum disorder vs typically developing
children undergoing outpatient surgery. Pediatr Anesth, 28, 142–8.
9 Wilkinson K, Cranston AJ (2018). Safeguarding for anaesthetists: working to protect children.
Anaesth Intensive Care Med, 19, 433–6.
10 Royal College of Anaesthetists, Association of Paediatric Anaesthetists of Great Britain and
Ireland (2016). Protecting children in theatre. M https://www.youtube.com/watch?v=JpxXd6C
1YrE&feature=youtu.be
11 Association of Anaesthetists, Association of Paediatric Anaesthetists of Great Britain and Ireland,
Royal College of Anaesthetists, College of Anaesthesiologists of Ireland (2019). Joint profes-
sional guidance on the use of general anaesthesia in young children. M https://rcoa.ac.uk/news/
joint-professional-guidance-use-general-anaesthesia-young-children
12 Kelly CJ, Walker RW (2015). Perioperative pulmonary aspiration is infrequent and low risk in
paediatric anaesthetic practice. Paediatr Anaesth, 25, 36–43.
13 Association of Paediatric Anaesthetists of Great Britain and Ireland (2018). APA Consensus
statement on updated fluid fasting guidelines. M https://www.apagbi.org.uk/news/
apa-consensus-statement-updated-fluid-fasting-guidelines
14 Thomas M, Morrison C, Newton R, et al. (2018). Consensus statement on clear fluids fasting for
elective pediatric general anesthesia. Pediatr Anesth, 28, 411–14.
15 The Royal Children’s Hospital Melbourne. Sedative premedication guidelines. M https://www.rch.
org.au/uploadedfiles/main/content/anaes/sedative_premedication_guidelines.pdf
16 Gaynor J, Ansermino JM (2016). Paediatric total intravenous anaesthesia. BJA Educ, 16, 369–73.
17 Schindler E, Schears GJ, Hall RS, et al. (2012). Ultrasound for vascular access in paediatric pa-
tients. Pediatr Anesth, 22, 1002–7.
18 Krishna SG, Bryant JF, Tobias JD (2018). Management of the difficult paediatric airway in the
pediatric patient. J Pediatr Intensive Care, 7, 115–25.
19 Humphries S, Schiber A (2020). Nasal high flow oxygen in pediatric anesthesia and airway man-
agement. Pediatr Anesth, 30, 339–46.
20 Park R, Peyton JM, Fiadjoe JE, et al. (2017). The efficacy of GlideScope® videolaryngoscopy com-
pared with direct laryngoscopy in children who are difficult to intubate: an analysis from the
paediatric difficult intubation registry. Br J Anaesth, 119, 984–92.
966 Chapter 36 Paediatric and neonatal anaesthesia
Oliver Dodd
Primary survey and resuscitation 971
Alex Wickham
Damage control resuscitation 982
Pregnancy and trauma 988
Edwin Clitheroe
Burns: early management 1013
Fleur Cantle
Major trauma in children 1019
Nicholas Freeman
Silver trauma 1025
See also
% Massive transfusion p. 460–1
968
The first two phases are carried out simultaneously, during which there is
multidisciplinary discussion and planning for the next steps of patient care,
e.g. theatre, CT, ICU or ward. The 2° survey (see % p. 980) is not started
until the patient has been adequately resuscitated and stabilised. Clear
documentation should be made of each stage of the process: examination
findings, investigations and treatment, including medications and transfu-
sion. Interruptions in care for investigations and handover between teams
(e.g. ED to theatre) are common, and outstanding tasks must be recorded
(e.g. 2° survey not complete) so they are not forgotten. As the anaesthetist,
you may accompany the patient from the ED, via imaging, to theatre and
onwards to the ICU, so you are uniquely placed to provide continuity of
care, ensuring that tasks are completed and details retained.
Primary survey and resuscitation 971
• Allocate clear roles: 1st intubator, 2nd intubator (if available), airway
assistant, drug administrator, cricoid pressure, MILS of the C-spine.
• Vocalise the airway plan and strategy for failed intubation. An intubation
checklist should be used.
• MILS of the C-spine: unless the trauma is an isolated penetrating injury,
full MILS C-spine immobilisation should be used during intubation. MILS
can be maintained from the side (ideal as the team member then does
not interfere with the intubator) or head-end of the patient. It should
be instituted prior to removal of the collar or blocks and continues
until they are replaced at the end of intubation. Traction must not be
applied.
• Preoxygenate: consider augmenting Mapleson C/circle circuit high
FiO2 and 5cmH2O PEEP with nasal O2 cannulae at 15L/min placed
pre-intubation if SpO2 <90%. If the patient’s ventilatory effort is
inadequate, gentle assisted ventilation, avoiding inflating the stomach,
can be used.
• Cricoid pressure, if used, should be two-handed (anterior and
posterior) to prevent displacement of any C-spine injuries.
• Induce anaesthesia. All induction drugs have the potential to cause
vasodilation and compound hypotension.
• Ketamine, fentanyl and rocuronium have become the drug
combination of choice in major trauma, for both prehospital and in-
hospital emergency use. The dose regimens should be sensitive to the
patient’s physiology.
• For the trauma patient without physiological compromise: 3
micrograms/kg fentanyl, 2mg/kg ketamine and 1mg/kg rocuronium is
appropriate (a ‘3-2-1 induction’).
• For physiologically unstable patients, reduce the doses to 1
microgram/kg fentanyl, 1mg/kg ketamine and 1mg/kg rocuronium (a
‘1-1-1- induction’).
• If the patient is critically unwell, ketamine in reduced doses and
rocuronium alone may be used.
• Alternative agents: thiopental can be used for normotensive head
injuries. Suxamethonium 1.5mg/kg can be used in the immediate
aftermath of trauma, even in patients with burns or spinal injury;
however, in patients with severe muscle injury or if there is a
suspicion of raised K+ from other causes, it should be avoided.
• Blood/fluid should be connected to a large-bore cannula and volume
given to compensate for the effects of anaesthesia.
• Laryngoscopy:
• Anticipate difficult laryngoscopy. Full C-spine immobilisation with
collar, blocks and tape limits neck movement to 5% of the normal
range, resulting in Cormack and Lehane grade III or IV views in 64%
of patients. Removing the anterior portion of the hard collar and
using assistant-provided MILS makes it easier, but 22% of patients will
still have grade III views at laryngoscopy.7
• VLs with hyperangulated blades are the preferred method for
intubation to reduce movement of the atlanto-occipital and
atlantoaxial joints.
974
Massive haemothorax
• Defined as 1000–1500mL of blood in the thoracic cavity in an adult. It
causes both hypovolaemia and impaired ventilation.
• It usually occurs 2° to a laceration of the intercostal artery or vein and
less commonly from a mediastinal vessel.
• Signs: reduced chest wall movement and stony dull percussion can be
supported by thoracic ultrasound which reveals a large collection of
blood above the diaphragm.
• Immediate treatment includes:
• High-flow O2
• Large-bore IV access × 2
• Chest drain insertion
• Blood product resuscitation via a rapid infusor device (see % p. 460).
Start the transfusion as the haemothorax is released.
• Caution is needed with chest drain insertion as this procedure may
dislodge a clot and cause further active bleeding.
• Ongoing drainage of blood from the intercostal drain of 100–200mL/h
over the subsequent hours will indicate the need for thoracotomy or
interventional radiology.
Flail chest
• A flail segment occurs when two or more adjacent ribs are fractured in
two or more places.
• Patients will present with pain and, if conscious, shallow and painful
respiration.
• Signs: paradoxical movement of the chest wall may not always be
present (some flails are only seen radiologically), but there will
be tenderness, bruising, crepitus and underlying lung contusion ±
pneumothorax.
• The principles of treatment are as per pulmonary contusion (see
% pp. 995–6.
• Rib fixation within 3–5d of injury has demonstrated shorter length of
hospital stay and better analgesic outcomes.8
Airway disruption
• Patients with major airway disruption will often asphyxiate at the scene.
Survivors may present with severe surgical emphysema, pneumothorax,
haemothorax, pneumomediastinum, pneumopericardium and
pneumoperitoneum. These injuries are often the consequence of high-
energy transfer and shear forces.
• Diagnosis is often made by the anaesthetist when trying to manage
blood in the airway, difficult intubation and, once intubated, a major
air leak.
• Fibreoptic bronchoscopy or, if stable enough, CT are diagnostic.
• Depending on the level of disruption, management may be surgical or,
for some small bronchopleural fistulae, conservative.
976
Cardiac tamponade
• Cardiac tamponade should be considered in any trauma patient who
has sustained a penetrating injury to the chest, neck or upper abdomen.
Cardiac tamponade can also occur in blunt trauma, especially in patients
taking oral anticoagulants, but this is rare.
• Beck’s triad (hypotension, distended neck veins and muffled heart
sounds) is unreliable, especially in a noisy ED. Thoracic ultrasound will
demonstrate diastolic RV collapse and blood in the pericardial space.
This is diagnostic of cardiac tamponade.
• The initial management of cardiac tamponade involves improving
preload through volume resuscitation (blood products), while the TTL
arranges definitive surgical intervention.
• If the patient deteriorates in the ED despite this, a resuscitative bilateral
anterior (‘clamshell’) thoracotomy and pericardiotomy with repair of
the myocardium should be undertaken (see % pp. 1010–11).
Circulation and shock
During the 1° survey, always suspect and actively look for haemorrhage
and shock. Place pregnant patients in the left lateral position or manually
displace the uterus to the left. Shock is defined as inadequate delivery of
oxygenated blood to tissues. Causes are shown in Table 37.2.
• Suspicion of circulatory compromise may come from the pre-alert and
mechanism of injury, while recognition of shock should begin at the
rapid assessment and handover.
• The TTL will coordinate simultaneous:
• Circulatory assessment and identification of hypovolaemia
• Haemostasis
• Treatment of haemorrhage.
• During the 1° survey, HR, BP, RR, capillary refill time, conscious level
and pallor may help to identify patients with shock.
• Traditional ATLS® teaching classifies shock into grades I–IV; however,
this has been widely scrutinised, with fewer than half of European
ATLS® instructors declaring they would use this tool.9 Certain drugs,
being cold and some pre-existing medical conditions may lead to
overestimation of blood loss, while the tool underestimates blood loss
in children, pregnancy, blunt trauma and athletes.9
• A shock index (HR/systolic BP) of >1 can help identify shock in patients
with apparently relatively normal physiology.10
• Bedside use of ultrasound may help identify the presence of blood and/or
the cause of shock (e.g. pericardial fluid, an empty IVC, blood in the
abdomen or chest).
• Control of haemorrhage begins with direct pressure, indirect pressure,
tourniquets, pelvic and long bone splints.
• Large-bore IV (14 or 16G), IO or central access is attained in major
trauma patients as early as possible.
• Send blood samples for: venous blood gas (lactate), FBC, G&S or X-
match, electrolytes, coagulation profile (TEG® or ROTEM® if available).
POCT can be extremely useful.
• If significant bleeding is suspected or evident, tranexamic acid is
given within 3h of injury (1g over 10min), if not already given by the
prehospital team, followed by 1g over 8h.
• If the patient is known to be on anticoagulants with ongoing bleeding,
use of factor concentrates or reversal agents may be indicated.
• Major trauma patients are at risk of the ‘lethal triad’ of acidosis,
coagulopathy and hypothermia. Pay attention to keeping the patient
warm—measure temperature, limit exposure to that which is required
for assessment/procedures and use active warming and warmed blood
products.
Resuscitation goals
• The goals of resuscitation are to optimise tissue oxygenation (Box
37.3).11,12 Acute shocked trauma patients are in a dynamic situation and
should be reassessed regularly.
• Patients with haemorrhagic shock will respond in one of three ways to
blood product administration:
• Improve
• Transiently improve, then deteriorate, requiring further fluid
resuscitation
• Not improve.
• Practically, until major bleeding has been stopped, volume resuscitation
should be titrated to maintain palpable central pulses,8 systolic BP
of 80–90mmHg, MAP of 50–60mmHg3 and diastolic pressures of
25–35mmHg (to achieve coronary perfusion).1 Conscious level is a
good indicator of cerebral perfusion in awake patients. Young, healthy
patients may tolerate a lower BP, while elderly patients may need
a higher BP—this is up to the clinical judgement of an experienced
anaesthetist/TTL on an individual basis13 (see % p. 1026).
(See % p. 1020 for paediatric parameters.)
• In the complex patient with traumatic brain or spinal cord injuries
and ongoing haemorrhage, the BP target depends on the dominant
condition. If haemorrhagic shock is the predominant problem,
restrictive volume resuscitation should be employed. If traumatic brain
injury is the predominant issue, a less restrictive approach, targeting SBP
of 100–110mmHg and MAP of ≥80mmHg, should be used to maintain
cerebral perfusion prior to surgery.3,11,14,15
• Patients who do not have a sustained improvement require further
blood product resuscitation and definitive management of their
haemorrhage. This can be achieved by surgery (see % pp. 982–3) or
interventional radiology (see % p. 824) with ongoing correction of
coagulopathy.
978
• Formal assessment of GCS (see % Table 37.4, p. 990) and gross motor
function bilaterally will alert the TTL to major spinal and intracranial
injuries. This needs to be accomplished prior to intubation.
• If not already administered, tranexamic acid should be given in isolated
head-injured patients with reduced GCS (9–12) prior to CT brain if
within 3h of the injury.19
• Ensure that blood glucose level and analgesia have been addressed by
this point.
Source: data from Hunt B et al. (2015) A practical guideline for the haematological management
of major haemorrhage British J Haematology 170(6), 788–803.
Exposure
• It is important to expose the patient completely and inspect the axillae,
back and groin for penetrating injuries (a ‘stab check’), while making
attempts to avoid hypothermia.
• Often a log roll is not performed prior to a trauma CT (if indicated),
but the TTL should have an appreciation of all major obvious wounds.
Imaging
(See % Table 37.3 and Box 37.5.)
• Imaging should aid in decision-making and the early planning phase of
the patient journey, as well as provide diagnoses.
• X-rays of the chest and pelvis may be performed as part of the 1° survey.
• Ultrasound can be performed quickly in the ED to identify free fluid
(blood) in the perihepatic and perisplenic regions indicating abdominal
haemorrhage. eFAST is a structured assessment looking for:
• Blood in the perihepatic, perisplenic, pericardial and pelvic areas
• Air (pneumothoraces) via anterior thoracic windows.
• Ultrasound can be used to identify blood in the abdomen but should
not be used to rule out the presence of blood, as there is significant
operator dependency and, even in experienced hands, retroperitoneal
and small volumes of blood can be missed.20 Even if no fluid is identified,
this does not rule out other abdominal injuries which may require
surgical intervention.
980
Ultrasound CT scan
Indication Screening for free fluid in unstable Diagnosis of organ injury
patients in haemodynamically stable
patients
Advantages Fast, sensitivity 83–87%, can Most specific for injury (92–
detect free fluid and some solid 98%), will also demonstrate
organ injury perforation
Dis- Operator-dependent; misses Takes time and involves
advantages diaphragm, bowel and some transfer away from resus
pancreatic injuries room
May delay CT
Log roll
If the patient is stable, a log roll may be appropriate prior to moving on to
the 2° survey. The purpose of the log roll is to ensure the back has been
visualised and if a full trauma scan has not been done, the TTL will assess
the spine for tenderness and sensation.
The secondary survey
The 2° survey requires a systematic head-to-toe examination of the patient.
It will also include management of peripheral injuries, an ECG, complete
neurological examination and, if required, a formal orthopaedic review, a
urinary catheter and American Spinal Injury Association (ASIA) chart com-
pletion. The 2° survey often occurs outside the ED in major trauma, after
resuscitation, surgery or transfer to critical care, and formal documentation
of this step, when it occurs, is important.
Primary survey and resuscitation 981
Response Score
Best motor Obeys commands 6
response Localises pain 5
Normal flexion withdrawal (stimulus to supraorbital 4
notch)
Abnormal flexion to pain 3
Extension to pain 2
No motor response 1
Best verbal Orientated 5
response Confused 4
Inappropriate words 3
Inarticulate sounds 2
No verbal response 1
Eye opening Eyes open 4
Eyes open to speech 3
Eyes open to pain 2
No eye opening 1
Reprinted from The Lancet, 304:7872, Teasdale G, Jennett B, Assessment of coma and impaired
consciousness, pp. 81–84, Copyright (1974), with permission from Elsevier.
Response Score
Best motor response Obeys commands (>2y) 6
Localises to pain (<2y) 5
Normal flexion to pain (>6mo) 4
Abnormal flexion to pain 3
Extension to pain 2
No motor response 1
Best verbal response Orientated (>5y) 5
Words (>1y) 4
Vocal sounds (>6mo) 3
Cries (<6mo) 2
No verbal response 1
Eye opening Eyes open 4
Eyes open to speech 3
Eyes open to pain 2
No eye opening 1
Using this scoring system, the maximum GCS is 9 at 0–6mo, 11 at 6–12mo, 13 at 1–2y and 14
at 2–5y.
Source: data from Reilly PL, et al., Assessing the conscious level in infants and young children: a
paediatric version of the Glasgow Coma Scale, Childs Nerv Syst, 1988:4(1):30–3.
Head and traumatic brain injury 991
Airway
Patients with reduced GCS may have impaired laryngeal reflexes and be
unable to protect their airway. Indications for intubation are as per major
trauma (Box 37.2) but, in addition, may include:
• Spontaneous hyperventilation causing PaCO2 <4.0kPa
• To enable CT scan
• Recurrent seizures uncontrolled by simple benzodiazepines.
The ETT should be secured with tape, rather than with ties, to prevent
compromising cerebral venous drainage and risk increasing ICP.
Breathing
Adequate oxygenation and ventilation will reduce the risk of 2° brain injury.
CBF is affected by extracellular pH which is, in turn, related to PaCO2 (see
% p. 559).
Once intubated, initial ventilatory strategies should aim for:
• Normocapnia: PaCO2 4.5–5.0kPa. Be mindful that ETCO2 will be
70.5kPa lower than PaCO233—take note of the ABG value. Reducing
PaCO2 will result in vasoconstriction and d cerebral perfusion.
Hyperventilation to PaCO2 of 4.0kPa (avoid lower) is recommended as a
temporising measure to reduce i ICP, but should be avoided, if possible,
during the first 24h after injury as CBF is often critically reduced.34
• Normoxia: SpO2 >95% and PaO2 ≥8kPa. Recent AoA guidance for
transfers recommends PaO2 ≥13kPa.35
• VT of 6–7mL/kg. While lung-protective strategies are preferred, VT can
be i, if needed, to prevent hypoxia or hypercapnia.36,37
• PEEP ≤5cmH2O: changes to intrathoracic pressure (PEEP) should be
minimised to reduce the effects on venous drainage and MAP, and thus
ICP and CBF, respectively.
Circulation
• The injured brain can lose the ability to autoregulate blood flow and is
dependent on systemic pressures. H A single episode of hypotension
(systolic BP <90mmHg) confers a doubling of mortality and an increase
in morbidity during acute management.
• In isolated head injury, aim for MAP of >90mmHg. Mortality may be
reduced and outcomes improved if systolic BP is maintained at:
• ≥100mmHg in patients 50–69y
• ≥110mmHg in patients 15–49y and >70y.34
• The recommended target for CPP (CPP = MAP –ICP) is
60–70mmHg.34
• Trauma patients often present clinical conundrums with opposing
treatment strategies for different injuries. Treatment of the most
life-threatening injury takes precedence. If a trauma patient has
uncontrolled haemorrhage, a systolic BP of 100mmHg is preferred until
haemorrhage control. A systolic BP <90mmHg is associated with poor
outcomes.33
• The correct fluid of resuscitation will depend on other injuries, but
avoidance of hyponatraemia is important. If haemorrhagic shock is
the dominant condition, continue restrictive volume resuscitation; if
traumatic brain injury is the dominant condition, use a less restrictive
volume resuscitation approach to maintain cerebral perfusion. Be
92
mindful that significant blood loss can occur from isolated scalp wounds
and during operative management of isolated head injuries. Be prepared
to transfuse these patients.
• In isolated head injury with GCS of 9–12, 1g tranexamic acid should be
given if within 3h of injury and any anticoagulants should be reversed
promptly.19
Disability
The Glasgow Coma Scale, pupillary examination and motor function are key
to neurological assessment and prognostication in traumatic brain injury.
• Eyes should be examined for:
• Signs of orbital trauma
• Pupillary response to light
• Pupillary size (>4mm is recommended as a measure of dilated
pupil).34
• Anaesthetists are well positioned at the trauma call to look in the ears
for haemorrhage and CSF indicative of base of skull fracture.
• Analgesia, sedation and adequate NMB are essential in the management
of traumatic brain injury to reduce cerebral metabolism and straining.
TCI propofol is acceptable for maintenance of anaesthesia.
• Keep the neck in the midline and tilt the bed/trolley to a 30° head-up
position to reduce ICP by improving venous return.
Other considerations
• The use of high-dose barbiturates is only recommended for control of
raised ICP refractory to standard medical and surgical treatment and
can cause significant haemodynamic instability.34
• Post-traumatic seizures are common (up to 12%). Seizure prophylaxis
with phenytoin or levetiracetam should be started, dependent on local
guidelines.
• Seizures in awake patients are managed as normal but would highlight
the possible need for intubation.
• Hyperglycaemia should be avoided.
• Maintain normothermia. There is no evidence supporting early
hypothermia.38 Hyperthermia should be managed aggressively.
• Ensure laxatives are prescribed.
Emergent management of raised ICP
• ICP should be kept <22mmHg. Prior to direct measurement
(intraventricular or intraparenchymal), elevated ICP may be identified
by clinical signs or at head CT with ventricular and sulcal effacement,
compression of basal cisterns and herniation.
• Raised ICP is associated with pupillary and haemodynamic changes.
In severe traumatic brain injury, abnormalities of pupillary response
or pupil size asymmetries are often associated with neurological
deteriorations and are correlated with poor neurological outcome.39
• Classically, the Cushing reflex is described as hypertension, bradycardia
and apnoea in response to intracranial hypertension. The bradycardia is
often preceded by tachycardia.40
Head and traumatic brain injury 993
Imaging
Head and C-spine CT may form part of the trauma CT. In isolated head
injuries, NICE guidelines indicate the cohort of adult patients that should
be imaged (Box 37.6).41
Surgically significant abnormalities seen on CT should be discussed with
a neurosurgical unit.
Regardless of imaging, other reasons for discussing a patient’s treatment
plan with a neurosurgeon include:
• GCS <8 after initial resuscitation
• Unexplained confusion >4h
• Deterioration in GCS and progressive focal neurology
• A seizure without full recovery
• Definite or suspected penetrating injury
• A CSF leak.
Referral and disposition will depend on local guidelines. Transfer of critic-
ally ill patients with traumatic brain injury must be accompanied by a doctor
with suitable competencies and experience in brain injury transfer.35,42
Secondary survey
As part of the 2° survey, it is important to check the skull and eyes for other
injuries. Give antibiotics if open skull fractures are present. Base of skull
fractures, although treated conservatively, need to be highlighted such that
NGTs are not inserted.
94
Thoracic injury
In the prehospital environment, severe thoracic injury accounts for 25% of
trauma deaths.44 Thoracic trauma can occur after:
• Direct injury: e.g. seat belts, intrusion of vehicle wreckage,
penetrating trauma
• Rapid deceleration, resulting in shearing forces that may lead to
traumatic aortic and lung injuries.
The immediate life-threatening conditions (tension pneumothorax, open
pneumothorax, massive haemothorax, flail chest, airway disruption/ob-
struction and cardiac tamponade) need to be identified and treated rapidly
during the 1° survey; these are addressed on % pp. 974–6. There are six
further potentially life-threatening injuries, which can occur after thoracic
trauma:
• Pulmonary contusion and rib fractures
• Cardiac contusion
• Traumatic aortic injury
• Oesophageal injury
• Ruptured diaphragm
• Rupture of the tracheobronchial tree.
Pulmonary contusion and rib fractures
Pulmonary contusions and rib fractures are common following blunt thor-
acic trauma and are associated with a high risk of respiratory complications.
Mechanisms include impact, deceleration and seat belt injuries. Examination
may reveal external bruising and focal points of tenderness, indicating likely
underlying rib fractures. Young adults and children have i chest wall com-
pliance which may result in significant pulmonary contusion without rib frac-
tures, while elderly patients may suffer significant rib injuries after a simple
fall; these can be associated with considerable morbidity and mortality.45
Pulmonary contusions
The earliest indicator of pulmonary contusion is hypoxia.
• CXR may show patchy infiltrates over the affected area but is often
initially normal. It may, however, reveal other pathology which would
raise the suspicion of pulmonary contusion, e.g. rib fractures, flail
segment, haemo-or pneumothorax. Less than 50% of pulmonary
contusions are apparent on admission, compared to 92% at 24h.46
• Typically, hypoxia from lung contusion progresses over 24–48h,
associated with reduction in lung compliance and worsening respiratory
distress.
• If these patients are ventilated, they may require higher levels of PEEP
to maintain oxygenation. Lung-protective strategies and careful fluid
resuscitation are also important to avoid worsening lung injury.
Rib fractures
• Rib fractures (see % p. 553) are painful; they reduce chest wall
excursion, leading to hypoventilation, and impair coughing ability, leading
to sputum retention. These combine to cause atelectasis. Additionally,
gas exchange is impaired in injured lung tissue, causing V/Q mismatch.
H Inadequate analgesia worsens hypoxia associated with pulmonary
contusion and rib fractures by d ventilation, i atelectasis and i risk of
superimposed infection.
96
• Often patients with severe cardiac contusion will have other injuries
mandating their admission to HDU/ICU.
• Severe myocardial contusion may require the use of inotropic support,
and although late complications including heart failure, arrhythmia and
aneurysm have been reported, they are rare.
Traumatic aortic injury
Around 80% of patients with traumatic aortic injury will die at the scene.
Although deceleration and falls account for the majority of cases, pene-
trating trauma is also a recognised cause.49
A high index of suspicion and a low threshold for CT and angiography
are the best diagnostic tools. ‘Cardinal’ CXR signs such as widened medi-
astinum, pleural capping and blunting of the aortic knuckle are not always
present. Checking bilateral BP is of limited value.
The site of the injury will dictate where the blood may collect; damage to
the intrapericardial portion of the aorta will lead to a cardiac tamponade,
and injuries to the extrapericardial aorta will lead to mediastinal haematoma
and haemothorax.
Grade of traumatic aortic injury
• Type 1: intimal tear
• Type 2: intramural haematoma
• Type 3: pseudoaneurysm
• Type 4: rupture (e.g. periaortic haematoma, free rupture).
Management of traumatic aortic injury
• Type 1 injuries: non-operative management consisting of aggressive HR
and BP control and serial imaging. Systolic BP should be maintained at
100mmHg and HR <100bpm with β-blockers and vasodilators if not
contraindicated.50
• Type 2, 3 and 4 injuries: repair is recommended. Endovascular
intervention is becoming the mainstay of treatment if the anatomy is
favourable due to the significant morbidity associated with open repair.
While awaiting repair, control BP and HR as per type 1 injuries. Delayed
repair may be appropriate for patients who are haemodynamically
stable with severe coexisting injuries.51
Oesophageal injuries
Oesophageal trauma is uncommon due to the relative protection afforded
by the chest wall. Oesophageal injuries normally occur in two places:
• Lower portion (commonest) associated with severe blunt trauma to the
abdomen
• Cervical region (less common) 2° to penetrating trauma.
Oesophageal rupture leads to mediastinitis, pneumomediastinum and a left-
sided pneumothorax or pleural effusion. Severe pain out of proportion to
the apparent injuries, pain on swallowing and shock should alert the clin-
ician to the presence of an oesophageal injury. Oesophageal rupture carries
a high mortality and early use of antibiotics and surgical repair is recom-
mended52 (see % p. 553 for repair of oesophageal injuries).
98
Ruptured diaphragm
Diaphragmatic rupture can be caused by both blunt and penetrating trauma
to the abdomen. Up to 15% of penetrating thoracoabdominal trauma
will involve the diaphragm. The commonest cause of blunt diaphragmatic
trauma is due to seat belt injuries and is more common from side impact
than frontal collision.4 The left side is more commonly involved, but when
the right hemidiaphragm is involved, hepatothorax can occur. Underlying
vascular damage can initially be masked due to the effect of the liver in
the chest.
Some diaphragmatic injuries are asymptomatic, with the diagnosis made
after CT. However, it is not uncommon for bowel to be felt on finger
thoracostomy. Subsequent herniation and strangulation are a significant
complication. Diaphragmatic rupture requires surgical repair (see % p. 553
for repair of diaphragmatic injuries).
Rupture of the tracheobronchial tree
• Tracheobronchial injuries surviving to hospital treatment are rare.53
Blunt trauma causes include deceleration, hyperextension and shear
forces, while penetrating injuries usually occur in the cervical trachea.
• Although airway management is key to the 1° survey, tracheobronchial
injuries can be missed in 25–68% of patients.54 There should be raised
suspicion for tracheobronchial injury when SC emphysema is seen over
the neck, a pneumothorax fails to reinflate after insertion of a chest
drain or there is evidence of excessive air leakage.
• Patients with distress and clinical suspicion of airway injury should be
immediately intubated, preferably under FOB guidance to place the
ETT distal to the injury or facilitate one-lung ventilation. Methods of
intubation include orotracheal (direct or VL), fibreoptic, through open
neck wound or tracheostomy.
• Injuries of the intrathoracic airway are more challenging. The use of
long ETTs bypassing the injury for single-lung ventilation has been
recommended.
(See % p. 554 for repair of tracheobronchial injuries.)
Abdominal and pelvic injuries 999
Pelvic injuries
• Pelvic ring injuries occur in 8–9% of all blunt force trauma and mortality
rates range from 10% to 50%, depending on the extent of haemorrhage
and associated injuries.
• Life-threatening haemorrhage may result. Most bleeding is usually from
tearing and shearing forces on the venous plexus at the back of the
pelvis. A small proportion is from arterial injury (<10%) and bleeding
from the surface of the fractures themselves.
• Associated urological injuries can result in severe long-term disability
and are potentially fatal.
• Open fractures of the pelvis involving the vagina and rectum are
associated with a mortality of 30–50%. These injuries may be difficult to
diagnose initially.
Injury classification
The Young and Burgess classification of pelvic fractures uses three mechan-
istic descriptions, each with degrees of severity.
