CTSP 2020 by NHG IM (V2)

CTSP
2020
CALLED TO SEE PATIENT
NHG INTERNAL MEDICINE
Table of Contents
Jump to the chapter by clicking on the content page below
Foreword ........................................................................1
General Advice ...............................................................3
Cardiology ....................................................................11
Dermatology .................................................................29
Endocrinology ...............................................................56
Gastroenterology ..........................................................67
General Medicine .........................................................83
Geriatric Medicine (GRM) .............................................95
Haematology/Oncology............................................... 109
Infectious Diseases..................................................... 148
Neurology ................................................................... 157
Palliative Medicine ...................................................... 171
Rehabilitation Medicine ............................................... 181
Renal/Electrolytes ....................................................... 185
Respiratory Medicine .................................................. 206
Rheumatology, Allergy & Immunology ........................ 220
Acknowledgements..................................................... 227
Important Contact Numbers ........................................ 229
We dedicate this book to
Our patients, who are our greatest teachers;

Our mentors, who inspire and nurture us daily;
Our allied health colleagues, who make this journey enjoyable.
Without each of you, we would not be who we are today.
Foreword
It brings me great pleasure as the Internal Medicine Programme

Director to pen the foreword for this booklet titled “Called To See
Patient (CTSP)”, which embodies the tremendous effort of our
residents with guidance from Internal Medicine faculty over the past
many years. This booklet is created by our residents for our residents.
Our first edition was written in 2011 with refinements made annually
based on feedback from residents and input from Internal Medicine
Education Committee.
I am sure we can recall the helplessness, insecurity and anxiety on our

first day of work as a doctor, especially during our very first call. No
matter how much reading or hard work you have put in prior to starting,
you never felt secure enough. There seems to be myriad of acute
medical conditions you may encounter on call and you are lost just
thinking about what you need to read before your call. While online
references like UpToDate, soft copy medical textbooks are easily
available nowadays with your smartphone, they tend to be verbose
and difficult to refer when time is of essence, especially if you are
struggling with the 15th admission of the night with a few other sick
patients to attend to. These references also often do not take local
practices, guidelines and preferences into account.
In response to these needs, our residents have come together to write

this booklet that aims to provide a practical guide to many acute
medical conditions and survival tips developed from their cumulative
Click here to return to Page 1
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and collective experience over the years. Many of our residents have
benefitted from this booklet. By helping to improve this booklet
regularly, they hope to pay it forward by helping their newly joined
juniors manage the challenges on the ground better and ultimately
provide better patient care. This booklet will also serve as a useful
reading before starting calls, as it narrows down the common
conditions you may encounter and how to manage them on call. It also
includes tips on how to navigate the systems in Tan Tock Seng
Hospital and Khoo Teck Puat Hospital. These are the features which
make this booklet unique and practical.
All these would not be possible without the great effort and thought put
in by our past and present residents. I would like to commend our
residents for their hard work and I am very proud of their spirit of paying
it forward, which showcases our NHG spirit. I would also like to thank
the Internal Medicine faculty from Tan Tock Seng Hospital, Khoo Teck
Puat Hospital and National Neuroscience Institute for their unfailing
guidance and support. We hope that you will find this booklet useful
for your work and look forward to any suggestions to make it even
better!
Dr Ng Wee Khoon
Programme Director
NHG Internal Medicine Residency Programme
Disclaimer
This booklet serves as a brief guide to the management of acute

conditions commonly encountered in the ward. It is not meant to be
exhaustive and the reader should use standard reference text for
further reading. Every patient and situation will differ, hence the
information presented here should be used in context. When in doubt,
always consult a senior.

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GENERAL ADVICE FOR ON-CALL
TTSH General Medicine HO Call Advice
You will cover patients from the following departments:

CVM (passives only), Dermatology, Gastroenterology, General
Medicine, Geriatric Medicine, Haematology/Oncology, Infectious
Diseases, Palliative Medicine, Psychiatric Medicine, Rehab, Renal,
Respiratory Medicine, Rheumatology/Allergy/Immunology
* Neurology actives and passives are seen by NL MO
Active cases = New admissions

Passive cases = Issues arising from existing patients
PRE-CALL:
- Get enough SLEEP the night before
- Check HMS Daily On Call for which levels/wards you’re covering
(and any additional area e.g. Medical Ambulatory Centre on L2)
- Get the numbers of your MOs and contact them early to ask them
how they want to work (e.g. Whatsapp / SMS / call? Contact them
for new cases first or clerk first?)
- Activate your call room early (L1 security office) and get changed
into scrubs
- HAVE AN EARLY DINNER – the best time to eat is around 5 to
6pm before all the calls flood in
- Once call starts (5pm on Weekdays, 1230pm on Saturdays,
1030am on Sundays/PH), you will start to receive HANDOVERS
from your friends
- Important things to note down on paper
o DIL patients
o Things to trace - bloods/ECGs/scans/blue letters (find out
WHAT to do/expect with the results e.g. keep Hb > what)
o Investigations to be performed (eg. ABGs)
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o Review of sick patients usually handed over to MOs
- Log in and familiarize yourself with EDWEB (can pre-empt and pre-
clerk new patients coming up to wards you’re covering)
- Always carry a few add-test forms and KY gel with you
- Useful to carry green (heparin) for BOHB, toxicology, and grey
(floride) tubes for lactate with you (not all wards stock – and may
need for acute emergencies)
- Know where to find the TTSH empiric antibiotic guidelines and
renal dose adjust tables on intranet
- Develop a system of keeping track of the things you have done /
not done and prioritizing changes
- You may create a list of all the patients in your allocated wards on
call in CPSS2
ON-CALL:
- Got time sleep, got food eat, got water drink.
- Call starts from 5 pm to 8 am. It is advised that you inform your
team that you are on call, and if there is a late exit, to handover the
responsibility of exiting to your colleagues if possible.
- You are also responsible for patients up to 8 am. The primary team
may help with clerking new admits just before 8 am but the default
responsibility falls on the on call team.
- Handover: ask for 2 patient identifiers (usually name, NRIC, ward
and bed number). DIL patients should have the extent of care and
CCOD handed over to you. If asked to trace results, ask for the
estimated time results will be out and what to do if there are
abnormalities (e.g. blood transfusion targets, what to do if Trop I
elevated).
- Learn to PRIORITISE. You may be overwhelmed by the sheer
amount of work especially during the first few calls, but if you sieve
out what’s important and deal with those first, things become much
more manageable.
- In rough order of priority:
1. Patient COLLAPSE
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2. Urgent passives e.g. desaturation, hypotension, chest pain
etc.
3. New cases (generally try to see before your MO)
4. Tracing labs/investigations and acting on them (including
correction of electrolyte abnormalities – remember to put an
end date for regular mist KCL replacement)
5. Time sensitive bloods (e.g. cardiac enzymes)
6. Procedures (IDCs, IV cannulation). More urgent if: ARU x long
time with high RU/PVRU, IV cannula for dopamine etc
7. Non-urgent passives (cough syrup, sleeping pills, change med
order in eIMR, etc.)
8. Updating/speaking with relatives, unless DIL
- KNOW YOUR LIMITS, both in terms of experience and the
capacity to bear responsibility if something goes wrong
- If in doubt, call your MO early
- Refrain from copying and pasting ED notes onto admission
clerking sheet
- Take note of vitals and progress in ED and medications served in
ED to avoid duplication (eg. electrolyte replacement/abx)
- Check with a senior first before ordering certain investigations (e.g.
generally all scans, expensive blood ix) and interventions (e.g. blue
letters, high risk meds, listing for scopes)
- PLEASE be polite to the nurses! A bad call with incessant calls
from the nurses and never-ending admissions/passives will fray the
nerves and crush the souls of the hardiest of HOs. No matter what
though, nurses are your allies and friends: they can make or break
your call in more ways than one.
- When giving meds/ordering investigations/taking blood:
o Check it’s the correct patient when sending off blood tests!!
Always check that patient name on sticky label correlates with
order form
o Taking GXMs: Sign BOTH the sticky label and order form,
indicate on sticky label date and time the blood was taken
o Learn how to dispatch your own bloods using the pneumatic
tube system
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o Don’t dismiss complaints like headache and giddiness (always
remember to check vital signs and review labs, giddiness
could be BGIT or stroke for example)
o Simple bedside investigations like CBG, ECGs can be
performed quickly and yield important information
o Trace all investigations you’re asked to review – document in
CDOC as appropriate
- Please do not remotely order investigations/medications without

seeing the patients. There are certain situations where remotely
ordering is acceptable (e.g. ordering medications that was served
late). Generally, if you are making a change to the patient’s
management, please see the patient and document your impression
and plans. Do note that the location of your order can be traced on
the system.
Common types of cases encountered:

- GM, PSY; can be flooded by the sheer volume of admissions as all
the wards are C class wards (up to 42 patients per ward). 5A is an
MRSA cohort ward.
- GRM; Treat AMS with respect in the geriatric patients. Basic
geriatric history (baseline cognition, functional history) and
examination (DRE, palpating for bladder, bedside swallowing test)
are useful to remember.
- RAI admits are usually (1) Allergies, (2) Joint pains/flare of
underlying condition, (3) Elective admissions.
- RM and CVM cases – expect to trace many ECGs/cardiac
enzymes, do ABGs, receive calls for SOB/chest pain. You will be
called for abnormal telemetry readings. Take note of the rhythm,
vitals and assess pt for symptoms. Patients with (1) Potentially
dangerous rhythms that may require intervention, (2) Who are
symptomatic, or (3) Unstable vitals will need to be reviewed ASAP.
- Renal patients – note which side is the AVF (or planned for AVF
creation) and avoid blood taking on that arm. Do not take bloods
from PICC unless you have been trained. DO NOT cannulate an
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AVF. DO NOT take blood from a perm cath. Low threshhold to
perform septic workup and start antibiotics for unwell,
immunocompromised pts. AHU is an acute hemodialysis unit
located in 9A where pts undergo dialysis after office hours (or
undergo SLED in the daytime if they are not well enough for
regular dialysis at Renal Unit). AHU is taken care of renal MOs
during office hours and the HD MO after office hours. You should
not be called to see patients in AHU.
- HO (Half Calls) – You should stop receiving calls from the nurses
after 9pm. Do try to clear your tasks ASAP – you are still expected
to report to the wards the next day at the same time (i.e. no post
call). If bloods are ordered at 8.30pm, make sure that the
phlebotomist is aware. Please take the bloods if you are not sure
whether the phlebotomist will do the bloods (esp blood cultures).
- Carry coins with you for a quick coffee/coke break at the vending
machines
- Save important phone numbers into your work phone (see last
section of this book ‘Important Contact Numbers’) as you work – so
that you do not have to call “0” (for operator) and wait
- Accompanying DIL patients down for scans/procedures – know
what the resus status is and ensure appropriate equipment is
available (e.g. drugs, fluids, working IV plug available) – if for
active and unstable may want to carry defibrillator for continuous
ECG monitoring, ensure O2 tank has enough O2 to last the
journey. Help to push the heavy beds (the Ah-Mahs and nurses will
appreciate it).
Clerking new cases

- Review Drug Allergies/Adverse Drug Reactions in the CMIS tab on
the top right hand corner of CPSS
- Summarize PMHx and latest medication list from NEHR, CPSS,
CPRS (scroll through past few prescriptions – BOTH prescribed
and dispensed meds so as not to miss anything)

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- CDMR is a useful place to trace the latest HbA1c, lipid panel from
OPS
- Can try to ask nurses to prepare items you may need while you
type to save time (e.g. otoscope/ophthalmoscope, tendon tapper,
blood culture set/bottles, bag of ice for ABG/lactate)
Plan – have a system, order everything you can on Aurora

1. Nursing Orders
- Monitoring – frequency of paras/SpO2, CLC, CBG (TDS +
10pm vs Q6H if NBM)
- Intake/Output charts (strict?)
- Charts e.g. postural BP, daily weight, fit, hemoptysis, stool,
vomit, behaviour, sleep-wake
- Fluid restriction e.g. 1L/day, 1.2L/day
- NBM vs Diet
- Types of diet
o Therapeutic e.g. DM, low salt, low fat, low purine, HD
(haemodialysis), non milk/non spicy
o Consistency
Solids: regular, easy chew, soft moist, blended
Liquids: pudding, honey, nectar, thin
o NG feeding (find out regular regime e.g. Ensure/
Glucerna 200ml x 6 with 50ml water flushes,
supplements e.g. myotein)
- Fall precautions, suicide precautions, abscondment
precautions, low platelet precautions e.g. no teeth brushing,
no IM injection, Complete Rest In Bed (CRIB)
- CIWA scoring (first input must be made by doctor)
2. Investigations
- Add tests
- Bloods (phlebotomist is around until 9pm, after which blood
cultures will need be taken by doctors)

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o On Aurora, ‘Renal panel’ does not include urea/
chloride/ bicarb, ‘Liver panel’ does not include AST and
GGT – order separately as needed
- Imaging (select wheelchair / trolley / portable accurately for
XRs) –provide relevant history in the top right hand corner
of Aurora to help radiologists fine tune their report based on
the clinical concern
- Microbiology
- Others
3. Management
- Relevant drugs to treat patient’s condition
- IV antibiotics (rmb to calculate CrCl and check dose)
- Restart old medications (check for contraindications – e.g.
hold off antihypertensives if pt is hypotensive, review for
anticoagulant/antiplatelet in bleeding, hold off metformin if
awaiting contrasted scan/AKI – consider actrapid sliding
scale)
- Referrals to PT/OT/ST
POST-CALL:
- HANDOVER sick patients you encountered overnight to the
primary team, especially if they should be reviewed again early
- HANDOVER significantly abnormal lab/imaging results
- Try to grab a quick breakfast before AM rounds start
- Be sure to finish up ALL your morning round changes and
handover appropriately before you go post call at 12-1pm
- It can be of tremendous learning value to re-visit some of your
interesting admissions/passives over the next few days when time
is available. Diagnoses may change, signs may develop, cases will
evolve.
- Read up and reflect on your performance of that call. Aim to do
better the next call!
- Savour the post-call euphoria while you can. It’s back to work the
next day…
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CARDIOLOGY
(I) CHEST PAIN

- Over the phone: vitals, admitting diagnosis, ECG if not done, BP
on both arms, supplemental O2 if hypoxic
- Review CDOC: risk factors for IHD, previous ECG, diagnosis of
ACS/raised trop I in this admission
- Attend to patient within 15 minutes. Eyeball the patient: escalate
early if unstable / ill-looking
- Compare ECG with old ECGs: ST and T wave changes,
reciprocal changes, new LBBB/RBBB, new arrhythmias
- History: Typical cardiac pain is crushing, retrosternal,
exertional/at rest, not worse on truncal movement/palpation,
radiates to jaw/ left UL, >15mins, a/w diaphoresis, SOB
- Remember the life-threatening causes of chest pain:
1) CVS: ACS (STEMI/NSTEMI/UAP), aortic dissection
2) Respi: tension pneumothorax, pulmonary embolism
3) GI: perf viscus (e.g. peptic ulcer, oesophageal rupture)
- PE: vitals, GCS, BP on both arms, RR/RF delay, new murmur,
signs of fluid overload, acute abdomen
- Investigations
▪ Trop I x 2 sets 3-6hr apart (detectable within 4-6h, peak 12-
36h, normalise after 1-2 weeks). No need CKMB.
▪ If ongoing chest pain and first ECG unremarkable, repeat
ECG every 5 min for dynamic changes
▪ Consider: FBC (T2MI ppt by anaemia, sepsis), UECr,
Ca/Mg/PO4 (arrhythmias), PT/PTT (if for procedure e.g.
coros), ABG (if desaturation or strong suspicion of PE)

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Diamond Classification Typical Atypical Non-Anginal
Angina Angina Chest Pain
Retrosternal with
characteristic quality & YES
2 OUT OF 0 OR 1 OUT
duration
3 OF 3
Precipitated by
YES CRITERIA CRITERIA
physical/emotional stress
Relieved by rest/GTN YES

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CHEST PAIN EVALUATION PROTOCOL FOR HO/MO

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TTSH Clinical Guidelines CMB-GP-Chest Pain protocol 01 2013
(II) ACUTE CORONARY SYNDROMES:
CTSP for chest pain, SOB, desat, hypotension, trace ECG, Trop I
Inferior MI
- ECG: II, III, aVF STE >/=1mm with reciprocal STD in I, aVL
- Look for 3 things:
1. Concurrent posterior infarct (V1, V2 STD – flip ECG over to
see STE or perform posterior ECG i.e. V7, V8, V9)
2. Concurrent right sided infarct (V2R-V6R STE) –commonly
a/w hypotension (preload dependent).
3. Arrhythmias – Mobitz type II 2nd degree or 3rd degree heart
blocks (AV nodal artery from RCA in 80%)
Anterior MI
- ECG:
▪ STE in V1-V6 (precordial) and I & aVL (high lateral),
reciprocal STD in inferior leads (mainly III and aVF)
▪ Wellen’s syndrome (critical prox LAD stenosis): Precordial T
wave inversions or biphasic T waves in V2-V3
RV infarct
- Preload sensitive (poor RV contractility). Can develop severe
hypotension with
nitrates or preload
reducing agents
- Treat with aggressive
judicious fluid infusion
with guidance from
seniors.
- Suspect in all inferior MI
- ECG: STE in V1, STE in
V1 > V2, may have STD
in V2, STE in right sided
leads - V3R to V6R

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Posterior infarct
- ECG: V1-V3 show horizontal STD, upright T waves, tall broad R
waves, R/S ratio > 1 in V2; STE in posterior leads V7 to V9
Management of ACS
- Inform senior immediately
- Nursing orders: hourly paras, supplemental O2 if hypoxic, keep
NBM
- If diagnosis in doubt but suspicion high, serial ECG 5-10min
- Labs: FBC, UECr, Trop I x 2, GXM, PT/PTT, CXR
(cardiomegaly, pulmonary congestion, widened mediastinum),
telemetry
- Meds:
▪ S/L GTN 0.5mg up to 3x / GTN patch 5mg (instruct nurse to
omit if BP < 90/60)
▪ Aspirin 300mg STAT then 100mg OM (if no
contraindications e.g. recent major GI bleed, ICH, allergy)
▪ Please consult registrar before initiating dual
antiplatelet therapy and LMWH, i.e Clopidogrel 300 mg
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STAT then 75 mg OM / Ticagrelor 180mg STAT then 90mg
BD + PPI cover, SC Clexane (1mg/kg BD, must be renal-
adjusted)
▪ Atorvastatin 40mg (high dose statin for plaque stabilisation)
▪ Medications good to have if vitals are normal: Beta-blocker
(e.g. Atenolol 25mg / Bisoprolol 1.25-2.5mg) if no heart
failure, hypotension, bradycardia, severe reactive airway
disease; ACE-I (e.g. Enalapril, Lisinopril) OR ARB (e.g.
Losartan, Valsartan)
▪ Refer CVM for coronary angiogram (if no contraindication):
o STEMI: urgent Coros (Door to Balloon time should be
within 90 minutes)
o NSTEMI / UAP: urgent Coros if there is ongoing chest
pain / haemodynamic instability /tachyarrythamia
(III) ACUTE DECOMPENSATED HEART FAILURE

CTSP for SOB, desat
- Symptoms: SOB, orthopnoea, PND, LL swelling, cough when
supine; Signs: creps, rhonchi, S3/S4, elevated JVP, pitting
edema
- Consider non-cardiogenic causes of fluid overload - nephrotic
syndrome, cirrhosis; Other causes of symptoms - ARDS (e.g.
pneumonia), neurogenic (e.g. CVA)
- Identify precipitating factors:
▪ Cardiac: ischaemia, arrhythmias (e.g. AF), valvular disease,
uncontrolled hypertension
▪ Non-cardiac: medication non-compliance or recent change,
iatrogenic (e.g. fluid resuscitation, transfusions), fluid
indiscretion, sepsis, anaemia, uncontrolled thyroid
dysfunction
- Investigations: ECG (arrhythmias, AMI, LVH, markers of poor
EF: anterior Q waves, poor R progression, small limb leads),
CXR, FBC, UECr, CMP, LFT, Albumin, Trop I, ABG if
desaturation, Iron Panel
- Management:
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- Nursing: hourly paras, supplemental O2, nurse 45 degrees
head up, strict I/O (urosheath/IDC), fluid restrict 0.8-1L/day, low
salt diet, weigh once and daily weight
▪ Diuretics: IV Frusemide 40-80mg STAT (check baseline
Frusemide dose) and BD (watch BP, daily UECr); review
later to check response (symptoms, O2 requirement, creps,
urine output) KIV further Frusemide if needed
▪ K replacement e.g. span K 600mg for IV Frusemide 40mg
OM
▪ BB not to be initiated in ADHF. If already on BB before, no
need to stop unless patient is hypotensive
▪ Watch kidney function (can worsen in cardiorenal
syndrome) and avoid nephrotoxins. Kidney function can
worsen if too dry or too wet
(IV) HYPERTENSION
CTSP for BP >180/120
- Differentiate HTN urgency vs emergency (end organ damage)
1. Neuro: infarct / bleed / encephalopathy /papilloedema
2. CVS: AMI / APO / aortic dissection
3. Renal: AKI
- History: numbness, weakness, blurring of vision, headache,
nausea / vomiting, confusion, chest pain, SOB
- PE: vitals including BP on both arms, RR/RF delay, signs of fluid
overload, neuro exam, fundoscopy (papilloedema)
- ECG, CXR, bloods (e.g. FBC, UECr, Trop I) ± CT brain, CT
aortogram
- Management of HTN urgency:
▪ Serve anti-HTN meds earlier if near serving time
▪ Amlodipine 2.5-5mg / Hydralazine 10-20 mg / Captopril
6.25mg
▪ Aim to reduce BP gradually over the next 1-2 days
- Management of HTN emergency:
▪ Inform senior
▪ Nursing: hourly vitals, supplemental O2 if hypoxic, CLC
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charting
▪ HD/ICU review
▪ Start with medications above as for HTN urgency. If BP
persistently high, consider IV GTN 5mcg/min up to
100mcg/min or IV Labetalol 20mcg bolus then 20-80mg
Q10min or 0.5-2 mcg/min
▪ Aim to reduce SBP by 10% in 1st hour then additional 15%
in next 2-3h
- Avoid overcorrection of BP as it can cause systemic
hypoperfusion and ischaemic stroke
(V) HYPOTENSION
CTSP for BP <90/60
- Over the phone: manual BP, BP trend, other vitals (tachycardic

response), GCS, admitting diagnosis, resus status, do ECG
- Review patient STAT
- DDx: Think of 4 classes of shock –hypovolaemic (dehydration,
haemorrhagic), cardiogenic, obstructive (PE, cardiac
tamponade, tension PTX), vasodilatory (septic, anaphylactic,
neurogenic. Others: iatrogenic (anti-hypertensives), adrenal
crisis
- Targeted history: chest pain, SOB, giddiness
- Examine GCS, JVP, heart, lungs, fluid status, skin (temperature,
capillary refill), DRE for melena. Review I/O chart: Persistent
negative balance over past few days?
- Review case notes: Clues to diagnosis e.g. known BGIT.
Caution with fluid challenge i.e. reduced EF, ESRF. Whether any
fluid challenges given in the day.
- Investigations (as indicated): FBC, UECr, ECG, Trop I, ±
PT/PTT, GXM, septic workup, CXR
- Management:
▪ Nursing: hourly vitals, large bore IV, strict I/O
(urosheath/IDC)
▪ Supportive: Fluid resuscitation e.g. IV 0.9% NaCl /
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Hartmann‘s 500ml over 15-30mins (depending on fluid
status, EF, renal function). Blood products if indicated.
▪ Off all anti-hypertensives in eIMR
▪ Treat underlying cause e.g. antibiotics for infection, refer to
GE if active BGIT
▪ Escalate to senior KIV inotropes (dopamine up to
20mcg/kg/min in the ward) if high risk for or signs of fluid
overload, refractory hypotension despite fluid challenge >1-
1.5L
(VI) APPROACH TO TELEMETRY