• AP compression (‘open book’) I–III. Associated with frontal collisions.
• Lateral compression I–III. Associated with lateral collisions.
• Vertical sheer. Associated with falls from height.
Management
• Immediate management of the unstable patient with pelvic trauma is
placement of a pelvic binder, which reduces the potential space within
the pelvic cavity.61
• The pelvic binder can be left in place for several hours and, if an injury
is identified, should only be removed when personnel are available who
can repair the injury.
• After a pelvic binder is removed, repeat a pelvic X-ray.
• Haemorrhage control can be achieved by:
• Pelvic external fixation—will clamp both sides of the pelvis together,
reducing pelvic volume and tamponading bleeding. This will take
precedence over laparotomy in an open book or vertical shear
fracture.
• Pelvic packing to manage venous bleeding in the unstable patient.
• Selective angiography and embolisation to manage arterial bleeding.
• A single gentle attempt at catheterisation by an experienced doctor is
permissible, even if the CT findings suggest urethral injury.
• Note, multiple surgical teams may be operating at once in pelvic injuries.
021
Spinal trauma
Between 250 000 and 500 000 patients around the world suffer a spinal
cord injury each year. Of these, 790% are due to traumatic events such as
road traffic collisions, falls and violence. Outcome after a spinal cord injury
depends on the severity and location of the lesion. Below the level of in-
jury, there may be complete or partial loss of sensory/motor function. The
commonest level affected is C5.62 Patients with spinal cord injuries are 2–5
times more likely to die prematurely.63
The 1° spinal cord injury results from the initial traumatic event, directly
damaging ascending and descending pathways and blood vessels. The com-
monest 1° mechanism of spinal cord injury is an impact, followed by con-
tinued compression.64 The acute phase of 2° injury occurs within minutes of
the 1° event and results from the consequences of the 1° injury, including:
local haemorrhage, hypotension, vasospasm, hypoperfusion, ischaemia,
cytokine release, oedema and neurotransmitter accumulation.63,64
The principles of management of a spinal cord injury are similar to those
of traumatic brain injury. The aims are to preserve neurological function and
reduce further injury by minimising 2° injury. The most effective treatment
in this case is early surgical decompression within 8h of injury.65
Primary survey
• On arrival in the ED, the patient may be on a vacuum mattress, ‘scoop’
or spinal board. Historically, spinal boards have been used for transport,
but these are extrication devices only. They should be removed as soon
as possible in the ED to avoid pressure areas developing using a ‘log roll’
technique (see % p. 1003). Every movement of the patient should be
well coordinated.
• The mechanism of injury, signs and symptoms will alert the team to
the presence of a spinal cord injury. Polytrauma patients should always
be considered as having a spinal cord injury until formal assessment,
including radiological investigations, has been completed.
Airway and cervical spine control
• Patients should arrive in the ED with C-spine control and spinal motion
restriction; however, this is not always the case. When performing
MILS or placing a hard collar, no patient should have their head or
neck forced into a neutral spine position and no deformity should be
reduced.4
• Early intubation and ventilation may be required as high cervical injury
above C3 leads to apnoeic respiratory arrest. Patients with spinal cord
injury are also at a higher risk of aspiration.66 (See % pp. 972–4 for
information regarding intubating the immobilised patient.)
Breathing
Supported ventilation may be required in the patient who has a thoracic
injury or cervical injury sparing the diaphragm (C3–5) due to reduced
chest excursion. Respiratory effort may deteriorate over time in the supine
patient.
Spinal trauma 1003
Circulation
Neurogenic shock, due to sudden loss of autonomic tone, may develop in
a patient with a cervical or high thoracic injury. Bradycardia and hypoten-
sion (systolic BP <90mmHg) in the presence of cervical or high thoracic
trauma should be managed with fluid and vasopressor infusion to maintain
a spinal cord perfusion pressure >60–65mmHg,67 which in practice entails
maintaining a MAP >85–90mmHg for 5–7d after injury.62 Metaraminol is a
simple 1st-line choice, but central venous access to facilitate noradrenaline
is recommended. When the injury is associated with polytrauma, every ef-
fort must be made to avoid ongoing haemorrhage. It may not be possible
to differentiate between the two causes of shock, especially when there is
loss of sensation below the injury level.
Disability
• The ASIA chart is currently the most widely accepted and employed
clinical record for spinal cord injury. The ASIA chart is repeated at 48h
to ascertain if the injury is incomplete or complete. A complete spinal
cord injury is suspected when there has been no change in neurological
deficit in this time.
• The ASIA chart is performed as part of the 2° survey, and perianal
sensation and tone should be included as this may demonstrate sacral
sparing. Prognostication may be complicated by the presence of spinal
shock and should not be discussed as part of the initial assessment and
management.
Log roll
‘Log rolling’ a patient requires a minimum of five people: three to control
the patient’s body and limbs, ensuring minimal movement of the spine; one
to control the C-spine and lead the log roll; and one to inspect the back.
Often formal examination of the back is delayed until after the trauma CT.
Removing the trauma scoop should be done using a modified log roll, util-
ising the smallest tilt/brace required to remove the split board.
Spinal shock
Generally, this is a reversible condition where there is complete loss of
sensation, muscle tone, power, autonomic activity and areflexia below the
level of the injury. This can last anywhere from hours to a number of weeks.
(See also % p. 303.)
Autonomic dysreflexia
Rarely seen in the acute stage of spinal cord injury, but occasionally oc-
curs in the following days and weeks. Most often occurs with lesions
above T6. Defined as episodic hypertension and associated bradycardia
(baroreceptor-mediated) due to disorganised autonomic reflexes. Life-
threatening hypertension can occur, precipitated by noxious stimuli below
the level of the injury, most commonly bladder or bowel distension. Other
symptoms include headache, sweating, flushing and anxiety. Management is
focused around removing the stimulus and acutely managing the hyperten-
sion. Head-up positioning and short-acting agents such as GTN sublingual
spray (400 micrograms) and sublingual nifedipine (5–10mg) are all treat-
ment strategies.
041
Type Characteristics
Primary Mechanism: overpressurisation by the blast wave causes rapid
compression and expansion of gas-filled structures
Affects: gas-filled structures
Examples: blast lung, bowel haemorrhage and perforation
from shear forces, tympanic membrane rupture and middle
ear damage, globe rupture, traumatic brain injury without
signs of head injury
Secondary Mechanism: flying debris and bomb fragments
Affects: any part
Examples: penetrating ballistic (fragments) or blunt injuries,
eye penetration (± occult)
Tertiary Mechanism: individual thrown by, or crushed by structures
thrown by, the blast wind
Affects: typically blunt injuries to any body part
Examples: fractures and traumatic amputation, closed and
open traumatic brain injury
Quaternary Mechanism: all explosion-related injuries, illnesses or diseases
not due to the above. Includes exacerbation or complications
of existing conditions
Affects: any part
Examples: burns, inhalational injuries, crush injuries, closed
and open traumatic brain injury, respiratory disease from
dust, smoke or toxic fume inhalation, angina, hyperglycaemia,
hypertension
Quinary Mechanism: tissue contamination from post-detonation
environment
Affects: any part
Examples: nuclear, biological, chemical, bloodborne viruses,
human remains
Crush injury
Crush injuries are caused by physical compression leading to direct injury
or ischaemia.76 The limbs are most commonly involved (legs > arms), but
multiple injury patterns are possible. Injury severity is determined by the
magnitude and duration of the crush.
• Fractures and open injuries will require standard treatment of fixation,
debridement, tetanus toxoid and antibiotics.
• Compressive forces to the torso can cause a wide spectrum of blunt
or penetrating injuries, including organ contusions/rupture, vascular
damage, fractures, haemorrhage and evisceration. Standard treatments,
including lung-protective ventilation, pelvic binders and prompt
multimodal analgesia, are required.
Crush syndrome: if significant muscle mass is crushed, potentially life-
threatening systemic manifestations, known as ‘crush syndrome’, may
occur. Crush syndrome results from traumatic rhabdomyolysis and the re-
lease of intracellular contents (K+, myoglobin, phosphate, urate and CK)
into the circulation following reperfusion of the injured muscle/organ.
The systemic effects and their management include:
• Reperfusion can lead to acute hypovolaemia and hypotension.
Significant volume/fluid replacement may be needed to compensate
for fluid sequestration into the interstitium, to restore BP and to
maintain renal perfusion. Infusions and boluses should be titrated to the
individual patient and regularly reassessed.
• Rhabdomyolysis:
• AKI may occur from myoglobinuria. Mannitol may be needed initially
to encourage diuresis, but haemofiltration/dialysis may also be
required later.
• Electrolyte disturbances/metabolic abnormalities—h yperkalaemia
and hypocalcaemia. Observe for cardiac arrhythmias and correct as
required.
• Metabolic abnormalities: lactic acidosis resulting from ischaemic
tissues can exacerbate the electrolyte abnormalities.
• Sodium bicarbonate 8.4% 1mL/kg slow bolus, with further doses
titrated to effect, can help.
• Compartment syndrome can occur as injured tissues swell. Prophylactic
fasciotomies may be needed.
• In addition to the specific nuances of crush syndrome, multiorgan
failure, ARDS, TIC and sepsis can also occur.
Traumatic cardiac arrest 1009
Preparation
Achieving a good outcome from resuscitative thoracotomy relies on a
number of components:
• A clear goal:
• Release of cardiac tamponade
• Control of cardiac, vascular or pulmonary haemorrhage
• Occlusion of descending thoracic aorta to reduce haemorrhage
below the diaphragm and increase blood flow to heart and brain
• Control of air embolism
• Provision of open cardiac massage.
• Personnel should have the expertise to perform the procedure.
• It needs a team approach with clear direction. If the TTL is the only
individual skilled in resuscitative thoracotomy, they should temporarily
hand over team leadership to another senior team member to allow
them to task-focus. The anaesthetist is responsible for securing the
airway and may be required to gain large-bore or central venous access.
• There needs to be a clear chain of survival such that when ROSC is
achieved, ongoing care is planned and there is no hiatus in the flow of
treatment.
• It is important to recognise that once initiated, the ongoing management
of resuscitative thoracotomy and traumatic cardiac arrest will use a
large number of personnel and resources.
• TCA should not be attempted if:
• There are no signs of life within the previous 15min
• Trauma is incompatible with life, e.g. decapitation or brain tissue loss.
Traumatic cardiac arrest 1011
Procedure78
• Stop CPR.
• Ensure the patient has an ETT or SGA in place.
• Perform bilateral finger thoracostomy in the 4th or 5th
intercostal space.
• Connect the two thoracostomies with a clamshell incision, using heavy-
duty (e.g. TuffCutt®) scissors or similar, to cross the sternum.
• Insert a retractor to open the chest cavity to the maximal extent.
• Lift the pericardium with forceps and make a midline longitudinal inverse
‘T’ incision to the pericardium. This avoids the phrenic nerves which
pass laterally on the pericardial sac.
• Deliver the heart from the pericardial sac.
• Close any wounds to the cardiac muscle with staple or interrupted
sutures. If you are unsure what to do, you can put a finger in the hole
temporarily.
• A 2nd operator can provide pressure on the descending aorta.
• Concurrently infuse blood and blood products. The right atrial
appendage can be used if vascular access is not possible to obtain.
• Control any bleeding that may be evident after ROSC, especially the
internal mammary arteries.
• Resuscitation should be terminated as a team decision and should be
considered if:
• There is no ROSC after reversible causes have been addressed
• There is no evidence of cardiac activity in the absence of a
tamponade (if ultrasound is used prior to thoracotomy).
021
Fig. 37.1 Traumatic cardiac arrest algorithm. Local guidelines may be adapted to
include the use of ultrasound and variations for the gravid patient. Reprinted from
Resuscitation, 95, Truhlar A et al., European Resuscitation Council Guidelines for Resuscitation
2015, Section 4. Cardiac arrest in special circumstances, 148–201, Copyright © 2015, with
permission from the European Resuscitation Council and Elsevier.
Burns: early management 1013
Chemical burns
• Hands and upper limbs are the most frequently affected areas.
• Staff must protect themselves with gloves, apron and face mask.
• Remove contaminated clothing as early as possible and place in a secure
container for disposal.
• Industrial or household alkalis and acids are commonly used chemicals,
e.g. bleach, washing powder, disinfectants, drain cleaner, paint stripper.
Immersion in complex hydrocarbons (petrol, diesel) without ignition
may cause systemic toxicity. Phosphorus burns may result from
fireworks or military applications.
• Tissue damage continues until the chemical is neutralised or diluted with
water. Early, continuous and prolonged (1h) irrigation with cold water is
vital for burns (except elemental Na, K and lithium).
• Specific treatments include:
• Hydrofluoric acid: used in the glass industry, highly toxic. Burns of 2%
TBSA can be fatal. Tissue penetration by fluoride ions causes deep
chemical burns. Inactivate toxic fluoride ions by application of topical
calcium gluconate burn gel and 10% calcium gluconate injections
into the burn wound (0.5mL/cm2 of surface burn), extending 0.5cm
beyond the burn margin. Do not use calcium chloride; it is an irritant.
Consider intra-arterial (10mL of 10% calcium gluconate in 40mL of
5% glucose over 4h) or IV (Bier’s block; 10–15mL of 10% calcium
gluconate plus 5000 units of heparin, diluted up to 40mL in 5%
glucose).
• Phosphorus: white phosphorus ignites spontaneously when exposed
to air; it can be extinguished by water. Apply copper sulphate
solution, converting phosphorus to black cupric phosphide.
• Bitumen: common injury in the UK from road maintenance. It is liquid
at 150°C and causes thermal burns. Cool with water; remove the
bitumen with vegetable or paraffin oil.
• Cyanide: hydroxocobalamin 5mg IV or 12.5g sodium thiosulfate
should be considered in patients with features of cyanide poisoning.
These treatments are controversial but have fewer side effects than
dicobalt edetate which should be reserved for confirmed cases of
cyanide poisoning.
081
Electrical burns
• Low voltage (<1000V) causes a local contact burn. The 50Hz
alternating current (AC) domestic supply is particularly likely to cause
cardiac arrest. Muscle spasm may prevent release of the electrical
source. There is no associated deep tissue damage.
• High voltage (>1000V) causes flash burn or deep tissue damage due
to current transmission. High-voltage cables carry 11 000 or 33 000V;
electric shock produces an entrance and exit wound, which may require
fasciotomy under GA. Haemochromogens released from muscle and
damaged red cells may cause AKI.
• A direct strike by lightning (ultrahigh voltage, high current) has a very
high mortality. Current may flow up one leg and down the other,
producing an entry and exit wound. Respiratory arrest is common.
Side flash (nearby lightning strike producing current that flows over the
surface of the victim) causes superficial burns.
Table 37.9 Chest drain, NGT and urinary catheter size by weight
Cervical spine
C-spine injuries in children are rare, but when present, they more frequently
occur in the upper cervical spine (C1–4) due to the relatively higher head-
to-body size ratio and higher fulcrum. With increasing age, the fulcrum
lowers and lower cervical spine injuries become more common. The spinal
skeleton is relatively mobile and can be significantly distracted without an
underlying spinal fracture; this leads to SCIWORA. If plain X-rays or CT
scans do not reveal a bony injury, but the neurological exam is abnormal,
SCIWORA should be suspected and imaging with MRI is required.
Immobilisation
The cervical spine must, wherever possible, be stabilised until a C-spine
injury is ruled out.89
If attempts at immobilising the cervical spine are causing distress and agi-
tation, the risks and benefits of continued attempts must be assessed.
• In conscious children, use MILS whenever possible.
• In unconscious children or when MILS cannot be maintained,
immobilisation should be performed with a properly fitting collar, blocks
and tape.
• If no properly fitting collar is available, towels or blankets, etc. should be
used to improvise an immobilisation device.
Major trauma in children 1021
Disability
Pupils should be assessed and a measure of consciousness, such as AVPU,
documented and repeatedly assessed.
Exposure and environment
Full exposure and examination of the child while limiting heat loss are crit-
ical. Underbody forced air warmers and paediatric fluid warmers with re-
duced dead space are useful.
Primary survey imaging
• Children are believed to be more sensitive to high doses of radiation
and this, together with a growing body of evidence suggesting a
relationship between exposure to ionising radiation and a risk of
developing malignancy, leads to a more conservative approach to
imaging, compared to adult patients. The ‘as low as reasonably
achievable’ principle leads to an imaging strategy built around judicious
use of plain films and targeted CT + MRI. (See Box 37.8 for a useful
framework for imaging of children in major trauma.)6,91
• Whole-body CT scan is still appropriate in children with severe injuries
or injuries affecting >1 body region, where the overall risks and benefits
have been carefully considered. Imaging should not be prioritised at the
expense of careful examination, observation and stabilisation.
Imaging guidelines
Indications for CT head within 1h of ED presentation for children sustaining
a head injury are as per adults (Box 37.8), but with a number of additional
indications:41
• Suspicion of non-accidental injury
• GCS <14 (<15 in under 1y) on initial ED assessment
• Tense fontanelle
• Children <1y with presence of bruise, swelling or laceration of >5cm
on the head
• More than one of the following:
• Loss of consciousness lasting >5min
• Abnormal drowsiness
• ≥3 discrete episodes of vomiting
• Dangerous mechanism of injury
• Amnesia (anterograde or retrograde) lasting >5min.
Silver trauma
‘Silver trauma’ generally describes trauma in patients ≥60y. A fall from
standing is the commonest mechanism, and the commonest injury is a frac-
tured neck of femur. However, rib and fragility fractures, head injury and
major haemorrhage are also commonly seen.
Frailty, lack of physiological reserve, sarcopenia, comorbid disease and
medication all impact on the type and severity of traumatic injuries and
their presentation.93,94,95,96 Older people are at significant risk of losing their
pretrauma level of function. Improving outcomes and the process of re-
enablement begins at triage. The Trauma Audit and Research Network
(TARN) data consistently show that elderly patients are undertriaged, as-
sessed by more junior team members, may be denied interventions and
face delays to treatment and transfer to trauma centres.97 Use of compre-
hensive geriatric assessment and frailty screening tools is recommended to
facilitate more informed early decision-making in older trauma patients.98
The falls history
‘A mechanical fall’ is commonly documented as the mechanism of injury in
silver trauma. This overlooks an important consideration: what precipitated
the fall? Assessment, examination and investigation of these patients should
aim to determine both the reason for the fall, the trauma caused by the fall
and any associated injuries (e.g. burns, rhabdomyolysis caused by periods of
immobility)—the input of orthogeriatricians is invaluable. Establishing the
cause of the fall can be aided by the following sieve:
• Cardiac: chest pain, new breathlessness, collapse on exercise?
• Neurological: preceding loss of consciousness? Symptoms of CVE,
headache, seizures?
• Drug-related: alcohol, medication changes?
• Orthostatic: PD, DM, bleeding, sepsis, medication?
• Environment: ill-fitting shoes, postprandial or post-micturition,
emotional state?
Emergency assessment
The salient differences in injury and physiological patterns are summarised
below. Be mindful that major life-changing injuries to the head, neck and
chest can result from low-energy falls from standing.
Airway with C-spine control
Can be compromised or complicated by lack of, or displaced, dentures and
restrictions in neck movement due to arthritic or spondylytic changes.
• Presence of severe degenerative disease of the cervical spine puts
elderly patients at risk of worsening neurological outcome with poorly
fitting hard collars. Padding and tape may be more appropriate and help
avoid hyperextended positions and pressure sores.99
• Upper C-spine injuries are more common.
• Degenerative disease makes spinal contusion and central cord
syndrome more likely and interpretation of images more difficult.100
• Have a low threshold for C-spine imaging. NICE guidance indicates that
even without signs or symptoms of cervical spine injury, if there is the
potential for C-spine injury in a person >65y, then a CT head should be
performed.6 If there is a head or face injury, think neck injury too. If CT
head is indicated, so is CT cervical spine.
0261
Breathing
Multiple rib fractures, flail segments and haemo-/pneumothoraces may re-
sult from simple falls.
Chronic lung disease and reduced muscle mass may impair the patient’s
ability to increase respiratory effort, making d pO2 and i pCO2 more likely.
Circulation
• Anticoagulation for cardiac and vascular disease is common in the ‘silver
trauma’ patient, turning what may have been a small haemorrhage into
a major haemorrhage. Anticoagulant and antiplatelet history should be
specifically sought for all patients. POCT of coagulation and platelet
function (e.g. TEG® or ROTEM®) can be useful. Where bleeding is
suspected, reversal of anticoagulation should be initiated promptly if
possible (see % p. 272).
• Hypertension is common, so physiological parameters for activation
of major haemorrhage protocols should be adjusted. Systolic BP
<110mmHg and/or a pulse of >90bpm should raise suspicion of
hypovolaemia/haemorrhage. β-blocker use prevents/reduces the
tachycardia response to hypovolaemia, which can reduce clinical
suspicion of haemorrhage and also reduce the physiological method by
which cardiac output and tissue perfusion are maintained.
• Invasive monitoring and repeated measurement of lactate and base
deficit help guide resuscitation. Base deficit changes more acutely,
whereas lactate can lag behind the clinical picture.
Neurological assessment
• Cerebral atrophy increases the relative skull vault space such that
significant intracranial bleeding may go unnoticed, without an initial
decrease in GCS. Repeat re-evaluation and a low threshold for CT head
are necessary.
• Patients on antiplatelet or anticoagulant medications with a head injury
and a normal initial CT head may require a repeat scan.
Temperature
• Elderly patients have reduced metabolism and muscle mass and are
often discovered, having fallen some time ago, lying on the floor. These
considerations render them more susceptible to hypothermia. Active
warming begins in the ED and should continue until the patient is
normothermic.
Electrolyte disturbance
• Elderly patients are more likely to have deranged electrolytes due to
comorbidities (e.g. CKD) or medicines (e.g. diuretics).
Analgesia
Undertreated pain is a significant cause of delirium, so timely assessment
and provision of multimodal analgesia are especially important in this at-risk
group. NSAIDs are relatively contraindicated. Conversely, opioids can also
cause delirium; regular oxycodone is preferred over morphine because it
has better oral bioavailability and no active metabolites and does not ac-
cumulate in renal impairment. Laxatives should be co-prescribed. Regional
anaesthesia (single shot or via catheters), where suitable, is ideal for redu-
cing opioid needs.
Silver trauma 1027
Delirium
Delirium is a disorder in which there is an acute confusional state, usually
with a fluctuating course, characterised by disturbed consciousness, cog-
nitive function or perception. In older people, especially those with pre-
existing cognitive impairment, it is usual to find several factors contributing
to delirium.101
The ‘PInCH ME’102 mnemonic (Table 37.12) is a useful aide memoire
to use when reviewing patients, in order to screen for and treat causes
of delirium. The 4AT103 (M https://www.the4at.com) is a validated tool
that quickly and easily detects delirium in routine clinical practice. Patients
should be given their usual visual and auditory aids to allow them to engage
with their environment as soon as possible.
Risk factors
P Pain Fractures and injuries
In Infection Skin and chest wall injuries, surgical site
C Constipation Opioids and immobility
H Hydration Nil by mouth, unable to reach drinks or hold cups,
delirium
M Medication Polypharmacy and alcohol or substance withdrawal
E Electrolytes Glucose, Na+ and K+ derangement
Recovery
Surgery care bundles are helpful in silver trauma patients. These prompt
consideration of common issues during recovery and the inpatient stay, and
provide appropriate parameters for early warning scores (e.g. BP, HR, Hb).
Elder abuse
Can take many forms, e.g. physical, financial, sexual, neglect, emotional and
discriminatory. Be vigilant for the signs and if suspected, adhere to local
reporting mechanisms.
References
1 Moran CG, Lecky F, Bouamra O, et al. (2018). Changing the system—major trauma patients and
their outcomes in the NHS (England) 2008–17. EClinicalMedicine, 2, 13–21.
2 Slope R (2017). Exploration of handover communication in military and NHS emergency care settings
[thesis]. Southampton: University of Southampton. M https://eprints.soton.ac.uk/422197/1/
Final_Thesis.pdf
3 National Institute for Health and Care Excellence (2016). Major trauma: assessment and initial
management. NICE guideline [NG39]. M https://www.nice.org.uk/guidance/ng39
4 Mountain Al, Goode P, Thies K-C (2018). European Trauma Course: the team approach, 4th edn.
European Resuscitation Council.
5 American College of Surgeons (2018). Advanced Trauma Life Support®: student course manual,
10th edn. Chicago, IL: American College of Surgeons.
6 National Institute for Health and Care Excellence (2016). Spinal injury: assessment and initial man-
agement. NICE guideline [NG41]. M https://www.nice.org.uk/guidance/ng41
7 Austin N, Krishnamoorthy V, Dagal A (2014). Airway management in cervical spine injury. Int J
Crit Illn Inj Sci, 4, 50–6.
8 Iqbal HJ, Alsousou J, Shah S, et al. (2018). Early surgical stabilization of complex chest wall injuries
improves short-term patient outcomes. J Bone Joint Surg Am, 100, 1298–308.
9 Mutschler M, Paffrath T, Wolfl C, et al. (2014). The ATLS® classification of hypovolaemic shock:
a well established teaching tool on the edge? Injury Int J Care Injured, 45S, S35–8.
10 Koch E, Lovett S, Nghiem T, et al. (2019). Shock index in the emergency department: utility and
limitations. Open Access Emerg Med, 11, 179–99.
11 Spahn DR, Bouillon B, Cerny V, et al. (2019). The European guideline on management of major
bleeding and coagulopathy following trauma: fifth edition. Crit Care, 23, 98.
12 National Blood Authority Australia (2009). Patient blood management guidelines: module 1, critical
bleeding/massive transfusion. M https://www.blood.gov.au/pbm-module-1
13 Harris T, Rhys Thomas GO, Brohi K (2012). Early fluid resuscitation in severe trauma. BMJ,
345, e5752.
14 Picetti E, Rossi S, Abu-Zidan FM, et al. (2019). WSES consensus conference guidelines: moni-
toring and management of severe adult traumatic brain injury patients with polytrauma in the
first 24 hours. World J Emerg Surg, 14, 53.
15 Harris T, Davenport R, Mak M, et al. (2018). The evolving science of trauma resuscitation. Emerg
Med Clin North Am, 36, 85–106.
16 Huber-Wagner S, Biberthaler P, Häberle S, et al. (2013). Whole-body CT in haemodynamically
unstable severely injured patients—a retrospective, multicentre study. PLoS One, 8, e68880
17 Holcomb JB, Tilley BC, Baraniuk S, et al. (2015). Transfusion of plasma, platelets, and red blood
cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR random-
ized clinical trial. JAMA, 313, 471–82.
18 Hunt B, Allard S, Keeling D, et al. (2015). A practical guideline for the haematological manage-
ment of major haemorrhage. Br J Haematol, 170, 788–803.
19 The CRASH-3 trial collaborators (2019). Effects of tranexamic acid on death, disability, vascular
occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3):
a randomised, placebo-controlled trial. Lancet, 394, 1713–23.
20 Netherton S, Milenkovic V, Taylor M, Davis PJ (2019). Diagnostic accuracy of eFAST in the
trauma patient: a systematic review and meta-analysis. CJEM, 21, 727–38.
21 The Royal College of Radiologists (2015). Standards of practice and guidance for
trauma radiology in severely injured patients. M https://www.rcr.ac.uk/publication/
standards-practice-and-guidance-trauma-radiology-severely-injured-patients-second
Silver trauma 1029
22 Lamb CM, MacGoey P, Navarro AP, et al. (2014). Damage control surgery in the era of damage
control resuscitation. Br J Anaesth, 113, 242–9.
23 Rotondo MF, Schwab CW, McGonigal MD, et al. (1993). ‘Damage control’: an approach for im-
proved survival in exsanguinating penetrating abdominal injury. J Trauma, 35, 375–83.
24 Joint United Kingdom (UK) Blood Transfusion and Tissue Transplantation Services Professional
Advisory Committee (2013). Section 4.13: Transfusion of blood components. In: Norfolk D
(ed). Handbook of Transfusion Medicine, 5th edn. London: The Stationary Office.
25 Shoemaker WC, Peitzman AB, Bellamy R, et al. (1996). Resuscitation from severe hemorrhage.
Crit Care Med, 24, S12–23.
26 Bickell WH, Wall MJ Jr, Pepe PE, et al. (1994). Immediate versus delayed fluid resuscitation for
hypotensive patients with penetrating torso injuries. N Engl J Med, 331, 1105–9.
27 Doran CM, Doran CA, Woolley T, et al. (2012). Targeted resuscitation improves coagulation and
outcome. J Trauma Acute Care Surg, 72, 835–43.
28 Imperial College Hospitals NHS Trust (2015). Rapid resuscitation transit: pa-
tient pathway. M https://smh-gas.org.uk/wp-content/uploads/2016/10/
Rapid-Resuscitation-Transit-FINAL-JAN15-2.pdf
29 Paterson-Brown S, Howell C (2016). Managing Obstetric Emergencies and Trauma: The MOET
Course Manual, 3rd edn. Cambridge: Cambridge University Press.
30 Jain V, Chari R, Maslovitz S, et al. (2015). Guidelines for the management of a pregnant trauma
patient. J Obstet Gynaecol Can, 37, 553–71.
31 Greco PS, Day LJ, Pearlman MD (2019). Guidance for evaluation and management of blunt ab-
dominal trauma in pregnancy. Obstet Gynecol, 134, 1343–57.
32 [No authors listed] (2000). The Brain Trauma Foundation. The American Association of
Neurological Surgeons Joint Section on Neurotrauma and Critical Care. Early indicators of prog-
nosis in severe traumatic brain injury. J Neurotrauma, 17, 449–627.
33 Manley G, Knudson MM, Morabito D, et al. (2001). Hypotension, hypoxia, and head injury: fre-
quency, duration, and consequences. Arch Surg, 136, 1118–23.
34 Carney N, Totten AM, O’Reilly C, et al. (2017). Guidelines for the management of severe trau-
matic brain injury, fourth edition. Neurosurgery, 80, 6–15.
35 Nathanson MH, Andrzejowski J, Dinsmore J, et al. (2020). Guidelines for safe transfer of the
brain injured patient: trauma and stroke, 2019. Anaesthesia, 75, 234–46.
36 Arora S, Singh PM, Trikha A (2014). Ventilatory strategies in trauma patients. J Emerg Trauma
Shock, 7, 25–31.
37 Asehnoune K, Roquilly A, Cinotti R (2018). Respiratory management in patients with severe
brain injury. Crit Care, 22, 76.
38 Andrews PJ, Sinclair HL, Rodriguez A, et al. (2015). Hypothermia for intracranial hypertension
after traumatic brain injury. N Engl J Med, 373, 2403–12.
39 Chen JW, Gombart ZJ, Rogers S, et al. (2011). Pupillary reactivity as an early indicator of in-
creased intracranial pressure: the introduction of the neurological pupil index. Surg Neurol
Int, 2, 82.
40 Kalamar AF, Van Aken J, Caemaert J, et al. (2005). Value of Cushing reflex as a warning sign for
brain ischaemia during neuroendoscopy. Br J Anaesth, 94, 791–9.
41 National Institute for Health and Care Excellence (2019). Head injury: assessment and early man-
agement. Clinical guideline [CG176]. M https://www.nice.org.uk/guidance/cg176
42 Intensive Care Society (2019). Guidance on: the transfer of the critically ill adult. M https://www.
ficm.ac.uk/sites/default/files/transfer_critically_ill_adult_2019.pdf
43 Harris T, Rice S, Watts B, et al. (2010). The emergency control of traumatic maxillofacial haem-
orrhage. Eur J Emerg Med, 17, 230–3.
44 Association of Ambulance Chief Executives (2017). Thoracic trauma: pathophysiology. Thoracic
trauma guideline. M https://aace.org.uk/jrcalc-updates-2016/thoracic-trauma-pathophysiology
45 Bulger EM, Arneson MA, Mock CN, et al. (2000). Rib fractures in the elderly. J Trauma, 48,
1040–6.
46 Pape HC, Remmers D, Rice J, et al. (2000). Appraisal of early evaluation of blunt chest trauma:
development of a standardized scoring system for initial clinical decision making. J Trauma, 49,
496–504.
47 Battle C, Hutchings H, Lovett S, et al. (2014). Predicting outcomes after blunt chest wall trauma:
development and external validation of a new prognostic model. Crit Care, 18, R98.
48 Brewer B, Zarzaur BL (2015). Cardiac contusions. Curr Trauma Rep, 1, 232–6.
49 Igiebor OS, Waseem M (last updated 2021). Aortic trauma. Treasure Island, FL: StatPearls
Publishing. M https://www.ncbi.nlm.nih.gov/books/NBK459337
031
76 NHS England (2020). Clinical guidelines for major incidents or mass cas-
ualty events. Version 2. M https://www.england.nhs.uk/publication/
clinical-guidelines-for-major-incidents-and-mass-casualty-events
77 Slessor D, Hunter S (2015). To be blunt: are we wasting our time? Emergency department thora-
cotomy following blunt trauma: a systematic review and meta-analysis. Ann Emerg Med, 65, 297–
307.e16.
78 Wise D, Davies G, Coats T, et al. (2005). Emergency thoracotomy: ‘how to do it’. Emerg Med J,
22, 22–4.
79 Kalson NS, Jenks T, Woodford M, et al. (2012). Burns represent a significant proportion of the
total serious trauma workload in England and Wales. Burns, 38, 330–9.
80 Battaloglu E, Greasley L, Leon-Villapalos J, Young A, Porter K (2019). Faculty of Pre-Hospital Care
and British Burn Association expert consensus meeting. Management of burns in pre-hospital trauma
care. M https://fphc.rcsed.ac.uk/media/2621/burns-consensus-2019.pdf
81 Holst J, Sauaia A, Ivashchenko A, et al. (2015). Indications for intubation of the patient with
thermal and inhalational burns. Am J Respir Crit Care Med, 201, A1619.
82 O’Driscoll BR, Howard LS, Davison AG (2008). BTS guideline for emergency oxygen use in adult
patients. Thorax, 63 (Suppl 6), vi1–68.
83 Venter TH, Karpelowsky JS, Rode H (2007). Cooling of the burn wound: the ideal temperature
of the coolant. Burns, 33, 917–22.
84 Rajan V, Bartlett N, Harvey JG, et al. (2009). Delayed cooling of an acute scald contact burn injury
in a porcine model: is it worthwhile? J Burn Care Res, 30, 729–34.
85 Hostler D, Weaver MD, Ziembicki JA, et al. (2013). Admission temperature and survival in pa-
tients admitted to burn centers. J Burn Care Res, 34, 498–506.
86 Middleton PM, Simpson PM, Sinclair G, et al. (2010). Effectiveness of morphine, fentanyl, and
methoxyflurane in the prehospital setting. Prehosp Emerg Care, 14, 439–47.
87 NHS England (2018). Clinical commissioning policy: hyperbaric oxygen therapy for carbon monoxide
poisoning (all ages). NHS England reference: 170048P. M https://www.england.nhs.uk/wp-
content/uploads/2018/07/hbot-for-carbon-monoxide-poisoning-v2.pdf
88 The TARNlet Committee. The Trauma Audit and Research Network, England and Wales. 2
years of severe injury in children. January 2013–December 2014. M https://www.tarn.ac.uk/
Content/ChildrensReport2/files/assets/common/downloads/TARN%20Leaflet.pdf
89 The Royal College of Emergency Medicine (2017). Position statement: paediatric trauma—
stabilisation of the cervical spine. M https://www.rcem.ac.uk/docs/RCEM%20Guidance/
Paediatric%20Trauma%20-%20Stabilisation%20of%20the%20Cervical%20Spine%20(Aug%20
2017).pdf
90 Royal College of Paediatrics and Child Health (2012). Evidence statement: major trauma and the
use of tranexamic acid in children. M https://www.rcem.ac.uk/docs/External%20Guidance/
10k.%20Major%20trauma%20and%20the%20use%20of%20tranexamic%20acid%20in%20chil-
dren%20Evidence%20statement%20(RCPCH,%20Nov%202012).pdf
91 The Royal College of Radiologists (2014). Paediatric trauma protocols. BFCR(14)8. M https://
www.rcr.ac.uk/system/f iles/publication/f ield_publication_f iles/BFCR%2814%298_paeds_
trauma.pdf
92 Vassallo J, Nutbeam T, Rickard AC, et al. (2018). Paediatric traumatic cardiac arrest: the develop-
ment of an algorithm to guide recognition, management and decisions to terminate resuscitation.
Emerg Med J, 35, 669–74.
93 Hazeldine J, Lord JM, Hampson P (2015). Immunesenescence and inflammaging: a contributory
factor in the poor outcome of the geriatric trauma patient. Ageing Res Rev, 24, 349–57.
94 Kingston A, Robinson L, Booth H, et al. (2018). Projections of multi-morbidity in the older popu-
lation in England to 2035: estimates from the Population Ageing and Care Simulation (PACSim)
model. Age Ageing, 47, 374–80.
95 Resuscitation Council UK. ReSPECT for healthcare professionals. M https://www.resus.org.uk/
respect/respect-healthcare-professionals
96 Antunes AC, Araújo DA, Veríssimo MT, et al. (2017). Sarcopenia and hospitalisation costs in
older adults: a cross-sectional study. Nutr Diet, 74, 46–50.
97 The Trauma Audit and Research Network (TARN) (2017). Major trauma in older people. M
https://www.tarn.ac.uk/content/downloads/3793/Major%20Trauma%20in%20Older%20
People%202017.pdf
98 Royal College of Anaesthetists (2020). Chapter 16: Guidelines for the provision of anaesthesia
services for trauma and orthopaedic surgery 2020. London: Royal College of Anaesthetists.
99 London Major Trauma System (2018). Management of elderly major trauma patients, 2nd edn.
London: London Operational Delivery Networks.
0321
100 Fassett DR, Harrop JS, Maltenfort M, et al. (2007). Mortality rates in geriatric patients with
spinal cord injuries. J Neurosurg Spine, 7, 277–81.
101 British Geriatric Society (2019). Comprehensive geriatric assessment toolkit for primary care practi-
tioners. London: British Geriatric Society.
102 Raven D (2014). HECTOR. The Heartlands’ elderly care trauma and ongoing recovery programme
course manual. M https://www.embeds.co.uk/wp-content/uploads/2019/10/Hector-
manual.pdf
103 Saller T, MacLullich AMJ, Perneczky R (2020). The 4AT—an instrument for delirium detection
for older patients in the post-anaesthesia care unit. Anaesthesia, 75, 410.
104 Griffiths R, Beech F, Brown A, et al. (2014). AAGBI working party: peri-operative care of the
elderly 2014. Anaesthesia, 69 (Suppl 1), 81–98.
105 Salmasi V, Maheshwari K, Yang D, et al. (2017). Relationship between intraoperative hypo-
tension, defined by either reduction from baseline or absolute thresholds, and acute kidney
and myocardial injury after noncardiac surgery: a retrospective cohort analysis. Anesthesiology,
126, 47–65.
106 Hovaguimian F, Myles PS (2016). Restrictive versus liberal transfusion strategy in the periopera-
tive and acute care settings: a context-specific systematic review and meta-analysis of random-
ized controlled trials. Anesthesiology, 25, 46–61.
107 Docherty AB, O’Donnell R, Brunskill S, et al. (2016). Effect of restrictive versus liberal trans-
fusion strategies on outcomes in patients with cardiovascular disease in a non-cardiac surgery
setting: systematic review and meta-analysis. BMJ, 352, i1351.
Chapter 38 1033
Fig. 38.1 Tracheal intubation of critically ill adults. Reproduced from Difficult Airway
Society 2015 guidelines for management of unanticipated difficult intubation in adults. Difficult
Airway Society intubation guidelines working group, BJA, 115(6): 827–48 (2015) doi:10.1093/
bja/aev371. Permission for the use of these algorithms for commercial purposes must be sought
directly from Difficult Airway Society as they hold the copyrights.
Sepsis and septic shock 1035
10 Finfer S, Bellomo R, Blair D, et al. (2009). Intensive versus conventional glucose control in critic-
ally ill patients. N Engl J Med, 360, 1283–97.
11 Semler MW, Self WH, Wanderer JP, et al. (2018). Balanced crystalloids versus saline in critically
ill adults. N Engl J Med, 378, 829–39.
12 Finfer S, Bellomo R, Boyce N, et al. (2004). A comparison of albumin and saline for fluid resusci-
tation in the intensive care unit. N Engl J Med, 350, 2247–56.
13 Myburgh JA, Finfer S, Bellomo R, et al. (2012). Hydroxyethyl starch or saline for fluid resuscitation
in intensive care. N Engl J Med, 367, 1901–11.
14 Cavalcanti AB, Suzumura ÉA, Laranjeira LN, et al. (2017). Effect of lung recruitment and titrated
positive end-expiratory pressure (PEEP) vs low PEEP on mortality in patients with acute respira-
tory distress syndrome—a randomized clinical trial. JAMA, 318, 1335–45.
15 Guérin C, Reignier J, Richard JC, et al. (2013). Prone positioning in severe acute respiratory dis-
tress syndrome. N Engl J Med, 368, 2159–68.
16 Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A (2000). Ventilation
with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the
acute respiratory distress syndrome. N Engl J Med, 342, 1301–8.
17 Amato MBP, Meade MO, Slutsky AS, et al. (2014). Driving pressure and survival in the acute
respiratory distress syndrome. N Engl J Med, 372, 747–55.
18 Papazian L, Forel JM, Gacouin A, et al. (2010). Neuromuscular blockers in early acute respiratory
distress syndrome. N Engl J Med, 363, 1107–16.
19 Moss M, Huang DT, Brower RG, et al. (2019). Early neuromuscular blockade in the acute respira-
tory distress syndrome. N Engl J Med, 380, 1997–2008.
041
Emergency laparotomy
(See also % pp. 1035–9; % pp. 1044–5.)
Indications for laparotomy include: bowel obstruction, perforation, in-
fection, ischaemia and bleeding. Physiological derangement and organ dys-
function are associated with both the underlying disease process and the
surgery itself:
• CVS instability due to vasoplegia and altered CO due to d preload,
depressed myocardial function and arrhythmias exacerbated by
electrolyte dysfunction and acidosis.
• Impaired oxygenation from V/Q mismatching due to atelectasis, d
FRC, fluid extravasation into pulmonary interstitium, reduced lung
compliance, abdominal distension and/or pain, leading to i work of
breathing or i inspiratory pressures.
• Renal hypoperfusion, i abdominal pressures and septic mediators can
cause AKI.
• Coagulopathy which may be related to sepsis or major bleeding.
Anaemia and bleeding might be exacerbated by acidosis, dilution and
hypothermia.
• Stress-induced hyperglycaemia and altered drug metabolism. Tissue
hypoxia is a common cause of metabolic acidosis and demonstrated by
a high blood lactate and a high anion gap (>14).
The recurrent UK National Emergency Laparotomy Audit highlighted that
the 30d mortality of emergency laparotomy remains 710%. Outcomes are
worse in the elderly. The mortality benefit from standardisation of care
has plateaued and wider organisational changes may be required to achieve
further reductions.20
Multiple risk factors associated with mortality have been identified
(including age, ASA, emergency surgery and peritoneal soiling).21
Preoperative assessment
• While a period of preoperative resuscitation may benefit some
patients, this should not delay surgery which should be performed by an
experienced team.
• A validated risk scoring tool (e.g. the NELA risk calculator M https://
data.nela.org.uk/riskcalculator) and assessment of frailty should be
conducted preoperatively. This allows for discussion of individualised
benefit vs risk with the patient and family, mobilisation of consultant-led
services and ICU/HDU admission for those with an estimated mortality
of >5%.
• O2 should be administered preoperatively to all hypoxic patients.
• Peritonitis and sepsis are common. Prompt antibiotic cover within the
1st hour in line with local guidelines should be given to cover Gram-
positive, Gram-negative and anaerobic bacteria.22
• An NGT should be inserted in patients with intestinal obstruction.
• Administration of balanced crystalloids is encouraged to minimise
acidosis and AKI.23
• Investigations: FBC, electrolytes (including Mg2+), LFTs, amylase, clotting,
lactate, G&S, ECG and CXR where appropriate. Reported CT imaging
can assist surgical planning.
• Electrolytes will often be deranged and should be corrected as soon as
possible perioperatively.
Emergency laparotomy 1041
• Analgesia:
• Opioids remain the mainstay for intraoperative analgesia in most
institutions.
• Caution with remifentanil and associated bradycardia,
• Neuraxial blockade should be used cautiously due to risks of
infective complications, sympatholysis and septic or haematological
coagulopathy.
• Rectus sheath catheters can be inserted at the end of the procedure,
and LA administered postoperatively (see % p. 1133).
• Monitor lactate and ABGs throughout the case to help guide
perioperative response to therapies and aid decision-making on the
postoperative disposition.
Postoperative care
• Consider ICU/HDU in high-risk or at-risk patients. Elderly and frail
patients have a higher mortality and ideally would be admitted to critical
care. If an ICU/HDU bed is unavailable, patients should be kept in
recovery for ongoing observation, and the same level of care provided
with ongoing reassessment of organ dysfunction.20
• Assess for the risk of abdominal compartment syndrome. High
ventilatory pressures (>30cmH2O) with hypoxia at the time of closure
are concerning and should be discussed with the surgeon and intensivist
(laparostomy may be helpful).
• Urine output should target >0.5mL/kg/h. In patients with persistently
low urine output, assess fluid balance and reconsider vasoactive support
to minimise AKI. AKI might be multifactorial (e.g. hypoperfusion, septic
AKI, nephrotoxins, abdominal compartment syndrome). Continuous
renal replacement therapy might be required.
• Optimise analgesia and provide chest physiotherapy to reduce the
risk of hospital-acquired pneumonia (with early commencement of
antibiotics if suspected).
• VTE prophylaxis when surgeon happy.
• Consider antacid prophylaxis if patient not able to eat.
• Consider parenteral nutrition if patient to remain nil by mouth.
• Specialist geriatrician input is recommended for elderly and frail patients.
• Timely communication with the family is important as the patient’s care
progresses.
Emergency laparotomy 1043
References
20 NELA Project Team (2019). Fifth Patient Report of the National Emergency Laparotomy Audit,
December 2017 to November 2018. London: Royal College of Anaesthetists.
21 Eugene N, Oliver CM, Bassett MG, et al. (2018). Development and internal validation of a novel
risk adjustment model for adult patients undergoing emergency laparotomy surgery: the National
Emergency Laparotomy Audit risk model. Br J Anaesth, 121, 739–48.
22 Levy MM, Evans LE, Rhodes A (2018). The Surviving Sepsis Campaign Bundle: 2018 update.
Intensive Care Med, 44, 925–8.
23 Semler MW, Self WH, Wanderer JP, et al. (2018). Balanced crystalloids versus saline in critically
ill adults. N Engl J Med, 378, 829–39.
24 Finfer S, Bellomo R, Blair D, et al. (2009). Intensive versus conventional glucose control in critic-
ally ill patients. N Engl J Med, 360, 1283–97.
25 Jonker WR, Hanumanthiah D, O’Sullivan EP, Cook TM, Pandit JJ (2014). A national survey
(NAP5-Ireland baseline) to estimate an annual incidence of accidental awareness during general
anaesthesia in Ireland. Anaesthesia, 69, 969–76.
26 Myles PS, Bellomo R, Corcoran T, et al. (2018). Restrictive versus liberal fluid therapy for major
abdominal surgery. N Engl J Med, 378, 2263–74.
27 Rhodes A, Evans LE, Alhazzani W, et al. (2017). Surviving Sepsis Campaign: international guide-
lines for management of sepsis and septic shock: 2016. Intensive Care Med, 43, 304–77.
041
• Helicopters and, less so, ambulances are noisy and you may be
required to wear ear protectors. Alarms are unreliably heard, even at
their maximum setting, so monitoring should be visible. If there is a
paramedic more familiar with the environment than you are, ask them
to help en route, such that you are able to remain hands-off, if possible,
and maintain situational awareness.
Paperwork
• Take: a concise handover, photocopy of the patient’s notes and drug
charts, pertinent imaging and lab results.
• The transport record should document the patient’s clinical status
before, during and after transport, relevant medical conditions,
environmental factors, therapy given, adverse logistical events and
procedures undertaken.
• Perform a predeparture checklist (Table 38.2).
Further reading
Association of Anaesthetists of Great Britain and Ireland (2009). Inter-hospital transfer. London:
Association of Anaesthetists of Great Britain and Ireland.
Australasian College for Emergency Medicine (ACEM); Australian and New Zealand
College of Anaesthetists (ANZCA); College of Intensive Care Medicine of Australia
and New Zealand (CICM) (2015). Guidelines for transport of critically ill patients. M
https:// w ww.anzca.edu.au/ g etattachment/ b d5938d2- d 3ab- 4 546- a 6b0- 0 14b11b99b2f/
PS52-Guideline-for-transport-of-critically-ill-patients
Whiteley S, Mark J, Barratt H, Binks R (2011). Guidelines for the transport of the critically ill adult.
London: Intensive Care Society.
Chapter 39 1051
Anaesthetic emergencies
Andrew Kane, Richard Armstrong, Jerry P Nolan
and Jasmeet Soar
Adult basic life support 1052
Adult advanced life support 1055
Post-resuscitation care 1058
Severe bradycardia 1060
Tachycardia 1062
Severe hypotension in theatre 1065
Severe hypertension in theatre 1068
Sorcha Evans
Severe hypoxia in theatre 1070
Severe laryngospasm 1073
Air/gas embolism 1074
Aspiration 1076
Severe bronchospasm 1078
Pulmonary oedema 1080
Anaphylaxis 1081
Anaphylaxis follow-up 1084
Latex allergy 1086
Intra-arterial injection 1088
Incomplete reversal of neuromuscular blockade 1090
Local anaesthetic toxicity 1092
See also
% Airway assessment and management p. 361
% Paediatric emergencies pp. 951–64
0521
At-risk patients
• All patients should have prior decisions about CPR to prevent
inappropriate CPR attempts.
• Use an early warning scoring system (e.g. National Early Warning Score
2 (NEWS2)) to identify deterioration and escalate care.
Further reading
European Resuscitation Council. M https://www.erc.edu
Resuscitation Council UK. M https://www.resus.org.uk
Adult advanced life support 1055
High-quality CPR
• Ensure high-quality chest compressions with minimal interruption.
• Aim for <5s for all pauses for interventions.
Defibrillation
• When a shockable rhythm (VF/pVT) is seen, restart chest
compressions and charge the defibrillator.
• Pause to deliver the shock and immediately resume compressions.
• Ensure everyone is clear when shock is delivered.
• Use at least 150J in an adult. Follow defibrillator manufacturer’s
instructions. Escalate shock energy if initial shocks fail.
• Remove O2 face mask or bag–valve–mask to >1m.
• Leave O2 circuit connected for an SGA or tracheal tube.
• Continue compressions for 2min until the next rhythm check.
• Use three ‘stacked’ shocks for a witnessed VF/pVT where a
defibrillator is immediately available, e.g. cardiac catheter lab.
• Precordial thump has a low chance of success if no defibrillator
available.
• Change pad position (e.g. to anterior–posterior) if VF/pVT persists.
Airway management and ventilation
• Assess and open the airway; use head-tilt, chin-lift and/or jaw thrust.
• Use an oropharyngeal or nasopharyngeal airway if needed.
• Use suction to clear secretions and gastric contents.
• Give 100% inspired O2 during CPR. After ROSC, target SpO2 94–98%.
• Use a stepwise approach (bag–valve–mask, SGA or tracheal tube).
Use whichever technique works best to deliver high-quality CPR with
minimal interruption to compressions.
• When the patient’s trachea is intubated, give continuous compressions
at about 120/min and ventilate the lungs at ten breaths/min without
pausing compressions. This can also be done with an SGA when there is
a good seal.
• Use waveform capnography to confirm correct tracheal tube
placement. Remember even in cardiac arrest, ‘No trace = wrong place’.
• Use front of neck access for airway (see % pp. 381–3) if unable to
oxygenate.
Drugs in cardiac arrest
• Give 1mg of adrenaline IV or IO every 3–5min (10mL of 1:10 000
solution) during cardiac arrest.
• For VF/pVT, delay 1st dose of adrenaline until after the 3rd shock.
• Give amiodarone 300mg IV or IO after three shocks for VF/pVT.
• Lidocaine 100mg can be used if amiodarone is not available.
Treat reversible causes
• Use the ‘4 Hs and 4Ts’ approach: hypoxia, hypovolaemia, hyperkalaemia
(and other metabolic disturbances), hypothermia, thrombosis, tension
pneumothorax, tamponade and toxins.
• Consider anaesthesia-specific causes: malignant hyperthermia, LA
toxicity, bone cement implantation syndrome, CO2/air/amniotic fluid
embolism, anaphylaxis, adverse drug reactions.
Adult advanced life support 1057
Post-resuscitation care
Following cardiac arrest, ROSC is the 1st step in what may be a prolonged
period of treatment. Unless the duration of cardiac arrest is very short, the
patient will be unconscious and is likely to develop the post-cardiac arrest
syndrome, which is associated with a marked systemic inflammatory re-
sponse. The anaesthetist may be expected to initiate treatment in the ED,
the operating room, the critical care unit or on the general ward. The aims
of post-resuscitation care are to:
• Prevent a further cardiac arrest
• Define and treat the underlying disease process
• Limit organ damage
• Predict non-survivors.
Prevention of further cardiac arrest
• Optimise oxygenation. If fully conscious following a short-duration
cardiac arrest, give O2 via a face mask.
• Most patients will require assisted ventilation via a tracheal tube.
• After ROSC, once SpO2 can be measured reliably or ABG values are
obtained, titrate the inspired O2 to achieve a saturation of 94–98% or
PaO2 of 10–13kPa.
• Provide ventilation to maintain normocarbia. Excessive ventilation will
cause hypocarbia and may cause cerebral ischaemia from cerebral
vasoconstriction.
• Maintain sedation with a propofol infusion, combined with a short-
acting opioid.
• Avoid hypotension (MAP <65mmHg). Target MAP to achieve adequate
urine output (>0.5mL/kg/h) and normal or decreasing lactate.
• Correct electrolyte disturbances, particularly K+, Mg2+ and Ca2+.
• Control blood glucose—treat blood glucose with insulin if it exceeds
10mmol/L; maintain in the range of 4–10mmol/L.
Define and treat the underlying disease process
• Establish the patient’s pre-arrest medical condition.
• Confirm correct placement of ETT and exclude pneumothorax with
CXR ± ultrasound.
• Perform early echocardiography in all patients in order to detect any
underlying condition and quantify myocardial dysfunction.
• Consider CT brain and CT pulmonary angiography.
Limit organ damage
• ST-elevation on the 12-lead ECG is an indication for urgent coronary
angiography and PCI if indicated. In patients without ST-elevation
on the ECG, consider urgent coronary angiography if there is a
high probability of acute coronary occlusion (e.g. patients with
haemodynamic and/or electrical instability).
• Treat patients remaining comatose after ROSC with targeted
temperature management. Maintain a constant target temperature
between 32°C and 36°C for at least 24h.
• Avoid fever for at least 72h after ROSC in patients who remain in coma.
• Control seizures with propofol, benzodiazepines, levetiracetam or
sodium valproate.
Post-resuscitation care 1059
Prediction of non-survivors
• About 8% of all those sustaining an out-of-hospital cardiac arrest will
survive to hospital discharge; the figure for in-hospital cardiac arrest is
about 23%.
• Short duration of cardiac arrest/CPR achieves better neurological
outcomes.
• Prognostication in unconscious patients is unreliable for at least 72–96h
after ROSC.
• Ensure that sedative drugs have cleared and use multiple modalities:
clinical examination, imaging (CT and/or MRI), biomarkers (e.g. neuron-
specific enolase) and electrophysiology (EEG, somatosensory evoked
potentials).
• Myocardial, neurological and other organ function may all improve
slowly, given appropriate support over a period of time—at least 3–7d
of intensive care should be considered in the comatose patient with
ROSC following cardiac arrest.
Further reading
Nolan JP, Sandroni C, Böttiger BW, et al. (2021). European Resuscitation Council and European
Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation care. Resuscitation, 161,
220–69.
061
Severe bradycardia
(See Fig. 39.3.)
Tachycardia
(See Fig. 39.4.)
Unstable tachycardias
• For sinus tachycardia, ensure adequate anaesthesia and analgesia.
• Check ABCDE. Rapidly correct hypoxia, hypovolaemia and electrolyte
abnormalities (K+, Mg2+).
• In otherwise normal patients, a ventricular rate of up to 150/min
is normally well tolerated, but patients with impaired function may
decompensate at lower rates.
• For all tachycardias, assess for life-threatening adverse features:
syncope, shock, myocardial ischaemia and heart failure. If present,
perform synchronised direct current cardioversion. Patient may need
sedation/GA.
• For direct current cardioversion, use 70–120J for atrial flutter and
narrow complex tachycardia, and 120–150J for broad complex
tachycardia and AF.
• If direct current cardioversion fails, give 300mg IV amiodarone over
10–20min, then reattempt direct current cardioversion. Follow this with
900mg IV amiodarone over 24h.
• If cardiac arrest or pulseless VT, start ALS algorithm.
• If the patient is stable, aim to use pharmacological methods 1st line.
There is usually time to seek expert help (see % pp. 147–51).
Stable, regular broad complex tachycardia
• This is likely to be VT or a supraventricular rhythm with a bundle
branch block. Treat with amiodarone. Seek expert help.
Stable, irregular broad complex tachycardia
• Likely AF with a bundle branch block. Most cases should be treated as
AF (see % pp. 149–51).
• This may be polymorphic VT (i.e. torsade de pointes), but this is
likely to be seen with adverse features or cardiac arrest. Treat with
magnesium sulfate 2g IV and seek expert help.
Stable, regular narrow complex tachycardia
• Sinus tachycardia is a physiological response. Identify the underlying
cause and treat.
• Paroxysmal SVT (AV nodal re-entry tachycardia and AV re-entry
tachycardia) represents abnormal conduction pathways allowing rapid
ventricular rate. Atrial activity is often not visible on the ECG.
• Atrial flutter with variable AV conduction presents as a narrow complex
tachycardia. The atrial flutter rate is classically 300/min, and so a ratio
of 2:1 conduction gives a ventricular rate of 150/min.
• Try vagal manoeuvres.
• If ineffective, give IV adenosine, starting with 6mg, then 12mg (repeat
12mg; if necessary, consider 18mg).
• Differentiating narrow from broad complex tachycardia can be difficult,
especially at high ventricular rates. Vagal manoeuvres or adenosine
should slow AV conduction of an SVT, but not a VT.
Tachycardia 1063
Adult tachycardia
Risk factors
• Preoperative fluid deficit (dehydration, diarrhoea and vomiting,
blood loss).
• Mediastinal/hepatic/renal surgery (blood loss and caval compression).
• Pre-existing myocardial disease/dysrhythmia.
• Multiple trauma.
• Sepsis.
• Carcinoid syndrome with liver or lung tumour/metastases (bradykinin).
• ACE inhibitors and ARBs.
Differential diagnosis
• Measurement error: clinical assessment and manual palpation of the
distal pulse, while repeating NIBP. Check when pulsation returns
against the monitor deflation figure. If using intra-arterial BP, check the
transducer height is at the level of the heart.
• Check peripheral perfusion; warm peripheries may suggest sepsis.
• Raised intrathoracic pressure can be caused by a pneumothorax or
capnothorax (during laparoscopic surgery where the diaphragm is
breached by insufflated gas). If tension pneumothorax is suspected,
(particularly following central line insertion and IPPV), the trachea
will be shifted away from a hyperresonant lung field, which will
have diminished breath sounds. Neck veins may be engorged. Treat
immediately by decompressing the pleural cavity with a large-bore
cannula placed in the 2nd intercostal space in the mid-clavicular line, or
a thoracostomy.
061
Risk factors
• Untreated or ‘white coat’ hypertension preoperatively (i lability).
• Aortic surgery (cross-clamp may ii SVR).
• Drugs: MAOIs (plus pethidine), ketamine, ergometrine.
• Family history of MEN (type 2) syndrome, medullary thyroid carcinoma,
Conn’s syndrome.
• Acute head injury.
Differential diagnosis
• Hypoxia/hypercapnia: go through ABC, and check for patient colour
and SpO2.
• Inadequate depth of anaesthesia: check volatile agent concentration;
sniff test (smell gases); check TIVA pump, line and IV cannula.