- Level 5, 7, 8, 9, 11 and 13 have telemetry beds, so you may be
called to review abnormal rhythms
- Over the phone:
1. Vitals (HR, especially BP)
2. General condition (Distressed vs alert? If there is any sign
that something is wrong, it is important to review the
patient early)
3. Indication for telemetry, e.g. recent NSTEMI/severe
electrolyte imbalances
4. Ask for 12-lead ECG; ensure no concurrent ischemia
(telemetry only shows lead II)
Bradycardia
- Sinus bradycardia: HR <60 (Note: HR may be low in IHD patients
on beta-blockers / non-dihydropyridine CCB). If BP stable / patient
not in distress / no conduction block continue monitoring. Note:
HR may be diurnally low when the patient is sleeping.
- Sinus pause: Pacing is only indicated after consultation with
Cardiology and if vitals unstable. sinus pause > 4 sec during
awake hours may be significant.
- Look through medications list, and stop all rate limiting drugs (e.g.
BB)
- 1st degree AV block (prolonged PR >200ms): review meds. No
pacing needed.
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- 2nd degree AV block
▪ Mobitz Type 1: Usually benign. If asymptomatic: no
treatment. KIV stop AVN blocking agents (BB, CCB, digoxin)
if concerned.
▪ Mobitz Type 2: More likely to progress to 3rd degree heart
block. Stop AVN blocking agents. Escalate to senior re: KIV
need for pacing
- 3rd degree heart block: Ensure patient is stable. Stop AVN
blocking agents. Escalate to senior KIV pacing.
Tachycardia
- Simple approach for all tachyarrythmias:
1. Hemodynamically stable?
2. Check and correct electrolyte abnormalities
3. (UECr, Ca/Mg/PO4)
4. Symptomatic? (chest pain, SOB, palpitations)
- Sinus tachycardia: Ensure it is sinus tachycardia: Is there a P
wave before every QRS complex?
- DDx of sinus tachycardia:
▪ 4 classes of shock
▪ Hyperthyroidism
▪ Hypoglycaemia
▪ Electrolyte abnormalities
▪ Drugs (e.g. caffeine, salbutamol nebs, smoking)
▪ Fever, pain, anxiety (diagnoses of exclusion)
Treat underlying cause, e.g. dehydration / distress / pain /fever

- PACs: usually benign
- PVCs: review meds; KIV recheck/correct electrolyte
abnormalities (if no recent test). Causes: K / Ca / Mg imbalance,
hypoxemia, acidosis, theophylline / TCA use, ACS
- Multifocal atrial tachycardia: Usually a/w respiratory conditions
e.g. COPD / severe pneumonia.
- Non-sustained SVT: usually benign and self-limited; ensure BP
stable
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- SVT: check hemodynamic stability, carotid massage (if no
carotid bruit), valsalva manoeuvre. IV Adenosine 6 mg into a
good IV plug rapidly with IV flush. Ensure that patient attached to
cardiac monitor. If not cardioverted, repeat with 12 mg dose up
to max total 24mg. Escalate to senior.
- Ventricular Bigeminy/ trigeminy: May be associated with cardiac

ischemia or electrolyte imbalance. Ask patient for chest pain /
tightness / SOB and correct any electrolyte imbalances
- Non-sustained VT: (defined as VT <30 s), ensure BP stable.

Cause: e.g. recent ischemic event – is this another event?
Ensure electrolyte imbalances corrected. Monitor closely.
• Increase frequency of parameters
• History and physical exam
• Investigate for cause: U/E/Cr, Ca/Mg/PO4, ECG
• Attend to patient if you get called repeatedly
- VT / VF / asystole: Get crash trolley to patient STAT, review

IMMEDIATELY. Ascertain EOL. Start ACLS if for active mx. Call
senior.
Management of AF with rapid ventricular response / atrial flutter

Types of AF:
(i) 1st detected episode
(ii) paroxysmal (<7d)
(iii) persistent (>7d)
(iv) permanent (failed cardioversion / not attempted)
Consult senior before proceeding

- Determine if it is new onset (i.e. within 48 hrs): KIV
pharmacological / electrical cardioversion
- If haemodynamically unstable: sedate, electrical cardioversion
(50J, 100J, 150J)
- If stable, for rate control
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If patient in heart failure:
(i) IV amiodarone 150mg/300mg over 40 min, can be given regularly
TDS if not responding to bolus (watch for hypotension) OR
(ii) IV digoxin e.g. total loading dose of IV 500 mcg (IV 250 mcg if
elderly / renal impairment) – split into 3 administrations as follow:
o Give 50% of loading dose initially = 250 mcg
o Then administer the remaining portion as 25% fractions
(125 mcg) at 4-8 hours intervals
(Caution: WPW, AMI, AV block, thyroid disease, monitor with
defibrillator, also check electrolytes)
If not in overt heart failure:

(i) Beta Blockers, e.g. bisoprolol 1.25mg – 2.5 mg, atenolol 25mg
(caution: severe reactive airway disease) OR
(ii) Ca Channel Blockers, e.g. verapamil, diltiazem (caution: heart
block)
- Rhythm control (TRO thrombus, anticoagulate 3 weeks before /

TEE): electrical / chemical cardioversion (amiodarone, sotalol)
Others:
- Consider anticoagulation
- Calculate CHA2DS2-VASc score (if you have time)
(VII) POST CICU REVIEW

Patients that are transferred to GW from ICU are usually stable
enough to be managed there so do not panic. Also, please take the
time to flip through the ICCA notes and the discharge summary.
Before transfer out, the MOs in the CICU will update the summary
with the corresponding plans.
- Know the patient’s diagnosis so that you can note down
recurring symptoms or potential complications
- Ensure patient is haemodynamically stable and non-toxic
- Handover to your full shift HO if needed (especially if patient is
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DIL status)
- Guidelines for plans overnight
Monitoring
- Closer monitoring in the immediate period after transfer out: Q1H
paras + SpO2 for duration 4-6 hrs
▪ Inform doctor if SBP < 90, HR > 100, SpO2 < 95% or if
symptomatic (as per diagnosis)
- H/C: Q6H/TDS + 10pm
- +/-GCS depending on clinical setting
- I/O: nurses will want to know if they can off hourly urine
monitoring
▪ Read through the summary, usually can be held off, just
maintain strict I/O
Investigations
- Usually nothing overnight but help to check if any investigations
are required for the next day and order them
- ABG may be required overnight in some cases (e.g. just weaned
off BiPAP or for nocturnal BiPAP)
Management
- Follow Discharge summary plans. Do not attempt to change
patient’s management overnight unless patient’s clinical status
changes.
(VIII) POST COROS REVIEW

Post procedural review – must trace procedural notes for specific
instructions
Specific to coronary angiogram

- Checking site of puncture (usually radial but can be femoral)
▪ Check report (accessible on CCDR), if final report not
uploaded yet, check procedural notes in case file), or ask
the patient
▪ Look for bruising/oozing
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▪ Check pulse and capillary refill
▪ Document clearly
- Check for symptoms (e.g. chest pain/SOB/pulseless cold LL)
Guidelines for plans overnight

Monitoring
- Closer monitoring in the immediate period after: Q1H paras +
SpO2 x 4-6H
▪ Inform doctor if SBP < 90, HR > 100, SpO2 < 95% or if
symptomatic (as per diagnosis)
- If you are concerned about the puncture site, start neurovascular
charting and inform the Cardiology SR on call
- Tell the nurses to do STAT manual compression if oozing and
inform you STAT
Investigations
- For next morning: ECG +/- U/E/Cr
- If patient c/o chest pain: repeat ECG w Trop I
- If patient has co-existing conditions (e.g. anaemia, BGIT), KIV
repeat FBC
Management
- Ensure medications are already ordered on eIMR, especially
DAPT. Check procedure notes for medications
- Analgesia PRN
*** ESCALATE TO CARDIO MO/REG IF YOU ARE UNSURE***
(IX) DVT / PE
Clinical features of DVT: unilateral LL swelling, pain, tenderness,
erythema
Wells Score for DVT
- Paralysis, paresis, recent Ortho casting of LL 1
- Immobilisation >3 days / major surgery <4 weeks1
- Localised tenderness in deep vein system 1
- Swelling of entire leg 1
- Calf swelling >3cm other LL 10cm below tibia tuberosity 1
- Pitting edema greater in symptomatic leg 1
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- Collateral non-varicose superficial veins 1
- Active CA / CA treated <6 months 1
- History of DVT 1
- Alternative diagnosis more likely (e.g. cellulitis, Baker‘s cyst) -2
* Probability ≥3 – high, 1-2 – moderate, ≤0 – low
Investigations: FBC, PT/PTT, D-dimer (TRO if low risk) ±

thrombophilia screen (i.e. anti-cardiolipin, Protein C/S, APC
resistance, lupus anticoagulant – for unprovoked / recurrent venous
thromboembolism / young patients – need to be done before starting
anticoagulation (may not change Mx), US LL venous system
Management:
- SC Clexane 1mg/kg BD (check if any recent hx of bleeding, low
Hb). Adjust for renal dysfunction.
- Clexane dosing (CrCl > 30: BD, Crcl < 30, OM dose)
Wells Score for PE

- Symptoms of DVT (3)
- No alternative diagnosis that better explains disease (3)
- Tachycardia >100 (1.5)
- Immobilisation ≥3 days / surgery in <4 weeks (1.5)
- Previous Hx of DVT/PE (1)
- Presence of hemoptysis (1)
- Presence of CA (1)
*Probability: ≥7 – high; 2-6 – mod; ≤1 – low
Investigations: FBC, ABG, UECr, D-dimer (TRO if low risk

Wells score), ECG + CE, CXR (TRO other respiratory causes), CTPA
(need green plug), KIV TTE

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Management:
- If unstable – inform senior, ABC, transfer to HD/ICU, KIV refer to
CVM for thrombolysis. Vitals Q1H; fluids / inotropes as indicated
- If stable – SC Clexane 1mg/kg BD (renally adjust if needed)
- Clexane dosing (CrCl > 30: BD, Crcl < 30, OM dose) –
MAX initial dose of 100 mg (so if pt is > 100 kg, don’t give
> 100 mg clexane)

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ACLS protocols:
https://www.uptodate.com/contents/image?imageKey=EM%2F73862&topicKey=
EM%2F278&rank=1~150&source=see_link&search=ACLS
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https://www.uptodate.com/contents/image?imageKey=EM%2F63919&topicKey=
EM%2F278&rank=1~150&source=see_link&search=ACLS

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DERMATOLOGY
Most of the dermatology patients will now be admitted in the new NCID
building in Ward 12E. However, there may rarely be overflow
dermatology admissions to the main building.
Existing NSC patients’ dermatological histories (clinic consultation,

diagnosis, treatment and photographs) are stored in NSC’s ‘Versalius
system’. Only Dermatology residents and MOs will have the username
and password to access the system.
If patients have been admitted from NSC to TTSH Main Building,

please look for a memo written by the admitting NSC doctor for
treatment plans.
CONTENTS:
I. APPROACH TO RASH
II. DERMATOLOGICAL EMERGENCIES
III. COMMON DERMATOLOGICAL CONDITIONS REQUIRING
ADMISSION
IV. TOPICAL CORTICOSTEROID POTENCY CHART
I. APPROACH TO RASH
HOPC:
General history
1. Duration of disease (acute vs chronic)
2. Site of onset
3. Pattern of spread (e.g. symmetrical, unilateral, cephalocaudal,
centrifugal spread)
4. Character of lesions (what did the skin disorder look like?)
5. Course of disease: is it getting worse and spreading, or comes
and goes, or getting better, or remaining the same?
6. Associated symptoms: itch, pain, burning, fever, constitutional
symptoms
7. Aggravating/ relieving factors
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8. Any treatment sought
Directed history: usually you will need to take a more focused history
after reviewing the morphology of the patient’s dermatosis to form a
list of differential diagnoses
9. Past history of skin disorders
10. Drug history (including allergy): include OTC, herbs,
supplements & TCM; any contactants
11. Occupation history
12. Social history: hobbies/ leisure activities, pets, plants
13. Sexual history
14. Travel history
15. Sick contact history
16. Past medical history
17. Family history of skin disorders
Drug History
If a drug cause of rash is suspected, obtain details including:
name, content, mode of delivery of drug. Ask the patient for drugs
obtained from GP/OTC/TCM/herbal supplements/online sources. Ask
the family to bring the drugs or call up the GP to verify the drugs
prescribed. Duration of drug intake prior to rash (corroborate
prescribed medications on CPRS/NEHR to whether the patient actually
consumed the medication. Check for TCM use. Drug history should
begin at least 3 months before onset of rash. Include chronic
medications and whether patient has previously tolerated the drugs
before.
Draw up a complete drug chart in suspected cutaneous adverse drug
reactions
Physical Examination
1. Describe the rash

- Find a noun to describe the rash:
Macule, papule, plaque, nodule, pustule, vesicle, bulla/blister,
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erosion (was this preceded by a vesicle or bullae), ulcer
- Embellish the nouns with adjectives (i.e. ulcerating plaque, scaly,
acneiform, umbilicated)
- Describe the colour (White [depigmented, hypopigmented],
Brown-Blue-Black [hyperpigmented], Red [blanchable:
erythematous, salmon-pink, non-blanchable: purpuric,
haemorrhagic])
- Record the location
- Describe the extent [mucosal, ocular, genitalia involvement, and
total body surface area (BSA)%]
- Describe the distribution (acral, truncal, photo-exposed
- Observe for specific dermatological signs (e.g. impetiginisation –
possible superinfection of an underlying rash, Nikolsky’s sign,
Hutchinson’s sign)
2. Examine hair, nails, mucosal surfaces
3. Assess for systemic involvement e.g. lymphadenopathy,
hepatosplenomegaly, joint synovitis
N.B If the rash has disappeared, enquire if photos have been taken.
Where possible, obtain permission from patient to have
photographs taken of current rash (may store in patient’s own
handphone) to show the primary dermatology team the following day
as some dermatoses evolve in morphology rapidly.
APPROACH TO RASH(ii) DERMATOL
II. DERMATOLOGICAL EMERGENCIES
A. SJS/ TEN
B. DRESS
C. AGEP
D. Generalised exfoliative dermatitis/Erythroderma
E. Generalized pustular psoriasis
F. Eczema herpeticum
NB: Early referral to dermatologists should be done for these

dermatological emergencies
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**Cutaneous adverse drug reactions are covered under RAI section.
A. SJS/ TEN
Definition:
▪ SJS: Less than 10% total body surface area (TBSA)
involved
▪ SJS-TEN overlap: 10-30% TBSA involved
▪ TEN: More than 30% TBSA involved
▪ BSA calculation is based on detached and detachable
epidermis.
Causative agents:
▪ Drugs are implicated in 70-80% of SJS and TEN (ALDEN
score may be used for evaluation of drug causality).
Typical time duration is 4-28 days.
▪ Drugs with high risk to induce SJS/ TEN:
▪ Allopurinol
▪ Carbamazepine
▪ Co-trimoxazole (other anti-infective
sulfonamides and sulfasalazine)
▪ Lamotrigine
▪ Nevirapine
▪ NSAIDs (oxicam type; i.e., meloxicam;
etoricoxib; diclofenac)
▪ Phenobarbital
▪ Phenytoin
▪ Important to draw an accurate drug chart
▪ Herpes Simplex and Mycoplasma infections account for
the next most common triggers of SJS/TEN.
Typical course:
▪ Usually starts with a prodromal phase of fever, cough, flu-
like symptoms and malaise
▪ This is followed 1-3 days later by an acute macular
exanthema +/- atypical targetoid lesions, located
predominantly on the trunk and proximal limbs which
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evolve into confluent flaccid blisters with positive
Nikolsky’s sign
▪ Mucous membrane involvement seen in about 95% of
cases and can precede or follow the skin eruption
Pay special attention to:
Vital signs
Mucosal involvement (oral, ocular, urogenital): painful crusts and
erosions may occur on any mucosal surface
Painful skin lesions, targetoid lesions (3 zones of color change),
atypical targetoid lesions (only 2 zones of color change and/or
indistinct border), dusky skin lesions, blisters/erosions (Nikolsky’s
sign positive), mucositis, skin denudation
Investigations
General: FBC, LFT, U/E/Cr/Glucose, Ca/Mg/PO4, ECG, UFEME,
skin swabs for pyogenic culture
Full septic workup (high risk of secondary bacterial infection and
septicaemia); to repeat cultures every 3 days throughout acute phase
of disease
Acute complications:
▪ Dehydration
▪ Electrolyte imbalance
▪ Pre-renal azotemia
▪ Thermal dysregulation
▪ Hypercatabolic state
▪ Adult respiratory distress syndrome
▪ Bacteremia
▪ Insulin resistance
▪ Multiple organ dysfunction
Skin biopsy to be done by the Dermatology Senior Resident.
Treatment
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Prompt withdrawal of causative drug
Consider transfer to a specialized unit (e.g. SGH Burns Unit if vital signs
stable; HD/ICU if vital signs unstable) if SCORTEN 2 or higher; or
progression to BSA >10%
Parameters Scores SCORTEN Predicted

mortality
1. Age > 40 years Yes=1,
No=0
2. Malignancy Yes=1, 0-1 3.2%

No=0
3. Tachycardia Yes=1, 2 12.1%

(>120/min) No=0
4. Initial BSA of Yes=1, 3 35.3%

epidermal detachment No=0
>10%
5. Serum urea Yes=1, 4 58.3%

>10mmol/L No=0
6. Serum glucose Yes=1, 5 90%

>14mmol/L No=0
7. Bicarbonate Yes=1,
<20mmol/L No=0
On call, general supportive treatment will suffice as first line

treatment; a specialist opinion is required for specific adjunct
therapies
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Strict IO charting, insert urinary catheter to guide fluid resuscitation (aim
urine output 0.5-1ml/kg/hour)
Venous access ideally via 2 large bore peripheral lines at non-lesional
skin (consider central lines and transfer to HD/ICU if hemodynamically
unstable)
Insert nasogastric tube for feeding if eating is painful, refer dietician for
nutrition needs
Fluid and electrolyte replacement (consider electrolyte solution

(0.7ml/kg/% affected area) and albumin solution (5% human albumin,
1 ml/kg/% affected area)
Treat hyperglycemia
Keep the temperature of the patient’s room at 28-32 degrees Celsius
Antibiotics should only be initiated if there are signs of sepsis and
culture-directed
For patients with dysphonia or dyspnea (supraglottic or laryngeal
involvement), urgent referral to ENT. Supplementary oxygen or
assisted ventilation as necessary in hypoxia
For patients with ophthalmic involvement, saline rinses to clean
eyes/eyelids and preservative-free lubricants; Eye referral soon next
morning
Monitor pain score 4 hourly. Prescribe analgesics such as paracetamol
(can consider IV); tramadol PO/IM 50-100mg Q4-6h PRN and
morphine PO 10-30mg Q4h PRN may be administered when
necessary. Consider patient-controlled analgesia and pain team
referral.
For mucosal lesions, white soft paraffin for lips, Oral7 moisturising
mouth gel; oral toilet and hygiene, saline compress, chlorhexidine
wash, Difflam gargle for anaesthetic effect
Sterile handling essential. For non-infected skin, use non-adherent
dressings (e.g. jelonet, petroleum impregnated gauzes, silicone
dressings (e.g. Mepilex Silicone, Mepilex transfer, Mepitel) Secure
primary dressing with roller-gauze bandages and elastic tubular
dressings (e.g. Tubifast)

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For infected wounds, use dressings with antimicrobial properties such
as silver dressings e.g. Acticoat, Mepilex Ag, Aquacel Ag.
B. DRESS
DRESS is characterized by a pruritic maculopapular rash, fever,
lymphadenopathy, leukocytosis with eosinophilia or atypical
lymphocytosis, liver or renal dysfunction.
Periorbital, facial or neck edema with pinhead-sized pustules are also
characteristic features at the early stage. The maculopapular rash often
generalizes into a severe exfoliative dermatitis or erythroderma.
In severe cases, symptoms can continue to deteriorate or flare-ups
can be seen even weeks after stopping the offending drug.
Usual associated drugs:
• Anticonvulsants (Carbamazepine, Phenytoin,
Phenobarbital, Lamotrigine)
• Allopurinol
• Dapsone
• Sulfasalazine
• Trimethoprim-sulfamethoxazole
• Anti-TB drugs
• Minocycline
Typical course:
• 2 – 6 weeks, up to 12 weeks after initiation of drug.
Prognosis:
• Mortality is approximately 10% and is primarily associated
with systemic organ involvement e.g. liver dysfunction,
renal impairment and interstitial pneumonitis
Usually febrile
Morbilliform eruption (80%) that can progress rapidly to a diffuse,
confluent and infiltrated erythema
Facial swelling (including the earlobes)
Purpura
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Enlarged lymph nodes
Tender hepatosplenomegaly
Erythroderma or exfoliative dermatitis may follow in some patients
Mucosal involvement may occur (lips, mouth, throat, genitals)
Vesicles, tension blisters induced by dermal oedema or pustules can
also occur
Tachypnoea and hypoxemia on pulse oximetry
Investigations
General: FBC (looking for leukocytosis, absolute eosinophilia ≥ 0.7 x
109/L or atypical lymphocytes), LFT, U/E/Cr, glucose, TFT (looking
for thyroiditis), CK, CK-MB, Trop I, ECG (looking for myocarditis/
complete AV block), amylase, lipase, UFEME (looking for
proteinuria), CXR, HBsAg, anti-HBc total Ab, anti-HBs Ab, anti-HCV,
HIV (baseline investigations for use of corticosteroids)
Full septic workup including blood cultures should be considered in
presence of fever and/or infective symptoms
Acute complications:
▪ Hepatitis, up to 70% of patients
▪ Renal impairment, particularly in allopurinol-induced
DIHS/DRESS (>80% of patients)
▪ Pulmonary involvement rare e.g. abnormal pulmonary
function, acute interstitial pneumonitis, lymphocytic
interstitial pneumonia, acute respiratory distress
syndrome
▪ Cardiac involvement rare e.g. myocarditis, heart failure,
complete atrioventricular block. Myocarditis can develop
at the onset of the disease or approximately 40 days after
onset
▪ Gastrointestinal involvement e.g. acute GI bleeding from
CMV ulcers. Enterocolitis develops 4-7 weeks after
disease onset
▪ Reactivation of viruses e.g. CMV, EBV, HHV-7, HSV,
herpes zoster (relevant PCR tests may be sent after
specialist review)
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▪ (Neurologic involvement e.g. meningoencephalitis may
develop about 2-4 weeks after disease onset)
Treatment
On call, general supportive treatment with antihistamines, emollients
and topical corticosteroids will suffice as first line treatment; a
specialist opinion is required for use of systemic corticosteroids or
specific adjunct therapies
RegiSCAR DRESS validation score
C. AGEP
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AGEP is a rare pustular serious cutaneous adverse drug eruption
Usual associated drugs:
• Ampicillin/amoxicillin
• Quinolones
• Sulfonamides
• (Hydroxy)chloroquine
• Terbinafine
• Diltiazem
• Pristinamycin (macrolide)
Typical course:
• Less than 4 days (1 – 11 days) after initiation of drug
Prognosis:
• AGEP is a self-limiting disease with a favorable prognosis
in most cases
Acute oedematous erythema studded with small non-follicular sterile
pustules, usually first starting on the face or intertriginous and flexural
areas, which then becomes more widespread
Almost always accompanied by fever above 38c
Mild, non-erosive mucous membrane involvement (mostly oral) in
about 20%
Less common/atypical manifestations include marked facial oedema,
purpura, blisters or target-like lesions
Investigations
FBC (typically will have leukocytosis mostly due to neutrophilia > 7 x
109/L), UECr, LFT
Skin swab for pyogenic culture and fungal smear of a skin pustule
Treatment

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On call, general supportive treatment with antihistamines, emollients
and topical corticosteroids will suffice as first line treatment; a
specialist opinion is required for use of systemic corticosteroids or
specific adjunct therapies
D. Generalized Exfoliative Dermatitis (GED) / Erythroderma

Definition: Erythema and scaling of ≥90% total BSA
Determine aetiology, keeping in mind these common causes:
Exacerbation of underlying dermatological condition (most common
cause): Atopic dermatitis, Psoriasis, Pityriasis rubra pilaris.
N.B Abrupt withdrawal/non-compliance to immunosuppressants or
systemic steroids might may trigger flare. It will be important to
determine if patient is steroid dependent.
Drug eruption
Underlying malignancy [E.g. organ or haematological malignancy,
cutaneous T cell lymphomas (Sezary/Mycosis fungoides)]
Idiopathic: present in 1/3 of patients
Infections: crusted Norwegian scabies, dermatophytosis, candidiasis
Immune related disorders: pemphigus foliaceus, lichen planus, AIDS
Pay special attention to:
Mucosal involvement (in drug and immunobullous disease cause e.g.
pemphigus foliaceous)
Nails and joints (nail pitting clue to erythrodermic psoriasis)
Scaling between fingers or burrows involving web spaces (scabies)
Keratoderma of palms and soles (e.g. pityriasis rubra pilaris, Sezary
syndrome)
Lymphadenopathy or hepatosplenomegaly, per rectal exam, breast
and pelvic exam (in females) (underlying malignancy)
Bullae and mucosal involvement may indicate immunobullous
disease (e.g. pemphigus foliaceous)
Look for complications - superimposed skin infection,
hypo/hyperthermia, dehydration (low BP, tachycardia and decreased
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skin turgor), high output cardiac failure states (peripheral oedema,
bibasal lung crepitation), sepsis (fever, delirium with altered mental
state), hypoproteinaemia and malnutrition (cachexia, pedal oedema)
Investigations
Basic:
FBC looking for anaemia, leucocytosis and eosinophilia. If anaemia is
present, to send for anaemia work up (Fe, Ferritin, Transferrin, B12,
Folate, Peripheral blood film (PBF))
U/E/Cr, Ca/Mg/PO4 to look for complications of dehydration and
increased fluid loss
LFTs looking for complications from medications (Methotrexate,
cyclosporin are hepatotoxic)
HBA1c, fasting glucose especially if patient is on prednisolone
Full septic W/U: 2 sets of blood cultures, C-Reactive Protein, Pro-
calcitonin if febrile/having chills; ESR
CXR looking for any suspicious mass lesions, evidence of high
output cardiac failure
Non-urgent skin biopsies (at least 2 sites): Histology +/- direct
immunofluorescence (will be done by Dermatology registrar)
Where relevant, baseline perform an immunosuppressive screen: TB
T-spot, HBsAg, anti-HBs Ab, anti-HBc Ab, anti-HCV Ab, CXR, HIV.
Specific (as clinically indicated):

Lymphomatous: peripheral blood film, buffy coat for Sezary cells,
lymph node biopsy and imaging
Paraneoplastic: malignancy screen
Infections: urinalysis, skin scrape for hyphae or scabies, skin swab
for pyogenic culture if clinically infected (remove overlying scab to
swab underlying lesion, do not swab dry scab), HIV test, CD4/8 count
Treatment
Treatment depends on the underlying aetiology. If GED is due to a
flare of an underlying dermatosis, adjustment of topical and systemic

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immunosuppressants might help – however, this should be discussed
with a dermatologist
Stop all possible offending drugs and non-essential medications
Regular close monitoring of parameters and fluid balances (strict I/O
chart, weigh patient daily in high-output cardiac failure)
Correction of fluid and electrolyte abnormalities with regular
monitoring of electrolyte and protein balance
Correction of nutritional deficiencies and ensure adequate protein in
diet (consider referral to dietician)
Antibiotic cover if required – consider MRSA coverage if MRSA swab
is positive
Symptomatic treatment for itch – anti-histamines, Suu-balm cream
Topicals steroids and intensive moisturisers (refer to section IV and
section III.C Atopic Dermatitis for illustration)
Emulsifying ointment OD as soap
E. Generalized Pustular psoriasis
Acute eruption of psoriatic plaques studded with small pin-point

sterile pustules on an erythematous base. Associated with systemic
symptoms of fever, malaise, lethargy.
Clinical history should search for precipitating factors including

infection and abrupt withdrawal of oral or topical steroids.
A close differential diagnosis is Acute Generalised Exanthematous

Pustulosis. Hence, a detailed medication history in relation to onset
of pustular rash is warranted.
In addition to a general dermatological examination;
Document the extent using total BSA%.
Document the severity using PGA (Physician Global Assessment)
and Psoriasis Area and Severity Index (PASI)

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Investigations
FBC (leucocytosis, lymphopenia)
U/E/Cr (raised urea and creatinine secondary to dehydration)
Ca2+ (Hypocalcaemia might be present)
LFTs (hypoalbuminemia, transaminitis)
Anti-streptolysin antibodies (infection as a precipitant)
Skin swab for pyogenic culture if a superimposed skin infection is
suspected
Baseline immunosuppressive screen (if not done yet): TB T-spot,
HBsAg, anti-HBs Ab, anti-HBc Ab, anti-HCV Ab, CXR, HIV
Fasting lipids and LFT if patient is on acitretin
Urine pregnancy test to ensure that patient is not pregnant if she is
on acitretin/ MTX
Monitor blood pressure (cyclosporin)
UFEME to rule out proteinuria and haematuria (cyclosporin)
Management
Do not start systemic steroids
Hydrate and replace electrolytes accordingly
IV antibiotics if there is evidence of sepsis/superinfection
On call, topical steroids and emollients will suffice, although the first
line treatment for generalised pustular psoriasis is systemic therapy
Generally a moderate-severe potency steroid, together with Vitamin
D analogue is prescribed. The vehicle of cream depends on the
thickness of the scales.
Do not use urea cream (Aqurea) as it will be painful.
Continue systemic therapy: MTX / Acitretin / Cyclosporin if these are
patient’s existing medications. In the event that organ dysfunction is
present, there is no harm in with-holding them till the next day.

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F. Eczema herpeticum
Characterised by clusters of monomorphic erosions over eczematous
skin. It implies a superimposed HSV infection.
Look for evidence of systemic HSV infection – especially eye
involvement (test VA), HSV meningitis (mental state, neck stiffness,
photophobia)
Investigations
Routine laboratory (FBC, RP- especially looking at renal function to
calculate the creatinine clearance, CRP, LFT)
On call, it will be sufficient to order a HSV PCR Swab
N.B It should be taken from an unbroken blister, for the doctor/nurses
to prick. The base of vesicle should be swabbed.
Swabs for pyogenic c/s if clinically indicated
Management
Stop topical steroids
Antiviral medication:
PO acyclovir 400mg TDS for 7-10 days or
PO valacyclovir 1g BD for 7 – 10 days for immunocompetent patients
or
IV acyclovir 10mg/kg/dose q8H for 5 - 7 days in severe infection or
immunocompromised patients, may oralise treatment when lesions
begin to regress and continue until lesions have resolved completely
N.B All should be renal dose adjusted
Consider antibiotics for secondary skin infection
If ocular involvement is suspected or cannot be ruled out, a referral to
ophthalmology is required
Anti-itch therapy and moisturizers

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III. COMMON INPATIENT DERMATOLOGICAL CONDITIONS
A. Bullous pemphigoid
B. Psoriasis
C. Eczema/atopic dermatitis
D. Superficial fungal infections
E. Herpes Zoster
A. Bullous pemphigoid
This is a sub-epidermal blistering condition which commonly affects
the elderly. This is especially so in patients with previous or chronic
neurological disorders (Parkinson’s disease/old CVA). It may also be
drug-induced (e.g. gliptins, loop diuretics and NSAIDs)
Examination
Pre-bullous phase: Non-specific pruritus, urticarial and/or eczematous
lesions.
Bullous phase: Tense bullae and erosions with a predilection for lower
abdomen, flexures.
Mucosal lesions are rare. If mucosal lesions are present, to strongly
consider the close differential of Pemphigus vulgaris.
Document presence or absence of mucosal involvement and total
body surface area affected.
Investigations
1. Non-urgent skin biopsy: Histology, DIF
2. Serum indirect immunofluorescence (IIF)
3. Serum BP180/BP230 antibodies
4. Routine bloods: FBC, U/E/Cr, HbA1c/ fasting glucose, LFT, G6PD
5. If patient is a known case and is likely to start
immunosuppressants/biologics: TB T-spot, HBsAg, anti-HBs ab,
anti-HBc Total Ab, anti-HCV IgG, HIV screen, CXR, UFEME
Management
1. Daily blister charting – deblister but do not de-roof
2. Non-adhesive dressing to open wounds.
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3. Potassium permanganate compresses/soaks BD to erosions till
dry
4. Antibiotics when superimposed infections are suspected.
5. Potent topical corticosteroids (e.g. Clobetasol Propionate 0.05%
BD, please refer to section IV)
6. Tetracycline antibiotic monotherapy or combination with
nicotinamide (decision to start can wait till dermatology consult)
7. PO prednisolone with starting dose of 0.3 – 1mg/kg depending on
severity of disease
N.B If unsure, this can be held off till dermatology consult is made.
However, it will be good to ensure good glucose control, or a
baseline HBA1c/Fasting glucose if there is none done recently.
8. Hydrate and correct electrolyte abnormalities
B. Psoriasis
Types:
1. Chronic plaque
2. Guttate
3. Erythrodermic (please refer above)
4. Pustular (localised/generalised)
5. Palmoplantar
6. Scalp
7. Inverse
8. Nail
9. Psoriatic arthritis
10. Acrodermatitis continua of Hallopeau
Precipitants:
1. Infection e.g. Streptococcal throat infection typically triggers
guttate psoriasis, HIV
2. Drugs (beta blockers, sudden withdrawal of oral or topical
steroids, anti-malarial or calcium channel blockers etc.)
3. Trauma (Koebnerisation) – physical, chemical, electrical, surgical,
infective and inflammatory
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4. Alcohol
5. Metabolic e.g. hypocalcaemia (pustular psoriasis)
6. Stress
7. Environmental factors e.g. heat
Describe/document the flare in this manner:

1. Location
2. Severity: Thickness, Redness, Scaling
3. Extent of disease: TBSA and PASI score
4. Quality of life affected
Investigations:
1. Routine labs: FBC, U/E/Cr, Calcium (pustular psoriasis), LFTs
2. Metabolic screen: Fasting lipids, fasting glucose/HBA1c, Blood
pressure, BMI
3. Anti-streptolysin antibodies (infection as a precipitant)
4. Septic workup for suspected infection
5. Urine pregnancy test for females if necessary (some DMARDs,
systemics are teratogenic)
Management:
Treatment varies according to type of psoriasis, but the following
general principle remains:
1st line:
1. Topical corticosteroids (mod-high potency) +/- salicylic acid 2% or
5% for thicker plaques.
2. For scalp: Betamethasone 0.1% scalp lotion
3. For nails: Apply steroidal ointments to nail fold and underneath
nail plate
4. Coal tar
5. Vitamin D derivatives (Calcipotriol containing). Betamethasone
dipropionate combination is used only once daily.

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Adjunctive therapy: moisturisers and coal tar shampoo, bath or soap
2nd line: Phototherapy (NBUVB) if total BSA >/=10%

3rd line: Systemics (MTX, Acitretin, Cyclosporin)
May consider use of anti-streptococcal antibiotic e.g. Penicillin V or

erythromycin for streptococcal throat infection
If there is joint involvement (e.g. in psoriatic arthritis)

1. Start NSAIDs if there are no contraindications
2. Patient will invariably require DMARDs (MTX); but there is no
urgency to start them on call
C. Atopic Dermatitis
An acute, subacute of chronic pruritic dermatosis. Presents with
dryness, itchiness, excoriations and lichenification (Chronic cases).
History should focus on:

1. Baseline control
2. Possible trigger for flare (E.g. HSV/staph infection, non-
compliance, stress , irritants (allergen, contactants, food, climate))
3. Detailed steroid history. Look through medication prescription list
on NEHR/private GP to ascertain frequency of oral steroids
4. Associated atopic symptoms (Asthma, allergic rhino-sinusitis) and
family history of atopy
Examination
Either 1 of the 3 scoring systems (EASI, POEM and SCORAD) can
be used. In general, they take into account these factors:
1. Extent (total BSA%) %)
2. Severity of scaling/erythema
3. Effect on quality of life (especially sleep).
Look for complications

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1. Clusters of monomorphic umbilicated blisters to suggest Eczema
herpeticum
2. Superimposed Staphylococcus aureus infection (e.g.
Impetiginisation (golden crust) or extensive weeping)
Investigations
1. Routine bloods: FBC, U/E/Cr
2. If relevant: Swab vesicles for HSV PCR, Pyogenic c/s
(staph/strep)
3. Consider working up for atopy if there is a strong suspect of a
causative precipitant (Skin prick test, RAST (IgE))
Management
1. Emollients:
a. Aqueous cream TDS for face
b. White soft paraffin:liquid paraffin 3:2 TDS for body and
trunks
c. Emulsifying ointment OD as soap
d. Urea 10% cream (not for broken skin)
2. Wash:
a. Triclosan wash to face
b. Octenisan wash to body
3. Topical steroids (potency depends on severity).

a. Betamethasone valerate 0.1% cream BD to body and
limbs
b. Betamethasone valerate 0.025-0.5% BD to face, flexure and
genitalia
c. Consider Tacrolimus/Pimecrolimus BD to face/periorbital
region if steroid atrophy present (do counsel patient
regarding high cost)
4. Anti-histamines; preferably a sedating one at bedtime
5. Antibiotics if superimposed infection suspected
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6. Systemics: Corticosteroids, Ciclosporin
N.B No urgency to start overnight
7. Nursing instructions: Double pyjamas (call NCID Ward 12E
nurses for instructions)
N.B Maximum dose of topical steroids if patient is on double
pyjamas is Betamethasone valerate 0.1% cream BD
D. Superficial Fungal Infections

Common organisms and their usual clinical findings:
- Dermatophytes:
o 3 genera of dermatophytes: Trichophyton, Microsporum,
and Epidermophyton
o Conditions: Tinea corporis, pedis, cruris, capitis, barbae,
manuum
o Clinical findings: raised annular border with an advancing
edge but can also take the form of eczematous, pustular,
bullous, psoriasiform lesions or Majocchi’s granuloma.
- Yeasts
o Candida
o Malassezia
▪ Conditions: pityriasis versicolor (tinea versicolor),
Pityrosporum folliculitis
o Clinical findings:
▪ Cutaneous candidiasis usually presents in intertriginous
areas or moist occluded sites with erythematous
papules and plaque with statellite pustules.
▪ Pityriasis versicolor presents with scaly hypo- or
hyperpigmented, red or brown macules affecting the
trunk, neck, abdomen or proximal limbs
▪ Pityriosporum folliculitis is characterized by
monomorphic, perifollicular, erythematous papules and
pustules on the trunk, upper arms and neck.
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Investigations
1. LFTs – are important as a baseline especially if considering oral

therapy
2. Skin scrape to send for microscopy for fungal elements
3. Fungal culture of nail clippings can be sent if onychomycosis is
suspected.
4. HbA1c, HIV screening, especially in patients with
recurrent/recalcitrant cutaneous fungal infections
NB: Skin investigations should ideally be done prior to application of

antifungal topicals.
Management
If skin is macerated, affected skin can be compressed with potassium

permanganate (PP) solution BD for 5-7 days until it has dried up.
Optimize control of any underlying DM if poorly controlled
Tinea infections
- Topical 2% miconazole cream BD or 1% clotrimazole cream BD
- Oral anti-fungal therapy:
o Indicated if
▪ BSA >10%
▪ In tinea capitis, or tinea barbae
▪ Unable to tolerate or lesions fail to clear with topical
therapy
▪ Diabetics or immunocompromised host
o Options: PO terbinafine 250mg or PO itraconazole 100mg
OD for 2 weeks
Pityriasis versicolor and folliculitis

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- Add shampoo as therapeutic adjuvant
o 2.5% selenium sulphide shampoo to leave on for 10
minutes before washing off
o Ketoconazole shampoo to leave on for 5 minutes before
washing off
- If oral systemic therapy is indicated, consider PO itraconazole
200mg OD for 5-7 days or PO fluconazole 300mg once a week
for 2 weeks.
Cutaneous candidiasis
- Oral antifungal therapy is usually not needed.
- Adjunctive therapy:
o Keep skin folds dry and clean
o Turn patient regularly if patients is bedbound and rashes
involve the back or buttocks
o Consider use of drying agent such as potassium
permanganate compress
o Barrier cream in diaper dermatitis. Consider cradle
nursing care.
E. Herpes zoster
VZV/HHSV-3 reactivation. Characterised by a painful, dermatomal

vesicular eruption which may pustulate or crust. If vesicles are multi-
dermatomal or scattered, do consider disseminated zoster and
evaluate for immunocompromised host. Abnormal sensation such as
anaesthesia may be described along affected dermatomes.
Examination:
1. Crops of vesicles, bullae and pustules on an erythematous or
oedematous base in a dermatomal distribution.
2. Look for conjunctival infection or positive Hutchinson’s sign
(vesicles on tip of nose strongly suggests involvement of

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ophthalmic branch of V1 – herpes zoster ophthalmicus – refer
Eye early!)
3. Ramsay Hunt syndrome (facial nerve involvement with rashes in
the external meatus)
4. Look for complications: secondary bacterial infection, eye
(uveitis/keratitis) involvement, meningitis/encephalitis, Guillain-
Barre syndrome
Investigations:
1. Confirm diagnosis: Prick vesicle and swab the base for VZV PCR
2. Routine bloods: FBC, U/E/Cr (CrCl)
3. Complications: Swab for aerobic culture (secondary bacterial
infection)
Treatment:
1. Contact precaution. Air-borne if patient has disseminated zoster
2. Anti-virals:
a. PO acyclovir 800mg 5 times a day for 7-10 days or
b. PO valacyclovir 1g TDS 7 days or
c. IV acyclovir 10mg/kg/dose q8H for 7 days in severe
infection, immunocompromised states or other serious
complications such as herpes zoster ophthalmicus and
Ramsay Hunt syndrome.
N.B Please ensure renal-dose adjusted
3. Analgesia
a. WHO pain ladder
b. For post-herpetic neuralgia:
- Topical lidocaine 5% patch/2% gel QDS PRN if pain is
mild or systemic agents are contraindicated
- Topical Capsaicin ointment 0.05% QDS PRN if pain is
mild or systemic agents are contraindicated
- Tricyclic anti-depressants (Amitriptyline/Nortriptyline)
as first line systemic treatment except in elderly

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patients who are susceptible to anticholinergic side
effects
- Anti-convulsants: Gabapentin/Pregabalin as second
line treatment but may be first line treatment in
patients who are susceptible to anticholinergic effects
of tricyclic anti-depressants
- Opioids as third line option in patients with
contraindications to tricyclic anti-depressants or anti-
convulsants
4. Consider antibiotics for secondary infection.

5. Zoster vaccination for adults =/>60years old
IV. TOPICAL STEROIDS POTENCY CHART

In general: ointments stronger than creams
Only creams available in TTSH/NSC included.
Topical Drug Suitable for

steroid face/flexures?
class
I – super Clobetasol propionate 0.05% No

potent ointment/cream/gel
Betamethasone dipropionate No
0.05% + salicylic acid ointment
(Diprosalic)
II – potent Betamethasone dipropionate No

0.05% ointment (Diprosone)
Betamethasone valerate 0.1% No

ointment
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III – upper Betamethasone dipropionate No
mid- 0.05% cream
strength Mometasone furoate 0.1% No
(Elomet) ointment
Clobetasone butyrate 0.05% No

ointment/cream
Mometasone furoate 0.1% Yes
IV – mid-
strength (Elomet) cream
Fluocinolone acetonide 0.025% No
ointment
Triamcinolone acetonide 0.1% No
cream
Betamethasone valerate 0.1%

V – lower cream No
mid- Betamethasone valerate 0.05%
strength cream/ointment o
corticoster Fluocinolone acetonide 0.025%
oids cream Yes
Desonide 0.05% cream/ointment Yes

VI – mild Fluocinolone acetonide 0.01%
corticoster cream
oids Yes
Betamethasone valerate 0.25%
cream/ointment
Yes
Hydrocortisone 1%
VII – least cream/ointment Yes
potent

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ENDOCRINOLOGY
RELEVANT GUIDELINES ON: May be found on TTSH hospital

intranet
• NBM (T1 VS T2DM)
• DKA/HHS
• Hypoglycemia
• High bedtime capillary glucose
(T1 VS T2DM)
APPROACH TO DKA/HHS (METABOLIC EMERGENCIES)

• Diagnosis → Cause → Complications → Prevention
• Symptoms:
o GI: Nausea, vomiting, diffuse abdominal pain
o Hyperventilation with deep rapid breathing (Kussmaul’s
breathing)
o Altered mental state / confusion / agitation
o Fairly asymptomatic with unexplained metabolic acidosis
▪ CBG level can be normal in euglycemia DKA
(especially with poor PO intake or SGLT2-inhibitor
usage)
• Inform MO on call of patient’s location and your assessment
ASAP

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• Workup:
o FBC (sepsis, DIC), renal panel (acute renal impairment,
hypokalemia), Cl/Ca/Mg/PO4, ABG (pH/HCO3), BHOB,
serum osmolality, serum glucose, lactate
o HbA1c
o LFT (sepsis), amylase/ lipase (pancreatitis can cause DKA),
o Baseline ECG +/- troponin I
o Septic workup: inflammatory markers including CRP,
UFEME, Urine culture, Blood culture
o Imaging: CXR, CT brain/MRI brain (altered mental status)
• Causes (5Is):
o Infection: Sepsis (respiratory, GIT, UTI, abscesses)
o Insulin:
▪ Non-compliance or inadequate treatment
▪ New onset DM / previously undiagnosed DM
o Infarction: Acute myocardial infarction, cerebrovascular
accident
o Iatrogenic: Drugs (glucocorticoids, atypical antipsychotics,
TCM, SGLT2 inhibitors)
o Others: Pancreatitis/ Alcohol misuse/Trauma
o Idiopathic

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TREATMENT (As per TTSH Intranet DKA/HHS Guidelines)
PILLAR DETAILS
IV hydration Fluid deficit
To correct 1L in 1h → 1L in 2h → 1L in 4h → 1 litre
hypovolemia/resto every 6 to 8 hours
re perfusion Watch for fluid overload inpatients with
poor cardiac/hepatic or renal functional
Choice of drip: 0.9% NaCl until CBG <
14mmol, then change to dextrose
containing drip
Corrected Na: Measured serum Na +
[venous glucose (mmol/L) – 5.5]/ 3.5
• Corrected serum Na > 140 mmol/L:

Use 0.45% NaCl
• Corrected serum Na ≤ 140 mmol/L:
Use 0.9% NaCl
IV insulin Usually Insulin scale 3 or 4 based on
To reverse patient’s weight and titrate based on the
ketoacidosis/ CBG readings
hyperglycemia