• Inadequate analgesia: if in doubt, administer opioid (e.g. alfentanil 10–20
micrograms/kg) and observe effect. Consider remifentanil infusion.
• Measurement error: palpate the distal pulse manually, while repeating
NIBP; check when pulsation returns against the monitor deflation figure.
Invasive BP: check the transducer height.
• Iatrogenic drug response: cocaine, wrong drug (such as ephedrine and
adrenaline), or wrong dilution (remember surgical drugs, e.g. adrenaline
with LA, Moffett’s solution, phenylephrine).
• Pre-eclampsia: if over 20w pregnant, check for proteinuria, platelet
count ± clotting studies and LFTs.
• Thyroid storm causing elevated T4 and T3 levels.
• Phaeochromocytoma causing elevated plasma catecholamine levels.
• Cushing response: hypertension and reflex bradycardia (baroreceptor-
mediated). This intracranially mediated response maintains cerebral
perfusion in the presence of i ICP (see % pp. 559–60).
Severe hypertension in theatre 1069
Immediate management
• ABCDE approach: identify and treat the underlying cause.
• Keep calm and aim for an acceptable safe BP value based on patient’s
age and comorbidities.
• Avoid alternating between severe hypertension and severe
hypotension. The aim is to minimise myocardial stress leading to MI,
arrhythmia or failure (Takotsubo cardiomyopathy), and to minimise the
risk of hypertensive stroke and surgical bleeding.
• If difficult BP to control, insert an arterial line for continuous BP
monitoring early.
• Consider the following drug options to decrease SVR and control HR.
The choice of drug will depend on availability:
• Vasodilators (may cause tachycardia): i volatile concentration,
but beware of increasing desflurane which may cause sympathetic
activation at >1.5 MAC. Hydralazine 5mg slow IV every 15min.
GTN (50mg/50mL; start at 3mL/h, and titrate to BP) or sodium
nitroprusside (50mg/50mL and titrate with care for fine control).
Magnesium sulfate 2–4g slow IV (8–16mmol) over 10min, followed by
infusion of 1g/h.
• β-blockade (particularly in the presence of i HR or dysrhythmias):
esmolol 25–50mg bolus doses, then 50–200 micrograms/kg/
min. (Note that esmolol is supplied as 10mg/mL and 250mg/mL
solutions.) Labetalol 5–10mg IV PRN (1–2mL increments from a
100mg/20mL ampoule). β:α block ratio = 7:1.
• α-blockade (particularly in the presence of normal or d HR):
phentolamine 1–2mg IV PRN (10mg ampoule made up to 10mL).
• Calcium channel blockade with IV nicardipine in 2.5mg increments.
Subsequent management
• Phaeochromocytoma crisis, or thyroid storm, may require prolonged
treatment and ICU admission. Liaise with endocrinologist to ensure the
correct samples are taken for investigation, and further treatments (e.g.
antithyroid drugs, iodine, steroids for thyroid storm).
• Check for evidence of MI and myocardial injury (troponin, 12-lead ECG,
echocardiography).
• Patient may require longer-term medication for BP. For
phaeochromocytoma, this includes an α-blocker (phenoxybenzamine or
doxazosin), and if they have tachycardia, a β-blocker.
071
Risk factors
• Reduced FRC (obesity, intestinal obstruction, pregnancy) reduces O2
reserves.
• Failure to preoxygenate exacerbates airway difficulties at induction.
• Laryngospasm can result in negative-pressure pulmonary oedema.
• Head and neck surgery (shared access to the airway) increases the risk
of undetected disconnection.
• History of CHD or detection of a heart murmur (left-to-right
communication).
• Chronic lung disease.
• Methaemoglobinaemia (interpreted as deoxyhaemoglobin by pulse
oximeters).
• Systemic absorption of patent blue dye.
Differential diagnosis
• Inappropriate FiO2: use an O2 analyser at all times.
• Signal error: reduced peripheral perfusion in hypovolaemic,
hypotensive, hypothermic patients or AF, Raynaud’s. Does the patient
appear cyanotic?
• Obstruction of airway equipment: check for kinks (e.g. during
positioning of gag during tonsillectomy), foreign bodies in filter/ETT,
water in circuit.
• Ventilation problem: is ETT same depth as it was? Has it been dislodged?
Look for chest movement with auscultation over the stomach and in
both axillae. Is the patient hypoventilating? Look at minute ventilation
Severe hypoxia in theatre 1071
Hypotension/hypovolaemia
Use fluid/blood/vasopressors as needed. During laparoscopy, check insuf-
flation pressures and ask surgeon if they can be reduced if needed.
Severe right-to-left shunt
Severe hypoxia occurs when blood starts flowing through a congenital heart
defect in the presence of low SVR, thus bypassing the pulmonary circula-
tion. The resultant hypoxaemia exacerbates the problem by causing hyp-
oxic pulmonary vasoconstriction which increases PVR and the tendency for
blood to shunt across the cardiac defect. Treatment is therefore twofold:
(1) to increase SVR by lifting the legs/Trendelenburg and giving adrenaline
plus IV fluid, especially in sepsis; and (2) to minimise PVR by removing PEEP,
avoiding high intrathoracic pressure and maximising FiO2.
Other considerations
• In chronic bronchitis, the bronchial circulation can shunt up to 10% of
the CO.
• The foramen ovale remains patent in 20–30% of patients but is normally
kept closed, because the left atrial pressure is usually higher than the
right atrial pressure. IPPV, PEEP, breath-holding, CCF, thoracic surgery
and PE can reverse the pressure gradient and result in shunt.
• Always check the SpO2 probe is well positioned and has a good trace.
However, this should not be presumed to be the offending problem
until other causes have been excluded!
Severe laryngospasm 1073
Severe laryngospasm
Condition Acute glottic closure by the vocal cords
Presentation Crowing or absent inspiratory sounds and
marked tracheal tug
Immediate action 100% O2, CPAP
Larson’s manoeuvre (vigorous jaw thrust)
Remove irritants from the airway
Deepen anaesthesia
Follow-up action Muscle relaxation if intractable
Also consider Bronchospasm
Laryngeal trauma/airway oedema
Recurrent laryngeal nerve damage
Tracheomalacia
Inhaled foreign body
Epiglottitis; croup
Risk factors
• Light anaesthesia, especially in anxious patients.
• Intense surgical stimulation: anal stretch, cervical dilation, etc.
• Extubation of a soiled airway.
• Thyroid surgery.
• Hypocalcaemia (neuromuscular irritability).
• Multiple crowns, poor dentition (inhaled foreign body).
Immediate management
(See % p. 370.)
• Remove the stimulus that precipitated the laryngospasm.
• Check that the airway is clear of obstruction or potential irritants,
including airway adjuncts in the light patient.
• Administer 100% O2 and CPAP.
• If unsuccessful, deepen anaesthesia with propofol or sevoflurane.
• If this fails, muscle relaxant is required. Suxamethonium 0.25–0.5mg/kg
IV or 3mg intralingual/submental or 4mg/kg IM thigh.
• Monitor for pulmonary oedema. Decompress stomach with an OGT.
Other considerations
• Risk may be reduced by co-induction with IV opioids, IV lidocaine, or by
topical lidocaine spray prior to laryngoscopy.
• Unilateral recurrent laryngeal nerve trauma results in paralysis of one
vocal cord and causes hoarseness, ineffective cough and the potential to
aspirate. Bilateral vocal cord paralysis is more serious, leading to stridor
on extubation. This may mimic laryngospasm but does not get better
with standard airway manoeuvres. The patient will require reintubation,
and possibly tracheostomy.
• Tracheomalacia is likely to cause more stridor with marked negative
inspiratory pressure, so treat initially with CPAP.
0741
Air/gas embolism
(See also % pp. 584–5.)
Condition Venous gas produces an airlock in RV and ob-
structs pulmonary capillaries
Presentation d ETCO2
d SpO2
Hypotension and loss of palpable pulse
i CVP, then d CVP
PEA
Immediate action Stop insufflating gas
Ensure open wound lower than heart
Flood wound and compress drainage veins
Follow-up action i venous pressure; turn off N2O; left lateral head-
down tilt; CVS support
Investigations Auscultation; Doppler; ECG; CXR
Also consider Breathing circuit disconnection
Other causes of PEA (4Hs and 4Ts)
Cement reaction
Pulmonary thromboembolism
AFE
Immediate management
ABC
• Eliminate possibility of breathing circuit disconnection; give 100% O2;
check the ECG trace and pulse.
• Increase venous pressure with rapid IV fluids ± vasopressors.
• If PEA arrest occurs, commence the ALS protocol for non-VF/VT
cardiac arrest.
Prevent further gas/air entrainment
• Surgeon to apply compression to major drainage vessels, flood the
surgical field with irrigation fluid or cover with damp pack, stop
reaming, etc.
• Decompress any gas-pressurised system/cavity, e.g. the abdomen
during laparoscopy.
• Lower the operation site to below the heart level.
Turn off N2O
• N2O will expand any intravascular gas volume.
Central venous line
• Classic teaching is to tip the patient head-down in the left lateral
position, to keep the bubble of gas in the right atrium or apex of the
RV. It can then be aspirated via a central line advanced into the right
atrium or will eventually dissolve. In practice, even if a CVP line is in situ,
aspiration is likely to be difficult.
Moderate CPAP
• Advocated as a means of rapidly increasing the intrathoracic pressure,
and therefore CVP, in the event of a gas embolus. While this
manoeuvre may limit the extent and progress of an air embolus, it
must be borne in mind that 10% of patients may have a patent foramen
ovale. Sustained rise in right atrial pressure may then lead to a right-to-
left shunt and paradoxical air embolism to the cerebral circulation.
Subsequent management
• Ask the surgeon to apply bone wax to exposed bone edges.
• Correct any pre-existing hypovolaemia.
• Perform a 12-lead ECG to look for ischaemia. Air in coronary arteries is
suggestive of paradoxical air embolism.
• Consider hyperbaric therapy, if available. i ambient pressure (3–6 bar)
will decrease the volume of gas emboli.
Other considerations
CO2 is the safest gas to use for laparoscopic insufflation. It is non-flammable
and more soluble than other agents. Should a gas embolus occur, it will dis-
solve over time. The priority of management should therefore be to limit
the extent and central progress of the gas ‘bubble’, thereby minimising its
systemic CVS effect.
0761
Aspiration
Condition Chemical pneumonitis; foreign body obstruction and
atelectasis
Presentation d SpO2, i RR, i HR, d lung compliance
Immediate action Minimise further aspiration
Secure the airway
Suction
Follow-up action 100% O2 and consider CPAP
Empty the stomach
Investigations CXR; bronchoscopy
Also consider Pulmonary oedema
Embolus
ARDS
Risk factors
• Full stomach/delayed emptying (many causes, including opioids, recent
trauma, DM, CKD).
• Known reflux.
• Raised intragastric pressure (intestinal obstruction, pregnancy,
laparoscopic surgery, high BMI).
• Anaesthesia—topically anaesthetised airway, LMA (especially 1st
generation), light anaesthesia.
• Oral/nasal surgery where ‘coroner’s clot’ may be aspirated from
nasopharynx on extubation.
• Steep Trendelenburg position.
Diagnosis
• Clinical: auscultation may reveal wheeze and crepitations.
• CXR: diffuse infiltrative pattern, especially in the right lower lobe
distribution (but often not acutely).
Immediate management
• Avoid a GA in high-risk situations, if possible.
• Use of an RSI when appropriate.
• Administer 100% O2, and minimise the risk of further aspirate
contaminating the airway.
• If light anaesthesia: suction and put into recovery position.
• If under GA, suction; consider securing the airway with ETT ±
cricoid pressure (controversial—avoid if actively vomiting, as risk of
oesophageal rupture or when it distorts the view on laryngoscopy).
Subsequent management
• Empty the stomach with a large-bore NGT prior to extubation.
• Monitor respiratory function and arrange a CXR. Look for evidence of
oedema, collapse or consolidation.
• If SpO2 remains <90%, despite 100% O2, there may be solid food
material obstructing part of the bronchial tree. Consider performing a
bronchoscopy.
Aspiration 1077
Severe bronchospasm
Presentation i airway pressure
Sloping expiratory capnograph trace
Wheeze or silent chest
i HR
Immediate action 100% O2
Salbutamol 250 micrograms IV/2.5mg neb;
aminophylline 250mg slow IV
Magnesium sulfate 2g IV
Follow-up action Hydrocortisone 200mg
Investigations CXR; ABG
Also consider Breathing circuit obstruction
Kinked ETT/cuff herniation
Endobronchial intubation/tube migration
Foreign body in airway
Anaphylaxis
Pneumothorax
Risk factors
• Asthma; particularly with previous acute admissions, especially to ICU,
and/or systemic steroid dependence.
• Paediatric: prematurity and LBW.
• Trigger exposure: smoke, allergens.
• Intercurrent respiratory tract infection.
• Carinal irritation by ETT.
Diagnosis
• i airway pressure, i expiratory phase of capnography waveform.
• Central trachea, with bilaterally hyperexpanded and resonant lung fields
± expiratory wheeze (absent if severe).
• Severe bronchospasm is a diagnosis of exclusion. The quickest method
of ascertaining the source of i airway resistance is to connect a self-
inflating bag directly to the ETT (not HME) and manually ventilate. If the
inflation pressure still feels too high, the problem is due to airway/ETT
obstruction or reduced compliance.
• Eliminate ETT obstruction by passing a suction catheter. Perform gently
to prevent further bronchospasm via carinal irritation.
Immediate management
ABC
• 100% O2.
Increase the volatile agent concentration
• Sevoflurane is the least irritant and is less likely to precipitate
dysrhythmias in the presence of hypercapnia. However, this may be
insufficient in severe bronchospasm.
Specific treatment
• Salbutamol and aminophylline (see Table 39.1).
Severe bronchospasm 1079
Adult Paediatric
Salbutamol: IV (slow) 250micrograms 15micrograms/kg
Salbutamol: nebulised 2.5–5mg every 15min 2.5–5mg every 15min
Salbutamol: puffs Ten puffs Ten puffs
Ipratropium bromide 0.25–0.5mg 4–6h 0.25mg 4–6h
(nebulised)
Aminophylline (IV) 250mg slowly 5mg/kg slowly
Ketamine (IV) 2mg/kg 0.5–1mg/kg
Magnesium (IV) 2g slowly 40mg/kg slowly
Adrenaline (IV) 10micrograms 1microgram/kg
Hydrocortisone (IV) 200mg 4mg/kg
Subsequent management
• If immediate treatment fails, consider ipratropium bromide, adrenaline
IV boluses, ketamine or magnesium (Table 39.1).
• Give hydrocortisone.
• Check for drug allergies to agents already administered.
• Arrange CXR—check for pneumothorax and ETT tip position
(withdraw if carinal).
• Check ABGs and electrolytes (prolonged use of β2-agonists causes
hypokalaemia).
• Refer to ICU.
Other considerations
• Gas trapping: i mean intrathoracic pressure may result from IPPV in the
presence i expiratory time. If pulse pressure falls and neck veins appear
distended, consider obstructed venous return and a dependent fall in
CO. Disconnect the ETT from the circuit and push on chest; preload
should be restored as intrathoracic pressure is d, and pulse pressure
and VT should improve.
• Ventilator settings in bronchospasm: 100% O2, low RR and prolonged
expiration (I:E ratio 1:3 or 1:4); accept i ETCO2, provided SpO2 is
adequate (permissive hypercapnia).
Further reading
British Thoracic Society, Scottish Intercollegiate Guidelines Network (2008). British guideline on the
management of asthma. A national clinical guideline. Revised July 2019. M https://www.brit-
thoracic.org.uk/quality-improvement/guidelines/asthma/
081
Pulmonary oedema
Condition i hydrostatic pressure
i vascular permeability
d plasma colloid osmotic pressure
Negative interstitial pressure
Obstructed lymphatic drainage
Presentation Pink frothy sputum, i HR, i RR, d SpO2, i CVP,
i PAOP
Immediate action 100% O2, sit up/reverse Trendelenburg. Opioids,
diuretics and vasodilators
Investigations CXR; ECG; ABG; echocardiography
Also consider Asthma
MI
ARDS
Aspiration
Risk factors
• Cardiogenic: MI, severe hypertension, CCF.
• Non-cardiogenic: airway obstruction (negative pressure), neurogenic,
sepsis, aspiration, pre-existing lung disease, impairment of lymphatic
drainage and rapid lung expansion.
Diagnosis
• Clinical: wheeze; pink, frothy sputum; fine crackles; quiet bases; gallop
rhythm; i JVP; liver engorgement.
• i HR; i RR; d SpO2; i airway pressure; i CVP; d PAOP.
• CXR: basal shadowing; upper lobe diversion; hilar haze; bronchial
cuffing; pleural effusions; septal/interlobar fluid lines.
• ECG: evidence of right heart strain; evidence of MI.
Immediate management
ABC
• If awake and breathing spontaneously: sit up to offload the pulmonary
vasculature and improve FRC; 100% O2 via mask/HFNO/CPAP
5–10mmHg.
• If anaesthetised and intubated: commence IPPV with PEEP (5–
10cmH2O), 15° head-up position to reduce atelectasis and improve
FRC; aspirate free fluid from the trachea intermittently.
Medication
• Furosemide 50mg IV.
• Diamorphine 5mg IV.
• Vasodilator if hypertensive (e.g. GTN 0.5–1.5mg sublingually or 10mg
transcutaneous patch. IV GTN only if arterial line in situ).
Anaphylaxis 1081
Anaphylaxis
Condition Immunoglobulin E-mediated type 1 hypersensitivity
reaction to an antigen, resulting in histamine and
serotonin release from mast cells and basophils
Presentation i HR, d BP, rash, wheeze, oedema
Immediate action Remove trigger
100% O2
Elevate legs and fluid resuscitation
IV adrenaline 20–50 micrograms
Follow-up action Chlorphenamine 10–20mg
Hydrocortisone 100–300mg
Investigations Plasma tryptase; directed allergy testing, ABG
Also consider Airway obstruction
Asthma
Tension pneumothorax
Anaphylactoid reaction
Sepsis
Histamine release (atracurium)
Cardiogenic shock
Risk factors
• IV administration of the antigen.
• Note that cross-sensitivities with NSAIDs and muscle relaxants mean
that previous exposure is not always necessary.
• True penicillin allergy is a reaction to the basic common structure
present in most penicillins (the β-lactam ring).
• Antibiotics (46%), muscle relaxants (33%), chlorhexidine (10%) and
patent blue are the most frequent triggers.
Diagnosis
• CVS collapse (51%)
• Erythema (45%)
• Bronchospasm (40%)
• Rash (13%)
• Angio-oedema (12%)
• Urticaria (8.5%).
Immediate management
ABC
• Stop any potential triggers, particularly IV agents. Be aware of
chlorhexidine-coated central lines.
• Call for help.
• 100% O2; maintain the airway and consider intubation.
• Lay the patient flat, with the legs elevated/Trendelenburg position.
• Give adrenaline in IV increments every 1–2min. Alternatively, give
adrenaline IM, repeated after 5min, if necessary (Table 39.2).
• Give IV crystalloid fluids 20mL/kg.
0821
Subsequent management
• Adrenaline infusion (1st line): 0.05–0.1 micrograms/kg/min or
noradrenaline 0.05–0.1 micrograms/kg/min (see % p. 1209).
• Resistant hypotension: consider glucagon in those on a β-blocker (1–
2mg IV every 5min); vasopressin (IV bolus 1–2 units, then 2 units/h).
• Antihistamines: consider PO non-sedating antihistamine when awake.
Alternatively, IV/IM chlorphenamine; however, evidence to support
their use is weak.
• Corticosteroids may help prevent or shorten protracted reactions.
• Consider bronchodilators (see % p. 1071) for persistent bronchospasm.
• Pregnancy: consider left uterine displacement or CS within 4min if
arrest or periarrest.
• Check for the presence of airway oedema by letting down the ETT cuff
and confirming a leak prior to extubating.
Other considerations
• NMBAs are responsible for 60–70% of serious anaesthetic adverse drug
reactions (AADRs), frequently on 1st contact.
• The quaternary ammonium group found in neuromuscular-blocking
drugs is present in other drugs, foods, cosmetics and hair care products.
Previous sensitisation is possible, predominantly in ♀ .
• Clinically, anaphylactic reactions may be indistinguishable from
anaphylactoid responses. Isolated cutaneous erythema is commonly
seen following IV thiopental or atracurium. If there are no further
histaminoid manifestations, investigation is unwarranted.
• Timing is important. Onset is usually rapid following an IV drug
bolus. Slower onset is expected if, for example, gelatin infusion, latex
sensitivity or diclofenac suppository is responsible.
Anaphylaxis 1083
Further reading
Royal College of Anaesthetists (2018). Anaesthesia, surgery and life-threatening allergic reactions. Report
and findings of the Royal College of Anaesthetists’ 6th National Audit Project: perioperative anaphyl-
axis. M https://www.nationalauditprojects.org.uk/NAP6Report#pt
Australian and New Zealand College of Anaesthetists (ANZCA) and Australian and New Zealand
Anaesthetic Allergy Group (ANZAAG) (2016). Perioperative anaphylaxis management guide-
lines. M https://www.anzca.edu.au/getattachment/ce1ac7fb-45c3-434c-9da9-7a61f14916b8/
Anaphylaxis-management-guidelines
Resuscitation Council UK (2008). Emergency treatment of anaphylactic reactions. Revised 2016. M
https://www.resus.org.uk/anaphylaxis/emergency-treatment-of-anaphylactic-reactions/
0841
Anaphylaxis follow-up
Investigation of reactions
Referral to anaesthetic allergy clinic
Referral to an allergy clinic is the responsibility of the anaesthetist and
should include:
• Anaesthetic chart
• Drug chart
• Timings of all administered substances
• Tryptase results and timings.
A list of specialist clinics is available on the British Society for Allergy and
Clinical Immunology website (M https://www.bsaci.org).
Serum tryptase evaluation
Tryptase is a neutral protease released from secretory granules of mast
cells during degranulation. In vivo half-life is 3h (compared with 3min for
histamine), and it is stable in isolated plasma or serum.
• Take three venous blood samples—immediately after resuscitation, at
1–2h (not later than 6h) and baseline levels at 24h. Serum should be
separated and stored at –20°C and sent to an appropriate laboratory.
• Basal plasma tryptase concentration is usually <11 nanograms/mL.
Levels of up to 15 nanograms/mL are seen in pseudoallergy, e.g.
anaphylactoid reactions. In patients with low baseline tryptase levels,
even if levels remain within normal limits, a level of >2 nanograms/mL +
1.2 × baseline is indicative of anaphylaxis.
Radioallergosorbent/C AP tests
• Radioallergosorbent tests (RASTs) for antigen-specific immunoglobulin
E antibodies have now been largely superseded by the CAP system
(Phadia®).
• Currently, only helpful in confirming penicillin, suxamethonium,
chlorhexidine and latex allergy. Sensitivity is low, and a negative result
still requires skin testing.
Skin testing
• Diagnosing an AADR depends on skin prick test or intradermal testing.
In proven neuromuscular-blocking drug anaphylaxis, no in vitro test has
been shown to have comparable specificity and sensitivity.
• Tests should take place at 4–6w post-event to allow the regeneration of
immunoglobulin E.
• Antihistamines should not have been given within the last 5d.
• Testing is required to all drugs given before the event. Remember
antibiotics, latex, chlorhexidine and lidocaine, if mixed with propofol.
Suspected LA allergy is best tested by challenge.
• Negative control is with 0.9% sodium chloride (to exclude
dermographia). Positive control is with a commercially available
histamine solution. The latter demonstrates a normal skin response.
Wheal and flare give a reference for reactions to test drugs.
• Wheal >2mm wider than the 0.9% sodium chloride control is
interpreted as positive. Positive test with undiluted drug is repeated
with 1:10 dilution to reduce the chance of a false positive.
Anaphylaxis follow-up 1085
Latex allergy
Latex is derived from the sap of Hevea brasiliensis (rubber tree). Hev b
proteins within latex act as the major allergens (there are 14 types—Hev
b1–14). Latex, although previously commonly found in much anaesthetic
and surgical equipment, has significantly lessened with the awareness of the
prevalence of latex allergy. However, this should not result in complacency
in preventing such reactions.
Classification of reaction
Irritant contact dermatitis
Non-allergic, irritant contact dermatitis, presenting over minutes to hours.
Damage to skin due to exogenous substance causing irritation.
Contact dermatitis
Type 4 (delayed) hypersensitivity reaction, based on allergic sensitisa-
tion mediated by T-lymphocytes. Presents over 48–72h with an eczema-
tous eruption. This can progress to lichenification and scaling on chronic
exposure.
Type 1 hypersensitivity
Development of latex sensitivity is dependent on previous exposure.
Immunoglobulin E-mediated type 1 hypersensitivity has been attributed to
Hev b proteins in latex. The three main presentations are:
• Contact urticaria: particularly of health care workers, typically 10–
15min following, and usually at the site of, exposure. This may develop
into a more severe reaction
• Asthma and rhinitis: characterised with bronchospasm and secretions.
Inhalation of airborne latex particles from powdered gloves has been
implicated
• Anaphylaxis: this is more commonly encountered intraoperatively.
IV and membrane inoculation are the commonest triggers; however,
donning of gloves and indirect contact have also been described.
High-risk individuals
Eight per cent of the population are sensitised to latex; however, 1.4% of
the population exhibit a latex allergy. Latex anaphylaxis appears to be more
common in ♀. There are certain groups at particular risk of developing
latex sensitivity.
Multiple surgical procedures
Patients with repeated exposure to latex have an i risk.
Neural tube defects, including spina bifida
Incidence of latex sensitivity due to recurrent bladder catheterisation is
20–65%.
Associated medical conditions
Patients with atopy, asthma, rhinitis and severe dermatitis have an i inci-
dence of sensitivity.
Health care workers
Prevalence of sensitivity can be between 3% and 12%.
Latex allergy 1087
Occupation
Rubber industry workers, occupations involving the use of protective
equipment (policemen, hairdressers, service food workers).
Fruit allergens
Patients allergic to fruit have an 11% risk of a latex reaction. Crossreactivity
has been demonstrated with certain fruit allergens (banana, chestnut, avo-
cado, passion fruit, tomato, grape, celery, peach, watermelon, cherry and
kiwi fruit).
Prevention of latex anaphylaxis
• All team members need to be alerted if a patient has a latex allergy.
• The operating theatre should be prepared the night before as this
reduces the number of latex particles in the air. The patient should be
scheduled 1st on the list.
• ‘Latex allergy’ notices should be placed on theatre doors.
• Only use latex-free equipment.
• Remove non-essential equipment from the vicinity of the patient.
• Limit staff traffic during surgery.
• Resuscitation equipment must be latex-free.
• There is no evidence to support prophylactic use of antihistamines and
corticosteroids.
Clinical features of latex anaphylaxis
Onset is normally 20–60min following exposure and progressively worsens
over 5–10min. Treat as for anaphylaxis (see % pp. 1081–3).
Further reading
Lieberman P, Nicklas RA, Oppenheimer J, et al. (2010). The diagnosis and management of anaphyl-
axis practice parameter: 2010 update. J Allergy Clin Immunol, 126, 477–80.
Bousquet J, Flahault A, Vandenplas O, et al. (2006). Natural rubber latex allergy among health care
workers: a systematic review of the evidence. J Allergy Clin Immunol, 118, 447–54.
Suli C, Lorini M, Mistrello G, Tedeschi A (2006). Diagnosis of latex hypersensitivity: comparison of
different methods. Eur Ann Allergy Clin Immunol, 38, 24–30.
Cullinan P, Brown R, Field A, et al.; British Society of Allergy and Clinical Immunology (2003). Latex
allergy. A position paper of the British Society of Allergy and Clinical Immunology. Clin Exp Allergy,
33, 1484–99.
Hepner DL, Castells MC (2003). Latex allergy: an update. Anesth Analg, 96, 1219–29.
081
Intra-arterial injection
Condition Unintentional intra-arterial injection of medication
can cause: paraesthesiae, pain, motor dysfunction,
compartment syndrome, gangrene and limb loss
Presentation Intense burning pain on injection; distal blanching;
blistering
Immediate action Stop injection, label cannula, flush with 0.9% sodium
chloride and maintain tissue perfusion
Follow-up action Anticoagulation and specialist referral
Investigations APTT
Also consider Extravasation
Dilution error of drug administered
Immediate management
Empirical, aimed at maintaining distal perfusion and symptomatic relief.
• Stop injecting and keep the cannula in situ, labelled clearly, and place an
IV cannula.
• If the drug administered was highly irritant, flush the vessel with 0.9%
sodium chloride or heparinised 0.9% sodium chloride and then maintain
cannula patency with slow infusion.
• Initiate anticoagulation with heparin (APTT 1.5–2) and discuss with
vascular surgeon.
• Administer LA via the cannula to reduce vasospasm and pain.
• Give analgesia.
• Administer a vasodilator (e.g. papaverine 40mg) through cannula or
consider prostacycline analogue (iloprost) IV.
• Once the immediate reaction has subsided, if the hand is well perfused
and pink, remove the cannula and apply sufficient pressure to the
puncture site to minimise local haematoma formation.
• Inform the patient of what has happened and document all actions
clearly.
Subsequent management
• To reduce pain, consider a sympathetic blockade (via stellate ganglion or
brachial plexus) or guanethidine block (consult a chronic pain specialist).
• Anticoagulation with heparin to reduce the risk of late arterial
thrombosis.
• Re-establishment of blood flow to extremity if necessary.
• Treat sequelae of tissue hypoperfusion (fasciotomy/amputation/skin
graft).
• Rehabilitation and follow-up.
091
Risk factors
• Type of LA:
• Short- vs long-acting
• Ester vs amide (prilocaine is an ester which is rapidly metabolised by
the liver with less risk of LA toxicity)
• Intrinsic vasoconstrictive effects (reduces systemic absorption and
thus improves safety, e.g. ropivacaine)
• Formulation (bupivacaine is a racemic mixture with the R-enantiomer
binding more firmly and released more slowly from the myocardium).
• Site of block: intercostal > central neuraxial > brachial plexus > SC.
• Single vs infusion/multiple dosing (i overall dose).
• Conduct of block: not visualising needle tip with ultrasound scanning,
overly firm pressure with probe causing compression of veins
preventing their identification, failure to aspirate causing inadvertent IV
administration; not using incremental dosing or test dose; performance
on anaesthetised patient rather than awake.
• Comorbidities: cardiac failure (susceptible to myocardial depressant),
liver disease (reduced metabolism), renal disease (reduced clearance).
• High-risk groups: elderly, paediatric and pregnant.
Presentation
• Light-headedness, dizziness, drowsiness, tingling around the lips and
fingers, or more generalised, metallic taste, tinnitus, blurred vision.
• Confusion, restlessness, incoherent speech, tremors or twitching,
leading to convulsions, with loss of consciousness and coma.
• Bradycardia, hypotension, CVS collapse and respiratory arrest.
• ECG changes (prolongation of QRS and PR interval, AV block and/or
changes in T-wave amplitude).
Local anaesthetic toxicity 1093
Immediate management
• Discontinue injection.
• Call for help.
• ABC and administer 100% O2.
• Intubation may be required to prevent hypoxic CVS collapse.
Hyperventilation may help by i pH in metabolic acidosis.
• CPR if pulseless—commence the ALS protocol (see % pp. 1055–7).
• Treat convulsions with IV:
• Midazolam 3–10mg
• Diazepam 5–15mg
• Lorazepam 0.1mg/kg
• Propofol 20–60mg
• Thiopental 50–150mg.
Fig. 39.5 Unanticipated difficult tracheal intubation. Reproduced from Difficult Airway
Society 2015 guidelines for management of unanticipated difficult intubation in adults. Difficult
Airway Society intubation guidelines working group, BJA, 115(6): 827–48 (2015) doi:10.1093/
bja/aev371. Permission for the use of these algorithms for commercial purposes must be sought
directly from Difficult Airway Society as they hold the copyrights.
Can’t intubate, can’t oxygenate 1095
Scalpel cricothyroidotomy
Equipment: 1. Scalpel (number 10 blade)
2. Bougie
3. Tube (cuffed 6.0mm ID)
This flowchart forms part of the DAS Guidelines for unanticipated difficult
intubation in adults 2015 and should be used in conjunction with the text.
Fig. 39.6 Can’t intubate, can’t oxygenate. Reproduced from Difficult Airway Society
2015 guidelines for management of unanticipated difficult intubation in adults. Difficult Airway
Society intubation guidelines working group, BJA, 115(6): 827–48 (2015) doi:10.1093/bja/aev371.
Permission for the use of these algorithms for commercial purposes must be sought directly from
Difficult Airway Society as they hold the copyrights.
0961
Malignant hyperthermia
(See also % pp. 322–3.)
Risk factors
• Family history.
• Exposure to suxamethonium or volatile agents (even if previous
exposures were uneventful).
• Heat stroke, exercise-induced rhabdomyolysis, central core disease.
• Some neuromuscular diseases have idiosyncratic MH-like reactions.
Diagnosis
• Sustained jaw rigidity after suxamethonium (masseter spasm).
• Unexplained i ETCO2 (IPPV) or i minute ventilation (SV), plus
unexplained i HR; accompanied, or followed, by an increasing core
temperature.
• Falling SpO2, despite i FiO2.
• CVS instability, dysrhythmias, especially multiple ventricular ectopics,
peaked T-waves on ECG.
• Generalised muscle rigidity.
Immediate management
Turn off volatile agent, stop giving suxamethonium
ABC
• Declare an emergency. Ask for help and dantrolene immediately.
• Hyperventilate with 100% O2, preferably not from the anaesthetic
machine containing volatile agent. Prepare an alternative method of
keeping the patient anaesthetised (e.g. propofol infusion).
• Ask the surgical team to conclude surgery as quickly as possible.
Malignant hyperthermia 1097
Dantrolene
• Give dantrolene 2.5mg/kg. Select dose based on actual body weight to
maximum 300mg per dose.
• Repeat dose every 10min until PaCO2 <6kPa and decreasing body
temperature. No cumulative ceiling dose. (Mortality associated with
insufficient dosing.)
Activated charcoal filters
• If available, place on inspiratory and expiratory limbs of the circle
breathing system.
Temperature
• Reduce temperature by exposing the patient, ice to the groin and
axillae, cold fluids and extracorporeal heat exchange if available.
Monitoring
• Check ABGs and K+, and correct acidosis/hyperkalaemia.
Subsequent management
• Place invasive monitoring (arterial line and CVP line).
• Send a clotting screen for DIC and serum CK assay.
• Promote diuresis with fluids and mannitol. Monitor for AKI.
• Avoid calcium channel blockers; treat arrhythmias with magnesium or
amiodarone or metoprolol.
• Will require HDU/ICU admission for at least 24h after resolution of
metabolic derangement.
• Monitor for recrudescence; likelihood increases with increasing
metabolic derangement during initial episode.
• Monitor for rhabdomyolysis and compartment syndrome.
• Refer to the MH investigation unit for follow-up.
Other considerations
• There are two formulations of dantrolene: Dantrium® 20mg (mixed
with 60mL of sterile water) and Ryanodex® 250mg (mixed with 5mL of
sterile water). Ryanodex® is currently unavailable in Europe. A 100kg
adult requires 12 ampoules of Dantrium® per dose.
• The use of visual aids for task prioritisation, such as prepared task cards
allocating roles, improves team performance during an MH crisis (see
M http://malignanthyperthermia.org.au/mh-task-cards/)
• Follow-up involves DNA testing for ryanodine receptor RYR1
mutations. If DNA negative, a muscle biopsy will be offered with in vitro
halothane and caffeine contracture tests.
• Beware of using bicarbonate to correct acidosis if the acidosis is
principally respiratory, since the reaction with H+ produces an i
CO2 load.
Anaesthesia for known or suspected MH-susceptible
patients
• MH patients should not be denied surgery solely because of MH.
• Preoperative questioning about personal and family anaesthetic history
is essential to identify potential MH patients.
• It is not essential to test suspected cases prior to surgery, provided
individual assessment has been made of the risks involved.
0981
Useful contact
UK MH Investigation Unit, Academic Unit of Anaesthesia, Clinical Sciences Building, St James’s
University Hospital, Leeds LS9 7TF. Emergency telephone number 07947 609601.
Chapter 40 1099
Regional anaesthesia
Mark Fairley
Fundamentals of safe practice 1100
Local anaesthetics and adjuncts 1102
Finding nerves 1104
Needle design 1108
Continuous regional anaesthesia 1108
Regional anaesthesia and coagulation disorders 1109
Regional anaesthesia and nerve injury 1112
Nerve blocks: central neuraxial blocks 1114
Nerve blocks: neck 1118
Nerve blocks: upper limb 1119
Nerve blocks: trunk 1128
Nerve blocks: lower limb 1135
Resources 1145
01
All trainees should focus on learning a small number of basic blocks that
cover the vast majority of surgical procedures. A proposed list of these
high-value basic blocks that all general trainees should learn has recently
been published1 (Table 40.1).
Regional anaesthesia fellowships and diplomas are formal training path-
ways added on to general training for those wanting advanced skills in
regional anaesthesia.
Personal audit
Regional anaesthetists should keep a record of the blocks they perform.
Difficulties encountered, success rates and complications should be re-
corded and should be both compared with available published data and dis-
cussed in an appraisal process. Lower success rates or higher complication
rates than are currently accepted, or any serious complications, should be
discussed with an appropriate colleague.
012
Drug Characteristics
Dexamethasone Prolongs long-acting LA block by 4–8h.4 Also has
similar effects when given IV. Possibly incompatible with
ropivacaine as crystallisation demonstrated in vitro. Can
increase blood sugar level. Dose 4mg
Clonidine Prolongs block by 1.5–2.5h.4 Effective in epidural,
caudal, spinal and peripheral nerve blocks. Use is limited
by hypotension, bradycardia and sedation. Dose 150
micrograms
Dexmedetomidine Prolongs block by 3–4h.4 Longer than clonidine, but not as
long as dexamethasone. i risk of sedation, bradycardia and
hypotension. Suggestion that it may cause more differential
block (sensory greater than motor) and may have some
neuroprotective effects. Dose 50–60 micrograms
Bicarbonate Added to reduce pain from SC injection and to increase
speed of onset by increasing pH of solution, and therefore
fraction of unionised LA. Add 1mL of 8.4% to every
10mL of lidocaine or 20mL of bupivacaine. Discard LA if
precipitate forms
Opioids Proven synergism with intrathecal and epidural LA. Beware
delayed respiratory depression with intrathecal morphine.
All opioids have been used. Of doubtful benefit in
peripheral blocks. Intrathecal remifentanil is contraindicated
due to the presence of glycine
Glucose Used to increase baricity of LA for intrathecal use.
Hyperbaric bupivacaine contains 80mg/mL of glucose.
Allows more consistent spread of block and provides the
opportunity to control spread by altering patient position
Hyaluronidase Used in eye blocks to enhance LA spread. Dose 15 units/mL
014
Finding nerves
Anatomical landmark techniques
The safe practice of regional anaesthesia is based on a detailed knowledge
of anatomy and its variations. Although most techniques based solely on
surface anatomy and the palpation of deeper structures have now been
superseded by PNS and ultrasound, several purely anatomical landmark-
based blocks are still effective and practical, e.g. spinal. Ultrasound and
PNS techniques still require good anatomical knowledge for their safe and
effective use.
Clicks, pops and loss of resistance
Some fascial plane techniques, e.g. fascia iliaca block, have relied upon the
sensation of a blunt or blunted needle passing through a fascial plane to
identify the correct anatomical location for injection. These ‘clicks’ and
‘pops’ take experience to appreciate and have a significant failure rate. With
ultrasound availability, most of these techniques have been superseded.
However, they still have a role where ultrasound is not available or not
practical. Loss of resistance has been used successfully for many decades to
identify the epidural space correctly and remains the technique of choice.
Paraesthesia
Direct contact between needle and nerve may result in an unpleasant ‘elec-
tric shock’ sensation that is felt in the distribution of the target nerve. This
is termed ‘paraesthesia’ and, before the introduction of nerve stimulation,
was often sought as confirmation of needle proximity to a nerve. With the
availability of PNS and ultrasound machines, paraesthesia is now seen as
an unnecessary needle–nerve contact that could potentially increase the
risk of nerve damage. However, in experienced hands and in the absence
of nerve stimulators and ultrasound machines, this technique may still be
effectively used.
Nerve stimulation
The use of nerve stimulators dominated the art of nerve location in the
final 20y of the last century and is still widely practised. The production of
evoked muscle contractions at low current levels (0.2–0.5mA) is thought
to confirm the placement of a needle near a nerve, while the production
of evoked contractions at very low current thresholds (<0.2mA) is thought
to indicate possible intraneural needle tip placement. If the target nerve
contains sensory fibres, the sensation may be unpleasant. The use of nerve
stimulators remains popular, either on their own, if no ultrasound machine
is available, or in combination with ultrasound. When used with ultrasound,
they can provide the anaesthetist with reassurance that the structure on the
screen is the target nerve, demonstrate twitches and functional anatomy to
educate trainees and, as an additional monitor, can help exclude intraneural
needle tip placement.
Finding nerves 1105
reimage the needle tip as it is advanced. OOP needling is popular for vas-
cular access as catheters need to be advanced along the long axis of the
vessel. IP needling is popular for most nerve blocks as the needle tip can
be imaged as it is advanced. Inexperienced ultrasound users are probably
safer using the IP needling technique. Experienced operators can use either
IP or OOP safely.
Developing skills
Manipulating the ultrasound probe and needle in 3D, while looking at the
2D image on the screen, can be a difficult skill to acquire. Some tips that can
accelerate your passage from novice to expert include:
• Get taught properly by experienced ultrasound users.
• Learn from all available media: online videos, mobile apps, ultrasound
and cadaver courses and phantoms, as well as books.
• Do not only practise when performing a block. Practise scanning
easily accessible aspects of yourself, colleagues and consented patients
whenever you can to become familiar with the knobology, probe
manipulation and identification of the sonoanatomy. Practise needle
imaging with commercially available or easily made phantoms or meat
models.
Using ultrasound
• Plan the ergonomics. Position yourself, your hands and the screen in a
line, so you can easily look from your needle and probe to the display.
This usually means the machine is on the opposite side of the patient.
Make sure you know which end of the probe corresponds to the left
and right side of the display.
• Make small, slow movements of the probe. Like a torch beam, a small
change in angle sweeps the beam through a large arc.
• Perform a prescan to identify the sonoanatomy; tilt the probe to make
the image of the nerve bright (anisotropy), then maintain that probe
tilt by holding the probe low and stabilising your hand on the patient.
Look at your hands and insert the needle from the near end of the
probe, making sure the needle trajectory is aiming along the centre of
the ultrasound beam. Once the needle has advanced under the probe,
look at the screen and slide (do not change the tilt) the probe slightly as
required to bring the needle into view.
• The needle needs to be in the 1mm-wide ultrasound beam to be
seen. Echogenic needles and needle imaging software can make a
needle image brighter but will not help if the needle is not in the
ultrasound beam!
• You should not advance the needle or inject if you cannot see its tip.
• Beware of obliquely imaged needles which will give a false tip
appearance. Ensure you can recognise an obliquely imaged needle.
• You should see the LA distending the tissues as soon as you inject the
first mL. If you do not, stop injecting as either you are not imaging your
needle tip or you may be in a compressed vessel.
Finding nerves 1107
Needle design
Many types of needle design are commonly used for regional anaesthesia,
whether PNBs or central neuraxial blocks.
• Long-bevelled needles (usually 10–15°) are sharp and pass readily
through tissues, without giving the operator a clear sensation of passage
of the needle through tissue planes and fascial layers. These are more
likely to enter nerves than short-bevelled needles; hence they are
rarely used.
• Short-bevelled needles (18–45°) are less likely to enter individual
nerves, making them safer. They also provide the operator with more
feel of the passage of the needle through fascial layers. They are
currently the most popular tips for PNBs.
• Pencil-point needles are popular for spinal anaesthesia, as they are
thought to separate the fibres of the dura mater, rather than cut them
as would a bevelled needle. They are associated with a lower incidence
of PDPH than the use of the bevelled alternative (often called the
Quincke-tip needle). Pencil-point needles are rarely used for PNBs as
they are too difficult to pass through intact skin and fascial planes.
• Tuohy needles were originally designed to allow epidural
catheterisation, but the tip design has also been adapted for use in
placing peripheral nerve catheters. They also provide a lot of resistance
to passing through fascial planes, enhancing the feel of ‘pops’ used in
some landmark techniques.
• Insulated needles are coated with a non-conducting material that allows
current flow only from a small area at the tip of the needle. This can
improve accuracy of nerve location with PNS.
• Echogenic needles have been designed to more effectively reflect
ultrasound waves, via geometric indentations on their shaft, enhancing
visibility, especially at steeper angles of insertion.
to a neurologist, nerve conduction studies, MRI and EMG can all assist
in the identification of the severity and location of the injury. There
is little that can be done to hasten the recovery of nerve function or
to minimise the extent of the nerve injury once harmed. If there is
acute compression from a haematoma, especially in the spinal canal,
urgent surgical decompression is indicated. If there is neuropathic pain,
appropriate antineuropathic pain medications should be prescribed.
• Recovery of neurological function is mercifully the norm. More than
90% of cases of neuropathy thought to have resulted from regional
anaesthesia recover within 3mo, and >99% within a year.10
Awake or asleep?
• PNBs are currently performed in awake, sedated or asleep patients.
Controversy exists as to whether performing blocks on anaesthetised
patients places the patient at i risk.
• In theory, awake patients may get symptoms of needle–nerve contact
and warn the anaesthetist before further needle advancement or
injection is performed, possibly averting nerve injury. Awake patients
may also complain of early symptoms of LA toxicity from inadvertent
intravascular injection, warning the anaesthetist to cease further
injection and possibly averting a major LAST event.
• However, needle–nerve contact and intraneural injection are known
to not always cause symptoms. Patient symptoms cannot therefore
be relied upon and other monitors of needle–nerve contact and
intraneural injection should be used. These are ultrasound visualisation
of intraneural needle tip placement, LA injection causing distension of
the nerve with separation of fascicles, low-threshold currents if using
a PNS, failure of evoked contraction disappearance on injection of
the LA and difficulty with injection/high injection pressure. Paediatric
anaesthetists argue that for most of their patients, ‘awake’ is not an
option; they are perhaps fortunate that the incidence of nerve damage
associated with PNBs in children is very low.
• The performance of PNBs on the non-anaesthetised patient need
not be unpleasant for the patient. Many anaesthetists successfully use
sedation with small doses of a benzodiazepine (e.g. midazolam) and/
or an opioid (e.g. fentanyl) or infusions of small amounts of propofol
or remifentanil. The increasing use of ultrasound for nerve location is
known to improve patient comfort if the evoked contractions produced
by nerve stimulators are avoided. It is therefore relatively easy to
perform ultrasound-guided blocks on patients who are lightly sedated.
• While there is currently no hard evidence to support either ‘awake’ or
‘asleep’ PNBs, it seems prudent to perform them in responsive patients
when possible.
(See also % p. 927.)
14
Absolute contraindications
• Local sepsis
• Patient refusal
• Anticoagulation (see % pp. 269–75).
Local anaesthetic drugs and doses for spinal anaesthesia
• Dosing of LA in adults depends upon age and pregnancy. The older
the patient, the less drug will be needed. This is thought to be due
to degenerative changes of the vertebral column and i sensitivity of
neural tissue to LA. Pregnant patients need less than their non-pregnant
counterparts, due to epidural vein engorgement compressing the
thecal sac.
• Bupivacaine 0.5% is usually used. ‘Heavy’ is hyperbaric and contains 8%
glucose. ‘Plain’ is isobaric at body temperature.
• Due to spread to the dependent part of the thoracic kyphosis in the
supine position, hyperbaric solutions can be used to achieve a higher
block and provide an ability to influence height with position changes of
the patient.
• A volume of 2.5–3.0mL of a hyperbaric solution of LA will reach
T6–T10 in most non-pregnant young adults placed in the recumbent
position shortly after spinal injection.
• Pregnant patients require less, often 1.8–2.2mL (see % p. 857).
• The volume of plain LA needed tends to be a little higher.
• Lidocaine is associated with a risk of cauda equina syndrome, transient
radicular irritation and transient neurological symptoms.
• Ropivacaine can be used but does not come in a ‘heavy’ preparation
and has a shorter duration of action than bupivacaine.
• Opioids are often added to improve the quality of the block. (See
% p. 1166; Table 41.9.)
• Ensure any drug preparations intended for intrathecal use do not
contain preservatives.
Clinical tips
• If there is difficulty at L3/4, ideally go down, not up, as the level of
termination of the conus is variable. Surface identification of the L3/
4 interspace is inaccurate; 70% of clinicians mark it as a higher space.
Ultrasound can be used to improve accuracy.
• A sitting position increases CSF pressure, and hence improves CSF flow
with fine needles. It is also easier to find the midline in obese patients in
this position.
• A lateral position offers patient comfort and the possibility of sedation.
• Problems are often due to the lumbar spine not flexed enough, or a
short introducer not inserted enough and a too flexible needle. When
difficulty is encountered in an elderly, osteophytic patient, consider a
22G Quincke-tip needle. PDPH is rare in this patient group.
• When hitting bone at a superficial level, this can only be the top of
spinous processes. This is a good sign that you are midline and need to
keep walking the needle cephalad or caudad.
16
• When hitting bone at a deep level, this is more likely to be lamina. Ask
the patient to identify on which side you are. If they can identify one
side, you are out of the midline and need to redirect to the opposite
side. If they state ‘middle’, you could be deep on a spinous process and
could continue walking cephalad or caudad, recheck landmarks or try
another level.
Complications
• Hypotension (due to sympathetic block), bradycardia (if block extends
to the mid-thoracic region): can progress to cardiac arrest.
• High block (compromising breathing, may extend to ‘total spinal’ with
loss of consciousness, apnoea and cardiorespiratory arrest).
• Urinary retention.
• Nerve damage (see % pp. 1112–13).
• PDPH (see % pp. 848–51).
• Infection: abscess, meningitis.
• Spinal canal haematoma: more likely in patients with disorders of
coagulation. Can cause spinal cord compression and permanent
paraplegia if not urgently decompressed with laminectomy.
• The serious complications of spinal and epidural anaesthesia have been
the subject of a nationwide audit in the UK—The RCoA’s 3rd National
Audit Project (NAP3) 2009. The incidence of permanent injury due
to neuraxial blocks was 1:25 000–1:50 000, with an incidence of death
or paraplegia of 1:50 000–1:140 000. The incidence of complications
in children, obstetric patients and those undergoing chronic pain
procedures was very low. There was an excess incidence of serious
complications in elderly patients with epidurals used during and after
surgery, and in patients undergoing CSEs, a finding supported by other
large studies (M http://www.rcoa.ac.uk/nap3).
Ultrasound for central neuraxial block
• Ultrasound for CNB is usually used to prescan the anatomy and
identify landmarks before performing the procedure. Ultrasound allows
identification of the midline, the accurate spinal level, an estimation of
the depth to the ligamentum flavum, the angle of insertion needed to
reach the space and the level with the widest interlaminar space for
needle passage. It can increase success and decrease technical difficulty,
the number of needle reinsertions and redirections and the risk of
traumatic procedures, and may therefore improve safety.11
• While this technique may not be of benefit to all patients, it may be
particularly useful in those with abnormal anatomy or in those whose
bony landmarks are not palpable. It is, however, a difficult skill in the
difficult patient (e.g. morbid obesity) where it is most useful. Practice is
required to become competent.
• Ultrasound can also be used as a teaching aid as it allows demonstration
of the anatomy by the instructor and confirmation to the student that
they have identified the correct insertion point and maximum depth to
insert the needle (Fig. 40.1).12
Nerve blocks: central neuraxial blocks 1117
Fig. 40.1 Low lumbar transverse interlaminar sonoanatomy. Erector spinae (E),
psoas (P), interspinous ligament, facet joints and vertebral body (tan), posterior and
anterior complexes (orange), spinal canal (yellow). Courtesy of Mark Fairley.
Fig. 40.2 Cervical plexus sonoanatomy. Cervical plexus (yellow), carotid artery
(red), internal jugular vein (blue), C5 transverse process (tan), muscles (burgundy),
C5 nerve root (R), SCM (S), needle path (white line), LA spread (cyan). Courtesy of
Mark Fairley.
Fig. 40.3 Interscalene brachial plexus sonoanatomy. C5 (5), C6 (6), C7 (7) roots
(yellow), carotid artery (C), internal jugular vein (J), vertebral artery and vein (V), C7
transverse process (tan); muscles (burgundy), scalenus anterior (A), scalenus medius
(M), phrenic nerve (P), needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
Tips Colour-flow Doppler is advised to identify all vessels close to, or passing
through, the plexus. Avoid in patients with severe respiratory disease and
contralateral phrenic nerve palsy because of risk of phrenic nerve block.
Injection should include the angle between the artery and the 1st rib (the
‘corner pocket’) to increase success rate of blocking the lower trunk. The
suprascapular nerve (needed for shoulder coverage) has often just left the
plexus at this level and may be seen travelling posterolaterally under the
omohyoid.
Infraclavicular paracoricoid brachial plexus block
Indications Analgesia or anaesthesia for elbow, wrist or hand.
Positioning Supine with the arm adducted and resting by the side.
Ultrasound The ultrasound probe should be positioned in a parasagittal
plane just medial to the coracoid process. Deep to the pectoralis muscles,
the axillary artery is seen cephalad to the vein, with the lateral, medial and
posterior cords around the axillary artery. The cords of the brachial plexus
can be deep and difficult to visualise. Using an IP technique from cephalad,
the needle tip should be advanced until it lies posterior to the artery
(Fig. 40.5).12
Volume 20–30mL.
Side effects Nil.
Complications Vascular puncture, intravascular injection, pneumothorax.
Tips Never angle the needle medially as this can increase the risk of
pneumothorax.
Axillary brachial plexus block
Indications Anaesthesia for hand surgery; analgesia for forearm, wrist or
hand surgery.
Positioning Supine with the arm abducted to 90°.
Ultrasound The ultrasound probe should be positioned high in the axilla
along the axillary crease, imaging the axillary artery in short axis. Three
nerves sit adjacent to the artery. The median nerve is usually superficial and
anterior, the ulnar nerve superficial and posterior, the radial nerve deep and
posterior. The musculocutaneous nerve is more anterior, most commonly
in the plane between the biceps and the coracobrachialis, or in the body of
the coracobrachialis (Fig. 40.6).12
Fig. 40.6 Axillary brachial plexus sonoanatomy. Median nerve (M), ulnar nerve (U),
radial nerve (R), musculocutaneous nerve (Mc), axillary artery and compressed veins
(red, blue), humerus (tan), coracobrachialis (C), triceps (T), needle path (white), LA
spread (cyan). Courtesy of Mark Fairley.
Volume 10mL.
Complications Vessel puncture.
Tips Needle can be inserted from cephalad or caudad end of probe.
Intercostobrachial nerve block
Indications Anaesthesia of skin to upper medial arm. Commonly added
to brachial plexus blocks for vascular surgery at ACF that may extend
proximally to medial aspect of arm or for tourniquet tolerance.
Positioning Arm abducted 90°.
Ultrasound Place probe transversely in axillary crease to image axillary
vessels. Slide probe posteriorly, placing vessels on anterior edge of image.
Insert needle IP from anterior to infiltrate from vessels posteriorly and
superficial to deep fascia of arm (superficial to muscles). Nerve not easily
identified. Infiltrate plane and surround any nerve-like structures.
Landmark technique Palpate axillary artery in axillary crease. Perform SC
infiltration from artery posteriorly.
Complications Vessel puncture.
Tips Intercostobrachial nerve block can also be achieved via a high
superficial serratus anterior plane block; however, more volume will be
required.
Median, ulnar and radial nerve blocks in the forearm
Indications Anaesthesia or analgesia of hand.
Positioning Supine with arm abducted 90°.
Ultrasound Allows these nerves to be blocked anywhere along their course
from the axilla to the wrist.
Nerve blocks: upper limb 1125
Median nerve Commonly traced proximally from carpel tunnel and blocked
mid forearm between superficial and deep flexor digitorums. Alternatively,
in the ACF, it sits medial and slightly deep to the brachial artery between
the brachialis and pronator teres. In the medial aspect of the upper arm, it
is superficial, adjacent to the brachial artery (Fig. 40.9).12
Fig. 40.9 Median nerve mid-forearm sonoanatomy. Median nerve (yellow), ulnar
and radial arteries (red), ulnar and radius (tan), deep flexor digitorum (D), superficial
flexor digitorum (S), flexor carpi radialis (F), needle path (white), LA spread
(cyan). Courtesy of Mark Fairley.
Radial nerve Commonly blocked in lateral aspect of distal upper arm where
it leaves the spiral groove of the humerus and travels in the plane between
the brachialis and brachioradialis before dividing into superficial and deep
branches around the level of the lateral epicondyle of the humerus (Fig.
40.10).12
Fig. 40.10 Radial nerve ACF sonoanatomy. Radial nerve (yellow), brachial artery
(red), cephalic and cubital veins (blue), brachioradialis (Br), brachialis (B), needle path
(white), LA spread (cyan). Courtesy of Mark Fairley.
Ulnar nerve Commonly traced up from the medial wrist where it is found
adjacent to the ulnar artery. The nerve and artery separate from each
other two-thirds of the way up the forearm, which is a commonly blocked
location. Alternatively, in the medial aspect of the upper arm, it is superficial
and posterior to the brachial artery and median nerve where it courses with
the ulnar collateral vessels before passing deep towards the cubital tunnel
of the elbow (Fig. 40.11).12
216
Fig. 40.11 Ulnar nerve mid-forearm sonoanatomy. Ulnar nerve (U), ulnar artery
(red), ulnar (tan); deep flexor digitorum (D), superficial flexor digitorum (S), flexor
carpi ulnaris (F), median nerve (M), needle path (white), LA spread (cyan). Courtesy
of Mark Fairley.
Landmark technique
Median nerve Position the patient with their arm slightly abducted, elbow
slightly flexed and forearm supinated. Feel the brachial artery at the
antecubital fossa crease. The median nerve lies medial and deep to the ar-
tery. A pop may be felt on passing through the fascial plane to reach the
nerve. It usually lies at 1–2cm depth.
Radial nerve Position as above. Radial nerve lies between the insertion of
the biceps and brachioradialis, proximal to the flexor crease in the ACF. It is
slightly deeper than the median nerve at 2–4cm depth.
Ulnar nerve The elbow should be slightly flexed, with the arm abducted
at the shoulder and externally rotated to expose the ulnar groove at the
elbow, or with the hand on the contralateral shoulder and arm across the
chest. The ulnar nerve lies in the groove between the medial epicondyle of
the humerus and the olecranon process. Pressure neurapraxia may develop
from blocking at the groove, so the point of injection is often 2–3cm
proximal to this, at a depth of 1–3cm.
PNS twitches
Radial Thumb, wrist or finger extension.
Ulnar Adduction of the thumb, little finger flexion.
Median Finger and wrist flexion and pronation of the wrist.
Volume 5mL per nerve.
Complications Artery puncture.
Wrist block
Indications Analgesia or anaesthesia for hand surgery.
Landmark technique
Median nerve Passes between the palmaris longus (look for the tendon
in the middle of the wrist when clenching the fist and flexing the wrist)
and the flexor carpi radialis. Inject 2–3cm proximal to the wrist creases, at
71cm depth
Nerve blocks: upper limb 1127
Ulnar nerve Runs between the ulnar artery and flexor carpi ulnaris, deep to
both. Inject 1–2cm proximal from the wrist creases from the ulnar side of
the wrist towards the radius underneath the flexor carpi ulnaris, 1cm depth.
Radial nerve Becomes SC 3–5cm proximal to wrist joint. Can be blocked by
infiltrating SC 72–3cm proximal to the anatomical snuffbox at the base of
the thumb over the dorsum of the radius.
Tips Avoid median nerve block and wrist block in patients with carpal tunnel
syndrome.
Digital (ring) block
Indications Distal finger or toe surgery.
Landmark technique The nerves run on either side of the phalanges, two on
the palmar side and two on the dorsal side of each finger.
• Insert a 25G needle just distal to the metacarpophalangeal joint from
the dorsal side (less painful), past the proximal phalanx on either side of
the finger to be blocked.
• Inject 2–4mL of LA (non-adrenaline-containing) on either side, while
withdrawing the needle.
Complications Vascular puncture, digital ischaemia.