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Monitor and Consider telemetry
correct Aim to keep potassium within 4-5 mmol/L
electrolytes • Correct hypokalemia (<3.3mmol/L)
K+ and PO4 before initiating IV insulin
• K < 3.3: Omit insulin, give drip that
contains 10 mmol of KCl per 500ml
of NaCl 0.9% and give IV KCL
10mmol x 2 cycles
• K 3.3-5.2: IV drip eg. NaCl 0.9% with
KCl 10 mmol per 500 ml
• K > 5.2: Do not give K replacement,
recheck K in 2 hours
Find and treat Antibiotics if bacterial infection
precipitating Give sodium bicarbonate if pH persistently
factor < 6.9 after IV hydration (IV 8.4% NaHCO3
100 ml STAT with ongoing potassium
replacement) (check with senior before
giving!)
Consider high dependency/medical ICU
referral if hemodynamically unstable
Nursing Q1H vitals, NBM (sips of water for comfort
instructions IF ALERT), CBG Q1H, CLC chart Q1H,
Strict IO charting, insert IDC
Ensure positive balance

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Bloods: Q4-6H RP, HCO3, BOHB, serum
osmolality, venous glucose (no need ABG
usually)
TIPS
• Do not transit IV to SC insulin

• DKA can exist even when patient is tested negative for urine
ketones as the urine dipstick test detects only acetoacetate and
not beta-hydroxybutyrate (hence, always check serum BOHB)
APPROACH TO HIGH CBG AT BEDTIME (T2DM)

Exclude diabetic emergencies (DKA/HHS)
1. Was the CBG a post-meal reading? (last meal < 2hours ago)
2. Assess patient for signs / symptoms of DKA/HHS: Vitals,
kussmaul’s breathing, AMS, abdominal pain, vomiting, signs of
crisis
3. Bloods: Renal panel, serum glucose, BOHB, serum osmolality
and either VBG/ABG
4. Review eIMR –OHGA/insulin or SCSI
a. Have old medications been restarted?
5. Check I/O charts: Last meal, type of diet, outside food, any
snacks/drinks
a. Common causes of hyperglycemia: post meal reading,
dietary indiscretion, pain, sepsis
b. Iatrogenic: peritoneal dialysis (glucose containing dialysate),
steroids usage

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TIPS
• Recheck CBG in 2H-4H to ensure downtrend (with or without
insulin being given)
• Avoid high doses of short- acting insulin eg. actrapid (which may
bring CBG down too fast) → Hypoglycemia, difficult to assess at
night. Insulatard is preferred.
• Beware of insulin stacking
• T1DM: Ensure that patient has been served basal insulin for the
day. Basal insulin cannot be omitted in T1DM even when patient
is kept NBM. Assess for DKA if basal insulin has been omitted.
Lower threshold to serve SC Insulatard. (If > 16.0, see T1DM
high bedtime CBG guideline)
APPROACH TO HYPOGLYCEMIA
Correct hypoglycemia, establish cause
1. Is the patient alert? Is the patient symptomatic?
2. Can patient take orally?
a. YES: Nurse led protocol, PO Glucose drink 15g, repeat
CBG in 15 min
b. NO: IV dextrose 50% 40ml STAT (ensure IV access patent),
repeat CBG in 15 min
3. Check for precipitating cause
a. EIMR → What OHGAs/insulins? (OHGA-meal mismatch)
b. Poor oral intake – review IO charts
c. Worsening hepatic/renal function
d. Alcohol intake
4. Review:
a. Diabetic medications – stop/reduce doses of medications
(especially sulphonylurea and insulin doses)
b. Drip (dextrose containing or not. Start IV dextrose
containing drip if patient taking poorly)
c. Diet (serve next meal / feeds if not contraindicated, consider
top up supplements / biscuits / milk / bread if taking < ½
share
d. Lab results – renal function
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5. Consult your on-call MO if unsure
6. Handover to primary team the following day
TIPS
• Type 1 diabetics will need their basal dose of Insulin, DO NOT
completely withhold it, but instead reduce the dose
• Do not give phone orders, especially for insulin
Special scenarios to consider:

• NBM status
• Patients on oral feeds only
• Patients on parenteral nutrition
• Patients on continuous NG feeding
• Patient near end of life > refer to “terminally ill patient with DM”
guideline
THYROID STORM
- Sudden severe exacerbation of hyperthyroidism with multi-organ

decompensation
- Precipitating factors: sepsis, surgery, contrast agents, trauma
- Presentation:
o Fever
o Tachycardia out of proportion to fever/sepsis
o Accentuated thyrotoxic symptoms and signs
o Multi-organ dysfunction
▪ CNS – AMS, agitation, psychosis, stupor, coma
▪ GI – abdominal pain, diarrhoea, vomiting, jaundice (if liver
dysfunction)
▪ CVM – hypertension, hypotension, heart failure, rapid AF,
atrial flutter

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- Labs:
o High free T3 and/or T4, low TSH, mild hyperglycemia,
hypercalcemia, abnormal LFT, leucocytosis/leucopenia
- Scoring: Burch-Wartofsky (estimate likelihood of thyroid storm)
- Management:
o Inform MO/reg on call of patient’s location and your
assessment ASAP
o Will need to be monitored in ACA/HD/ICU
o Urgent referral to Endocrine
o The following treatment plans consist of high-alert medications
and will need to be discussed with your seniors
- Hourly paras, NBM except for medications
- PO Carbimazole 40mg stat then 20mg q4h/
Propylthiouracil 400-600mg stat PO/PR (if CI to feeding
eg perforated viscus) followed by 200mg q4h (PTU also
blocks peripheral conversion of T4 to T3)
- PO Lugol’s Iodine/ IV Sodium Iodide: inhibits release of
thyroid hormone (must give no earlier than 1H post-
thionamides)
- Beta-blockers
o PO propranolol/ bisoprolol (if no heart failure
/cardiomegaly/cardiomyopathy – can
precipitate CVS collapse)
o IV esmolol (ultra short-acting, give in HD/ICU)
- IV Hydrocortisone 100mg q8h (also blocks conversion of
free T4 to T3)
- IV hydration
- Avoid aspirin-based antipyretics → release free T4 and
free T3 from protein-bound sites
▪ Treat precipitating factors
*Avoid Amiodarone for AF treatment due to Amiodarone high iodine

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Myxedema Coma
- An uncommon and life threatening form of long-standing,

neglected, untreated hypothyroidism with physiological
decompensation
- Precipitating factors: infection, MI, CCF, stroke, trauma, non-
compliance with thyroid hormone treatment
- Presentation:
o Hypothermia
o CNS – confusion, lethargy, psychosis, seizures
o CVM – bradycardia, heart failure, pericardial effusion,
hypotension
o Hyponatremia
o Hypoventilation with respiratory acidosis
o Hypoglycemia
o Labs:
▪ Free T4, TSH, Cortisol (to exclude hypocortisolism before
replacing thyroxine)
- Management:
- Inform MO/reg on call of patient’s location and your
assessment ASAP
- Will need to be monitored in ACA/HD/ICU
- Urgent referral to Endocrine
- The following treatment plans consist of high-alert
medications and will need to be discussed with your
seniors
o Hourly paras, NBM except for medications
o Warming blanket (avoid external heating pads
as might lead to vasodilation and shock)
o Replace IV Hydrocortisone 50mg q8h first if
any concurrent hypocortisolism
o Thyroid hormone replacement
▪ PO L-Thyroxine 100mcg/day
orally / via NGT (if no ACS) /
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25mcg/day if myocardial ischemia
likely
• Discuss with
Endocrine for possible
need for IV T4 or
consider oral T3
▪ Treat precipitating causes and
complications

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GASTROENTEROLOGY
(I) APPROACH TO BGIT

CTSP: haematemesis, coffee ground vomitus, melena,
haematochezia
Over the phone

- Vitals, GCS - see IMMEDIATELY if unstable (HR>100,
SBP<100mmHg) or low GCS
- Ask nurse to keep a sample of the BGIT to confirm if true BGIT and
assess volume
Essential information
- Is patient stable? Vital signs (including tachycardia but be mindful
of b-blocker use ), GCS
- Is there true BGIT? Inspect vomitus/stool, DRE, aspirate NGT to
look for blood/coffee ground, differentiate BGIT from haemoptysis
/epitaxis or PV/PU bleeding
(check meds usage: fe/charcoal )
- Assess volume of overt bleeding
- Assess cause:
UBGIT vs LBGIT (haematemesis/coffee ground vomitus or melena
suggests UBGIT; haematochezia suggests LBGIT or massive UBGIT
if w hemodynamic instability) (Clots/fresh red blood likely lower GI)
o If UBGIT variceal vs non-variceal (cirrhosis – chronic hepatitis,
alcoholism suggests variceal)
- Assess complications: symptomatic anaemia, ACS
- Look at PMHx/comorbidities: previous BGIT, IHD (higher
transfusion target), CCF/ESRD (risk of fluid overload with aggressive
resuscitation), coagulopathic states/thrombocytopenia, medications
(antiplatelets/anticoagulants, steroids, NSAID)
Causes to consider
UBGIT Variceal: h/o varices(esophageal /gastric)

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cirrhosis – chronic hepatitis, alcoholism
Non-variceal
PUD: h/o PUD, h/o use of NSAIDs/ steroids
Esophagitis: odynophagia, h/o GERD, dysphagia
Mallory-Weiss tear: recent emesis/retching
Malignancy: constitutional symptoms, dysphagia/
early satiety
LBGIT Haemorrhoids: fresh PR bleed on wiping with toilet
paper, drops of fresh blood after passing motion
Diverticulosis: h/o diverticulosis, large amount of
painless fresh PR bleed, chronic constipation
Colonic source (colitis – post RT/infective/IBD,
malignancy): blood mixed with stool
Stercoral ulcer : especially elderly, prolong
immobilisation patient
Vascular ectasia
Physical Exam
- Abdominal examination: tenderness, guarding, masses
- DRE: iron stools vs fresh blood vs melena (fresh vs stale)
- Proctoscopy if fresh PR bleed to distinguish piles vs colonic bleed
Management:
- Q1h parameters and SpO2 monitoring
- NBM, note last meal timing
- Stool and vomit chart
- FBC (Hb may not drop acutely), UECr, PT/PTT/INR, GXM, ECG
CXR erect/ AXR
- Review medications: stop antihypertensives, antiplatelets (review
indication first – e.g. recent PCI), anticoagulants
- If unstable, escalate to senior immediately
o Insert 2 large-bore IV plug (green) and take above bloods
o Fluid resuscitation (e.g. IV normal saline), transfuse blood (if
patient unstable no need to wait for Hb to be reported)
o Intubation if massive haematemesis and unable to protect airway
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- Transfuse blood products if necessary
o Aim Hb >7, if known IHD aim >8, variceal usually 7-8
o If actively bleeding keep platelet >50
o FFP to correct coagulopathy
o Vit K replacement if INR > 1.5 (esp cirrhotics)
- Pharmacological therapy
o If suspect UBGIT, IV omeprazole 80mg STAT then
esomeprazole infusion 8mg/hr
o If suspect variceal bleed, IV somatostatin 250mcg STAT then
infusion 250mcg/hr + IV ceftriaxone 1g STAT and OM
o Stat dose IV erythromycin (check QTc) or metoclopramide 30mins
before scope if no CI ( improves endoscopic view)
- Intervention
o If diagnosis of BGIT questionable, or patient stable with
insignificant bleed may not need to refer GE overnight
o If patient unstable, significant or ongoing bleed – escalate to
senior, may refer GE bleeder on-call
o May elect to do urgent endoscopy or in cases of massive bleed
CT mesenteric angiogram (Duty Radio: 8131, IR suite: 8157) KIV
angioembolisation (will need green plug)
(II) APPROACH TO ABDOMINAL PAIN

- Over the phone: vitals, GCS - see IMMEDIATELY if unstable
- By bedside: TRO acute abdomen (i.e. abdominal pain due to life
threatening condition); making specific diagnosis is of secondary
importance
Causes:
- Epigastric/LHC – PUD, GERD/reflux esophagitis, pancreatitis,
cardiovascular (AMI, aortic dissection/ruptured AAA)
- RHC – liver (abscess, hepatitis, ruptured HCC), biliary
(cholecystitis, cholangitis, biliary colic), basal pneumonia,
diverticulitis, pyelonephritis

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- Lower abdominal – RIF (appendicitis, gynae/ genital causes)
diverticulitis, UTI, ureteric colic, pyelonephritis (with back pain),
constipation colic
- Generalized – constipation colic, acute abdomen, early appendicitis,
DKA, Porphyria, SBP, dengue fever, ischemic
History:
- SOCRATES
- GI symptoms: nausea, vomiting, constipation, abdominal distension
- NSAIDs use: perforated PUD
- Jaundice, dark urine, acholic stools: HBS pathology
- Hx EtOH use /gallstones: pancreatitis
- Previous surgeries, hernias: IO
- Fever / chills / rigors: intra-abdominal abscess, peritonitis,
cholangitis
- Sexual Hx, LMP: ectopic pregnancy / PID/ ovarian cyst rupture
- Urinary symptoms: UTI, cystitis, pyelonephritis
Physical Exam:
- Signs of peritonism: board-like rigidity, tenderness / rebound
- Masses? E.g. palpable bladder
- Bowel sounds: absent/sluggish (? ileus) vs active vs tinkling (IO)
- DRE: BGIT, impacted stools
- AF pulse
Investigations:
- FBC, UECr, LFT, Electrolytes, amylase ± CE, blood cultures / CRP /
procal (if febrile), PT/PTT, GXM, ABG / lactate (TRO ischaemic
bowel)
- Erect CXR (80% perforated viscus a/w gas under diaphragm),
supine AXR, KIV CTAP
- ECG
- UPT, UFEME, urine c/s
Exclude emergencies first – when to call a surgeon:

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- Acute abdomen – peritonitis, perforated viscus,ischemic bowel
- IO
- Unstable: tachycardic, hypotensive
- Severe unstable sepsis (e.g. cholangitis: KIV refer GE for ERCP
after senior consult)
**Keep in mind extra-abdominal causes of abdominal pain e.g. AMI,

(basal) pneumonia, DKA – treat accordingly
Management:
- Treat underlying cause
- Treat symptoms – analgesia ladder (avoid NSAIDs)
- As required: NBM + IV drip, vitals + SpO2 q1h
- If suspect HBS/intra-abdominal sepsis, start IV Augmentin/once
dose gentamicin as per TTSH ASP
- KIV PPI (e.g. IV omeprazole)
- IO: NGT + low intermittent suction
- Medication review
- Serial abdominal examination
Notes:
- Common cause of abdominal pain on call is constipation colic.
Confirm lack of BO, rule out acute abdomen. KIV AXR TRO IO. PR
Dulcolax to clear bowels (KIV fleet if Dulcolax ineffective/dilated rectum
on PR exam), consider judicious use of IM / PO Buscopan for severe
colicky pain relief.
- After giving laxatives to a patient who BNO for 3 days, it is normal for
them to have abdominal pain. This should resolve after BO. If it does
not, reassess patient again.
- Have a high degree of clinical suspicion for ischaemic bowel,
especially if the patient has high arteriosclerotic / embolic risk.
Remember “pain out of proportion of physical signs” If in doubt, do
lactate / ABG
- Remember to review results and patient clinical conditions, early
escalation if in doubt
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(III) PANCREATITIS
Diagnosis (2 out of 3 of the following)
- Characteristic epigastric pain +/- radiating to the back
- Elevation in serum lipase or amylase ≥3x ULN
- Characteristic findings of acute pancreatitis on imaging
Aetiologies
- Common: gallstones, alcohol, post-ERCP
- Less common: hypertriglyceridemia, hypercalcaemia, drugs
(diuretics, chemotherapeutics, sulphonamides,
valproate),autoimmune
Investigations
- Diagnostic: amylase or lipase ≥3x ULN
- Prognostic: FBC, UECr, Ca/alb, LDH, glucose, ABG, LFT
- Erect CXR and ECG TRO other cause of abdominal pain
- Aetiology: US HBS to look for gallstones (obstructive LFTs may
suggest), lipid panel if reason to suspect hyperTG, Ca/alb, alcohol
and drug history
Assessment of severity
Many models and scores eg Revised Atlanta, Glasgow, Ranson,
BISAP, APACHE II, CTSI (usually Atlanta or Glasgow used)
Revised Atlanta Classification

-Organ Failure : a score of 2 or more for one of the three organ systems
using Modified Marshall scoring system as below
-Local complications : acute pancreatic collections(can be infected),
GOO, splenic and portal vein thrombosis, colonic necrosis
- Systemic complications : exacerbation of pre-existing co-morbids

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Modified Glasgow score [on admission and at 48hrs]
(Mnemonic: PANCREAS)
Criteria Point scored
P: PaO2 < 8kPA 1
A: Age > 55 years old 1
N: Neutrophilia – WCC > 15 1
C: Ca < 2mmol/L 1
R: Renal Function – Urea > 16 1
E: Enzymes – LDH > 600 or AST > 200 1
A: Albumin < 32 1
S: Sugar – BSL > 10mmol/L 1
≥3 = severe pancreatitis
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Management
- Consider closer monitoring (e.g. ACA/high dependency) if Glasgow
score ≥ 3/severe acute pancreatitis
- NBM
- Strict I/O
- IV fluid replacement (Ringer’s lactate preferred)
- Adequate analgesia
- Treat underlying trigger:
o IV hydration for hypercalcaemia
o Stop any offending drugs
o Gallstone pancreatitis may need ERCP (consult senior)
o HyperTG (>5) may need endocrine input KIV IV insulin
o IV hydration for post-ERCP pancreatitis: escalate to senior, most
patients are already on post-ERCP pancreatitis prophylaxis – IV
Ringer’s lactate 20ml/kg bolus followed by 3ml/kg/h x 8h after
ERCP (usually included in post-procedure instructions)
- Complications: infected necrosis, pseudocyst formation, ARDS
(IV) APPROACH TO VOMITING

- First exclude regurgitation (return of oesophageal contents to the
hypopharynx with little effort) and rumination (return of food to the
mouth through voluntary contractions)
h/o bulbar dysfunction, Parkinson’s disease, MS
- Determine if vomiting is acute (<1 month) or chronic (>1 month)
- Obtain history to identify cause of vomiting:
GIT *Obstructive: adhesions, GOO, strangulated
hernia, volvulus
Organic: cholecystitis/ cholangitis, hepatitis,
*pancreatitis, *PUD, *mesenteric ischaemia,
peritonitis
Neurological Raised ICP: ICH, SOL, hydrocephalus,
meningoencephalitis
Normal ICP: Migraine, vestibulopathy
Cardiac *AMI
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Infectious GIT (gastroenteritis): viral, bacterial, bacterial
toxins, SBP
Non-GIT: pneumonia, UTI, otitis media
Iatrogenic Ethanol, intentional drug overdose
Anaesthesia, opiates, chemotherapy, antibiotics,
immunosuppressants, antiarrhthmics,
anticonvulsants
Metabolic Pregnancy, hypo- or hyperthyroidism, DKA,
uraemia
Others Acute glaucoma, benign intracranial HTN
*Life-threatening causes to be excluded via history, physical
examination and appropriate investigations
Investigate for causes:

- Investigations as per abdo pain section (II)
- Additional investigations to consider: CT brain/fundoscopy for raised
ICP
Look for complications:

- Fluid depletion, AKI: BP (postural), HR, skin turgor
- Hypokalaemia, metabolic alkalosis
- Perforated GIT: peritonism
- Oesophageal rupture/tear: fresh blood or coffee ground vomitus
Management: mainly supportive and directed to underlying aetiology

- Stop offending agent if applicable
- NBM as necessary, otherwise low-fat, non-milk, non-spicy diet
- Antibiotics/ urgent referrals as indicated
- Hydration: IV ± PO 1.5-2L/day (beware fluid status in e.g. IHD /
CCF, ESRF) & ORS
- Correct electrolyte abnormalities
- Trial of anti-emetics:
o Metoclopramide (beware oculogyric crisis in young females)
o Ondansetron for post-chemotherapy

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o Chlorpromazine/ prochlorperazine for vertigo/ migraine/ post-
chemotherapy (beware EPSE, sedation)
- Avoid anti-motility agents in suspected infective causes
(V) APPROACH TO DIARRHOEA

History:
- Frequency, loose stools, liquid stools, loss of sphincter control
(incontinence), increased stool volume/ Bristol stool chart
- Duration; chronic ≥ 4 weeks
- Colour, consistency, Blood/mucous/pus
- Pale/bulky/sticky/greasy (steatorrhea)
- Is it associated with constipation (spurious/overflow)
- Improves with fasting (osmotic vs secretory)
- How is it different from usual bowel habits
- Precipitating factors:
o Sick contacts
o Overseas travel
o Uncooked foods
- Targeted history based on differentials:
Gastroenteritis Bacterial/Viral/Parasitic
Inflammation IBD (Crohn’s, Ulcerative), Post RT
Malignancy CRC/functional NET
Drugs Antibiotics, Alcohol, laxatives
Malabsorption Short bowel syndrome
Bacterial overgrowth/blind loop syndrome
Coeliac disease
Pancreatic dysfunction/chronic pancreatitis
Bile salts malabsorption
Radiation enterocolitis
Endocrine Thyrotoxicosis
Diabetes mellitus (Autonomic neuropathy)
Addison’s disease
Dysmotility Spurious diarrhoea
Dietary
IBS
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- Abdominal examination: tenderness, guarding, masses, BS
- DRE to check for masses, faecal loading if suspect spurious
diarrhoea
Investigations: based on clinical suspicion

- Bloods: FBC/CRP (Raised WCC), Renal Panel and electrolytes
(Dehydration, electrolyte imbalances), TFT (If suspicion of
thyrotoxicosis), Glucose, Blood cultures (if septic/febrile)
- Stool tests: stool cultures/microscopy, O/C/P, CD toxin, stool fat
- Radiology: AXR (to see faecal loading if spurious diarrhoea)
Management:
- Supportive and directed to underlying aetiology
- Stop laxatives
- Low-fat, non-milk, non-spicy diet
- Hydration: IV ± PO 1.5-2L/day (beware fluid status in e.g. IHD / CCF,
ESRF) & ORS
- Most GE are viral but if suspect bacterial (raised TW with neutrophilia,
raised procalcitonin, prolonged fever): PO Ciprofloxacin or IV
Ceftriaxone 2g OM after blood cultures taken
- Symptomatic treatment: Lacteoforte, ORS
- Avoid antimotility agents if suspect bacterial gastroenteritis
In the nosocomial setting, common causes of “diarrhoea” are (1)

laxatives – therefore stop laxatives first; and (2) C diff colitis
Treatment of Clostridium difficile infection (CDI):

- Suspect CD colitis if exposed to antibiotics in the last few months and
present with ≥3 episodes of loose stools in 24h (may be associated
with abdominal pain, anorexia, fever, hemodynamic instability)
- Can range from acute watery diarrhoea to fulminant colitis (toxic
megacolon with ileus and/or bowel perforation)
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- Send stool for CD toxin only if symptomatic i.e. having diarrhoea
(formed stools will get rejected!)
- Stop offending antibiotics (usually cephalosporins, clindamycin,
fluoroquinolones) – but any antibiotics can cause CD colitis
- Supportive treatment with IV hydration
- Antibiotic treatment depends on severity of CDI
o Severe CDI = WBC > 15, Cr > 132
o In non-severe disease: PO Metronidazole 400mg 8H x 10 days
o In severe disease: PO Vancomycin 125mg 6H x 10 days
o In fulminant disease with hypotension, ileus, megacolon: IV
Metronidazole + PO Vancomycin
- Look out for ileus/toxic megacolon – listen for sluggish/absent bowel
sounds, do AXR. Diarrhoea may “resolve” due to ileus!
- If worsening (ileus, toxic megacolon, bowel perforation, peritonitis,
septic shock) consider urgent surgical consult
(VI) DECOMPENSATED LIVER CIRRHOSIS