Intravenous regional anaesthesia—Bier’s block
Indications Anaesthesia for superficial arm surgery or fracture reduction.
Maximum operation length limited to about 30min. Can be used for
lower limb.
Technique Measure the patient’s BP. Insert one IV cannula into the limb
requiring surgery, and one into another limb. Apply a double-or single-
cuff tourniquet to the upper arm. Reliable arterial compression cannot be
obtained over the forearm as vessels will be held open between the radius
and ulna. The limb should be exsanguinated with a compression bandage or
by elevation if fractured. The cuff should then be inflated to 50–100mmHg
above the patient’s systolic BP. A non-adrenaline-containing LA with low
systemic toxicity, such as prilocaine 0.5%, should be used. Inject slowly:
40mL for small, 50mL for medium and 60mL for a large arm. Alternatively,
lidocaine 0.5% can be used, maximum dose 250mg. Other LAs are not
appropriate. The patient should be warned that the arm will begin to feel
warm and appear mottled. Surgery can start within a few minutes. On no
account should the tourniquet cuff be deflated before 15min for prilocaine
and 20min for lidocaine. Potentially devastating systemic toxicity can occur if
large volumes of LA are released before it becomes bound or metabolised.
If tourniquet pain is experienced during the procedure and a double cuff
is used, the distal cuff can be inflated before deflating the proximal cuff.
The tissue under the distal cuff should be anaesthetised at this stage. The
technique is contraindicated if pre-existing circulatory difficulties, e.g. crush
injury, homozygous SCD, peripheral vascular disease. A reliable tourniquet
and resuscitation equipment are essential.
Complications LAST.
218
Fig. 40.12 Thoracic paravertebral sagittal view. Pleura and lung (pink), superior
costotransverse ligament (orange), transverse processes (superficial, tan) rib necks
(deep, tan), trapezius (T), erector spinae (E), needle path (white), LA spread
(cyan). Courtesy of Mark Fairley.
Volume 20–30mL.
Complications Pneumothorax, LA toxicity, sympathetic block, epidural
spread.
Tips Can be performed bilaterally and at multiple levels.
A useful option if paravertebral considered too difficult.
Pectoserratus plane (PSP) and interpectoral plane (IPP)
blocks
Indications Analgesia to breast, axilla, pectoral muscles and anterolateral
chest wall.
Positioning Supine with arm abducted 45–90°.
Nerve blocks: trunk 1131
Fig. 40.15 PSP and IPP sonoanatomy. Pleura and lung (pink), ribs (tan), pectoralis
major (PM), pectoralis minor (Pm), serratus anterior (S), needle path (white), LA
spread (cyan). Courtesy of Mark Fairley.
Volume 20–30mL.
Side effects Some surgeons have objected to PSP and IPP for breast cancer
surgery as LA tracks to the axilla, distorting fascial planes and there is a risk
of needle trauma to malignant nodes.
Complications Vessel puncture, pneumothorax, LAST.
Tips IPP block involves placing LA between the pectoralis major and minor
only. This only blocks the medial and lateral pectoral nerves innervating the
pectoral muscles. Useful for breast implants or pacemaker insertions that
are deep to pectoralis major. PSP and IPP also blocks the lateral cutaneous
branches of the intercostal nerves, providing analgesia to the anterolateral
chest wall, the intercostobrachial nerve innervating the axilla and the long
thoracic nerve innervating the serratus anterior.
Ilioinguinal and iliohypogastric block
Indications Analgesia for inguinal hernia, orchidopexy or hydrocele surgery.
Positioning Supine.
Ultrasound The ilioinguinal and iliohypogastric nerves are branches of the
lumbar plexus. The nerves run initially in the TAP before piercing first the
internal oblique (IO) and then the external oblique (EO) muscles to provide
sensory innervation over the lower abdomen and upper thigh. Ultrasound
can be used to identify the correct planes, or it may be possible to locate
specific nerves. Place the probe between the ASIS and the umbilicus, and
scan caudally. Blood vessels may lie with the nerves and aid in identification.
Use an IP technique with the needle from either end of the probe. The
nerves most commonly lie between the transversus abdominis (TA) and IO,
but variations are common (Fig. 40.16).12
312
Fig. 40.16 Ilioinguinal and iliohypogastric nerves sonoanatomy. External oblique (E),
internal oblique (I), transversus abdominis (T), iliacus (IL), ilium (tan), peritoneum
(green), ilioinguinal and iliohypogastric nerves (yellow), needle path (white), LA
spread (cyan). Courtesy of Mark Fairley.
Fig. 40.19 Suprainguinal fascia iliaca sonoanatomy. Fascia iliaca (orange), deep
circumflex iliac vessels (red, blue), anterior inferior iliac spine (tan), internal oblique
(IO), sartorius (S), iliacus (I), needle path (white), LA spread (cyan). Courtesy of Mark
Fairley.
316
Fig. 40.20 Femoral nerve sonoanatomy. Femoral nerve (yellow), femoral artery
and vein (red, blue), fascia iliaca (orange), iliopsoas (IP), pectineus (P), needle path
(white), LA spread (cyan). Courtesy of Mark Fairley.
PENG block
Indications Analgesia of hip joint. This is a new block still needing clinical
trials to clarify indications.
Ultrasound Place transverse probe over ASIS. Scan caudally and medially a
few cm to image the anterior inferior iliac spine. Rotate medial end of probe
45° and tilt caudally to image the ilium from the anterior inferior iliac spine
to the iliopubic eminence as a continuous hyperechoic line. Too distal and
the femoral head and joint space will be imaged. Identify femoral vessels and
femoral nerve. Psoas tendon is often seen as a hyperechoic area deep in
psoas muscle. Insert needle from lateral end of probe. Target is plane deep
to psoas and psoas tendon immediately anterior to bone between anterior
inferior iliac spine and iliopubic eminence (Fig. 40.21).12
Volume 10–20mL.
Complications Vessel puncture, femoral nerve injury, bladder or ureter injury.
Tips If the femoral head is imaged, you are too distal and need to slide
the probe proximally to image the ilium from anterior inferior iliac spine to
iliopubic eminence.
Lateral femoral cutaneous nerve
Indications Analgesia for incisions on lateral thigh.
Ultrasound Place the probe transversely just distal to the ASIS and slide a
few cm caudally. Identify the sartorius medially as the most superficial, more
echogenic, boat-shaped muscle. Laterally is the tensor fascia lata. Superficially
between the two is often a small, triangular, fat-filled compartment containing
the small hyperechoic nerve. The nerve often divides as it is traced distally and
usually runs superficial to the sartorius as it is traced proximally. The needle
can be passed IP from the lateral end of the probe or OOP (Fig. 40.22).12
Landmark technique The nerve runs under the inguinal ligament, just
medial to the ASIS and superficially over the sartorius muscle. The nerve
can be blocked 2cm medial and 2cm caudal to the ASIS. Insert the needle
perpendicular to the skin to a depth of 1–3cm, until you feel the needle pass
through the fascia lata, and inject here.
318
Fig. 40.22 Lateral femoral cutaneous nerve sonoanatomy. Sartorius (S), tensor
fascia lata (T), rectus femoris (R), lateral femoral cutaneous nerve (yellow), fat-
filled triangular fascial compartment (orange), needle path (white), LA spread
(cyan). Courtesy of Mark Fairley.
Volume 5–10mL.
Complications Nerve injury.
Tips If you are unable to visualise the nerve, you can infiltrate the plane
superficial to the sartorius, just distal to the ASIS where the nerve
usually runs.
Subgluteal sciatic nerve block
Indications Rarely indicated as more distal block usually preferred. Analgesia
for ankle or foot surgery, or for lower limb amputation. Combined with
femoral nerve block for analgesia of the leg.
Ultrasound Place a curvilinear probe midway between the greater
trochanter and ischial tuberosity in an oblique transverse orientation.
Identify the gluteus maximus superficially, the greater trochanter laterally,
the ischial tuberosity medially and the quadratus femoris deep. The sciatic
nerve is usually a flattened hyperechoic structure in the fascial plane joining
these two bony landmarks deep to the gluteus maximus, superficial to the
quadratus femoris. Nerve stimulation is helpful in confirming nerve location.
IP needle from lateral side (Fig. 40.23).12
Fig. 40.23 Subgluteal sciatic sonoanatomy. Sciatic nerve (yellow), gluteus maximus
(G), quadratus femoris (Q), femur (F), ischium (I), needle path (white), LA spread
(cyan). Courtesy of Mark Fairley.
Nerve blocks: lower limb 1139
Fig. 40.24 Popliteal sciatic sonoanatomy. Tibial nerve (T), common peroneal nerve
(C), popliteal artery and vein (red, blue), biceps femoris (B), semimembranosus (S),
needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
410
Landmark technique Lateral approach, supine, with the knee slightly flexed,
mark the groove between the vastus lateralis (above) and biceps femoris
(below). Draw a line down from the superior border of the patella where
it crosses this groove. Insert a 22G 100mm needle, directed posteriorly
25–30° and slightly caudally. The needle passes through the biceps femoris
into the popliteal fossa, initially encountering the common peroneal nerve,
then the tibial nerve.
PNS twitches Common peroneal nerve, f oot dorsiflexion and eversion; tibial
nerve, foot plantarflexion and inversion.
Volume 20mL.
Tips If this junction location is too deep and imaging poor (due to obesity),
the nerves can be blocked more distally where they are more superficial
and easily imaged as two separate nerves. Branches to the sural nerve may
have come off and be missed if too distal. Anisotropy is prominent with
these nerves; tilt probe to maximise brightness of nerve.
Saphenous nerve block
Indications Provides analgesia for the medial lower leg and ankle.
Usually combined with popliteal sciatic to complete coverage of lower
leg and ankle.
Ultrasound The saphenous nerve is small and difficult to image in the leg. The
adductor canal block is therefore usually performed.
Landmark technique The patient should be supine, with the leg externally
rotated. Identify the tibial tuberosity and inject 10–15mL SC from the tibial
tuberosity towards the medial tibial condyle.
Adductor canal and distal femoral triangle blocks
Indication Usually performed to achieve saphenous nerve and nerve to
vastus medialis block for total knee replacement or combined with popliteal
sciatic to complete lower leg coverage.
Positioning Supine with hip slightly flexed and externally rotated.
Ultrasound Place probe transversely over anteromedial aspect of mid thigh.
Identify the femoral artery with the sartorius muscle superficial to it. The
sartorius is usually a small, boat-shaped muscle slightly more echogenic
than other muscles. The target is the area lateral to the artery deep to the
vasoadductor membrane (bright fascial plane between the sartorius and
the artery). The saphenous nerve is sometimes able to be visualised in this
location. Pass the needle IP from the lateral end of the probe (Fig. 40.25).12
Volume 10mL.
Complications Artery puncture.
Tips Ensure LA spreads deep to vasoadductor membrane lateral to artery.
Usually performed at mid thigh level which is usually a distal femoral triangle
block. Sliding more distally becomes an adductor canal block which blocks
saphenous nerve only.
Nerve blocks: lower limb 1141
iPACK block
Indication Posterior capsule analgesia for total knee replacement, often
combined with distal femoral triangle or adductor canal block for motor-
sparing analgesia.
Positioning Supine, hip flexed and externally rotated, knee slightly flexed.
Ultrasound Place curvilinear probe over medial aspect of distal thigh
just above level of proximal patella. Identify femur and popliteal artery.
Target plane is between artery and femur. Slide probe posteriorly into a
posteromedial location, so needle trajectory is parallel to posterior surface
of femur. Insert needle from medial end of probe, and advance between
femur and popliteal artery until 2cm lateral to artery. Inject a few mL here
and remainder while withdrawing to infiltrate plane between artery and
femur (Fig. 40.26).12
Fig. 40.26 iPACK block sonoanatomy. Femur (tan), popliteal artery and vein (red,
blue), sartorius (S), semimembranosus (Sm), biceps femoris (B), vastus medialis (V),
needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
Volume 10–20mL.
Complications Artery puncture, tibial or common peroneal nerve block.
Tips Easily combined with distal femoral triangle or adductor canal block.
412
Ankle block
Indications Analgesia or anaesthesia to the foot.
Positioning Depending on the nerve to be blocked, position as convenient in
figure 4 position, supine or lateral.
Ultrasound
• The tibial nerve is blocked first due to slowest onset. Place probe
proximal to medial malleolus between tibia and Achilles tendon. Identify
posterior tibial artery and veins. The tibial nerve usually lies posterior to
vessels lying on the flexor hallucis longus muscle and sheath. The flexor
hallucis longus tendon within the muscle should not be confused with
the nerve. Trace these structures proximal and distal to confirm their
identity. Pass needle IP from posterior end of probe (Fig. 40.27).12
Fig. 40.27 Tibial nerve ankle sonoanatomy. Tibial nerve (yellow), posterior tibial
artery and veins (red, blue), great saphenous vein (S), tibialis posterior tendon (T),
flexor digitorum longus (D), flexor hallucis longus (H), tibia medial malleolus (tan),
needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
• The saphenous nerve is usually the most difficult to image. Place the
probe transversely over the anteromedial ankle with light pressure (or
use a tourniquet) to identify the greater saphenous vein. Slide the probe
proximally and distally on the vein to identify the saphenous nerve
running in close proximity. It may be divided around the vein. Pass the
needle from the posterior end of the probe to surround the vein if
nerve not identified (Fig. 40.28).12
Fig. 40.28 Saphenous nerve ankle sonoanatomy. Tibia medial malleolus (tan),
posterior tibial vessels and tibial nerve (P), great saphenous vein (S), saphenous nerve
(yellow), flexor digitorum longus (D), tibialis posterior (T), flexor hallucis longus (H),
needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
Nerve blocks: lower limb 1143
Fig. 40.29 Deep peroneal nerve ankle sonoanatomy. Tibia (tan), deep peroneal
nerve (yellow), anterior tibial artery and veins (red and blue), tibialis anterior (T),
extensor hallucis longus (H), extensor digitorum longus (D), needle path (white), LA
spread (cyan). Courtesy of Mark Fairley.
Fig. 40.30 Superficial peroneal nerve sonoanatomy. Fibula (tan), tibialis anterior (T),
extensor digitorum longus (D), peroneus longus and brevis (P), superficial peroneal
nerve (yellow), needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
41
• The sural nerve can be blocked by placing the probe transversely over
the posterolateral leg just proximal to the lateral malleolus. Identify
the peroneus brevis anteriorly, the Achilles tendon posteriorly and the
lessor saphenous vein in the fascial plane between them. Use light probe
pressure to avoid squashing the vein. The nerve is difficult to see but is
usually near the vein. The nerve can be traced from mid-posterior calf
where it exits the deeper planes between the medial and lateral heads
of the gastrocnemius and then travels laterally in the SC tissues towards
the lateral malleolus. Pass the needle IP from anterior or posterior,
surrounding the vein if nerve not seen (Fig. 40.31).12
Fig. 40.31 Sural nerve ankle sonoanatomy. Fibula (tan), peroneus brevis (P), flexor
hallucis longus (H), soleus (S), lesser saphenous vein (blue), sural nerve (yellow),
needle path (white), LA spread (cyan). Courtesy of Mark Fairley.
Resources
Illustrations
• Sensory innervation (Figs. 40.32–40.35)
• Cutaneous dermatomes (Fig. 40.36).
Websites
• American Society of Regional Anesthesia and Pain Medicine (ASRA).
M https://www.asra.com/
• European Society of Regional Anaesthesia and Pain Therapy (ESRA).
M https://esraeurope.org/
• New York School of Regional Anesthesia (NYSORA).
M https://www.nysora.com/
• Regional Anaesthesia United Kingdom (RA-UK).
M https://www.ra-uk.org/
• Ultrasound for Regional Anesthesia. M http://www.usra.ca
Mobile applications
• AnSo Anaesthesia Sonoanatomy. Sumo Enterprises Pty Ltd. 15-1-2020.
Version 1.1. Apple App Store. M https://apps.apple.com/au/app/
anso-anaesthesia-sonoanatomy/id1202779264
• Regional anesthesia Reference. University of Washington. 6-3-20. Version
2.1.1. Apple App Store. Google Play. M https://play.google.com/
store/apps/details?id=com.awalters.regionalanestheiaatlas&hl=en
• Echo Blocks. WaveWeb. 6-3-20. Version 1.0.5. Apple App Store.
M https://waveweb.pt/echoblocksapp/
YouTube channels
• Ki-Jinn Chin. M https://www.youtube.com/channel/
UC8oN4lw8d7uGzhARRrGZjiQ
• Vicente Roqués Escolar. M https://www.youtube.com/channel/
UCd6XscTpV0qK4DDEvfM3saQ
• LSORA Videos. M https://www.youtube.com/channel/UCV8d6B_
W6KmPoL_bWXeYiqQ
References
1 Turbitt LR, Mariano ER, El-Boghdadly K (2020). Future directions in regional anaesthesia: not just
for the cognoscenti. Anaesthesia, 75, 293–7.
2 Neal JM, Brull R, orn J-L, et al. (2016). The Second American Society of Regional Anesthesia and
Pain Medicine evidence-based medicine assessment of ultrasound-guided regional anesthesia:
executive summary. Reg Anesth Pain Med, 41, 181–94.
3 Neal JM (2016). Ultrasound-guided regional anesthesia and patient safety update of an evidence-
based analysis. Reg Anesth Pain Med, 41, 195–204.
4 Desai N, Albrecht E, Ei-Boghdadly (2019). Perineural adjuncts for peripheral nerve block. BJA
Educ, 19, 276–82.
5 Marhofer P, Harrop-Griffiths W, Kettner SC, Kirchmair L (2010). Fifteen years of ultrasound
guidance in regional anaesthesia: Part 1. Br J Anaesth, 104, 538–46.
6 Ilfeld BM (2017). Continuous peripheral nerve blocks: an update of the published evidence and
comparison with novel, alternative analgesic modalities. Anesth Analg, 124, 308–35.
7 Horlocker TT, Vandermeuelen E, Kopp SL, et al. (2018). Regional anesthesia in the patient re-
ceiving antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and
Pain Medicine Evidence-Based Guidelines (Fourth Edition). Reg Anesth Pain Med, 43, 263–309.
8 Tsui BCH, Kirkham K, Kwofie MK, et al. (2019). Practice advisory on the bleeding risks for periph-
eral nerve and interfascial plane blockade: evidence review and expert consensus. Can J Anesth,
66, 1356–84.
416
9 Working Party; Association of Anaesthetists of Great Britain & Ireland; Obstetric Anaesthetists'
Association; Regional Anaesthesia UK (2013). Regional anaesthesia and patients with abnormal-
ities of coagulation: the Association of Anaesthetists of Great Britain & Ireland The Obstetric
Anaesthetists' Association Regional Anaesthesia UK. Anaesthesia, 68, 966–72.
10 Lalkhen AG, Bhatia K (2011). Perioperative peripheral nerve injuries. Contin Educ Anaesth Crit
Care Pain, 12, 38–42.
11 Perlas A, Chaparro LE, Chin KJ (2016). Lumbar neuraxial ultrasound for spinal and epidural anes-
thesia. Reg Anesth Pain Med, 41, 251–60.
12 Sumo Enterprises Pty Ltd. AnSo Anaesthesia Sonoanatomy. 15-1-2020. Version 1.1. Apple App
Store. M https://apps.apple.com/au/app/anso-anaesthesia-sonoanatomy/id1202779264
Declaration of interest
The author is the producer of the AnSo Anaesthesia Sonoanatomy mobile application.
Fig. 40.35 Leg sensory innervation. Copyright American Society of Regional Anesthesia
and Pain Medicine. Used with permission. All rights reserved.
Resources 1149
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C4 C8
C5 T1
T2
T1 T3
T2 T4
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T2 T3 T6
T4 T7
T3 T9
T4 T5 T9
T6 T10
T5 T11
T6 T7 T12
T7 T9 L1
T8 T9 L2
T9 L3
L1 T10 L4
T10 T11
L2 T11 L5
L3 T12 S1
L4 T12 S2
L1 S4
S2 S1 C5 S2 S3 S5
C7 C8 L2
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L5
Acute pain
Adrian Dashfield
Introduction 1152
Analgesic drugs 1155
Patient-controlled analgesia 1162
Epidural analgesia 1164
Continuous peripheral nerve blockade 1167
Abdominal wall blocks 1168
Stimulation-produced analgesia: transcutaneous electrical nerve
stimulation and acupuncture 1169
Non-opioid adjuvant analgesic drugs 1170
Long-term opioid use and the opioid-dependent patient 1176
Specific patient groups 1179
David Kibblewhite
Persistent pain patients in acute pain 1173
512
Introduction
Problems with inadequate acute pain management
Kehlet1 identified the aim of postoperative pain relief was firstly to provide
subjective comfort, secondly to reduce the magnitude of the surgical stress
response and thirdly: ‘to enhance restoration of function by allowing the
patient to breathe, cough and move easily’. Severe postoperative pain and
the stress response to surgery cause i morbidity and mortality.
• CVS: tachycardia, hypertension and i peripheral vascular resistance
cause i myocardial O2 consumption/demand and myocardial ischaemia.
Altered regional blood flow (sympathetic stimulation), reduced mobility,
venous stasis and i clotting cause venous thrombosis.
• Respiratory system: abdominal/thoracic pain results in diaphragmatic
splinting and weakened cough. Reduction in lung volumes, atelectasis
and sputum retention cause chest infections and hypoxaemia.
• GI: delayed gastric emptying and reduced intestinal motility. This can be
a direct effect of pain or as a side effect of opioids and surgery.
• Genitourinary: urinary retention.
• Metabolic/endocrine: release of vasopressin, aldosterone, renin,
angiotensin, cortisol, glucagon, growth hormone and catecholamines
and reduction in insulin and testosterone lead to i protein breakdown,
impairment of wound healing/immune function, Na+ and water
retention, i fibrinogen and platelet activation and i metabolic rate.
• Chronic pain: there is increasing evidence that patients who suffer from
acute pain are more likely to develop chronic pain.
• Psychological: poor acute pain management can lead to patient anxiety,
sleeplessness, fatigue and distress well into the postoperative period.
• Cancer survival: surgical stress produces an environment that favours
tumour growth and metastasis.
• Despite these insights, there remains compelling evidence that pain
after surgery is often poorly managed, and up to 40% of patients report
severe pain that negatively impacts on their recovery.2
Measurement of pain
Verbal rating scales Stratify pain intensity according to commonly used
adjectives such as ‘mild’, ‘moderate’ and ‘severe’. They are widely applied
and easy for patients to use. The semiquantitative nature makes them less
suitable for research purposes.
Numerical rating scales Take the two extremes of the pain experience and
have a numerical scale in between ‘no pain’ and ‘worst imaginable’, for
example. These scales are robust, reproducible and easy for patients to
understand. A disadvantage is that a digital scale reduces the capacity to
detect subtle changes, as the digits act as anchoring points.
Visual analogue scales Similar to numerical rating scales, with two extremes
of the pain experience on either end of the scale. The patient is asked to
mark across a line of standard length (usually 100mm). The distance along
this line is used. The continuous data generated make analysis easier than
with verbal or numerical rating scales.
Introduction 1153
1154
Chapter 41
Acute pain
Analgesic drugs
Paracetamol
The action of paracetamol is via a number of central mechanisms, including
effects on prostaglandin production and serotonergic, opioid, NO and can-
nabinoid pathways. Analgesic and antipyretic, without anti-inflammatory
activity. Excreted renally after glucuronide and sulphate conjugation in the
liver. A hepatotoxic metabolite N-acetyl-p-benzoquinoneimine is normally
inactivated by conjugation with hepatic glutathione. In paracetamol over-
dose, this pathway is overwhelmed, leading to hepatic cell necrosis. Toxicity
may occur in certain patients, even within the recommended dose range,
because of altered metabolism.
• Usually given PO or PR, but available as an IV preparation. Particularly
effective when administered IV.
• Recommended dose 4g/d in adults. Most effective when prescribed
regularly, rather than PRN. The MHRA licensed dose of paracetamol
is the same for all routes of administration in adults over 50kg. In
July 2010, the MHRA issued a Drug Safety Update for dosing IV
paracetamol in neonates, infants and children, following a number of
cases of accidental overdose. The dose in children weighing ≤10kg is
now 7.5mg/kg (>10kg: 15mg/kg).
Non-steroidal anti-inflammatory drugs
Analgesic, anti-inflammatory, antiplatelet and antipyretic actions are due to
inhibition of the enzyme COX, and consequently the synthesis of prosta-
glandins, prostacyclins and thromboxane A2 from arachidonic acid.
• Two types of COX: C OX-1 is normally present in the kidney, GI
mucosa and platelets where prostaglandin contributes to normal organ
function. COX-2 is associated with inflammatory mediators following
tissue damage. COX-2 inhibitors may be associated with fewer adverse
effects than COX-1.
• NSAIDs have some central, as well as peripheral, activity. Absorption
from the upper GI tract is rapid. Metabolised in the liver, excreted in the
kidney.
• Opioid-sparing effect of between 20% and 40%. May be used as the
sole analgesic for mild to moderate pain. Side effects with NSAIDs are
relatively common.
• The VIGOR study,4 in which patients on low-dose aspirin were
excluded, found an i risk of MI for patients given rofecoxib, compared
to naproxen. Rofecoxib and some other COX-2 inhibitors have been
withdrawn from clinical practice because of further concerns about the
risks of CVS events, including MI and CVE. Celecoxib and etoricoxib
remain available in the UK for the relief of pain in osteoarthritis, RA and
ankylosing spondylitis. IV parecoxib remains a useful analgesic drug in
the perioperative period.
• In January 2010, the MHRA assessed the i thrombotic risk at three
additional events per 1000 patient-years. The i risk relates mainly
to MI and includes CVE and peripheral events in some studies. For
the majority of patients, the potential increase in the thrombotic risk
is small. In patients with pre-existing risk factors for, or a history of,
cerebrovascular disease, the risk may be higher (Table 41.1).
516
Opioids
Opioid drugs act as agonists at opioid receptors, found mainly in the brain
and spinal cord, but also peripherally. The opioid system comprises four
types of receptor: mu-, delta-and kappa-opioid and nociceptin. Opioid
receptors all have selective endogenous peptides. Analgesia elicited by
clinically applied opioids act predominantly via the mu-opioid receptor.
Tolerance to mu-opioid receptor analgesics may be attenuated by both
nociceptin and delta-opioid receptor antagonism.
Morphine Remains the gold standard against which all new analgesics are
compared. It is the least lipid-soluble opioid in common use. Metabolised in
the liver, with only 10% excreted unchanged by the kidney. The metabolite
morphine-6-glucuronide is more potent than morphine. The other main
metabolite is morphine- 3-glucuronide which has no analgesic activity.
Both metabolites are excreted in the kidney. Accumulation can occur after
prolonged use in patients with impaired renal function. Dose ranges and
dose intervals vary according to the route of administration.
Diamorphine A prodrug (diacetylmorphine) rapidly hydrolysed to 6-
monoacetylmorphine and then morphine. Diamorphine is much more
lipid-soluble than morphine and thus has a more rapid onset of action than
morphine when given by epidural or IV route.
Fentanyl Highly lipid-soluble synthetic opioid with a short duration of action
because of rapid tissue uptake. The high lipid solubility makes it suitable for
transdermal administration. Metabolites of fentanyl are inactive. Fentanyl is
commonly administered IV, epidurally, intrathecally, buccally or via the nasal
mucosa as a spray.
Pethidine Analgesic with anticholinergic and some LA activity. Primarily
metabolised in the liver, with metabolites excreted in the kidney. One of the
main metabolites is norpethidine with a half-life of 15–20h. Norpethidine is
a potent analgesic. High blood concentrations can lead to CNS excitation.
Patients with impaired renal function are at risk. Pethidine can be used to
treat postoperative shivering associated with volatile anaesthetic agents and
epidural and spinal anaesthesia.
Codeine A prodrug for morphine. Usually administered for the treatment
of mild to moderate pain. About 10% of the dose is converted to
morphine. Metabolism to morphine requires an enzyme (CYP2D6) which
is part of the cytochrome P450 system; 8–10% of Caucasians lack this
enzyme, obtaining little or no benefit. This variable metabolism results in
an unpredictable analgesic efficacy, a high NNT and a concurrent risk of
inadvertent overdose. Subsequently, codeine is not recommended for use
in children, pregnancy or breastfeeding mothers.
Tramadol Synthetic, centrally acting opioid-like drug. Less than half of its
analgesic activity is at the mu-opioid receptor. It inhibits noradrenaline
and serotonin uptake at nerve terminals. Lower tolerance and abuse
potential, less respiratory depression and constipation reported, compared
to other opioids. Metabolised in the liver and excreted in the kidney. The
main metabolite of tramadol is O-desmethyltramadol (M1) which is more
potent. Formation of M1 also depends on the presence of CYP2D6 within
the cytochrome P450 system.
518
All opioids are equianalgesic if adjustments are made for the dose and
route of administration. Allowance should be made for long-term opioid
therapy, incomplete cross-tolerance between opioids, differing half-lives
and interpatient variability (Table 41.2).
Opioids have a similar spectrum of side effects. There is considerable
interpatient variability, and some patients may suffer from more side effects
with one particular drug compared to another.
Side effects include respiratory depression (d RR and VT and irregular
respiratory rhythm), sedation, euphoria, dysphoria, nausea and vomiting,
muscle rigidity, miosis, bradycardia, myocardial depression, vasodilation,
delayed gastric emptying, constipation and pruritus.
Patient-controlled analgesia
PCA refers to self-administration of IV opioids and helps overcome the
marked variability in response to postoperative opioids. Patients titrate their
plasma opioid concentration to remain in the analgesic window (above the
minimum effective analgesic concentration and below the minimum toxic
concentration). The inherent safety of PCA lies in the fact that excessive
doses of opioid will not be delivered, should the patient become sedated.
No one but the patient is allowed to operate the PCA demand button.
Patient-controlled analgesia regimens
• The most commonly used opioid is morphine. Fentanyl, pethidine,
tramadol and other opioids have also been used. No opioid is
noticeably superior to any other, although a greater incidence of
pruritus may be seen with morphine; on an individual basis, one opioid
may be better tolerated than another.
• The optimal bolus dose consistently results in analgesia without side
effects. Initial values for PCA variables are given in Table 41.6.
• For paediatric use of PCA, see % pp. 926–7.
Complications
• Equipment malfunction is rare. Interference in pump operation has been
reported following current surges and static electricity. Modern PCA
pumps have a number of fail-safe design features where the program
defaults to the lowest setting possible for a bolus dose. Most machines
have a battery backup lasting up to 8h. Failure of antireflux valves has
led to cases of respiratory depression.
Patient-controlled analgesia 1163
Sedation score
0 Patient wide awake
1 Mild drowsiness. Easy to rouse
2 Moderate drowsiness. Easy to rouse
3 Severe drowsiness. Difficult to rouse
4 Asleep but easy to rouse
614
Epidural analgesia
Regional anaesthesia reduces acute pain and chronic pain after some sur-
gical procedures and can reduce length of hospital stay.7 Other benefits of
epidural analgesia are:
• The incidence of postoperative atelectasis and pulmonary infection is
reduced, improving oxygenation. Effective pain relief allows the patient
to cough, breathe deeply and cooperate with physiotherapy. Epidural
analgesia combined with GA reduces pulmonary complications in
thoracic, abdominal and lower limb procedures, and is of proven benefit
in patients with pulmonary disease.8,9
• The hypercoagulable response to surgery is attenuated, and fibrinolytic
function is improved by attenuation of the stress response. This has
been shown to be of benefit for graft survival in patients undergoing
lower limb revascularisation.
• Epidural analgesia reduces pain and opioid consumption, and has been
shown to reduce the duration of both ileus and time to 1st flatus.
There has been concern that epidural analgesia increases the risk of
anastomotic leakage perhaps caused either by gut hypoperfusion or by
an increase in peristalsis 2° to associated sympathectomy, but this has
not been consistently demonstrated.
• Reduction in surgical site infections.9
• There is, however, no survival benefit in high-risk patients, despite being
beneficial in terms of pain relief and respiratory function.10
Contraindications
• Patient refusal, staff untrained in epidural care on wards and
contraindications to catheter or needle placement (local or general
sepsis, hypovolaemia, coagulation disorders, concurrent treatment with
anticoagulant drugs and some central neurological diseases).
Troubleshooting
Breakthrough pain
Consider:
• Adding regular PO/PR/IV NSAID and paracetamol, if not
contraindicated.
• Bolus dose (3–5mL), followed by i infusion rate.
• Check all connections and insertion site.
• Check the block level (with ice or touch). If block patchy or unilateral,
withdraw the catheter to 2cm in space.
• Bolus dose of opioid only (fentanyl 50–100 micrograms, diamorphine
2–3mg).
• Pruritus; give naloxone (50–100 micrograms), and consider adding 300
micrograms to infusion fluids or removing the opioid from the epidural
infusion. Antihistamines may give some relief.
• Hypotension: check fluid status of the patient who is probably relatively
hypovolaemic. Check block height. Consider reducing the infusion rate.
If acute/severe, raise the legs; give fluid bolus and vasopressor.
• Motor block: reduce the infusion rate. Consider reducing LA
concentration.
• Complications of epidural analgesia are summarised in Table 41.8 (see
also % p. 844).
Epidural analgesia 1165
Intrathecal opioids
Opioids can be administered intrathecally, in combination with LA,
during spinal anaesthesia. The opioid is delivered directly into the CSF, so
avoiding distribution into epidural fat and blood vessels. Consequently, the
doses used are much smaller, compared to epidural or parenteral routes
(Table 41.9).
• The more lipid-soluble the drug, the more rapid the onset and the
shorter the duration of action.
• Pethidine has LA, as well as opioid, properties. It can be used as the sole
drug for spinal anaesthesia (requires higher doses).
• Delayed or late respiratory depression can occur with the less lipid-
soluble drugs (particularly morphine). Increasing patient age, high doses
of opioid administered intrathecally, concurrent use of sedatives and
systemic opioids are associated with i risk of respiratory depression.
• Diamorphine (if available) offers the best combination of duration of
analgesia with fewest side effects.
Spinal infection
Extreme vigilance is needed for all patients who have had epidural anal-
gesia because of the risk of spinal infection.11,12 Only 13% of patients with
an epidural abscess present with the classical triad of fever, backache and
neurological signs and symptoms. Back pain is the initial symptom in 75% of
cases. Fever occurs in 66% of cases. Only two out of three patients have
leucocytosis. A raised ESR (>30mm) is a consistent finding. If there is suspi-
cion of infection, a full infection screen and blood cultures are mandatory.
The epidural catheter should always be removed immediately and sent to
the laboratory for microbiological investigation. Ninety per cent of spinal
infections are bacterial, mainly Staphylococcus aureus. MRI with gadolinium
is the investigation of choice. The whole spine should be scanned early,
before neurological signs and symptoms occur. Once muscle weakness is
present, only 20% of patients regain full function, even after spinal surgery.
Poor recovery is predicted by patient age (older patients do worse), extent
of cord compression and duration of neurological symptoms (<36h has
better prognosis). Mortality from an epidural abscess is 10%. Treatment is
based on surgical or percutaneous abscess drainage and antibiotics. Steroids
are contraindicated.
Continuous peripheral nerve blockade 1167
Table 41.10 Typical bolus and infusion rates for peripheral nerve blockade
Stimulation-produced analgesia:
transcutaneous electrical nerve
stimulation and acupuncture
Stimulation techniques activate the body’s pain modulation systems. The
gate control theory of pain by Melzack and Wall in 1965 provided a model
to explain this phenomenon.
• Incoming noxious pain signals are reduced by presynaptic and
postsynaptic inhibition in laminae 1–5 in the dorsal horn of the spinal
cord. Modulatory input arrives via the descending pathways and
lateral branches from myelinated afferent A-fibres. A-fibres arise in
low-threshold mechanoreceptors activated by TENS, and in high-
threshold mechanoreceptors activated by needles used in acupuncture
techniques.
• TENS: A-fibres are recruited at 50–200Hz and respond to low-intensity
stimulation, increasing levels of the inhibitory neurotransmitters
dynorphin A and B in the dorsal horn. Pain relief occurs immediately
but lasts only as long as stimulation continues.
• Acupuncture: A-fibres are recruited at 2–4Hz, responding to high-
intensity stimulation by increasing inhibitory neurotransmitter met-
enkephalin levels in the dorsal horn. Pain relief takes 20–30min but lasts
hours or days.
710
higher doses or a longer duration for pain control, then discuss with a
pain specialist.
• Lidocaine infusions:14 1–2mg/kg/h or combined with ketamine, e.g.
25mg of ketamine added to 20mL of 2% lidocaine running at 0.1mL/
kg/h.
• Antineuropathic medications. These include TCAs (amitriptyline 10mg
nocte, NNT of 3–4) and gabapentinoids (e.g. gabapentin 300mg tds,
NNT of roughly 7).
• Psychotropic drugs. This group can be particularly useful for
management of distress. Haloperidol 2.5–5mg IV or PO is probably
most familiar to anaesthetists, but the atypical antipsychotics quetiapine
(12.5–25mg) or risperidone ( 0.5–1.0mg) are also helpful.
• Benzodiazepines are also useful to manage distress. Consider lorazepam
(1–2mg), temazepam or diazepam.
Non-drug management
On occasion, despite best management, no relief from pain can be
obtained. It is important to eliminate ongoing tissue damage and request a
surgical review if necessary. Once this has been ruled out, then it is useful
to bear in mind the concept of total pain and explore these avenues. This
can be very rewarding if you are comfortable in this area, but equally it may
be appropriate to ask for psychiatric consultation.
Predictability
Sometimes a patient in this group has less pain than predicted and follows
a relatively normal clinical pathway, but most commonly pain is a major
problem. As a simple rule of thumb, this group will need three times the
analgesia for three times as long and be three times as sore, no matter what
you do.
Distress management
Distress and anxiety compound pain are often manifest as out-of-control
pain, even in those in whom you would not expect such a response.
Reassurance or sometimes specialist pain or psychiatric input may be re-
quired. Refer to the flow chart in Fig. 41.2.
Plan and progress
It is important that all members of the treating team are consistent in their
approach to analgesic management. A well-documented plan is key. It is ac-
ceptable to change the plan, but communicate with all members of the team
and the patient. Sometimes patients can play on the lack of consistency and
split the team. Remember to start discharge planning well in advance.
Persistent pain patients in acute pain 1175
Out-of-control pain
Yes
Try simple measures such as
Is anxiety a major feature?
breathing techniques
Yes
Add analgesics carefully Can you safely add more
analgesics?
Fig. 41.2 Aide memoire for approaching persistent pain patients with acute
perioperative pain.
716
Naltrexone
A long-acting competitive opioid antagonist with a duration of action of
748–72h. Chronic use results in i sensitivity to morphine-induced analgesia
and a doubling of brain mu-and delta-opioid receptors, which may return
to baseline in 76d post-treatment. It is recommended to stop naltrexone
72h prior to surgery, and it is important to note that although patients may
be resistant to opioids while taking naltrexone, they may then become
extremely opioid-sensitive once stopping it. It is therefore imperative to
maximise opioid-sparing strategies (e.g. regional anaesthesia) and consider
managing the patient in a high dependency setting in the postoperative
period, to ensure appropriate monitoring of treatment. Usual maintenance
dose is 25–50mg daily.
Buprenorphine
This partial opioid agonist is used in the treatment of opioid addiction.
Commonly prescribed doses are 8–32mg. The high receptor affinity and
long half-life of buprenorphine result in difficulty obtaining effective an-
algesia by simply adding further opioid. At high doses of Suboxone®
(buprenorphine and naloxone), e.g. 22–32mg, there is a theoretical con-
cern that buprenorphine will antagonise the effect of a full agonist. There
are very few reports describing perioperative pain management of patients
administered high-dose buprenorphine. Strategies in this situation have
included continuing the usual dose of buprenorphine and either (1) pro-
viding additional full opioid agonists or (2) prescribing supplemental doses
of buprenorphine. An alternative strategy involves rotating to a full agonist
before surgery such as methadone. The author recommends continuing the
patient’s usual dose of buprenorphine, maximising the use of opioid-sparing
adjuncts, and using conventional full opioid agonists to treat acute pain. The
doses of opioid required for analgesia may be appreciably higher than one
would expect for other opioid-tolerant patients and in view of this, it may
be advisable to monitor the patient in a high dependency environment.
Specific patient groups 1179
References
1 Kehlet H (1994). Postoperative pain relief: what is the issue? Br J Anaesth, 72, 375–8.
2 Gerbershagen HJ, Aduckathil S, van Wijck AJ, et al. (2013). Pain intensity on the first day after sur-
gery: a prospective cohort study comparing 179 surgical procedures. Anesthesiology, 18, 934–41.
3 Scott DA, McDonald WM (2008). Assessment, measurement and history. In: Macintyre PE,
Rowbotham D, Walker S (eds). Clinical Pain Management: Acute Pain, 2nd edn. London: Hodder
Arnold; pp. 135–53.
4 Bombardier C, Laine L, Reicin A, et al. (2000). Comparison of upper gastrointestinal toxicity of
rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR Study Group. N Engl J Med,
343, 1520–8.
5 Ross JAS (2000). Isoflurane entonox mixtures for pain relief during labour. Anaesthesia, 55,
711–12.
6 National Institute for Health and Care Excellence. British National Formulary. M https://bnf.nice.
org.uk/
7 Schug SA, Palmer GM, Scott DA, et al. (2015). Acute Pain Management: Scientific Evidence. 4th
edn. Melbourne: Australian and New Zealand College of Anaesthetists and Faculty of Pain
Medicine.
8 van Lier F, van der Geest PJ, Hoeks SE, et al. (2011). Epidural analgesia is associated with im-
proved health outcomes of surgical patients with chronic obstructive pulmonary disease.
Anesthesiology, 115, 315–21.
9 Smith LM, Cozowicz C, Uda Y, et al. (2017). Neuraxial and combined neuraxial/general anes-
thesia compared to general anesthesia for major truncal and lower limb surgery: a systematic
review and meta-analysis. Anesth Analg, 125, 1931–45.
10 Hopkins PM (2015). Does regional anaesthesia improve outcome? Br J Anaesth, 115, Suppl 2,
ii26–33.
11 Royal College of Anaesthetists (2009). National audit of major complications of central neuraxial
block in the United Kingdom. Report and findings. M http://www.rcoa.ac.uk/nap3
12 Joshi SM, Hatfield RH, Martin J, et al. (2003). Spinal epidural abscess: a diagnostic challenge. Br J
Neurosurg, 17, 160–3.
13 Chin KJ, McDonnell JG, Carvalho B, et al. (2017). Essentials of our current understanding: ab-
dominal wall blocks. Reg Anesth Pain Med, 42, 133–83.
14 Cowlishaw PJ, Kotze PJ, Gleeson L, et al. (2017). Randomised comparison of three types of
continuous anterior abdominal wall block after midline laparotomy for gynaecological oncology
surgery. Anaesth Intensive Care, 45, 453–8.
15 Schug SA, Bruce J (2017). Risk stratification for the development of chronic postsurgical pain. Pain
Rep, 2, e627.
16 van Helmond N, Olesen SS, Wilder-Smith OH, et al. (2018). Predicting persistent pain after sur-
gery: can predicting the weather serve as an example? Anesth Analg, 127, 1264–7.
17 Laskowski K, Stirling A, McKay WP, et al. (2011). A systematic review of intravenous ketamine
for postoperative analgesia. Can J Anaesth, 58, 911–23.
18 McCartney CJL, Sinha A, Katz J (2004). A qualitative systematic review of the role of N-methyl-
D-aspartate receptor antagonists in preventive analgesia. Anesth Analg, 98, 1385–400.
19 Verret M, Lauzier F, Zarychanski R, et al. (2020). Perioperative use of gabapentinoids for the
management of postoperative acute pain: a systematic review and meta-analysis. Anaesthesiology,
133, 265–79.
20 Reddi D (2016). Preventing chronic postoperative pain. Anaesthesia, 71, 64–71.
21 Barreveld A, Witte J, Chahal H, et al. (2013). Preventive analgesia by local anaesthetics: the re-
duction of postoperative pain by peripheral nerve blocks and intravenous drugs. Anesth Analg,
116, 1141–61.
22 Blaudszun G, Lysakowski C, Elia N, Tramer MR (2012). Effect of perioperative systemic α-2
agonists on postoperative morphine consumption and pain intensity: systematic review and
meta-analysis of randomized controlled trials. Anesthesiology, 116, 1312–22.
23 Borghi B, D’Addabbo M, White P, et al. (2010). The use of prolonged peripheral neural blockade
after lower extremity amputation: the effect on symptoms associated with phantom limb syn-
drome. Anesth Analg, 111, 1308–15.
24 Loftus RW, Yeager MP, Clark JA, et al. (2010) Intraoperative ketamine reduces perioperative
opiate consumption in opiate-dependent patients with chronic back pain undergoing back sur-
gery. Anesthesiology, 113, 639–46.
25 Naa-Afoley Quaye A, Zhang Y (2019). Perioperative management of buprenorphine: solving the
conundrum. Pain Med, 20, 1395–408.
26 Zollinger PE, Tuinebreijer WE, Breederveld RS, Kreis RW (2007). Can vitamin C prevent
complex regional pain syndrome in patients with wrist fractures? A randomized, controlled,
multicenter dose-response study. J Bone Joint Surg Am, 89,1424–31.
Chapter 42 1181
Drug formulary
Andrew Bradley
Drug formulary 1182
Infusion regimes 1209
812
1182
Chapter 42
Drug formulary
(See Table 42.1.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Drug formulary
Adenosine Endogenous nucleoside with 2nd- or 3rd-degree Flushing, dyspnoea, 1mo to 1y: 0.1mg/kg fast 6mg fast IV bolus,
antiarrhythmic activity. Slows heart block. Long headache, AV block, IV bolus, increasing by followed by 12mg at
conduction through AV node. QT. Asthma/COPD. transient angina 0.05–0.1mg/kg every 1– 1–2min, then further
Treatment of acute paroxysmal Reduce dose in 2min to max 0.5mg/kg 12mg at 1–2min, as
SVT (including WPW) or heart transplant or (max 12mg ). >12y: as necessary. Reduce to
differentiation of SVT from VT. dipyridamole treatment adult quarter of dose if giving
Duration 10s with dipyridamole
Adrenaline Endogenous catecholamine Arrhythmias, especially Hypertension, 1. Refer to paediatric 1–3. IV/IM/ETT 1mL
with α and β action: with halothane. Caution tachycardia, anxiety, anaphylaxis emergency aliquots of 1:10 000
1. Treatment of anaphylaxis in elderly. Via central hyperglycaemia, (see % pp. 1081–3) up to 5–10mL
2. Bronchodilator catheter whenever arrhythmias. Reduces 2. ETT 0.1mL/kg (0.5–1mg). Infusion
possible uterine blood flow of 1:1000 (100 2–20 micrograms/min
3. Positive inotrope (0.04–0.4 micrograms/
micrograms/kg)
4. Given by nebuliser for croup kg/min)
3. Infusion 0.05–1
5. Prolongation of LA action. micrograms/kg/min 4. Nebulisation 5mL of
1:1000 contains 1mg/mL, 1:1000 (max 5mg)
1:10 000 contains 100 4. Nebuliser 0.5mL/kg
(up to 5mL) of 1:1000 5. Max dose for
micrograms/mL, 1:200 000 infiltration
contains 5 micrograms/mL 5. Maximum dose
for infiltration 2 micrograms/kg
6. Cardiac arrest 6. 1mg (10mL of
2 micrograms/kg
6. 10 micrograms/kg, 1:10 000), every
refer to cardiac arrest 3–5min
(see % pp. 1052–4)
Alfentanil Short-acting, potent opioid Use IBW Respiratory Injection: 5–20 250–750 micrograms
analgesic depression, micrograms/kg, then 10 (5–10 micrograms/kg).
Duration 10min bradycardia, micrograms/kg boluses Attenuation of CVS
Sedation in ICU hypotension. Infusion: 10–100 response to intubation:
Prolonged half-life in micrograms/kg over 10–20 micrograms/kg
neonates 10min, then 0.5–1 Sedation: infusion 2mg/h
micrograms/kg/min
DRUG FORMULARY
(Continued)
1183
814
1184
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Amiodarone Mainly class III antiarrhythmic, Via central catheter. Commonly causes >1y IV: 5mg/kg over 5mg/kg over 20–
useful in treatment of Sinoatrial heart block, thyroid dysfunction 20–120min. Infusion: 120min, followed by
Chapter 42
supraventricular and ventricular thyroid dysfunction, and reversible corneal 5 micrograms/kg/min, infusion if required,
arrhythmias pregnancy, porphyria, deposits max 1.2g/24h. 5mg/kg max 1.2g in 24h.
iodine sensitivity. Dilute slow IV bolus for defib- 300mg slow IV bolus for
in glucose 5%, not 0.9% resistant VF/VT defib-resistant VF/VT
sodium chloride
Atenolol Long-acting, cardioselective Asthma, heart failure, Bradycardia, 0.05mg/kg every 5min, 5–10mg over 10min
β-blocker AV block, verapamil hypotension, max four doses
treatment d contractility
Drug formulary
Atracurium Benzylisoquinolinium NDMR. Potentiated by Mild histamine release Intubation: 0.3–0.6mg/kg Use IBW
Undergoes Hofmann aminoglycosides, loop and rash common with Maintenance: Intubation: 0.3–0.6mg/kg
elimination plus non-specific diuretics, Mg2+, higher doses. Flush 0.1–0.2mg/kg Maintenance:
enzymatic ester hydrolysis. lithium, d temp, with 0.9% sodium Infusion: 0.3–0.6mg/kg/h, 0.1–0.2mg/kg
Useful in severe renal or d K+, d pH, prior use chloride before and monitor blockade
hepatic disease. of suxamethonium, after Infusion: 0.3–0.6mg/kg/h,
Duration 20–35min volatile agents. monitor NMB
Store at 2–8°C
Atropine Muscarinic acetylcholine Obstructive uropathy Decreases secretions IV: 10–20 micrograms/kg. 300–600 micrograms.
antagonist. Vagal blockade at and CVS disease. and lower oesophageal Control of muscarinic Prevention of muscarinic
AV and sinus node increases HR Glaucoma, myasthenia sphincter tone, relaxes effects of neostigmine: effects of neostigmine:
(transient decrease at low doses gravis bronchial smooth 20 micrograms/kg. IM/ 600–1200 micrograms
due to weak agonist effect). muscle. Confusion in SC: 10–30 micrograms/kg.
Tertiary amine, therefore elderly PO: 40 micrograms/kg
crosses blood–brain barrier
Bicarbonate Alkaline salt used for Precipitation with Alkalosis, Dependent on degree of Dependent on degree of
(sodium) correction of acidosis and to calcium-containing hypokalaemia, acidosis. 1mL/kg of 8.4% acidosis. Resuscitation:
enhance onset of action of solutions, i CO2 hypernatraemia, solution (1mmol/kg) 50mL of 8.4%, then
LAs. 8.4%, 1000mmol/L. Dose production, necrosis hypocalcaemia recheck blood gases.
(mmol) in acidosis: weight (kg) on extravasation. Via Bicarbonation of LA:
× base deficit × 0.3 central catheter if 1mL of 8.4% to 20mL
possible of bupivacaine. 1mL
of 8.4% to 10mL of
lidocaine/prilocaine
Bupivacaine Amide-type LA used for Greater cardiotoxicity Toxicity: tongue/ Infiltration/epidural: max 0.25–0.75% solution.
infiltration and epidural and than other LAs. Do circumoral numbness, dose dependent upon Infiltration/epidural:
spinal anaesthesia. Slower not use for IVRA. restlessness, tinnitus, injection site; 2mg/kg/4h max dose dependent
onset than lidocaine. Duration Adrenaline-containing seizures, cardiac arrest recommended upon injection site;
3–6h (slightly prolonged by solutions contain 2mg/kg/4h (2mg/kg
adrenaline ), pKa 8.1 preservative and do not with adrenaline). 0.75%
prolong action solution contraindicated
in pregnancy
Buprenor- Opioid with both agonist and May precipitate Nausea, respiratory 6mo to 12y: IV 3–6 Slow IV/IM: 300–600
phine antagonist actions. Duration 6h withdrawal in opioid- depression, micrograms/kg tds (max micrograms qds.
dependent patients. constipation 9 micrograms/kg) Sublingual: 200–400
Only partially reversed 12–18y: IV 300–600 micrograms qds
by naloxone micrograms tds
Calcium Electrolyte replacement, Necrosis on Arrhythmias, 0.1mL/kg of 10% 2–10mL of 10% solution
chloride positive inotrope, extravasation. hypertension, solution, slow IV (10mg/kg, 0.07mmol/kg)
hyperkalaemia, Incompatible with hypercalcaemia
hypermagnesaemia. Calcium bicarbonate
chloride 10% contains Ca2+
680 micromoles/mL
DRUG FORMULARY
(Continued)
1185
816
1186
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Calcium As calcium chloride. Calcium Less phlebitis than As calcium chloride 0.3–0.5mL/kg of 10% 6–15mL of 10% solution
Chapter 42
gluconate gluconate 10% contains Ca2+ calcium chloride solution (max 20mL) (30mg/kg, 0.07mmol/
225 micromoles/mL kg)
Carboprost Synthetic prostaglandin F2α Asthma, DM, epilepsy, Fever, bronchospasm. Never give IV.
analogue used to treat severe jaundice, anaemia, Nausea, vomiting, 250 micrograms deep
postpartum haemorrhage glaucoma. Large doses flushing. May cause IM or directly into
due to uterine atony (after may cause uterine CVS collapse myometrium. Repeat,
ergometrine and oxytocin rupture if needed, after at least
failed) 15min.
Drug formulary
(Continued)
DRUG FORMULARY
1187
81
1188
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Dexametha- Prednisolone derivative Interacts with See Prednisolone IV/IM/SC: 83–333 IV/IM/SC: 3.3–6.6mg.
sone corticosteroid. Less Na+ anticholinesterase micrograms/kg, Cerebral oedema:
Chapter 42
retention than hydrocortisone. agents to increase 1–2 divided doses 8–16mg initially, then
Cerebral oedema, oedema weakness in myasthenia (max 20mg/d). Cerebral 5mg qds (use 3.8mg/mL
prevention, antiemetic gravis. Dexamethasone oedema: see BNF for preparation)
0.75mg, Children. Croup: Antiemetic: 3.3–6.6mg
prednisolone 5mg 150 micrograms/
Different kg ± repeat at 12h.
formulations available Antiemetic:
(dexamethasone 150 micrograms/kg (max
Drug formulary
(Continued)
1189
910
1190
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Ephedrine Direct and indirect Caution in elderly, Tachycardia, 3–6mg repeated (dilute
sympathomimetic (α-and hypertension and CVS hypertension 30mg in 10mL of 0.9%
Chapter 42
(Continued)
1191
912
1192
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Glyceryl Organic nitrate vasodilator. Remove patches before Tachycardia, 10–30 micrograms/kg/h, Infusion: 0.5–10mg/h.
Chapter 42
trinitrate Controlled hypotension, defibrillation to avoid hypotension, starting dose up to 300 Sublingual tabs: 0.3–1mg
angina, CCF electrical arcing headache, micrograms/kg/h. Max PRN. Sublingual spray:
nausea, flushing, 600 micrograms/kg/h 400 micrograms PRN.
methaemoglobinaemia Patch: 5–10mg/24h
Glyco- Quaternary ammonium Caution in glaucoma, Paradoxical 4–10 micrograms/kg 200–400 micrograms.
pyrronium anticholinergic agent. CVS disease. Unlike bradycardia in small Control of muscarinic
bromide Bradycardia, blockade atropine, does not doses. Reduces lower effects of neostigmine:
(glyco- of muscarinic effects cross blood–brain oesophageal sphincter 200 micrograms for each
Drug formulary
(Continued)
DRUG FORMULARY
1193
914
1194
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Insulin Human soluble pancreatic Monitor blood glucose Hypoglycaemia, Ketoacidosis: 0.1–0.2 Ketoacidosis: 10–20 units,
Chapter 42
(soluble) hormone facilitating and serum K+. hypokalaemia units/kg (max 20 units), then 5–10 units/h. Sliding
intracellular transport of Store at 2–8°C then 0.1 units/kg/h scale (see % pp. 218–19).
glucose and anabolism. DM, (max 5–10 units/h) Hyperkalaemia (see %
ketoacidosis and hyperkalaemia pp. 240–1)
Intralipid® 20% emulsion used in See % pp. 1092–3 for 1.5mL/kg bolus, followed 1.5mL/kg bolus,
treatment of severe LA toxicity LA toxicity guidelines by 15mL/kg/h followed by 15mL/kg/h
Ketamine Phencyclidine derivative Emergence delirium Bronchodilation. Induction: IV 0.5–2mg/kg, Induction: IV 1–2mg/kg,
producing dissociative reduced by i, BP, uterine tone, IM 5–10mg/kg. Infusion: IM 5–10mg/kg. Infusion:
Drug formulary
(Continued)
DRUG FORMULARY
1195
916
1196
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Magnesium Essential mineral used to treat: Potentiates muscle CNS depression, 1. Hypomagnesaemia: 1. Hypomagnesaemia:
Chapter 42
(Continued)
1197
918
1198
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Morphine Opioid analgesic. Prolonged risk of Histamine release, PO: 0.05–0.3mg/kg IV: 2.5–10mg. IM/SC:
Half-life 2–4h respiratory depression, hypotension, 4-hourly. IV boluses: 50– 5–10mg 4-hourly. PO:
Chapter 42
Naloxone Pure opioid antagonist. Can be Beware renarcotisation Common: 5–10 micrograms/kg. 200–400 micrograms,
used in low doses to reverse if reversing long-acting Arrhythmias, dizziness, Infusion: 5–20 titrated to desired
pruritus associated with opioid. Caution in headache, hyperten- micrograms/kg/h. effect. Treatment of
epidural opioids and as depot opioid-dependent sion, hypotension, IM depot in newborn: opioid/epidural pruritus:
IM injection in newborn of patients, may nausea, vomiting 200 micrograms. Pruritus: infusion rate 0.25–1
mothers given opioids precipitate acute 0.5 micrograms/kg micrograms/kg/h
withdrawal. Duration ± bolus of
of action 30min 40–100 micrograms
Neostigmine Anticholinesterase used for: Administer with Bradycardia, nausea, 50micrograms/kg with 1. 50–70 micrograms/kg
1. Reversal of NDMR antimuscarinic agent excessive salivation atropine 20 micrograms/ (max 5mg) with
2. Treatment of (muscarinic effects) kg or glycopyrronium atropine 10–20
myasthenia gravis 10 micrograms/kg micrograms/kg or
glycopyrronium
Duration 60min IV (2–4h PO) 10–15 micrograms/kg
2. PO: 15–30mg at
suitable intervals
Neostigmine Combination of neostigmine See Neostigmine See Neostigmine 0.02mL/kg (dilute 1mL 1–2mL over 30s
and glyco- metilsulfate (2.5mg) and with 4mL of 0.9% sodium
pyrronium glycopyrronium (500 chloride, give 0.1mL/kg).
micrograms) per 1mL Max 2mL
Omeprazole PPI. Reduction in gastric acid Liver disease, max Headache, diarrhoea, PO: 0.7–1.4mg/kg up to PO/slow IV: 20–40mg/d.
secretion 20mg od prolonged QT 40mg od. IV: 0.5mg/kg/d Premedication PO:
40mg. Bleeding peptic
ulcer: 80mg bolus, then
8mg/h for 3d
Octreotide Somatostatin analogue used Pituitary tumour GI disturbance, SC: 1–5 micrograms/kg SC: 50 micrograms
in treatment of carcinoid, expansion, reduced gallstones, hyper-and 6- to 8-hourly od/bd, i up to 200
acromegaly and variceal need for antidiabetic hypoglycaemia micrograms tds. IV: 50
bleeding (unlicensed use) treatments micrograms diluted in
0.9% sodium chloride
(ECG monitoring)
Ondanse- Serotonin (5-HT3) receptor QT interval Hypotension, >1y: slow IV Slow IV/IM/PO: 4–8mg
tron antagonist antiemetic prolongation headache, flushing 100 micrograms/kg tds
(max 4mg) qds
Oxycodone Opioid used for moderate Porphyria, acute Nausea, vomiting, PO: Oxynorm® >1mo: PO: Oxynorm® 5mg
pain, often in palliative care. abdomen dysphoria, drowsiness initially 200 micrograms/ 4- to 6-hourly, i as
IV preparation available: dose kg (max 5mg) 4-to 6- required. Oxycontin®
1–10mg 4-hourly hourly. >12y: adult doses 10mg bd, i as required
(Continued)
DRUG FORMULARY
1199
201
1200
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Oxytocin Nonapeptide hormone which Avoid rapid Vasodilation, Postpartum slow IV:
stimulates uterine contraction. administration. Fetal hypotension, flushing, 5 units, followed, if
Chapter 42
stimulation
Pantoprazole PPI used to inhibit gastric acid Liver disease, Headache, pruritus, NR PO/slow IV: 40mg od
secretion pregnancy. Renal bronchospasm (max 80mg)
disease
Paracetamol Mild to moderate analgesic and Neonates: PO Liver damage in Slow IV: 15mg/kg qds Slow IV: >50kg, 1g qds;
antipyretic 10–15mg/kg 6-hourly overdose (max 60mg/kg/d) <50kg, 15mg/kg qds.