- Cirrhotic patients may get admitted for episodes of decompensation
= jaundice, variceal bleed (see above), ascites, encephalopathy
- Important points to note when admitting cirrhotic patients:
o Sodium restriction: low salt diet, avoid 0.9% NS drip; many
have hyponatremia due to fluid overload and this should be
corrected by correcting overload (e.g. ascitic drainage) rather
than giving drip
o Patients with alcohol-related cirrhosis may still be drinking;
check last drink, if recent – start CIWA score 4H, IV thiamine,
tailing dose of lorazepam for DT prophylaxis
o Investigations to do for all: FBC (anaemia from bleed,
thrombocytopenia), UECr (hyponatremia), LFT (raised bilirubin),
PT/PTT (deranged INR more than baseline)

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Specific complications
Hepatic Encephalopathy
- Always suspect in AMS for cirrhotic patients
- Always rule out other causes of AMS as well
- May present early as personality change, sleep-wake reversal; later
as lethargy or coma
- Check for asterixis; perform a neurological exam
- Ammonia levels are not useful
- Look for precipitant: constipation, infection (septic workup if
necessary), variceal haemorrhage, alcohol, sedative medications,
electrolyte disturbances, surgery (including post TIPSS)
- Labs: FBC, UECr/Ca/Mg/PO4, PT/PTT, LFT, glucose, +/- ABG;
septic workup if suspect infection; KIV CT brain TRO other causes of
AMS (especially if there is focal neurology)
- Treatment:
o CLC and behavioural charting
o NBM if too drowsy to take orally
o Correct precipitant (e.g. treat underlying sepsis)
o Clear bowels with lactulose; if already on lactulose previously
can increase dose further
Symptomatic Ascites
- Common precipitants: non-compliance to medications, non-
compliance to sodium restriction, on regular ascitic drainage but turned
symptomatic before next scheduled drainage, SBP
- Consider SBP if TW raised, febrile, abdominal tenderness
- Most patients will require ascitic drainage the next day by the primary
team; what you can do overnight before that would be:
o Note the 3 general points about cirrhotic patients as above
o No need to keep patients NBM for ascitic drains
o Stop the patient’s diuretics (usually held off for ascitic drainage
to avoid hypotension)
o If SBP is suspected, blood cultures (and other septic workup as
indicated) and start IV ceftriaxone 1g OM (check ASP
guidelines on intranet)

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o If patient is extremely symptomatic overnight, consult senior to
see if wish to do ascitic drain overnight
o LVP will require albumin infusion as per guideline in intranet.
- You may also be asked to remove ascitic drains overnight as ascitic
drains inserted as grey plugs can only be left in 8 hours after insertion.
- How to remove grey plug ascitic drain: clamp drain, remove
tape/tegaderm/medicine cup, aseptic technique, clean site with
chlorhexidine, remove drain with tip intact, manual compression, apply
gauze and pressure dressing. There are usually no stitches to cut.
Document ascitic fluid drained in total.
Detailed guideline on diagnostic tapping, percutaneous and US guided

guided LVP is available in document: CMB-GP-Abdominal
Paracentesis-02
(VIII) ABNORMAL LIVER ENZYMES

- Look at the clinical context in which the LFTs were done
- Recognise the overall pattern:
o Predominantly raised AST/ALT = hepatocellular cause (AST≥2x
ALT suggests alcoholic hepatitis, ALT>AST suggests viral
hepatitis/NASH)
o Predominantly raised bilirubin/ALP/GGT = cholestatic cause
o Isolated raised ALP with normal GGT may suggest bone
cause (e.g. vitamin D deficiency – check vitamin D levels,
calcium etc.)
o Isolated raised bilirubin other than considering liver causes,
also rule out haemolysis! (anaemia, high LDH, low haptoglobin,
PBF showing schistocytes)
- Check R factor (use medical calculator): R factor >5 suggests
hepatocellular, <2 suggests cholestatic, 2-5 suggests mixed

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Common causes
Hepatocellular Viral Hepatitis (send acute hepatitis panel; EBV
or dengue if clinically suggestive)
Alcoholic hepatitis (take alcohol history)
Non-alcoholic steatohepatitis
Ischaemic hepatitis (history of hypotension;
avoid further hypotension and hepatotoxic
drugs)
Medications (TB drugs, macrolides,
nitrofurantoin, minocycline, AEDs, NSAID)
Autoimmune
Cholestatic US HBS is investigation of choice
Choledocholithiasis/cholangitis/HBS
malignancy
PSC/PBC
Medications (Augmentin, Bactrim)
Remember to check liver synthetic function (INR, alb, bilirubin)

If cholangitis: blood c/s, IV antibiotics
(IX) ENDOSCOPIC PROCEDURES
Preparation:
- Anti-thrombotic/anti-coagulant use -> please refer to guidelines and
consult relevant disciplines if in doubt
- OGD – NBM 12mn, list + consent (can allow early breakfast if for
PM slot)
- Sigmoidoscopy – fleet enema (contraindication: eGFR<30, HD) on
morning of procedure, list + consent
- Colonoscopy – low residue diet for 1-2 days, stop iron 5 days to 1
week before, PEG 2L evening before + 1L on morning of procedure,
NBM 12mn (or 6h before scope), list + consent
- ERCP – FBC, PT/PTT, ± UECr/ECG/LFT day before procedure,
NBM 12mn, list + consent
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- GA Cases -> should be kept NBM from 12MN generally
Risks (refer to intranet guidelines):

- OGD – perforation, bleeding (0.01%)
- Colonoscopy – perforation, bleeding (0.1%)
- ERCP – perforation (0.5%), bleeding (1-2%), infection, pancreatitis
(<5%), cholangitis (1-5%), stenting +/- repeat ERCP
- Sedation risk – MI, CVA, death (1%)
Post procedure review:

- Assess for possible complications – e.g. drowsiness from sedation,
perforation (beware of retroperitoneal perforation, e.g. OGD reaching
duodenum / ERCP – air under diaphragm will not be seen on erect
CXR, KIV urgent CTAP), post-ERCP pancreatitis
- Follow POT in the endoscopic report
- Generally, for OGD, sigmoidoscopy, colonoscopy – vitals q1h x4
then q4h if well, DOC as tolerated when alert (beware of
contraindications to start feeding e.g. Forrest 1a ulcer found and
clipped – keep NBM in case of rebleed)
- Generally, for ERCP NBM 6 hrs post procedure then allow diet
- If suspecting perforation: inform senior
- If suspecting post ERCP pancreatitis: inform senior, manage as per
pancreatitis (refer to section iii)

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GENERAL MEDICINE
CTSP: Fever (with elaboration on sepsis)
1. Overview
We usually deem fever significant if ≥ 38.0 °C

Broad causes of fever:
• Infection*
• Inflammation – including autoimmune conditions, crystal
arthropathy
• Drugs – can range from benign conditions like drug fever
to serious conditions like neuroleptic malignant syndrome
• Malignancy
• Thrombosis*
• Others e.g. Atelectasis
*Infection/thrombosis usually necessitate prompt treatment overnight
Sepsis = life-threatening organ dysfunction caused by a dysregulated

host response to infection; ↑SOFA score by ≥2
2. Evaluation of fever
History
Characteristics of fever: onset, duration, continuous vs. intermittent,
Tmax, diurnal variation (if any)
Associated symptoms
Corroborative history if pertinent
Look at vital signs & mental state
Generally guided by history
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• General systems to cover: cardiovascular, respiratory,
abdominal, neurological, musculoskeletal, dermatological
• Also important: checking calves, looking at indwelling
lines/catheters
• If appropriate: doing cervical/axillary/inguinal LN
examination
Investigations
Guided by history and physical examination
Not advisable to add test Ca/Mg/PO4, thyroid function
Inflammatory markers (CRP/Procal): generally useful only if a)
changes management e.g. will start antibiotics if raised and/or b)
used to guide clinical response (especially if not easily observed e.g.
deep seated infections)
3. Pertinent points for sepsis management
1. Stabilize the patient - ABC: Airway, Breathing. Circulation

Airway
• Look for signs of airway obstruction
• Call airway team if necessary
Breathing
• Supplementary oxygen to maintain desired SpO2 –
generally can be divided into a) nasal prongs b) venturi
mask c) non-rebreather mask
• Consider performing ABG if patient in significant
respiratory distress
Circulation
• Consider fluid resuscitation or inotropic support to
maintain adequate perfusion
• Fluid resuscitation:
o No significant difference between crystalloids,
colloids & products mimicking human plasma
e.g. plasmalyte; crystalloids often 1st choice in
general ward
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oDecide on a) volume and b) rate
oExercise caution in the elderly and patients
with significant cardiac and renal disease
• Inotropic support:
o Not a substitute for fluids in a dehydrated
patient
o In general ward, dopamine (range is 5-
20mcg/kg/min) is typically used; will need to
key in estimated weight in EIMR
o May not be suitable for patients who have
ongoing tachyarrhythmia > may need ICU/HD
admission for noradrenaline
2. Treatment/management
• Septic workup:
o 2 sets of peripheral blood culture (10ml each)
o Blood culture from line – let the senior doctor
assess & decide
o UFEME, urine culture, CXR usually required
o Wound swab – superficial swabs are often not
useful and may reflect commensals; often not
required overnight
o Repeat septic workup if a change of IV
antibiotics is deemed desirable overnight
• Antibiotics
o Prompt administration is key (ideally within
1hr)
o Always check ED notes to check if any given
(and at what time)
o In general, choice/dose of antibiotics will
depend on:
▪ Any prevailing drug allergy – good
to ascertain on top of checking
CMIS

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▪ Suspected source (IE, joint
infection and CNS infection will
require higher dose in general)
▪ Renal function
▪ Previous microbiology results (in
relevant cases)
o Refer to ARUS-C on the intranet if unsure
• Review other drugs
o Hold off anti-hypertensives if BP is a concern
(do not need to wait till hypotensive)
o Beware of drugs which are not primarily
intended as anti-hypertensives but have BP
lowering effects e.g. madopar, alpha blockers
(alfuzosin, tamsulosin)
• Source control
o There are several instances whereby
emergent source control is important
▪ In patients with features of severe
sepsis + indwelling lines
(especially dialysis lines) + without
any other apparent source,
escalate to your senior early.
Prompt removal of line may be
required
▪ Surgical causes: necrotizing
fasciitis, wet gangrene, Fournier’s
gangrene
3. Monitoring
• Monitoring of vital signs paramount – decide on frequency
• Monitoring of end organ perfusion may provide greater
amount of information:
• Clinical: mentation, urine output (decide on the degree of
strict IO charting required)
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o Biochemical: lactate, renal function, liver
function
o Pulse oximetry may not be accurate in
patients with hypotension – due to peripheral
shut down; correlate with ABG if required
CTSP: GIDDINESS
Differentials for giddiness are wide

Diagnostic considerations for an existing inpatient may be slightly
different from that of a new admission

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CTSP: DELIRIUM TREMENS & HIGH CIWA SCORE
Delirium Tremens
1. Overview
Alcohol is a CNS depressant. In patients with alcohol dependence,

abrupt cessation unmasks adaptive responses to chronic ethanol use,
resulting in CNS over-activity (i.e. sympathetic overdrive)
2. Diagnosis
• Alcohol withdrawal is a clinical diagnosis.
• Main risk factor for DT = previous occurrence(s) of DT
• Important history re: current alcohol use

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o What do they drink
o How much are they drinking currently
o How often do they drink
o Date/time of last drink
3. Physical Examination (minimum)
No. To Assess Rationale
1 Vital signs Ensure stability of patient
*Tachycardia may reflect

sympathetic overdrive but
do consider other causes
e.g. hypotension
2 GCS Establish baseline – helpful

in longitudinal assessment
Mental state
Prompt consideration of
brain imaging (if indicated)
Assess risk of patient to

himself/herself and others
3 Neurological examination Prompt consideration of:
a) brain imaging (if

indicated)
b) alternative neurological
diagnoses (if clinically

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suggestive)
4 Stigmata of chronic liver Help to decide between use

disease or lorazepam vs. diazepam
4. Look out for concomitant condition(s)

• Actively assess and exclude common coexisting
conditions:
o Falls, Head Injury & Seizures
o Dehydration & Electrolyte Derangements
o Alcoholic Gastritis/pancreatitis/hepatitis
o Concurrent substance abuse
(Benzodiazepines, etc.)
o Wernicke encephalopathy
• Concurrent alcohol and benzodiazepine withdrawal can be
additive in severity
5. Investigations to consider (on top of FBC/renal panel done by

ED)
No Investigations Rationale
1. Extended electrolytes – Risk factor for subsequent DT
Ca/Mg/Po4 and refeeding syndrome
2. Urine drug screen Look for concurrent
polysubstance abuse
If concurrent BZD withdrawal
→ may need higher doses of
lorazepam/diazepam
3. Brain imaging Especially for unknown
circumstances leading up to
drowsy state
4. Septic workup (if Intercurrent illness may
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indicated) precipitate unplanned alcohol
cessation
6. Pharmacological management
Please refer to intranet > “All work is part of a process” (top

of intranet; middle panel) > Clinical Guidelines (4th from top)
> Guidelines, Directives & Circulars (CMB’s face) > search
“Delirium Tremens” after excel sheet pops out
7. Salient points of management

• Please differentiate acute alcohol intoxication from alcohol
withdrawal
• DT typically occurs between 48 to 96 hours post last drink
• If persistent delirious after D5-7 of last drink → consider
other causes of delirium
• CIWA scoring only validated for pure alcohol withdrawal;
inaccurate in the presence of other causes of delirium
• Main stay of pharmacological treatment –
benzodiazepines: a) CNS inhibition b) anti-seizure
• User needs to decide between lorazepam vs. diazepam
• In general – use lorazepam for elderly patients & patients
with liver cirrhosis; additionally, to consider in patients with
significant pulmonary disease (less likely to tolerate
respiratory depression)
• IV benzodiazepines have to be given by doctors i.e. you
• Low threshold for empiric high dose IV thiamine - IV
thiamine 500mg TDS x 3/7

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CTSP High CIWA Score
1. Overview
• CIWA score
o Score range 0 – 67
▪ < 9 (absent/minimal AW) - consider
monitoring withdrawal symptoms
without initiating
▪ benzodiazepines regime
▪ 10-20 (mild-moderate AW) - start
treatment with BZD and monitor
withdrawal symptoms
▪ >20 (severe) – assessment for
HD/ICU
• CIWA not validated for other forms of delirium
• Helpful to look at which specific domain the high score
comes from → may hint at alternate diagnoses
2. Suggested algorithm

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CTSP re: ↑CIWA
Assess patient Consider

• CNS event e.g. ICH
• ARU
• Constipation
• Drugs
Exclude other causes of • Infection
delirium • Electrolytes
• Concomitant
withdrawal e.g. BZD
• Others
Most likely due to worsening

alcohol withdrawal
Manage accordingly
Patient not cooperative with Not sedated sufficiently after Was sedated sufficiently but
oral meds (BZD) previous dose wears off too fast
Consider higher dose: Conside

Conside
Lorazepam – max 2mg r
r
Diazepam – max 10mg shorteni
lorazep
ng am →
dosing diazepa
interval
m*
(no
shorter
Escalate to senior
Consider parental administration (if so lorazepam may be preferable as it is shorter

acting)
ClickConsider
here toHD/ICU
return care
to if regular and/or high dose parental sedation needed; last resort = continuousPage
IV
94
infusion
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GERIATRIC MEDICINE (GRM)
CLERKING NEW GRM CASES

- GRM cases may present undifferentiated, atypically, or in the form
of Geriatric syndromes
- Common Geriatric syndromes: falls, functional decline, delirium,
cognitive impairment, incontinence, inanition/malnutrition
- Effort should be made to take a corroborative history from the
patient‘s caregiver and/or nursing home staff EVEN on call
especially if the patient is unable to give history. Remember to ask
about recent drug allergies
- Domains to be included in clerking:
A. Pre-morbid functional status
- This means the patient’s usual functional status before the acute
illness
- Assessment of the premorbid status is paramount as any acute
change in function usually indicates acute pathology
B. Swallowing
- Perform swallowing assessment for every patient on oral feeding
(if not too drowsy)
- Note special feeding requirements – NGT, diet and fluid
consistencies
- Check notes for previously prescribed diet consistency
o If not available and patient cooperative, always do bedside
swallowing test
o If unable to or in any doubt, consider thickened feeds VS
NGT VS NBM + IV drip till ST reviews
- How to perform bedside swallowing test
o Bedside swallowing test: 30ml of water in small plastic
cup with patient seated upright – look for drooling,
coughing, change in voice quality after swallowing, SOB,
delayed / multiple swallows, desaturations (put patient on
O2 probe when assessing). If patient was on modified diet
prior to admission, assess swallowing with thickener
- Order diet and modified fluid regimen as required
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o Do not keep patient fasted unless there is significantly
reduced conscious state or on high flow oxygen (>40%).
o If keeping patient with history of DM fasted, remember to
order dextrose containing drip and to follow intranet DM
NBM protocol
- If the patient is on NGT feeding, and CXR is done on admission
always review the position of the NGT tip on CXR before
commencing feeding. If the tip of the NGT is not below the
diaphragm, inform the nurses to either adjust it as per protocol
or reinsert it
C. DRE
- Constipation is common in the elderly and a precipitant or
complication of several geriatric syndromes, thus an integral
part of geriatric assessment
(I) FALLS
- The patient should be seen and assessed ASAP
- Assess vitals, ABCs and mental status (compare with baseline if
possible)
- Is it a syncopal fall versus a non-syncopal fall?
- Evaluate subsequently for causes (precipitating factors) and
complications
- History: witnessed vs unwitnessed, time of fall, mechanism of fall,
location of fall, aetiology (pre fall symptoms: chest pain, SOB, BOV,
focal neurological symptoms, giddiness, headache), extent of injury,
sinister symptoms after fall (BOV, nausea / vomiting, severe pain,
ability to ambulate post fall > beware occult fractures/ osteoporotic
fractures), number of falls in last one year (first fall vs recurrent falls)
- Speak to family/caregiver for further history as history may
sometimes be inconsistent
Causes:
(I) Predisposing factors:

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- Intrinsic: muscle weakness due to old stroke, vision/ hearing
impairment, poor balance/ vestibular dysfunction, postural
hypotension, peripheral neuropathy, dementia with poor safety
awareness
- Extrinsic: drugs (including recent change in meds), environmental
hazards, inappropriate footwear
(II) Precipitating factors:

- E.g. acute medical illness (e.g. sepsis, ACS, stroke, arrhythmias),
electrolytes imbalances, seizure
Complications:
E.g. fractures / dislocation, intracranial bleed – especially if on
anticoagulation)
- Neuro: GCS, pupils, reflexes, power, gait, cerebellar signs
- CVS: murmurs, arrhythmias (ECG), carotid bruit
- Lungs: to look for signs of infection
- Abdo: tenderness, DRE (if suspect BGIT / anaemia as a
precipitating cause for the fall)
- Pressure sores
- Postural blood pressure
- Secondary survey: cephalohematoma, chest/pelvic compression,
spinal tenderness, hip tenderness, other joint pain/deformities,
bruising, abrasions
- Swallowing test
- Gait assessment
Orders (as indicated)

- Vitals, CLC monitoring, postural BP (including standing), PVRU, fall
precaution
- Hypocount STAT, ECG
- Fall precaution, allied health referrals will be initiated after primary
team’s review
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- Review meds (e.g. sedatives, anticoagulants, anti-HTN), KIV
withhold
- Analgesia if required
- Fill in the Fall Assessment form (if fall occurs in the ward). Nurses
will also raise IRIS for falls occurring in the wards
- Depending on the circumstances of the fall, consider:

• Bloods: FBC, UECr, Ca/Mg/PO4, CE, LFT, TFT, CK if prolonged
lie is suspected, septic workup if suspicious of infection as
precipitating factor
• Imaging: XR of affected parts (e.g. AP pelvis, hip, wrist), plain
CT brain (TRO bleed), MRI brain (TRO stroke)
• Update main spokesperson on call if there are serious injuries –
otherwise, primary team can update cm
• Escalate to MO if you are ordering urgent scans / suspecting
serious pathology
What to do for head injury as result of fall?

a) When to order urgent CT brain (<1hr)
- Reduced level of consciousness
- Recurrent vomiting
- New focal neurological deficit/ seizure
- Suspected skull fracture
b) Non urgent CT brain

- Delirium
NB.Any unwitnessed fall requires thorough neurological examination
and observation even if there is no evidence of head injury
(II) FUNCTIONAL DECLINE

In clerking – need to specify which component of function has
deteriorated, duration of decline, chronicity (acute, subacute,
chronic). This is important in identifying the cause of functional
decline Identify main caregiver.

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Functional Assessment
- Mobility how much assistance is required, walking aids (e.g. WS,
WF), wheelchair-bound, bed-bound
- ADLs: DEATH – dressing, eating, ambulation, transfer, hygiene
- IADLs: SHAFTTT – shopping, housework, accounting, food
preparation, transport, taking meds, telephone
- Swallowing
- Cognition
- Continence
(III) COGNITIVE IMPAIRMENT IN THE ELDERLY PATIENT

- Most important thing to determine is whether this change in
cognition is acute / chronic (i.e. delirium vs dementia)
- High index of suspicion for delirium if patient has precipitating
factors (e.g. sepsis, ACS, CVA, recent change in meds, urinary /
faecal retention, metabolic / electrolyte abnormalities, uraemic /
hepatic encephalopathy)
Delirium Dementia
Presence of (1 and 2 + 3 OR Presence of the following:
4) (a) Amnesia (short/long term
1. Acute onset and fluctuating memory loss)
course AND
2. Inattention
3. Disorganised thinking (b) ≥1 of the following:
4. Altered level of • Apraxia
consciousness • Aphasia
• Agnosia
• Executive dysfunction
AND
Significant impairment / decline

accustomed community functioning /
home functioning / self-care

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Confusion assessment AMT/ CMMSE (no need to do
method (CAM) CMMSE on call)
AMT (1 point each for each questions answered correctly)

1. What is the year?
2. What is the time (+/- 1 hour)
3. What is your age?
4. What is your year of birth?
5. What is your home address? (includes block number, street, unit
number)
6. Count backwards from 20 to 1
7. Where are we now?
8. Who is our country’s current Prime Minister?
9. What is his/her job? (points to nurse)
10. Recall memory phrase “37 Bukit Timah Road”
How to take a cognitive history (NOT to do for all patients on call,

only when indicated)
- Purpose: to assess the severity and duration of cognitive decline
with corroborative history from the patient‘s family
- Cognition:
1. Amnesia (consider onset, progression, duration)
o Short term memory loss (e.g. repetitive questioning, forgets
conversation/recent events/meals, misplaces objects,
forgets to turn off light/stove/tap, difficulty remembering appt
dates)
o Long term memory loss (e.g. death of a loved one, unable
to remember childhood incidents)
2. Apraxia (e.g. cannot button clothes or assist in dressing,
problems with using utensils, problems with manipulating TV
remote control button)
3. Aphasia –word finding difficulties, incoherent speech/slurred
speech, unable to follow through conversations, inappropriate
answers to questions, appears less chatty
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4. Agnosia (e.g. cannot recognise close family members or familiar
objects and places, calls relatives by the wrong name)
5. Executive dysfunction (e.g. unable to handle finances and buy
things, draw money from ATM, unable to use the remote control
to turn on the television/switch between channels when
previously able to, unable to pack/distribute red packets during
CNY, unable to plan / prepare meals when previously able to,
unable to learn new knowledge, failed judgement)
6. Functional impairment in the community / at home / problems
with self-care (how has the day-to-day function been affected
due to cognitive difficulties)
7. BPSD
o Behaviour / mood (e.g. depression, agitation, hallucinations,
delusions etc)
▪ Reports of feeling down/sad/low mood?
▪ Stopped doing hobbies/things that they like?
o Sleep (e.g. timing and duration, sleep wake reversal,
difficulty falling asleep)
o Appetite
o Care giver stress
(IV) DEALING WITH A DELIRIOUS PATIENT ON CALL

- Risk factors for delirium: age ≥65yo, underlying cognitive
impairment / dementia, current hip fracture, pain, severe illness e.g.
sepsis
- Reversible causes of delirium:

• Drugs, dehydration, discomfort (pain)
• Electrolyte abnormalities (e.g. hypo/hypernatraemia,
hypercalcaemia, hypoglycaemia), environmental changes
• Lungs (hypoxia), liver (hepatic encephalopathy), lack of sleep
• Infection, infarction (cardiac, cerebral), iatrogenic events
• Restraints, restricted movement / mobility, renal failure (uraemia)
• Impaired sensory input (visual / hearing impairment), intoxication
(alcohol)
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• Urinary retention / faecal impaction
• Medication changes
Management of delirium
1. Treat underlying cause! (E.g. ARU: clear bowels, insert IDC)
Orders (depending on cause)
- CLC (if clinically indicated), behavioural monitoring and sleep-
wake chart
- STAT hypocount
- Bloods (if indicated): FBC, electrolytes, septic w/u if suspicious
of new infection, ECG+CE (if indicated), CT brain/MRI brain if
indicated (please kindly discuss with your seniors before doing
so)
- Palpate for bladder, ask for PVRU/RU
- DRE TRO fecal impaction
- Review medications – bear in mind some pain meds TRIGGER
delirium as well; consider stopping such meds if not required
(e.g. tramadol)
2. Non-pharmacological:
(Below measures are modelled after the 1HELP (Hospital Elder Life Program – established
multimodal delirium prevention in elderly patients))
- Effective communication and frequent re-orientation to the
unfamiliar ward environment
- Minimise sensory impairments (ensure spectacles or hearing
aids by patient’s side)
- Ensure adequate hydration
- Encourage mobility with early mobilisation; avoid physical
restraints as much as possible
- Encourage family members to visit often and talk to patient
Bright light therapy2 (only in Geriatric Monitoring Unit (GMU))
1K. Singler, C. Thomas. "HELP - Hospital Elder Life Program - multimodal delirium prevention in elderly
patients”, Internist vol. 58 (2), 125-131.
2Chong, Mei Sian et al. “Bright light therapy as part of a multicomponent management program improves sleep and
functional outcomes in delirious older hospitalized adults.” Clinical interventions in aging vol. 8 (2013): 565-72.
3. Pharmacological (rule of thumb: start low and go slow, oral first)

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- PO haloperidol 2 drops BD / PRN if patient is
agitated/aggressive – avoid in Parkinson‘s disease as it may
worsen rigidity / Lewy body dementia as it might precipitate
neuroleptic malignant syndrome
▪ Check QTc is not prolonged before giving haloperidol
- PO quetiapine 6.25mg ON / PRN (check ECG to ensure QTc is
not prolonged)
- DO NOT use anti-histamines / anticholinergics (e.g.
chlorpheniramine) as these can worsen delirium, cause urinary
retention and postural hypotension
*This can also be found on intranet (e-bulletins/notice board --> Geriatric med notice board → Guides on Geriatric
Syndromes chapter on delirium)*
TREATMENT ALGORITHM FOR MANAGEMENT OF AGITATION

IN MEDICAL SETTING
STEP 1: INITIAL ASSESSMENT AND INTERVENTION
Assessment
- Medical History/ Surgical Issues
- Past Medical History
- Psychiatric History
- Forensic and Illicit Drug History
- Recent investigations on:
▪ Substance intoxication/withdrawal
▪ Metabolic/ electrolyte/intracranial pathology
- Review of previous medication/ response/ allergy/ side effects
- ECG (QTc), CK if indicated
- Urine toxicology for new admissions
Interventions
- Environmental interventions & De-escalation
- Consider urgent medical emergencies for:
▪ Delirium

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▪ Substance Intoxication or Withdrawal (including Delirium
Tremens)
▪ Seizures
- Start Behavioural Charting
- Activate Security and colleagues early
- Least restrictive use of physical restrainers
STEP 2: IF NON-PHARMACOLOGICAL APPROACHES

UNSUCCESSFUL

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STEP 3: IF NO DESIRED RESPONSE AFRER 30-60 MINUTES
1. Seek advice from Consultant or Specialist On Call

2. Give another dose of initial agent tried/ alternative agent
provided maximum therapeutic limits not reached ( exercise
caution with intramuscular medication eg Haloperidol)
3. Consider escalation to high-dependency unit where moderate
sedation may be undertaken
* It is important to treat the underlying medical condition giving rise to

the agitation. Early referral to the appropriate Medical specialty is
needed, with consult to the Psychiatrist On Call as appropriate.
WORKFLOW FOR POTENTIAL ESCALATION OF DISTURBED,

AGGRESSIVE AND VIOLENT (DAV) INPATIENTS TO HIGH
DEPENDENCY (HD) OR INTENSIVE CARE UNIT (ICU)

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Clinical Qn: Are there peculiar characteristics of DAV
patients which may make them hard to evaluate?
• History may be limited
• Agitation may interfere with vital signs assessment
e.g. BP may be spuriously high or "normal"
• Agitation falsely paints a picture of a "well" patient
• Possible delay in performing important investigations
- ECG, blood tests
Clinical Qn: What are the overall goals of care in

managing DAV patients?
• Stabilization of vital signs
• Minimize harm to themselves, other patients and
healthcare workers
• Uncover and manage etiology of aggression
Clinical Qn: What are the broad principles to consider

when determining suitability for HD/ICU admission?
• Can be divided into
1. Complications of illness
2. Complications of treatment
1. Complications of illness
- Manifestations of sympathetic discharge, especially in patients
with known end organ damage/failure e.g. ischemic heart
disease (less physiological reserves; higher risk of
decompensation)
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- Hemodynamic instability
- Severe metabolic acidosis - serum bicarb <16, BE <10
- Known chronic lung disease - either airway or parenchyma
(higher risk of CO2 retention with sedation)
- Fluctuating GCS – especially if GCS <10
- Suspected poisoning (may confound clinical picture; also
represents blind spot for many physicians)
- Suspected serotonin syndrome/neuroleptic malignant
syndrome
2. Complications of treatment
- Need for continuous infusion parental sedation
- Repeated and/or high doses of sedation – either oral* or parental
*Typically includes benzodiazepines and antipsychotics

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HAEMATOLOGY/ONCOLOGY
(I) Approach to anemia on call

Definition: Hb < 13g/dL (men) or < 11 g/dL (women)
Approach:
Assessment
1. Vitals
2. Look for obvious source of bleeding ie. hematochezia, malena,
hematuria, hemoptysis, petechaie/purpura
3. Symptoms of anemia ie. SOBOE, chest pain, palpitations,
giddiness
4. Etiology:
- Trace old notes to find baseline Hb, comorbidities (e.g.
CKD, IHD, previous history of BGIT, alpha/beta
thalassemia), any scopes done before
- Use of NSAIDs/steroids/TCM, recent surgery/procedures,
menstrual hx, dietary hx
- Jaundice (hemolysis)
Investigations

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1. FBC, PBF, reticulocytes, Cr/urea (raised urea in active GI bleed),
PT/PTT, GXM (if planned to transfuse), Fe panel (Fe, Fe sat,
transferrin, ferritin), B12, folate, TFT
2. In acute Hb drop consider excluding haemolysis (FBC, PBF, LDH,
bilirubin, haptoglobin, reticulocytes – to consider sending Direct
Coombs test later if haemolytic markers raised) and acute
bleeding (perform per rectal examination to look for features
suggestive of bleeding GIT)
(II) Appproach to bleeding disorders on call

Platelet disorder
A. Quantitative: Thrombocytopenia
- Is the thrombocytopenia real: repeat FBC, PBF – platelet
clumping (also to look for other cell line involvement)
- Is the thrombocytopenia new: check old platelet counts and
previous workup
- Etiology:
▪ Fever: Fever, infection, DIVC
▪ Hepatosplenomegaly: Possible liver disease with
hypersplenism, lymphoma
▪ Neurological findings: Possible TTP, HUS, drug
induced thrombotic microangiopathies, ie heparin
induced thrombocytopenia, Vit B12 deficiency
▪ Lymphadenopathy: infection, malignancy, lymphoma
▪ Thrombosis: HIT, APS, paroxysmal nocturnal
hemoglobinuria (PNH)
▪ Idiopathic thrombocytopenia (ITP – dx of exclusion)
B. Qualitative: Platelet function disorders (refer Haem)

- Von-willebrand disease
- Ix: Ristocetin Cofactor Assay, Von Willebrand’s Factor,
Antigen, Factor VIII

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C. Drug-induced platelet dysfunction (from use of antiplatelet
agents)
Coagulopathy
A. Bleeding from coagulopathy vs platelet disorder
Bleeding Platelet disorder Clotting factor
characteristics deficiency/inhibitor
Major sites of Mucocutaneous Deep tissue , soft
bleeding tissue hematomas
Petechiae Common Uncommon
Ecchymosis Small superficial Large
Excessive bleeding Yes Not usually
after minor cuts
Excessive bleeding Ofter immediate, Often during
after degree varies with procedure, can be
surgery/invasive severity of defect delayed
procedures

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B. Etiology
PT APTT N Inherited
Factor VII deficiency
Acquired
Mild Vit K deficiency
Liver disease
Warfarin
DIC
PT APTT Inherited
N Factor VIII, IX, XI deficiency
Factor XII, prekallirein or HMW
kinninogen
Von willebrand disease
Acquired
Heparin, dabigatran , direct factor Xa
inhibtiors
Acquired inhibitor of factor VIII, IX, XI or
XII
Acquired von willebrand syndrome
Lupus anticoagulant
PT APTT Inherited
Deficiency of prothrombin, fibrinogen,
factor V or factor X
Combined factor deficiencies
Acquired
Liver disease
DIC
Severe Vit K deficiency
Anticoagulants
Acquired inhibitor of prothrombin,
fibrinogen, factor V or X
Amyloidosis associated factor deficiency

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**If isolated prolonged APTT (normal PT), consider sending APTT
mixing studies. If not corrected and with clinical bleeding/bruising
present, consider excluding acquired haemophilia and send off
Factor 8, 9, 11. Lupus anticoagulation test should also be considered
with non corrected APTT mixing studies (to call Haem lab ext: 8955
for APTT mixing studies if unsure of how to interpret)
C. Vascular abnormalities
- E.g. Hereditary hemorrhagic telengectasia (HHT), Ehlers-
Danlos, Osteogenesis imperfecta, HSP
(III) Blood transfusions
Packed cells Anemia or bleeding (1 unit

increases Hb by approximately 1
g/dL)
Irradiated blood Indicated for patients

products (Packed - Hodgkin lymphoma
cells, platelets) - Post allogeneic stem cell
transplant
- Antithymocyte globulin (ATG),
- Pt receiving purine analogues
(fludaribine and cladribine and
bendamustine)
Leucocyte depleted Minimise HLA sensitisation and

red cell platelet refractoriness in chronic
transfusion, CMV transmission,
febrile non hemolytic reactions

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Washed red cells Indicated for patients with recurrent
or severe allergic or febrile
reactions to red cells, and severely
IgA-deficient patients with anti-IgA
antibodies
Fresh frozen plasma FFP is indicated for the following:

Massive hemorrhage or
replacement of more than 1x blood
volume in <24h, especially with
evidence of microvascular bleeding
and significantly prolonged PT and
APTT.
–Coagulopathy due to acquired or
congenital clotting factor deficiency
PLUS bleeding or impending/recent
major invasive procedure.
•PT >1.5x ULN, APTT >1.5x ULN,
INR >1.5 or coagulation assay
<25% activity are generally
accepted to be able to cause
coagulopathic bleeding.
•Common acquired factor
deficiencies are liver disease,
disseminated intravascular
coagulation, trauma-induced
coagulopathy and dilutional
coagulopathy from large volume
transfusion
•Congenital factor deficiencies
when no specific factor

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concentrates are available e.g.
factor XI, factor V deficiency.
•Reversal of warfarin when there is
bleeding or impending emergency
surgery.
–4-factor prothrombin complex
concentrate is more appropriate in
most settings and should be
considered before FFP –consult
hematologist
–Vitamin K should be concurrently
given for sustained reversal
•Plasma exchange for TTP or HUS

•Replacement of rare plasma
proteins when specific concentrates
are not available e.g. C1 inhibitor
deficiency, anti-thrombin
Cryoprecipitate Adult dose is two pooled units (ten

donor units – approximately 3 g
fibrinogen).
Indications include:
- Acute DIC with bleeding and
fibrinogen <1.5 g/L
- Severe liver disease with
bleeding
- Prophylaxis for surgery when
fibrinogen <1.5 g/L
- Hypofibrinogenaemia
associated with massive
transfusion (maintain >1.5 g/L).
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Platelet (All leucocyte 1 pooled platelet unit (equivalent to
reduced) 4 random units) or 1 CSP unit
should increase platelet count by
30-50 x 109/L, unless there is
ongoing consumption
Apheresis platelets: Are collected

from one donor and therefore limit
the number of donor
Pooled platelets: Are obtained from
a pool of buffy coats from 4 donors.
There are pooled and re-
suspended to create one unit of
pooled platelets
Indication for red cell transfusion
Condition Hemoglobin threshold for

transfusion
Symptomatic patient e.g. 10 g/dL
myocardial ischemia
Hospitalized patient
Pre-existing coronary artery 8 g/dL
disease
Acute coronary syndromes 8 to 10 g/dL
Intensive Care Unit 7 g/dL
(hemodynamically stable)
Gastrointestinal bleeding 7 g/dL
(hemodynamically stable
Non-cardiac surgery 8 g/dL
Cardiac surgery 7.5 g/dL
Ambulatory outpatient
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Oncology patient in treatment 7 to 8 g/dL
Palliative care settings As needed for symptoms;
hospice benefits may vary
Source: Uptodate
Decision to transfuse should be based on assessment of the patient’s

clinical situation and not simply on a fixed threshold.
Factors to consider include:

- Any active bleeding and rate of bleeding, estimated extent of
blood loss
- Any significant symptoms and/or signs attributable to tissue
hypoxia secondary to anemia
- Acuteness of the fall in hemoglobin
- Individual’s particular hemoglobin threshold below which
symptoms occur
- Any coronary artery disease (CAD) or CAD risk equivalent e.g.
ESRF, multiple cardiovascular risk factors (see table above)
- Actively bleeding patients with significant, ongoing blood loss
should be transfused in an expeditious manner. Hb may not
reflect the extent of blood loss until hours later. Massive
hemorrhage protocol (MTP) or urgent blood ordering protocol
should be utilized when indicated.
Patients with significant signs and symptoms of anemia e.g. stable or

unstable angina, dyspnea, tachycardia or hypotension not due to
hypovolemia, should be transfused with the minimum required to
alleviate symptoms/signs of anemia.
- In the majority of non-bleeding patients, one unit transfusion at a

time should be adopted, with clinical assessment and check of
post-transfusion hemoglobin to determine the need for additional
units. Patients with unstable angina and active myocardial
infarction benefit from transfusion to Hb above 9-10 g/dL.

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- Patients who have chronic compensated anemia with mild
symptoms e.g. dizziness or palpitations alone, may not need
transfusion even at low Hb if anemia can be effectively corrected
via medical means, e.g. iron deficiency, Vit B12 deficiency.
- For patients who are not acutely bleeding and have no
symptoms/signs of anemia, evidence based thresholds derived
from randomized controlled trials should be followed.
Indications for platelet transfusions
Thrombocytopenia does not always correlate with bleeding, hence
the decision for platelet transfusion should not be based on platelet
counts alone. Other factors to take into account in the decision on
whether or not to transfuse include:
- Other risk factors for bleeding e.g. other coagulopathies,
coexistent liver disease and renal failure
- Anti-platelet effects of concomitant medications (e.g. aspirin,
plavix, GPIIb/IIIa inhibitors, NSAIDS, serotonin-reuptake inhibitor
anti-depressants, amphotericin etc.)
- Nature of impending (in next 24h) or recent (<48h) invasive
procedure and its bleeding risk
- Fever and sepsis
- Cause of thrombocytopenia
- Any congenital or acquired platelet dysfunction
The cause of thrombocytopenia should always be established

before considering platelet transfusion, unless there is life
threatening bleeding.
Platelet transfusions should be given as close to the procedure
as possible for the best hemostatic effect.
1 Platelet Count of < 20 x 10^9/L (Patients with
thrombocytopenia due to impaired bone marrow
function can be transfused when platelet count < 10 x
109/L in the absence of bleeding, sepsis, fever or other
coagulopathy)

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2 Active bleeding in presence of significant platelet
dysfunction (regardless of platelet count)
3 Platelet count < 50 x 10^9/L with active bleeding, or
undergoing invasive procedure or surgery in the next
24hrs, or major surgery in the past 48hrs, or massive
transfusion
4 Platelet count <80 x 10^9/L with massive transfusion, or
bleeding from multiple trauma or large volume
transfusion at risk of consumptive thrombocytopenia, or
epidural catheter insertion/removal in next 24hrs, or
undergoing high bleeding risk procedure/surgery or
procedures at hard to control sites in next 24hrs
5 Platelet count < 100 x 10^9/L with massive transfusion,
or CNS or intraocular bleeding, or undergoing
neurosurgery to CNS/spine or posterior eye surgery in
next 24hrs.
When platelets should not be given

Contraindicated for thrombocytopenia due to platelet activation
e.g. Thrombotic thrombocytopenic purpura, Hemolytic uremic
syndrome, Heparin induced thrombocytopenia, unless patient has
significant or life threatening bleeding
Not indicated for thrombocytopenia due to immune- mediated
platelet destruction e.g. autoimmune thrombocytopenia (AITP) and
post- transfusion purpura, unless patient has significant or life
threatening bleeding. Haematologist should be consulted
For spontaneous intracranial bleed on aspirin, platelets are not
indicated
[PATCH Trial. The Lancet. 2016;387(10038): p2605-2613]
Do not reduce major bleeding in stable non-bleeding adult dengue

patients without other risk factors, and are associated with side
effects

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Transfusion related reactions
The following steps should be taken in all patients suspected of having
a transfusion reaction
- Immediately STOP the transfusion; save the remaining bag and
tubing for potential analysis- this should be sent to the blood bank
for post transfusion workup of the transfusion reaction with
transfusion reaction worksheet.
- Maintain a patent IV access with IV NS.
- Confirm the correct product was transfused to the intended patient
based on product labeling and patient identification; also assess
the product for gross color changes or bubbles suggestive of
bacterial contamination.
- Assess the patient, including symptoms of fever, respiratory
distress, chest pain, back pain, itching, angioedema, vitals
- Contact the Blood bank to discuss the appropriate evaluation and
initial management.
Type of reaction Signs and Management

symptoms
Acute haemolytic Life threatening and ABCs
anaemia/AHTR worst reaction Start IV hydration
Often clerical issue +- diuretics
(Preformed Abs vs (ABO FBC, RP, Dipstick
donor RBCs) incompatibility) Inform BTS and
return transfusion
Occurs within pack and tubing
minutes Escalate to Senior,
KIV send to
Symptoms: Chills, MHD/ICU
SOB, Flushing,
Abdo/flank pain,
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Pain at site of
reaction
Signs: Fever,
SBP<90, Dark
urine, Oozing from
IV plug sites, Overt
bleeding
Transfusion Life threatening ABCs

associated Escalate to Senior,
circulatory Occurs during or KIV end to
overload, TACO 6hrs after MHD/ICU
transfusion ABG and put on O2
(Increase in if sp02< 94%
circulating volume) Symptoms: SOB, ECG/CXR
orthopnea IV lasix 40mg once
and assess
Signs: HTN, ↑ HR, response
Edema, Lung KIV NIV, eg CPAP
creps, Wheeze, ↑ KIV resume
JVP transfusion at
slower rate
BNP elevated
Transfusion related Life threatening ABCs
lung injury, TRALI Escalate to Senior,
Occurs during or KIV end to
(Donor Abs vs 6hrs after MHD/ICU
recipient WBCs, ↑ transfusion ABG and put on O2
lung capillary if SpO2 < 94%
permeability) Symptoms: SOB, ECG/CXR
orthopnea Start IV drip/IV
dopamine if
Signs: Shock, persistently
Fever, Rigors,
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Edema, Lung hypotensive(Start
creps, Wheeze, ↑ at 10mcg/kg/min)
JVP, Pink frothy No role for steroids
sputum BNP not elevated
Transfusion Life threatening ABCs

transmitted Inspect blood bag
bacterial infection, Symptoms: Chills, for bubbles, foul
sepsis myalgia, lethargy smell, aggregates.
Full septic work up.
Signs: Fever, Send Urine/Blood
Rigors, Shock, cultures.
↓GCS Cover with IV
Piptazocin and IV
Vancomycin(MRSA
) ± Amikacin(Gram
neg)
Start IV drip/IV
dopamine if
persistently
hypotensive(Start
at 10mcg/kg/min)
Allergic reaction- Life threatening ABCs(Ensure
Anaphylactic patent airway)
Occurs within Escalate to Senior,
(Reaction to seconds to minutes KIV end to
transfused MHD/ICU
proteins) Symptoms: SOB IM 0.3mg
epinephrine stat
Signs: IV hydrocortisone
Angioedema, 100-200mg stat
Wheeze, Stridor, Start IV dopamine if
Shock, in shock(Start at
10mcg/kg/min)
Antihistamines
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Delayed Occurs 5-7 days Supportive
transfusion reaction after transfusion management
Diagnosis important
(Undetected allo- Symptoms: Often for future
Abs vs minor asymptomatic transfusions
antigens)
Signs: Fever,
Jaundice, Dark
urine
Febrile non Occurs 0-6 hrs after Slow rate of
haemolytic transfusion. transfusion
reaction, FNHTR Paracetamol
Symptoms: Chills, If fever persistent,
(Abs vs donor Nausea, Myalgia consider sending
WBCs and off haemolytic
cytokines in blood Signs: screen or septic
products) Fever(Temperature work up if infective
increase of > 1.0), symptoms present
Rigors Irradiated blood
transfusion
(IV) Reversal of warfarin, NOACs and heparin

Reversal of Warfarin
A. Risk factors for bleeding: Age >65. Prior stroke. Previous
severe hemorrhage. Renal dysfunction. Hepatic dysfunction.
Anemia. Bleeding disorders (e.g coagulation defect,
thrombocytopenia)
B. Assessment:
i. Haemodynamic stability, please escalate to senior early in
case of major bleeding. Clinically significant bleeding
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includes: intracranial, retroperitoneal, intraocular bleeding,
muscle hematoma with compartment syndrome.
ii. indication for anticoagulation.
iii. Compliance with medication and any recent change in
medications
.
C. Management
Minor bleeding and no significant drop in hemoglobin level

INR Recommendation
< 4.5 Monitor more frequently, consider omitting 1 to 2
doses then resuming at original dose or lowering dose
for a short period till hemostasis secured.
4.5 -7 Omit 1 to 2 doses, monitor more frequently, consider
low dose oral vitamin K 2mg if there is no evidence of
bleeding and resume therapy at a lower dose when
hemostasis secured.
>7.0 Omit warfarin and administer 1–3 mg of oral vitamin
K. Check INR in 24 hours. If INR remains high,
administer additional 1–2 mg of oral vitamin K.
Resume therapy at a lower dose when INR is within
therapeutic range.
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Major bleeding
- Consider haematology consult

- Hold warfarin therapy and administer 5-10mg vitamin K by slow
IV infusion
- Rapid reversal with 4-factor prothrombin complex concentrate(4
factor PCC, available in TTSH Blood Bank as Octaplex®
- Exact Dosing of Octaplex is dependent on INR of patient
- If 4 factor PCC is not available, please also consider reversal
with fresh frozen plasma 15ml/kg or prothrombin complex
concentrate 30 to 50IU/kg (dose is dependent on INR)
- Check INR every 6 hours and repeat the procedure if necessary,
depending on the INR.
Reversal of Novel oral anticoagulants (NOACs)
NOACs include Dabigatran, Rivaroxaban and Apixaban.
There is reversal agent available for Dabigatran (Idarucizumab,

i.e.Praxbind®). For major bleeding with Dabigatran, consider sending
off Dabigatran levels, Thrombin Clotting Time (TCT), PT/PTT before
administration of reversal agent Idarucizumab.
There is currently no specific reversal agent for rapid reversal of

rivaroxaban/apixaban in the event of major or life-threatening
bleeding or emergency surgery. High quality evidence from published
data is not available to guide the management of these patients.