(5mg/kg if jaundiced). (10–50kg, max 60mg/kg; PO: 0.5–1g qds
Max 60mg/kg/d. >50kg, max 4g/d). PO/
<10kg: IV 7.5mg/kg PR: 20mg/kg for 1st
6-hourly. dose, then 10–15mg/kg
Max 30mg/kg/d qds (max 75mg/kg/d,
up to 4g/d). PR loading
dose: 30–40mg/kg
(>44w post-conception)
Paraldehyde Status epilepticus Dilute neat solution Rash Deep IM: 0.2mL/kg. Deep IM: 5–10mL.
with equal volume of PR: 0.3mL/kg PR: 10–20mL
olive oil before PR
administration
Parecoxib Prodrug of valdecoxib. Severe renal GI upset, thrombotic Not evaluated for use IV/IM: 40mg, then
COX-2 inhibitor. Licensed for impairment, peptic events in <18s 20–40mg 6- to 12-hourly
acute pain ulceration, IHD (max 80mg/d)
and inflammatory
bowel disease.
Hypersensitivity to
sulphonamides and
aspirin. Reconstitute
with 0.9% sodium
chloride
Pethidine Synthetic opioid: Seizures possible in Respiratory >12y: IV/IM/SC: 0.5–1 IM/SC: 25–100mg
1. Analgesia high dosage: max daily depression, mg/kg (max 100mg). 3-hourly. IV: 25–50mg.
2. Postoperative shivering dose 1g/d hypotension, Infusion: 5mg/kg in 50mL PCA: 10mg/5min
(20mg/kg/d). MAOI dysphoria of 5% glucose at 1–3mL/h lockout. Shivering:
(100–300 micrograms/ 10–25mg
kg/h)
Phentol- α1- and α2-adrenergic Treat excessive Hypotension, 0.1mg/kg, then 5–50 2–5mg (10mg in 10mL
amine antagonist. Peripheral hypotension with tachycardia, flushing micrograms/kg/min of 0.9% sodium chloride,
vasodilation and controlled noradrenaline or 1mL aliquots)
hypotension. Treatment of methoxamine (not
extravasation. adrenaline/ephedrine
Duration 10min due to β effects)
DRUG FORMULARY
(Continued)
1201
201
1202
Phenyl- Selective direct-acting Caution in elderly Reflex bradycardia, 2–10 micrograms/kg, 20–100 microgram
ephrine α-adrenergic agonist. and CVS disease. arrhythmias then 0.1–0.5 increments (10mg in
Peripheral vasoconstriction Hyperthyroidism micrograms/kg/min 500mL of 0.9% sodium
and treatment of hypotension. chloride, 1mL aliquots).
Duration 20min IM: 2–5mg. Infusion:
30–60 micrograms/min
(5mg in 50mL of 0.9%
sodium chloride at 0–
30mL/h)
Drug formulary
Phenytoin Anticonvulsant and treatment Avoid in AV heart Hypotension, AV IV loading dose: 20mg/kg (max 2g) over
of digoxin toxicity. Serum block, pregnancy and conduction defects, 20mg/kg over 1h 1h (dilute to 10mg/mL in
levels 10–20mg/L (40–80 porphyria. Monitor ataxia. Enzyme 0.9% sodium chloride),
micromoles/L) ECG/BP on IV induction then 100mg tds.
administration Arrhythmia: 3.5–5mg/kg
(rate <50mg/min)
Potassium Electrolyte replacement Dilute solution before Rapid infusion can 0.5mmol/kg over 1h. 10–20mmol/h (max
chloride (see % pp. 238–9) administration cause cardiac arrest. Maintenance: concentration 40mmol/L
High concentration 1–2mmol/kg/d peripherally). With ECG
causes phlebitis monitoring:
up to 20–40mmol/h
via central line (max
200mmol/d)
Pregabalin Binds to voltage-dependent Avoid abrupt Dry mouth, Pain: 150mg 2–3
calcium channels and decreases withdrawal, severe constipation, oedema, divided doses with slow
release of neurotransmitters. CCF, renal impairment dizziness increase. Epilepsy: 25mg
Adjunct for focal seizures bd increasing
Prednisolone Orally active corticosteroid. Adrenal suppression, Dyspepsia and PO: 1–2mg/kg od. PO: initially 20–60mg od,
Less mineralocorticoid action severe systemic ulceration, Croup: 4mg/kg, then reduced to 2.5–15mg od
than hydrocortisone infections osteoporosis, 1mg/kg tds for maintenance
myopathy, psychosis,
impaired healing, DM
Prilocaine Amide-type LA. Less toxic than Adrenaline-containing Toxicity: tongue/ NR <6mo LA: 0.5–2% solution.
lidocaine. Used for infiltration solutions contain circumoral numbness, 6mg/kg/4h (max
and IVRA. Rapid onset. preservative. Significant restlessness, tinnitus, dose dependent upon
Duration 30–90min (prolonged methaemoglobinaemia seizures, cardiac arrest injection site); 9mg/kg
by adrenaline), pKa 7.9 if dose >600mg. with adrenaline
Use IBW
Prochl Phenothiazine antiemetic Hypotension on rapid Tardive dyskinesia >10kg: PO: 0.25mg/kg IM: 12.5mg tds. PO:
orperazine IV administration. and extrapyramidal tds. IM: 0.1–0.2mg/kg tds 20mg, then 5–10mg tds
Neuroleptic malignant symptoms
syndrome
Procyclidine Antimuscarinic used in acute Glaucoma, GI Urinary retention, dry <2y: 0.5–2mg. IV/IM: 5–10mg, repeat
treatment of drug-induced obstruction. Lower mouth, blurred vision 2–10y: 2–5mg. after 20min if needed
dystonic reactions (except dose in elderly >10y: adult dose
tardive dyskinesia)
(Continued)
DRUG FORMULARY
1203
2041
1204
Propofol IV induction agent. Rapid Reduce dose in elderly Apnoea, hypotension, Induction: 2–4mg/kg. Induction: 2–3mg/kg.
recovery and little nausea. or if haemodynamically pain on injection. Infusion: 4–15mg/kg/h. Infusion: 6–10mg/kg/h.
1° drug in TIVA unstable. Caution Myoclonic spasms, NR induction <1mo. TCI: initially 4–8
in severe allergy to rarely convulsions NR maintenance <3y micrograms/mL, then
peanuts, soya and 3–6 micrograms/mL
soybean oil (reduce in elderly)
Propranolol Non-selective β-adrenergic Asthma, heart failure, Bradycardia, 0.1mg/kg over 5min 1mg increments, up to
antagonist. Controlled AV block, verapamil hypotension, AV 5–10mg
Drug formulary
(Continued)
1205
2061
1206
Table 42.1 (Contd.)
Drug Description and perioperative Cautions and Side effects Dose (paediatric) Dose (adult)
indications contraindications
Sugammadex Specific cyclodextrin reversal Wait 24h after Binds with If two twitches present If two twitches
agent for rocuronium and use before using contraceptive pill from TOF, 2mg/kg. Full present from TOF, give
Chapter 42
methonium Rapid short-acting muscle plasma cholinesterase with 2nd dose IM: 3–4mg/kg Infusion: 0.5–10mg/min
paralysis. Phase II block deficiency,
develops with repeated doses hypokalaemia,
(>8mg/kg). Store at 2–8°C hypocalcaemia.
MH, neuromuscular
disorders. i serum K+
(normally 0.5mmol/L,
greater in burns,
trauma, upper motor
neurone injury)
Tapentadol Moderate to severe pain Reduce in hepatic Diarrhoea, dyspepsia, Consult tertiary >18y PO: 50mg 4-to 6-
managed only by opioids impairment weight loss consultant hourly, max 700mg
Temazepam Benzodiazepine.Sedation or d requirement for Respiratory depression PO: 0.3mg/kg PO: 10–40mg 1h
premedication. Duration 1–2h anaesthetic agents in combination with preoperatively. NR <12y preoperatively (elderly
opioids. Amnesia 10–20mg)
Thiopental Short-acting thiobarbiturate. Accumulation Hypotension.Necrosis Induction: neonate 2–4 Induction/cerebral
Induction of anaesthesia, with repeated if intra-arterial mg/kg, child 5–6mg/kg. protection: 3–5mg/kg.
anticonvulsant, cerebral doses. Caution in Status: 2–4mg/kg, then Anticonvulsant: 0.5–2
protection. Recovery due to hypovolaemia and 8mg/kg/h mg/kg PRN
redistribution elderly. Porphyria
Tramadol Analgesic thought to have Only 30% antagonised Nausea, dizziness, dry >12y: adult dose PO: 50–100mg 4-hourly.
less respiratory depression, by naloxone. Caution mouth. i side effects Slow IV/IM: 50–100mg
constipation, euphoria and in epilepsy. Previously in conjunction with 4-hourly (100mg initially,
abuse potential than other not recommended for other opioids then 50mg increments
opioids. Has opioid and non- intraoperative use. to max 250mg).
opioid mechanisms of action MAOI Max 600mg/d
Tranexamic Inhibits plasminogen activation, Avoid in Dizziness, nausea Slow IV: 10–15mg/kg tds. Slow IV: 0.5–1g tds.
acid reducing fibrin dissolution thromboembolic PO: 10–25mg/kg tds PO: 15–25mg/kg tds
by plasmin. Reduced disease, renal
haemorrhage in major trauma, impairment and
prostatectomy and dental pregnancy
extraction. Can be used for
surgical bleeding in obstetric
haemorrhage and prophylaxis
in arthroplasty
Vasopressin Synthetic ADH used in Extreme caution in Pallor, coronary Diabetes insipidus Diabetes insipidus SC/
treatment of diabetes insipidus, coronary vascular vasoconstriction, SC/IM: <12y, 0.1–0.4 IM: 5–20 units 4-hourly.
resistant vasodilatory shock, disease water intoxication micrograms/d; >12y, 1–4 Septic shock infusion:
variceal bleeding micrograms/d. See BNF 1–4 units/h. Variceal
for Children for specific bleed: 20 units over
indications 15min
DRUG FORMULARY
(Continued)
1207
2081
1208
Chapter 42
bd, twice daily; ET, endotracheal; IM, intramuscular; IV, intravenous; NR, not recommended; od, once daily; PO, per os (oral); qds, four times daily; SC, subcutaneous; SL, sublingual; tds,
three times daily. Doses are IV and dilutions in 0.9% sodium chloride, unless otherwise stated.
Infusion regimes
(See Table 42.2.)
Drug Indication Diluent Dose Suggested regime Infusion Initial rate Comments
(60kg adult) range (adult)
Adrenaline Treatment of 0.9% 2–20 micrograms/min 5mg/50mL (100 1.2–12+ 5mL/h Via central catheter. Suggest
hypotension sodium (0.04–0.4 micrograms/ micrograms/mL) mL/h 1mg/50mL for initial intraoperative
chloride, kg/min) use (or 1mg/500mL if no central
5% glucose access)
Alfentanil Analgesia 0.9% 0.5–1 micrograms/ Undiluted (500 0–8 mL/h 4mL/h 1–2mg can be added to 50mL of
sodium kg/min micrograms/mL) propofol for infusion
chloride,
5% glucose
Aminophylline Bronchodilation 0.9% 0.5mg/kg/h 250mg/50mL 0–6mL/h 6mL/h First 5mg/kg can be given over
sodium (5mg/mL) 20min if theophylline-naïve
chloride, Caution in patients already
5% glucose receiving theophyllines (serum
level 10–20mg/L); 0.6mg/
kg of aminophylline should
increase serum level by 1mg/L
Side effects include
tachydysrhythmias, tachypnoea,
seizures and nausea
INFUSION REGIMES
(Continued)
1209
201
1210
Table 42.2 (Contd.)
Drug Indication Diluent Dose Suggested regime Infusion Initial rate Comments
(60kg adult) range (adult)
Amiodarone Treatment of 5% glucose Loading infusion 5mg/kg 300mg/50mL 25–50 25mL/h Via central line (peripherally ‘in
arrhythmias only over 20–120min, then (6mg/mL) mL/h, extremis’). Max 1.2g in 24h. Adjust
Chapter 42
(Continued)
1211
21
1212
Ketamine ‘Trauma’ mixture 0.9% 0.5mL/kg/h 50mL mixture 15–45 30mL/h 200mg ketamine + 10mg
sodium (4mg/mL ketamine) mL/h midazolam+ 10mg vecuronium
chloride in 50mL
Lidocaine Ventricular 0.9% 4mg/min for 30min, 500mg/50mL 6–24 24mL/h After 50–100mg, slow IV bolus.
(lignocaine) arrhythmias sodium 2mg/min for 2h, then (10mg/mL, 1%) mL/h ECG monitoring
chloride 1mg/min for 24h
Lidocaine Postoperative 0.9% Loading dose 1.5mg/ 2% lidocaine neat 1.5–6 3mL/h Use IBW. ECG monitoring
(lignocaine) analgesia sodium kg over 2-4min (max. (20mg/mL) mL/h throughout. Avoid in hypotension,
chloride 20min), followed by hypovolaemia, heart block,
0.5–2mg/kg/h concurrent regional technique with
LA. Caution with renal, hepatic and
cardiac dysfunction. Monitor for
signs of toxicity and sedation
Morphine Analgesia 0.9% 0–3.5mg/h 50mg/50mL 0–3.5 2mL/h Monitor respiration and sedation
sodium (1mg/mL) mL/h hourly. Administer O2
chloride
Naloxone Opioid antagonist 0.9% >1 microgram/kg/h 2mg/500mL (4 100mL/h Rate adjusted according to
sodium micrograms/mL) response
chloride,
5% glucose
Noradrenaline Catecholamine 5% glucose 2–25 micrograms/min 4mg/40mL (100 1.2–12+ 5mL/h Via central line. Potentiated by
α-adrenergic (0.04–0.5 micrograms/ micrograms/mL) mL/h MAOIs and TCAs
agonist. kg/min, up to If infusion >0.5micrograms/kg/min
Treatment of 1 microgram/kg/min consider adding a second
hypotension in extremis, weaned as ionotropic agent
soon as possible)
Octreotide Somatostatin 0.9% 25–50 micrograms/h 500micrograms/ 2–5mL/h 5mL/h Use in variceal bleeding unlicensed
analogue sodium 50mL (10
chloride micrograms/mL)
Oxytocin Prevention of 0.9% 0.02–0.125 units/min 30units in 500mL 30–125 125mL/h Individual unit protocols vary
uterine atony sodium (10 units/h) (0.06 units/mL) mL/h
chloride,
5% glucose
Phenylephrine Treatment of 0.9% 30–60 micrograms/min 5mg in 50mL (100 18–36 30mL/h Gaining popularity for regional
hypotension sodium micrograms/mL) mL/h Caesarean
chloride,
5% glucose
INFUSION REGIMES
(Continued)
1213
241
1214
Index
Note: Tables, figures, and boxes are indicated by an italic t, f, and b following the page number.
A acute kidney injury adult basic life support
see AKI 1052–4
AAA repair 592–4 acute laryngotra breathing 1053
emergency 595–6 cheobronchitis 949 chest compressions 1053
ABC acute liver failure 202–4 defibrillation 1053
air/gas embolism 1075 anaesthetic see also resuscitation
anaphylaxis 1081 management 206 Adults with Incapacity Act
burns patients 1013–14 causes 203t (Scotland) (2000) 328
elderly patients 1025–6 subtypes 203t advance directives 42
paediatric emergencies transplant referral Jehovah’s Witnesses 462
951, 959 criteria 210b psychiatric patients 328
pulmonary oedema 1080 acute motor axonal advanced life support
severe bronchospasm 1078 neuropathy 312t adult 1055–7
severe hypertension 1069 acute motor-sensory paediatric 951, 953f
severe hypotension 1066 axonal neuropathy Advanced Trauma Life
severe hypoxia 1071 (AMSAN) 312t Support (ATLS) 969–70
see also resuscitation acute pain 1152 children 953f
abciximab 277–8, 279t acute renal failure see AKI see also resuscitation
regional anaesthesia 1110t adalimumab 248 aeromedical
abdominal hysterectomy 752 Addison’s disease 228 transfer 1046–7
abdominal injuries 999–1000 perioperative AF 149–51
children 1021 management 228 ablation 832–3
abdominal wall blocks 1168 Addisonian crisis 229 anticoagulant
abdominoperineal resection adductor canal block 1140 therapy 269–75
672t, 678t adenosine 149, 1182t heart failure 113
abdominoplasty 650t in porphyria 261t hyperthyroidism 223
ABG 165t thallium scintigraphy 105 management 149–50, 150t
chronic liver disease 206 adenosine diphosphate/ prevention 150t
COPD 179 P2Y12 inhibitors 277 risk stratification 270t
restrictive pulmonary ADHD 328 AHI 109
disease 185 adjuvant analgesia in AIDS 228
ablation perioperative air embolism 135, 584–5,
intracardiac 832–3 care 1170–2 1074–5
endometrial 747t adrenal crisis 229 blast injuries 1006
tumours 733, 824 adrenalectomy 233 paradoxical 585
abortion 749 see also airborne respiratory
acarbose 219t phaeochromocytoma viruses 403–4
accidental awareness during adrenaline 758, 1182t airway 971–4
GA see awareness anaphylaxis 1081, assessment 363–7
under anaesthesia 1082t, 1082 burns patients 1013
ACE inhibitors bronchospasm 1079t cannot intubate, cannot
and breastfeeding 867t children 962t, 963–4 oxygenate 381, 1095
heart failure 113 drug interactions 331–2 cricothyroi
ischaemic heart infusion 1209t dotomy 381–3
disease 106–7 in porphyria 261t rescue techniques 381–3,
in pregnancy 894 pulmonary 382f
achondroplasia 252 hypertension 143t children 921
acromegaly 222 resuscitation 1056 face masks 908
ACTH sepsis and septic nasopharyngeal 908
Cushing’s syndrome 232 shock 1037 oropharyngeal 908
activated charcoal filters 1098 adrenocortical stabilisation prior to PICU
acupuncture 1169 insufficiency 228–9 transfer 961
acute epiglottitis 949–50 see also Addison’s disease supraglottic airway
acute intermittent adult advanced life support 908, 909t
porphyria 260 1055–7 trauma 1019
281
1218 Index
1220 Index
1222 Index
cardiac resynchronisation heart murmurs see heart cerebral blood flow 559
therapy see CRT murmurs cerebral ischaemia,
cardiac stress testing 29 hypertension 116–17 delayed 576
cardiac surgery 508–27 pulmonary 139–44 cerebral palsy, fetal
CABG see CABG ischaemic heart neuroprotection 870
controversies 526–7 disease 102–8 cerebral perfusion
CPB 511–12, 514 myocardial pressure 558
DHCA 521–2 infarction 109–10 cerebrovascular disease 298
IABP 523 obesity 71 cerebrovascular event
preoperative pericardial disease 128 see CVE
considerations 508–9 in pregnancy 891–2 certolizumab 248
drugs 509 transplanted heart 132–3 cervical cerclage 896
pulmonary valvular heart disease see cervical spine
hypertension 524–5 valvular heart disease elderly patients 1025
redo 517–18 cardiovascular history 24 emergency care 971–4
risk scoring 509 cardiovascular system, children 1020
routine elective 513–15 preoperative fusion 630t
RV function 524–5 examination 27 CHA2DS2-VASc score
specific cardioversion 828 269, 270f
considerations 516–18 carotid Charcot–Marie–Tooth
TOE 510 endarterectomy 601–3 syndrome 322
valve surgery 518t, 518 awake 602–3 drug considerations 324t
cardiac tamponade 976 carpal tunnel release CHD 134–5
cardiogenic shock 976t 640t, 650t adults with 138
cardiology procedures, carvedilol 113 ASD 136
anaesthesia for 826–7 cataract extraction 812 Eisenmenger’s
angiography 829 catheter syndrome 135
cardiac device insertion central venous 360 Fontan circulation 137
and removal 830–1 epidural 842, 845, HLHS 137
cardioversion 828 1108, 1165 non-cardiac
electrophysiology suprapubic 726t surgery 134–5
procedures 832–3 Tenckhoff 196–7 PDA 136
indications 826 urinary, by weight 1020t risk factors 134–5
TAVI 834–5 vascular, placement 825 tetralogy of Fallot 137
cardiomyopathy 129–31 caudal block 929–30 transposition of the great
alcoholic 338 advantages/ arteries 137
causes 129t complications 930 VSD 136
dilated 130 anatomy 930f checklists
HOCM 131 children 929–30 anaesthesia 4–6, 5f
restrictive 130 continuous caudal epidural drug administration 7–8
stress-induced 129 analgesia 930 intubating critically ill
cardiopulmonary bypass CCF 134–5, 136, 1072 patients 375f
see CPB cefalexin 261t patient transfer
cardiopulmonary exercise cefotaxime 963–4 1048t, 1049t
testing see CPET ceftriaxone 261t TIVA 416t
cardiopulmonary cell saver see intraoperative WHO 4–6, 5f
resuscitation see CPR cell salvage chemical burns 1017
cardiovascular cement implantation chest compressions 1053
disease 102–62 syndrome 615 see also CPR
arrhythmias, cementoplasty 823 chest drain,
perioperative 145–6 central cord syndrome 305t in children 1020t
narrow central nervous system tension
complex 147–51 elderly patients 90 pneumothorax 974
broad complex neonates 903 chest injuries 553–5,
arrhythmias 152–3 central neuraxial 974–6, 995–8
cardiomyopathy see anaesthesia 306 aortic injury 997
cardiomyopathy central venous cardiac contusion 996–7
CHD 134–5 cannulation 360 children 1021
CPET 105 femoral 580–1 diaphragmatic rupture
elderly patients 89 internal jugular 701 553, 998
heart failure 111–15 cephalosporins 867t life-threatening 974–6
241
1224 Index
1226 Index
1228 Index
1230 Index
1232 Index
1234 Index
1236 Index
labour and delivery (Contd.) accidental IV injection 846 in liver failure 211t
epidural analgesia 842–3 ATI 395 neuropathic pain 1171
complications 845–7 common adjuncts 1103t ophthalmic surgery 804
CSE 843 day surgery 488 in porphyria 261t
poorly functioning 844 and MAOIs 331–2 in pregnancy 895
regional anaesthesia 841–3 in myasthenia gravis 314 regional anaesthesia 1102t
remifentanil 852 ophthalmic surgery 802– resuscitation 1056
see also Caesarean section 3, 804–7 lignocaine see lidocaine
Lambert–Eaton regional anaesthesia 1102 limb fractures
syndrome 316 premedication 66 femoral neck 642–6
drug considerations 324t systemic major trauma 1004–5
lamotrigine 302t toxicity see LAST ORIF 625, 626t
laparoscopy 674–81 laser surgery 476–9 limb-girdle muscular
appendicectomy 678t, 681 laser wavelength/ dystrophy 321t
cholecystectomy colour 476t limb injuries 1004–5
678t, 680 microlaryngoscopy 773–5 children 1021
gas insufflation 675, 675t prostate surgery 729 compartment
gynaecological surgery 750 safety 478–9 syndrome 1005
hysterectomy 752 lasers 477 linezolid 331–2
patient positioning 674 LAST 1092–3, 1102 lipid emulsion therapy 1093
perioperative care 676 Lasting Power of Attorney liposuction 662–3
pneumoperitoneum see LPA liraglutide 219t
675, 675t lateral decubitus position literature searches 13
postoperative care 677 438–9, 438f lithium 332
preoperative lateral femoral cutaneous measurement of cardiac
assessment 676 nerve block 1137–8 output 431–2
robot-assisted latex allergy 1086–7 lithotomy position 436–7,
prostatectomy 737–8 anaphylaxis 1086 437f
sterilisation 750 clinical features 1087 lithotripsy, extracorporeal
surgical requirements 674 prevention 1087 shock wave 740
trauma 675 league table of liver
laparotomy 747t analgesics 1161t oesophageal bleeding,
emergency 1040–3 learning disabilities 95 acute 696–7
laryngeal mask airway communication 95 resection 704–7
see LMA leflunomide 247 transplantation 699–703
laryngeal view 365f legal proceedings ultrasound 140
laryngectomy 778–9 death on operating table variceal haemorrhage,
pharyn 505, 506 acute 696–7
golaryngectomy 333t major anaesthetic mishaps liver disease 202–13
laryngoscopy 505, 506 acute 202–4
airway 971–4 leukaemia 238, 288 anaesthetic
children 333t, 909 levetiracetam 301 management 206
difficult, predictors seizure management 992 transplant referral
of 364–6 levobupivacaine 1182t criteria 210b
grade of view 365f in porphyria 261t alcoholic 338
laryngoscopes 357–8 regional anaesthesia anaesthetic
microlaryngoscopy 773–5 1102t, 1102 management 205–10
videolaryngoscopy 357–8, thoracic surgery 531 Child’s classification
358f, 379–80 levodopa–benserazide 292t 205, 206t
bladed levodopa–carbidopa 292t chronic 202
videolaryngoscopes levosimendan 143t anaesthetic
357, 380 LFTs 207t management 205–
conduited videolaryn carcinoid syndrome 235 10
goscopes 380 chronic liver disease 206 coagulation disorders 266t
difficult, predictors of 366 LiDCOplus™ 431–2 drug metabolism 211, 211t
laryngospasm 370 lidocaine 186t, 1182t elderly patients 90
in children 371, 921–2 in CKD 197t hepatic
severe 1073 in G6PD deficiency 264t encephalopathy 204
laryngotracheobronchitis, induction of oesophageal varices 207
acute 949–50 anaesthesia 408 postoperative 212–13
LAs 1102 infusion 1209t safe drugs 211t
Index 1237
1238 Index
1240 Index
1242 Index
1244 Index
1246 Index
1248 Index
1250 Index
total knee joint replacement transposition of the great secondary survey 980
see TKR arteries 137 secondary survey 980
total pain 1173–4 transthoracic silver 1025–8
total spinal block 845–6 echocardiography 114 spinal 1002–3
tourniquets 616–17 transurethral resection teams/team leader 969
tracheal intubation see of bladder tumour 731 thoracic 974–6
intubation of prostate see TURP Trendelenburg position 436
tracheobronchial foreign transurethral vaporisation reverse 436
body 333t of prostate 729 treprostinil 141t, 143t
tracheobronchial injury transvenous pacing 156 triamcinolone 231b
554–5, 998 transversus abdominal plane tricyclic antidepressants
tracheoesophageal block see TAP block see TCAs
fistula 936 tranylcypromine 331–2 trifascicular heart block 155
tracheostomy 776–7 trapeziectomy 640t trigger finger release 640t
see also cricothyroidotomy trauma 968–1028 triple H therapy 576
tracheostomy tubes 777 abdominal injuries trisomy 21, see Down’s
train-of-four monitoring 999–1000 syndrome
423, 424t airway 971–4 troponins 109
tramadol 1157–8, 1182t blast injuries 1006–7 heart failure 114
in CKD 197t brain 989–94 trunk, nerve blocks 1128–34
contraindicated with burns 1013–18 erector spinae plane
MAOIs 331–2 cardiac arrest secondary block 1130
dosage 1158t to 1009–11 iliohypogastric
efficacy 1161t chest 553, 974–6, 995–8 block 1131–2
in epilepsy 301t children 1019–24 ilioinguinal block 1131–2
in G6PD deficiency 264t imaging 1022–3, midaxillary transversus
tranexamic acid 281, 1022b–3 abdominis plane
702, 1182t circulation and shock 976–8 block 1133
blood management 458–9 crush injuries 1008 pectoserratus plane (PSP)
cardiac surgery 526 elderly see silver trauma and interpectoral plane
transcatheter aortic valve exposure/environmental (IPP) blocks 1130
implantation see TAVI control 979 penile block 1132
transcutaneous electrical eye injury 815 rectus sheath
nerve stimulation fluid resuscitation 978, 979b block 1133–4
see TENS gunshot injury 1006 TAP block 932, 1133
transcutaneous pacing 156 head 989–94 thoracic paravertebral
transfer factor (diffusing imaging 979–80, 980t, 981 block 1128–9
capacity) 165t children 1022–3, tryptase 1084
transfusion-associated 1022b–3 TT, coagulation
circulatory overload immediate care 968–70 disorders 266t
(TACO) 456 induction of tuberculosis see TB
transfusion-associated anaesthesia 972–4 tubes 355
graft versus host intracranial chest, see chest drain
disease 456–7 haematoma 564–5 double-lumen see DLT
transfusion-related intubation 972–4, 972b–4 microlaryngeal 773
acute lung injury limbs and extremities misplaced 371
(TRALI) 456–7 1004–5 nasogastric see
transient ischaemic log roll 981 nasogastric tube
attack 296 maxillofacial 993–4 in children 909–10, 910t
transoesophageal neurological tracheostomy 777
echocardiography assessment 978–9 see also ETT
see TOE head injuries 992 tumour lysis syndrome 474
transplanted heart patient journey 968–70 tumour necrosis factor
anaesthetic pelvic injuries 1001 inhibitors 247–8
technique 133 prehospital care 968 tunnelled, cuffed CVCs 360
immunosuppression 132–3 pregnancy 988 Tuohy needle 1108
physiology 132 primary survey 971–80 TURP 728–30
risk factors 133 resuscitation TURP syndrome 729–30
transplantation, damage control 982–7 TUVP 729
kidney 742–4 haemostatic 983–4 tympanoplasty 771
transplanted lungs 188–90 primary survey 971–4 tyramine 331–2
Index 1251
1252 Index