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Direct thrombin FXa inhibitors
inhibitors (apixaban,
(dabigatran) rivaroxaban)
Non life- -Local hemostatic measures
threatening/minor -Delay or discontinue DOAC
bleeding -Investigate aetiology of bleeding and
treatment of underlying cause as per
standard clinical practice
-Consult hematology
• Estimate • Normalization of
normalization of plasma levels: 12–24
plasma levels: h
Normal renal function: 12–24 h
CrCl 50–80 mL/min: 24–36 h
CrCl 30–50 mL/min: 36–48 h
CrCl <30 mL/min: >48 h
• Maintain diuresis
Life-threatening - All of the above - All of the above

bleeding - Stop DOAC - Stop DOAC
- Consult - Consult
haematology haematology
- Hemodynamic - Hemodynamic
support: iv fluids, support: iv fluids,
blood products blood products
- Send FBC, GXM, - Send FBC, GXM,
RP, LFT, TCT, RP, LFT, TCT,
PT/PTT/fibrinogen: PT/PTT/fibrinogen
Normal Thrombin Normal PT means
Clotting Time less like therapeutic
(TCT) probably levels are present
excludes and does not exclude
dabigatran activity prophylactic levels
Normal APTT
means less likely

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therapeutic levels INR is not helpful and
are present and not meaningful for
does not exclude rivaroxaban
prophylactic levels - Measure
- Measure rivaroxaban/apixaban
dabigatran levels: levels:
send to TTSH rivaroxaban/apixaban
Haem lab anti-Xa to TTSH
- Consider dialysis Haem lab
for Dabigatran
•If last dose was • If last dose was
taken within the taken within the past
past 3 hours, 3 hours, consider
consider oral oral activated
activated charcoal(liquid
charcoal(liquid charcoal with sorbitol
charcoal with 50g) X 1 dose
sorbitol 50g) X 1 The use of non-specific
dose hemostatic agents is
• Direct reversal: off-label and based on
Idarucizumab 5 g clinical judgement:
i.v. in two doses a PCC, FEIBA,
2.5 g i.v. no more Novoseven
than 15 min apart
Consider
• Prothrombin complex concentrate (PCC,
Octaplex ®) 25-50 IU/kg (with additional 25
U/kg if clinically needed)
• Alternative agent: Activated PCC(FEIBA
®) 50 U/kg; max 200 U/kg/day: no strong
data about additional benefit over PCC. Can
be considered before PCC, if available

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Reversal of Low Molecular Weight Heparin ( Enoxaparin,
Tinzaparin)
Non-Urgent Urgent (Not Urgent (Bleeding)

Bleeding)
• Hold day of • Wait 12-24 hours if
procedure possible • Protamine sulfate
• Once-daily regimens • Consider protamine • Consider rVIIa
° 1⁄2 dose day prior sulfate
if delay not possible
• Twice-daily
for high bleeding risk
regimens
procedure
° Hold evening dose
day prior
• Protamine Dose for Reversal of Heparin and LMWH
Agent* Half-Life Protamine Sulfate Dosing for

Reversal
All Maximum dose is 50 mg

Heparin 1-2 hours • 1 mg per 100 units heparin if last
dose <30 min; 0.5mg per 100 units
heparin if last dose 30-60min;
0.25mg per 100 units if last dose
60-120 min.
Enoxaparin 4.5 hours • 1 mg per 1 mg Enoxaparin if last

dose< 8 hours, 0.5mg per 1mg
enoxaparin if last dose between 8-
12 hours, if last dose given more
than 12hours, no protamine

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* Half-life is longer with subcutaneous administration for all agents so
may require monitoring with PTT (heparin) or anti-Xa level (LMWH)
every 3 hours with repeat protamine (0.5 mg per indicated amount of
LMWH or heparin) if bleeding continues
• Protamine only partially affects anti-Xa levels

• Anti-Xa levels were useful to assess the amount of
anticoagulation before protamine administration but
unhelpful in assessing its effect
(V) FEBRILE NEUTROPENIA
An Oncological Emergency
Definition
Febrile neutropenia (FN) is defined as an oral temperature of

>38.3°C or two consecutive readings of >38.0°C for 2 h and an
absolute neutrophil count (ANC) of <0.5 × 109/l, or expected to fall

below 0.5 × 109/l. (ESMO guidelines)
- Neutropenia is usually defined as an ANC <1500 cells/microL, with

severe neutropenia defined as <500 cells/microl or an ANC that is
expected to decrease to <500 cells/microL over the next 48 hours.
- Severely ill patients or those on steroids may not be able to mount

fever; other signs of serious infection include tachycardia and
hypotension

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- The ANC can be calculated by multiplying the total WBC count by
the percentage of polymorphonuclear (PMNs) and band neutrophils.
History
a. Look broadly for sources of infection: Facial tenderness/sinus

discharge, oral or gingival ulcers, cough/flu, chest pain, vomiting
or diarrhoea, dysuria or urinary frequency, discharges or pain over
site of CVP lines or biopsy sites, MSK pain or swelling (skin,
bones).
b. Check the number of days from last chemotherapy (ANC nadir
typically at 7th-12th day)
c. Check to see if GCSF has been given and if so, when
d. Check previous culture results (if any) and if MRSA/CRE/VRE
status
e. Check for antibiotic allergies (if any)
Examination (head to toe)
• Palpate facial sinuses for tenderness

• Assess neck for neck stiffness, ± fundoscopy if needed
• Inspect oral cavity AND oropharynx for ulcers/thrush
• Examine the skin, including perineum (no per-rectal or per
vaginal examination as that may induce infection by
traumatising fragile mucosa)
• Inspect central lines / catheters
• Auscultate heart for murmurs and lungs for crepitations
• Palpate abdomen for tenderness, flanks for renal angle
tenderness
• Percuss spine (if complain of back pain)
• Examine the joints for warmth, effusion
Clinical Assessment
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MASCC Risk Scoring Index
Criteria Scoring
1. Burden of illness, choose one:
a. no or mild symptoms 5
b. moderate symptoms 3
c. severe symptoms 0
2. No hypotension (SBP >90mmHg) 5
3. No COPD 4
4. Solid Tumour or haematological 4
malignancy with no previous fungal
infection
5. No Dehydration 3
6. Outpatient at onset of fever 3
7. Age <60 years 2
NB: High risk patients include those with severe neutropenia (ANC
<500) for > 7 days with MASCC score of <21, with any signs of:
hemodynamic instability, hypoxemia, changes in mental state,
vomiting, diarrhoea, line infections, or evidence of renal/hepatic
dysfunction.
Investigations
1. FBC, UECr, LFT, CRP/procalcitonin

2. Septic workup: peripheral blood c/s at least 1 set if also drawing
blood from central line. If no central line, then at least 2 sets
(separate sites); if central line present – c/s x1 set from each
port/lumen (Differential Time to Positivity >120min suggests
CVC source) in addition, UFEME/urine c/s, CXR
3. Consider: sputum c/s, AXR, stool c/s, stool C-diff toxin if having
diarrhea, influenza PCR, lumbar puncture (if symptoms of CNS
infection present e.g. AMS, nuchal rigidity, headache); lactate
only if septic and unwell
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Management
- Vitals monitoring including SpO2, IV access
- Empiric broad-spectrum antibiotics: Gram-positive and Gram
negative (especially Pseudomonas) microbes
- (to adjust according to CrCl and to be administered once blood
cultures are taken, ideally within an hour):
a. IV Piperacillin-Tazobactam
b. If central line present, skin/soft tissue infection or prev
MRSA infection: empiric IV Vancomycin and check
trough levels accordingly
c. If concerned about Gram negative bacteremia (e.g.
urinary tract infection/HBS sepsis): once dose IV
Amikacin
d. If history of ESBL organisms and high likelihood of re-
infection: consider IV Meropenem
e. Do NOT follow ARUS-C/hospital guidelines blindly!
Check with senior resident if unsure!
- Ideally, septic workup should be completed before initiation of

antibiotics. However, in the event that it is really impossible to do
so, antibiotics should be administered as it is life-saving.
- If beta-lactam allergic: consider IV Meropenam if no
documentation of carbapenam allergy and if penicillin allergy is
not type I.: if unclear consider IV Aztreonam ± IV Vancomycin
- Unwell/deteriorating patients: in addition to above: consider
R3/R4 review for medical HD/ICU as per extent of care plans
- Subcutaneous GCSF has not been shown to have mortality
benefit: to discuss with primary team
- If very low risk MASCC (uncommon for inpatients): consider oral
antibiotics (PO Augmentin AND PO Ciprofloxacin). This should
not be decided while patient is admitted after office hours. Treat
all febrile neutropenic patients with IV broad spectrum
antibiotics.
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- New-onset fever in a patient being treated for neutropenic
sepsis:
If fever despite at least 48h of antibiotics:
▪ Retake history and physical examination to determine
possible source
▪ Repeat septic workup. KIV include fungal c/s (esp. if
treated for >4 days and/or severe prolonged neutropenia
>7days)
▪ If symptomatic and/or unwell, consider escalating
antibiotics and add IV Vancomycin and/or antifungals
- Consider CVC removal for patients with catheter-related
bloodstream infections caused by S aureus, P aeruginosa,
Candida spp, or rapidly growing nontuberculous mycobacteria
(discuss w senior)
- Keep Hb >8 and Plt > 20
- When patients are deep in the throes of neutropenia, they may
not be able to mount a response to an infection. As such, an
abscess may be found only when the white blood cells are
improving.
(VI) APPROACH TO ACUTE LEUKAEMIA ON CALL

- Types of acute leukaemia: ALL (commonly seen in children,
young adults) vs AML (adults, elderly). Usually transferred from
other hospital or flagged up as blasts on peripheral blood film in
the haematology laboratory
- Presentation:
▪ Symptoms: Malaise, arthralgia, myalgia, fever,
frequent/persistent infection, bleeding/bruising,
symptomatic anaemia (decreased effort tolerance, SOB,
chest discomfort/chest pain, dizziness, fatigue)
▪ Signs: splenomegaly, gum hypertrophy (acute monocytic
leukemia), lymphadenopathy (more common in ALL)

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History and Physical Examination
Look for complications, particularly
1. Infection – if patient has fever, for full septic workup and manage
as per febrile neutropenia. See Febrile Neutropenic guidelines.
2. Leukostasis – exclude this especially if TW count is high (>

50K for acute myeloid leukemia)
Poor prognosis, 20 – 40 % die within first week if present with
symptomatic hyperleukocytosis. Respiratory failure + neurologic
death rate at one week reaches 90%.
Most commonly seen in those with AML or CML in blast crisis.
This can manifest in the following clinical presentations:

- Lung: Dyspnea, hypoxemia, diffuse alveolar hemorrhage,
respiratory failure
- CNS: Confusion, dizziness, headache, coma, focal neurologic
deficits, stroke
- Eye: Impaired vision, retinal hemorrhage (perform fundoscopy)
- Ear: Tinnitus
- Heart: Myocardial ischemia/infarction
- Vascular: Limb ischemia, renal vein thrombosis, priapism, deep
vein thrombosis
3. Bleeding – Thrombocytopenia secondary to marrow

infiltration -> easy bruising/bleeding tendency
Send off DIVC screen. Suspect acute promyelocytic leukaemia if in
DIVC. Consider CT brain (low threshold for this if having headache
with thrombocytopenia or altered mental state/drop in GCS).
Investigations
FBC, Renal panel with bicarbonate, lactate, D-dimer, DIVC screen,
screen for tumour lysis (Calcium, Albumin, PO4, Creatinine,
potassium, uric acid),and LDH (also useful to help exclude TLS),
G6PD screen, GXM, CXR and ECG

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Management – Discuss all new cases with after office hour with
registrar on call (1st line) and consultant haematologist on call
1. If unwell, admit to High Dependency /ICU for closer monitoring
or Ward 9C (haematology ward 9C ACA)
2. Hydrate well, usually 1.5-2 L/day. For patients with leukocytosis
(>50 × 109/L), KIV 3L/day if no contraindications, with strict I/O
KIV Frusemide if positive balance >500-750 mL.
3. Start PO Allopurinol 300mg OM (if no contraindications, check
CrCl and renal dose adjust if needed). If already in tumor lysis
and patient has hyperuricemia, give IV Rasburicase 0.15 mg/kg
over 30 min after checking that patient is not G6PD deficient.
(Counsel family about cost, discuss with haematologist-on-call)
4. Start Cytoreduction with hydroxyurea/low dose cytarabine or
consider leukapheresis if having clinical leukostasis
(Haematology After Office hour registrar to be informed as 1st
line by on call team, case to be discussed with haematology
consultant on call)
5. Bone marrow examination/2D Echo (brief)/PICC line/HLA
typing/fertility preservation will be arranged by primary team the
next day or urgently if deemed critical by haematology after
office registrar/consultant haematologist on call
6. TLS management (see below)
7. Take baseline weight and height
8. Transfusion support: Keep platelet >20 x 109/L if febrile, or >10 x
109/L if afebrile, > 50x109/L if diagnosis of acute promyelocytic
leukemia is suspected or if leukostasis is suspected. Transfuse
platelets and correct coagulopathy with FFP/cryoprecipitate if
associated with active bleeding. Aim Hb>7g/dl and >8g/dl if
having ischaemic heart disease (should discuss transfusions to
correct bleeding diathesis with after office on call haematology
registrar)
9. Check Massive Transfusion protocol to determine if
cryoprecipitate is necessary.

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**Transfusion in the presence of high white cell count may
precipitate complications of leukostasis. Discuss with after
office hour registrar or on call haematologist.
Emergency
APML (Acute promyelocytic leukaemia)- clinical variant of AML
- High rate of early mortality, good prognosis after treatment
- Clinical presentation: symptoms related to complications of
pancytopenia, * bleeding secondary to DIVC
- Investigations: PML/RARA
* Consult haematologist on call urgently to decide if need to start
differentiating agents urgently.
APML is a medical emergency with a high rate of early mortality
if left untreated. It is critical to start treatment with ATRA without
delay as soon as diagnosis is suspected based on cytologic criteria.
APML is characterized by severe bleeding due to DIC and/or primary
fibrinolysis. Another common complication is differentiation syndrome
(=retinoid acid syndrome/cytokine storm) occurs in 25% of patients,
characterized by fever, peripheral edema, lung infiltrates, respiratory
distress, hypotension, renal and hepatic dysfunctions, serositis etc.
Early recognition is needed and treatment is with steroids
(Dexamethasone 10mg Q12H)/temporary stopping of ATRA or
arsenic trioxide, leukapheresis, cytotoxic chemotherapy (This should
be discussed with the primary haematologist on call).
(VII) APPROACH TO TUMOUR LYSIS SYNDROME (TLS)
An Oncological Emergency
If untreated, high mortality risks in event of cardiac arrhythmia, renal
failure, seizures
- Caused by massive tumor cell lysis and the release of K, PO4, uric
acid into systemic circulation. Deposition of uric acid/calcium
phosphate crystals in renal tubules can result in AKI/oliguria/anuria,
even acute renal failure requiring dialysis.
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- Symptoms and signs are non-specific- mainly secondary to
metabolic abnormalities and their complications
- If the patient has a background of renal impairment, he/she is also

more prone to developing TLS
Identification and prophylaxis is key. TLS may be spontaneous or

occur post-initiation of systemic cytotoxics in treatment-sensitive
disease:
A. Aggressive NHL (e.g. Burkitt’s, diffuse large B-cell lymphoma)

B. Acute Leukemia, ALL> AML (especially when TW>100K)
C. Some solid organ tumors such as small cell lung cancer, germ
cell tumor
As a guide, any tumor/malignancy that has any of the following

characteristics is at risk:
- fast-growing
- large
- sensitive to systemic treatment
Classified into biochemical and clinical criteria:
Metabolic Criteria for Criteria for

abnormality classification of classification of
laboratory TLS clinical TLS
( Cairo Bishop)
Hyperuricemia Uric > 475 umol/L
or 25 % from
baseline
Hyperphosphatemia Phosphate > 1.5
mmol/L or 25 %
from baseline

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Hyperkalaemia K > 6mmol/L or 25 Cardiac
% from baseline dysrhythmias
Hypocalcemia Corrected Ca Signs of
>1.75 mmol/L or neuromuscular
ionized calcium irritability eg
<1.12 or or 25 % Chvostek’s,
from baseline Trousseau’s,
hypotension. Heart
failure, seizure
AKI Increase in serum Oliguria
creatinine >26.5
umol/L or 1.5 x
upper limit of
normal if no
baseline available
*2 or more laboratory changes within 3 days before or seven days

after cytotoxic agent

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Management:
A. Prevention is key
- Risk-stratify your patients into low, moderate or high risk for TLS
- consider prophylactic Allopurinol or Rasburicase

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[Reference: Journal of Hematology and Oncology December 2012. Ali
McBride and Peter Westervelt. Recognizing and managing the
expanded risk of tumor lysis syndrome in hematologic and solid
malignancies]
B. Aggressive IV hydration
- At least 3-3.5 litres/day (check cardiac/renal status)
- Diuretics (Lasix) can be used to maintain good urine output- but
avoid in hypovolemia and obstructive uropathy
- Strict I-O charting- aim for a urine output of 2ml/kg/hr
C. Correct electrolytes
- Especially hyperkalemia (refer to protocol)
- Consider monitor renal panel 4-6 hourly in severe high-risk
cases
- Consider renal referral for dialysis in severely acidotic/refractory
cases or if unable to hyperhydrate, severe hyperphosphatemia
in the presence of symptomatic hypocalcemia.
- Careful correction of symptomatic hypocalcemia in the
presence of hyperphosphatemia, Be careful if solubility product
of Ca2+ and PO43- nears or exceeds 5.
D. Control of hyperuricemia
- Allopurinol PO 300mg daily (adjust renally) - (xanthine oxidase
inhibitor, reduces conversion of nucleic acid byproduct to uric
acid)
- Rasburicase IV 6mg in 50 mls NS to be administered over 30
min (0.1mg/kg ~$1000/dose) - ( recombinant urate oxidase,
converts uric acid to water-soluble metabolites, more rapid
onset)
▪ Must NOT be G6PD deficient
▪ Do not give with concurrent allopurinol

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▪ Check with senior resident/primary team before
administering
(VIII) APPROACH TO NEOPLASTIC CORD COMPRESSION
Introduction
- Most commonly due to lung, prostate, multiple myeloma, breast,
RCC, lymphoma
- Occurs when malignant process invades the epidural space and
compresses on the thecal sac
- Causes mechanical instability of spine and potentially irreversible
loss of neurological function
- Early recognition is key to prevent further progression of
neurological deficits
- The neurological prognosis is also dependent on how long the
symptoms have been. Symptoms can be irreversible when the
symptoms have been there for >48 hours.
History
- New onset/worsening back pain in an oncology patient **pain is
very often the first sign, neurological deficits might not even be
present
- Motor deficits- typically weakness, followed by gait dysfunction,
and then paralysis
- Sensory deficits
- Ask for bladder and bowel dysfunction (late sign) e.g. ARU,
constipation, incontinence
- Ask for onset of symptoms (if within or more than 48hours)
- NOT all patients will present with classic symptoms and signs
- Full neurological examination including DRE
▪ Cord compression classically causes a pyramidal pattern of
weakness [preferentially causing weakness of flexors in LL
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(below thoracic spine) and weakness of UL extensors (above
thoracic spine), hyper-reflexia, increased tone, extensor
plantar responses.]
▪ Cauda equina will typically cause more asymmetrical and
patchy weakness
▪ Sensory findings less common than motor but still present in
majority of patients- sensory level might be 1-5 levels below
actual level of compression
- Percuss for palpable bladder
- Palpate and percuss for spinal tenderness
- Document perianal sensation and anal tone (saddle
anesthesia/loss of anal tone)
- Document power and sensory levels DAILY (serial examinations)
Investigations (inform SR before ordering on-call)

- Imaging of entire spine – urgent MRI whole spine screening (done
at TTSH not NNI)
o CT myelography is the alternative imaging
option in patients who cannot undergo MRI
- Bedside PVRU
- FBC, renal panel, calcium/P04/PTH, 25OH-Vit D, PT-PTT, ±GXM
if for op
- Newly-diagnosed cases may need CT imaging to detect location
of primary tumour (non-urgent: may consult Med Onc)
- Consider MRI brain with contrast if signs and symptoms not in
keeping with Cord pathology
Referrals
1. Urgent Neurosurgical/Ortho referral (check HMS roster for spine-
on-call)
(Exception: pre-terminal, advanced cancer for best supportive care
with a prognosis of less than 6-months, non-surgical candidates)
- Most rapid method for relief of acute cord comp, esp if there is
spinal instability
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- Spinal Instability Neoplastic Score [SINS] may determine if
surgery is appropriate:
▪ Location of the tumor
▪ Presence or absence of pain relief with recumbence
▪ Lytic or blastic features
▪ Presence or absence of spinal deformity on imaging,
bone collapse, and tumor infiltration of the posterolateral
elements of the spine.
▪ Minimal score 0, maximal score 18: 0-6 stable spine, 7-12
indeterminate, warrants surgical consultation, 13-18
instability, warrants surgical consultation
2. Urgent Rad Onc referral for all cases
- Radiation administered after surgical decompression (typically 2-
3 weeks after op)
- In non-surgical candidates, lack of spinal instability: RT alone
Management (if acute onset <48h)

- IV dexamethasone 8mg STAT + 4mg q6h with IV Omeprazole
(in the on call setting, prompt administration of steroids is crucial)
o In the event that lymphoma is suspected,
please discuss with senior on duty before
administering steroids
- Optimise pain control (glucocorticoids may not be sufficient,
consider opioids)
- Spinal nursing
- Keep NBM until surgical review, blood sugar monitoring
- Consider DVT prophylaxis
- Insert IDC if evidence of urinary retention
- Other considerations: bisphosphonates/denosumab (if non-
urgent will need dental review first: risk of ONJ)
(IX) SVCO (SUPERIOR VENA CAVA OBSTRUCTION)
Oncological Emergency: risk of tracheal obstruction; laryngeal

oedema, cerebral oedema if left untreated
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- Causes: Intrinsic (tumour or clot thrombus) / Extrinsic (Malignant
from mass/nodes: lung, lymphoma, less common breast,
mediastinal germ cell tumor, thymoma); Benign causes: Infection,
RT, iatrogenic e.g. line related)
- Patients with SVCO due to underlying cancer may present without
a known diagnosis of malignancy
[Reference: NEJM 2007 Lynn Wilson et al. Superior Vena Cava

Syndrome with Malignant Causes]
History
- Common symptoms
▪ Facial swelling or head fullness
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▪ Headaches
▪ Dyspnea, oftentimes better with sitting up and leaning
forwards
▪ Cough
▪ Facial plethora
- Less common symptoms
▪ Syncope
▪ Confusion
▪ Giddiness
▪ Stridor
- Not all facial swelling and lip oedema is drug allergy especially if
chronic and/or no antecedent medication use
- Trace oncological history and latest CT scans (if known case)
- Severity of symptoms is important in deciding urgency of
intervention
- Signs
▪ Facial/UL edema (edema is of the taut and tight kind, different
from the edema that you get in fluid retention)
▪ Distended neck veins flushing
▪ Dyspnoea and cough
▪ Pemberton’s sign (do not do this if possible, can be very
uncomfortable for the patient)
▪ Hoarseness or a high-pitched nasal-type voice
Investigations (should not delay appropriate treatment)

- CXR (widened mediastinum, right upper zone mass),
- CT thorax urgent +/- CT neck
o Assess level of obstruction, identify cause of
SVCO, differentiate between tumor and
thrombosis
- FBC renal panel PT-PTT, calcium/phosphate, uric acid
- AFP b-HCG and LDH if germ cell tumour suspected

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Treatment
1. General
- Elevate HOB 45°, O2, Establish IV access in lower limbs FIRST
BEFORE removing any plugs on UL
- Steroids controversial – may consider ONLY if known case and/or
lymphoma is ruled out (to discuss with a senior first before
starting)
- Diuretics generally not used in this setting, but can be considered
- Call senior, establish extent of care. Regardless of status, try to
alleviate patient’s symptoms
- In these instances, it is usually fast-growing and a more centrally
located tumor. This makes it likely that some of the more common
tumors are lung cancer, lymphoma and germ cell tumor. This
would mean that they are potentially curable and are chemo-
sensitive. So with all intents and purposes, extent of care should
be active unless proven otherwise.
2. Relieve obstruction
- Consider VIR consult for percutaneous SVC stenting (KIV order
diagnostic CT neck/thorax to do in same setting).
- Complications include infection, pulmonary embolus, stent
migration, hematoma at the insertion site, bleeding, and, very
rarely, perforation.
- If airway compromise: consider intubation or monitoring in
mHD/MICU if for active management
3. Oncologic therapy
A. Refer Rad Onc for RT (non-urgent)
- Urgent cases need stenting ± intubation
- Patient must be hemodynamically stable and be able to
lie supine or at least 45 degrees for RT to be
administered
B. Refer Med Onco to discuss systemic treatment if not admitted

under Med Onco
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INFECTIOUS DISEASES
(i) WHERE TO FIND IMPORTANT INFORMATION

TTSH Intranet
- Notification forms for Infectious Diseases/Tuberculosis (right of
screen > Emerging Infectious Diseases); alternatively,
electronically through MOH CDLENS (CPSS toolbar > External
Apps)
- To access Antimicrobial Stewardship Programme (ASP)
guidelines: TTSH Intranet → Right side of screen → ASP
Guidelines
o Empiric Antibiotic Guideline
o Carbapenem and Tazocin Usage Criteria
o Renal Dose Table
o How-to Guide to ARUS-C
o Antibiotic Prophylaxis for Surgery
- The ASP Guidelines will be your lifeline in deciding the choice
antibiotic for your patient. It gives first and second-line antibiotic
options, duration of therapy, and options for de-escalating to oral
therapy.
ARUS-C (via eIMR)

- Will offer protocolised guidance on nearly all antibiotic
prescriptions, including renal dosing
- Notable exception is vancomycin dosing (consult
guidelines/pharmacist)
- Still requires you to get the diagnosis correct!
Vaccination Records
- NEHR > Medications > Immunisation
- Intranet > e-Bulletins/Notice Board > Pharmacy Notice Board >
Pre-discharge Vaccination Programme > Weblink to Vaccination
History (this is in active use, but requires you to activate your
account via the Pharmacy department)

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KTPH Intranet
- Intranet > Useful Links > Antimicrobial Stewardship Program OR
search ‘Antibiotic Guidelines’
- In addition to the equivalents of what is in TTSH Intranet, also
contains useful guidelines on treatment of infective diarrhoea and
UTI
(ii) DENGUE FEVER

- Features (have a high index of suspicion!): Fever, headache,
vomiting, myalgia, arthralgia, retro-orbital pain rash (classically
macular, blanching and confluent with islands of sparing;
occasionally petechial)
- Leukopaenia, thrombocytopaenia and transaminitis (AST > ALT)
are common laboratory findings, but may also occur in other viral
illnesses
- Diagnostic testing: “Dengue Duo” (IgM + IgG, and NS1 Ag)
- NS1 usually turns positive 24hrs after fever onset and peaks in
sensitivity by 72hrs; IgM usually reaches detection threshold by
day 5 of fever.
- Remember that dengue fever is an MOH notifiable disease
- Differential diagnoses to consider: Other viral haemorrhagic fevers,
Chikungunya, Zika, malaria (hence obtain travel history), even
gram negative bacteremia (which is also a differential of
leukopaenia and thrombocytopaenia)

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Triaging the dengue patient – WHO 2009 Classification

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- ASSESS ALL PATIENTS WITH DENGUE FOR WARNING
SIGNS/SEVERE DENGUE AND INDICATE THIS CLEARLY IN
YOUR WORKING DIAGNOSIS/ISSUES LIST
- eg. Diagnosis : Dengue fever, day __ of illness, in __ phase
(febrile/ critical/ defervescence), with /without warning signs
- Most patients present in the febrile phase or critical phase
(classically occurring after défervescence with a fall in platelet
count and onset of third spacing)
- ALL PATIENTS WITH DENGUE + WARNING SIGNS, OR
SEVERE DENGUE, MUST BE ESCALATED TO A REGISTRAR;
KIV MHD MANAGEMENT
- Signs of intravascular volume depletion include tachycardia,
postural hypotension (remember that BP can be normal until class
III shock!), narrowed pulse pressure (<20 mmHg) and an elevated
haematocrit.
- Ensure adequate hydration with fluid boluses but avoid
overcorrection (refer to the dengue E-Carepath for specifics);
consider ‘top-up’ boluses if haematocrit is > 50%.
- Recheck FBC at least daily; recheck FBC a few hours after a fluid
bolus if correcting for markedly elevated haematocrit.
- Platelet transfusions are not routinely required unless there is
severe bleeding
- Patients should be placed on thrombocytopenic precautions : no
IM injections, no brushing of teeth. To order chlorhexidine gargle
instead
- Where possible, avoid prescribing paracetamol in patients with
dengue, as this may worsen transaminitis. Tepid sponging for fever
and alternatives such as tramadol may be used for headache/
myalgia
- Encourage oral intake, Oral hydration is preferred over IV hydration
if patient can drink; as dengue patients are at risk of
thrombophlebitis
(iii) BETA-LACTAM ALLERGIES/ADRs

Must know
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1. Review the CMIS entry for all antibiotic allergies and try to verify
these with a brief history. A “beta-lactam allergy” can have
significant implications on your patient outcome.
2. ARUS-C (in eIMR) can take allergies into account when giving
antibiotic recommendations!
3. “Severe allergy” = anaphylaxis, angioedema; “Severe ADR” =
SJS-TEN, DRESS/DIHS.
If in doubt, consult a senior or the pharmacist on call.
4. DOCUMENT all new adverse reactions to antibiotics (whether
allergic or non-allergic) promptly in C-DOC. There is no rush to
make a CMIS entry as the diagnosis may evolve over time.
Good to know (In practice - discuss antibiotic choice with a

senior or specialist in the context of documented drug allergies)
- Beta-lactam antibiotics often have the best efficacy and/or side
effect profiles for treatment of many common infections. Try to
avoid unnecessary use of second-line agents.
- Cross-reactivity between penicillins and cephalosporins varies
between 1-25% for IgE-mediated reactions (anaphylaxis,
angioedema, urticaria), but mostly occurs with first-generation
cephalosporins. It is usually safe (<5% cross-reactivity) to
administer a 3rd/4th generation cephalosporin to patients with a
non-severe penicillin allergy.
- (The corresponding cross-reactivity rates for non-IgE-mediated
reactions (non-urticarial rashes, SJS-TEN, DIHS/DRESS) are
largely unknown.)
- Cross-reactivity between penicillins and carbapenems is reported
to be ~10-25%, but the actual rate is likely to be much lower. As
carbapenems are usually reserved for sick patients, their benefits
may still outweigh the risks (do discuss this with a senior).
- Cross-reactivity between cephalosporins and carbapenems is
reported to be <5%.
- Aztreonam (monobactam) is active against non-ESBL gram-
negatives and is a suitable choice for patients with severe
penicillin allergy who cannot tolerate all other 𝛽-lactam agents.
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However there is significant cross-reactivity with ceftazidime due
to their identical side chains.
(iv) COMMON INFECTIONS

Pneumonia
- In a patient with respiratory symptoms, If CXR changes are absent,
consider other respiratory differentials such as infective
exacerbations of asthma/COPD/upper respiratory tract infection
and alternative diagnosis (UTI, bacteremia etc,.)
- Patients with swallowing impairment are prone to aspiration;
consider swallowing assessment/temporary NBM. They require
anaerobic cover using antibiotics such as augmentin, tazocin
- Empiric treatment for CAP are augmentin +/- clarithromycin (for
atypical coverage)
- Empiric treatment for hospital acquired pneumonia are IV tazocin
(for Pseudomonal cover) PLUS once loading dose IV vancomycin
(for MRSA cover)
- Patients with bronchiectasis may require empiric anti-pseudomonal
therapy (tazocin, levofloxacin, ceftazidime).
UTI
- In truly infected patients, UFEME WBC should be >10/microL or
10,000/mL
- In patients with IDCs in-situ, first change the IDC, obtain a urine
sample from the new IDC, then start antibiotics to improve
microbiological yield
- Nosocomial/ Catheter associated/ post urological procedure: use
IV cefepime + once dose amikacin (use IV tazocin in KTPH, as
cefepime is non-formulary)
- Simple community acquired UTI: use ciprofloxacin (good prostatic
penetration if suspecting prostatitis) or augmentin
- S. aureus bacteriuria should prompt a search for S.aureus
bacteraemia (do blood cultures), do not disregard as a contaminant
especially in absence of IDC
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- Candiduria is almost always due to colonization and does not
require empiric antifungal treatment. This does not apply in
patients with in-situ foreign bodies (PCN, DJ stents) or neutropenic
patients.
Clostridioides/Clostridium difficile diarrhoea

- Should be suspected in patients with ≥3 loose stools/day with no
alternative explanation, in the setting of risk factors (recent
antibiotic use, hospitalization, and advanced age)
- First episode: PO metronidazole 400mg Q8H or if severe, then PO
Vancomycin 125mg Q6H for 10 days
- 2nd/recurrent episode: Oral vancomycin pulsed-tapered regimen
OR if metronidazole was used for the first episode: PO
Vancomycin 125mg Q6H for 10 days
- Fulminant disease (hypotension, tachycardia, ileus, megacolon):
PO Vancomycin 500mg Q8H + IV Metronidazole 500mg Q8H;
consider AXR and surgical consult
- No role for repeat testing within seven days of same episode of
diarrhoea, for test for cure, for testing in asymptomatic patients or
for patients receiving treatment
- Put on contact precaution; use soap (not hand rub) for hand
hygiene
- Consider stopping offending antibiotics if not necessary
Sacral sores
- Remember to turn the patient to examine for sacral sore
- Cultures of deep tissue or bone biopsies are most sensitive and
specific
- Do not take superficial swab cultures as they reflect surface
colonization and are not clinically useful
- Antibiotic therapy may not need to be started overnight in patients
who are clinically well with stable vital signs
- Look through old microbiology results of chronic wounds to help
guide empiric therapy if needed

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- IV Augmentin can be used as initial empiric antibiotic in clinically
well patients; to add IV vancomycin in MRSA patients
Cellulitis
- Empiric treatment with IV cefazolin; consider IV vancomycin if
patient has known MRSA colonisation
- If history of water exposure: add PO ciprofloxacin
- Do not take superficial swab cultures as they reflect surface
colonization and are not clinically useful
- Calculate the LRINEC score in patients who have lesions
suspicious of necrotising fasciitis
- Obtain surgical consult in patients with suspect necrotizing fasciitis
and/or drainable abscesses
- Look out for septic arthritis
Central Line-associated Blood Stream Infection (CLABSI)

- Take one set of cultures from the periphery and another through
the central line
- DO NOT take blood from a dialysis catheter → can be taken by
renal unit nurses just before next dialysis
- Memo microbiology lab to do Differential Time to Positivity (call lab
beforehand), and clearly label bottles “peripheral” and “line
(indicate which port)” with time taken
- Empirical treatment with vancomycin and amikacin
Neutropenic fever
- Reverse barrier nursing, full septic work up
- Empirical treatment with IV tazocin, amikacin +/- vancomycin (if
suspected catheter related infections, skin/soft tissue infection,
pneumonia, hemodynamically unstable)
- Consider G-CSF

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(v) BLOOD CULTURE ADVISORY SERVICE
- Bacteraemia/fungemia is a serious infection that has direct
implications on clinical outcome, especially for organisms like S.
aureus or Candida
- TTSH’s blood culture service offers early recommendations based
on blood culture results so as to improve clinical outcomes,
especially for time-sensitive antibiotic decisions
(vi) NEEDLESTICK INJURY

- Wash your wound with soap and running water
- Inform ward sister, document the incident in the case notes and
inform your senior (MO/reg)
- Arrange for a colleague to consent the source patient and take
their baseline bloods for HIV, HBsAg and HCV Ab. (Aurora order
pre-sets > IEM - SOURCE)
- Indicate on the request form that the blood draw is done under
needle stick injury protocol so that the patient does not get charged
for the tests. Also do get a quick history from the patient if possible
to determine the risk status.
- You will be given an appointment to see an ID consultant/registrar
- Claims for MOHH staff for ED visit and Post Exposure Prophylaxis
will be via Prosoft via Workplace Injury Compensation.
In TTSH:
- During office hours: go to Occupational Health clinic (CDC2
63577392/3, 63573965) to get your bloods taken.
- After office hours: go to ED
- IRIS the incident (last thing to do)
In KTPH:
- During office hours: Go to the HFLC (Health For Life Clinic) located
in Tower C, level 5 (C54); office number is 66023540, 66023058
- After office hours: go to ED
- Submit incident report on HITS (Hospital Incident Tracking System,
KTPH’s IRIS equivalent)

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NEUROLOGY
I. CEREBROVASCULAR ACCIDENTS
CTSP: GCS drop (“drowsier”, “sleeping a lot”), diplopia, slurring of

speech, new swallowing impairment, lateralizing
weakness/numbness, hypertensive episode +++ associated with
neurological symptoms, critical abnormal CT/MRI brain result
On the phone +/- on the computer:
- Vitals + GCS and its trend (if it suddenly nose dived, plan to
escalate once you have evaluated patient). There may be reflex
hypertension in acute stroke),
- When was patient last seen well?
- What was the patient admitted for?
- Request for STAT hypocount to be done (readily reversible stroke
mimic)
- Order for IV plug (preferably green) to be set and 4 tubes to be
taken if not yet done
- Receiving a handover for tracing a CT/MRI brain result: politely ask
for indications for scan, any contraindications to start anti-platelets
for patient, what they are looking for, what consultant’s plan is if it
is positive for an ischemic stroke
Broad questions to keep in mind when assessing patient (referenced

from Dr Lee SH notes):
1. Is this a stroke? Differentials to consider:
(a) CNS infections: Cerebral abscess,meningitis, encephalitis
(b) Structural intracranial lesions: Aneurysm,tumour,hematoma

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(c) Autoimmune: Multiple sclerosis
(d) Metabolic: Hypoglycemia, hypertensive and other

encephalopathies, hypo/hyperK periodic paralysis
(e) Others: Migraine, epilepsy (partial seizures or Todd’s paralysis),

Cervical myelopathy, LMN pathology (MG/GBS), labyrinthine
disorders which may cause acute vertigo/ataxia, psychological,
2. Is the patient within the window period for the following

interventions? (as per NNI treatment algorithm):
(a) 4.5 hrs: IV tPA +/- thrombectomy
(b) 6 hrs: thrombectomy
(c) 6-24 hrs: thrombectomy if deficit/infarct mismatch (i.e clinical

deficit disproportionately severe compared to volume of infarction on
imaging).
(c) 24 hrs: DAPT (with loading dose on D1) - for mild stroke i.e
NIHSS </= 3 and high risk TIA i.e ABCD >/= 4). Check with senior
before starting.
(d) 48 hrs: Aspirin, decompression for large MCA infarct
Initial assessment:
- Airway, Breathing, Circulation, Disability (GCS – please do the

GCS assessment yourself again; do not just rely on the nurse’s
assessment)
- Hypocount if not done yet
- History from patient/family/nurse/NEHR/CCDR:
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o Time of onset – “When was the patient last seen well?”
o Get a clock time (implication on treatment as above)
o Symptoms: giddiness, unsteady gait, diplopia, slurring of
speech, facial droop, dysphagia, weakness, numbness
o Headache/nausea/vomiting/seizing prior to neurological deficit
> suggestive of bleed
o Get a reliable witness – family member, nurse in charge who
called
o Tempo: gradual or sudden, Maximal at onset or not
o Any crescendo transient ischemic attack pattern
o Check for cardiovascular risk factors:
DM/HTN/HLD/CAD/AF/previous CVA, smoking, alcohol
o Long term meds and compliance
- Examination:
o GCS
o Pupils – Anisocoria (may be bleed or brainstem infarct),
pinpoint (pons), fixed mid-sized (midbrain)
o Cortical signs: aphasia, apraxia, neglect, gaze deviation,
extinction (sensory, visual), drowsiness, hemianopia.
o Blink to threat (visual fields)
o Reflexes, tone, UMN signs
o Sensation, power, posturing, focal neurological deficits,
pronator drift
o NIHSS scoring (usually done by neuro team)
o Look for Afib, mitral stenosis, prosthetic heart valves, stigmata
of IE, carotid bruit
o Swallow test if patient alert
Investigations to order:
- Q1hrly monitoring: vitals, CLC (inform if GCS drops by >2 points)

- Keep NBM, STAT hypocount then 6hrly hypocount; aim hypocount
7-10

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- Bloods: FBC, UECr, LFT, CE (only if clinically indicated – e.g.
CHEST PAIN), PT/INR, GXM,
- Bloods for CVRF: lipid panel, HbA1c, fasting glucose
- Bloods for young stroke work up only if indicated: ESR,
ACA(IgM&IgG), LA, fasting homocysteine, syphilis IgG LIA, RPR,
[thrombophilia screen, protein C/S, anti-thrombin III] – leave to
primary team if unsure
- Imaging: MRI/MRA brain stroke protocol (this has NO
CONTRAST, the MRA is a digital reconstruction of the vessels),
plain CT brain is of choice if <4.5h onset and need TRO
haemorrhagic stroke before starting to treat as for ischemic stroke
i.e. with IV thrombolysis
- CXR stat
- ECG STAT look for AF, new LBBB, any ST changes – if yes, order
Trop as well
- Call for telemetry if confirmed stroke for monitoring of paroxysmal
AF if it is not already known or not readily diagnosed by ECG or by
bedside evaluation; in suspected ischemic stroke
- Doppler US carotids cm if suspected ANTERIOR circulation
ischemic stroke (do not order for posterior circulation)
- Transthoracic Echocardiogram cm looking for cardiac thrombus,
in suspected ischemic stroke
Initial Management:
Ischemic Stroke
Nursing - If large stroke, keep head elevated to 30 degrees in view

of risk of elevated ICP, KIV NGT insertion for PO meds
Fluids – ***extremely important to improve perfusion to brain. avoid

giving dextrose, give isotonic saline. May give up to 1.5 – 2.5L/day, if
no CI
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Avoid hyperthermia – PO or rectal acetaminophen as required
Avoid hypoglycemia/hyperglycemia – aim 7-10
Permissive hypertension – control only if BP >220/120 in patients

not planned for IV thrombolysis; only if BP>180/105 in patients
planned for IV thrombolysis; do not restart antihypertensives in
known hypertensive unless significant large artery stenosis has been
ruled out with investigations
Hypertension more than acceptable – consider short acting agents

such as PO captopril (6.25-25mg TDS) or PO hydralazine 25mg stat
—check with senior if unsure
Revascularisation therapy – if <4.5h from time of onset and no

contraindications*, update senior, refer Neuro reg STAT, get ready
for thrombolysis; if <6h from time of onset, has large artery occlusion,
update senior, refer Neuro reg STAT, KIV endovascular
thrombectomy
Antiplatelets – aspirin loaded 300mg STAT then 100mg OM if no

hemorrhagic conversion; if it is a large stroke, consult senior before
loading aspirin in view of increased risk of hemorrhagic conversion.
DAPT* initiation to be decided by senior.
Statin – atorvastatin 40mg/80mg STAT
VTE prophylaxis – calf compressors
+/- Anticoagulation – only if patient has known cardiac thrombus

and defaulting treatment (no contraindications to anticoagulation, to
confirm with seniors/neuro reg), or if patient has diagnosed AF and

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the pattern of stroke is likely cardioembolic (need to confirm with
seniors/neuro reg)
*Contraindications to Thrombolysis (consult senior/neuro reg)
Inclusion Clinical diagnosis of ischemic stroke causing

Criteria measurable neurologic deficit
Onset of symptoms <4.5h before beginning
treatment
Age >=18yo
Exclusion Historical Onset of symptoms >4.5h ago
criteria Stroke/head trauma in last 3/12
Previous ICH
Intracranial
neoplasm/AVM/aneurysm
Recent intracranial or intraspinal
surgery
Lumbar puncture in last 7 days
Arterial puncture at
noncompressible site in
previous 7 days
Symptoms of post myocardial
infarction pericarditis or known
ventricular aneurysm
Clinical Symptoms suggestive of SAH
BP>185/110
CBG<2.8
Active internal bleeding
Acute bleeding diathesis

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Suggestion of subacute
bacterial endocarditis
Labs/Imaging Plt<100k
Current anticoagulant use
INR>1.8 or PT>15s
Heparin use within 48h and
aPTT>1.5x normal
Use of DOAC with affected
coags
Evidence of haemorrhage/mass
effect on CT
Extensive regions of obvious
hypodensity consistent with
irreversible injury
Relative <3h Only minor and isolated
exclusion neurologic signs (e.g. pure
criteria sensory, isolated dysarthria,
isolated facial weakness,
isolated ataxia etc.)
Rapidly improving stroke
symptoms
Major surgery or serious trauma
in previous 14 days
GI or urinary tract bleeding past
21 days
Myocardial infarction last 3
months

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Seizure at onset of stroke with
post-ictal neurological
impairments
Pregnancy
Between 3- >80yo
4.5h Oral anticoagulant use
regardless of INR
NIHSS > 25
Combination of both previous
ischemic stroke and DM
CT findings involving more than
1/3 of MCA territory (as
evidenced by hypodensity,
sulcal effacement or mass
effect)
Haemorrhagic Stroke
Refer to NES STAT for review (discussed with senior before
referring)
Nursing - NBM, nurse with head elevation at 30 degree, monitoring
as above
Stop offending medications - Stop all antiplatelets/anticoagulants
Blood pressure control - Keep SBP <160mmHg
If requires IV Labetalol, will need IA line insertion and at least HDU
stay – need to arrange logistics
Correct any coagulopathy – PCC and Vit K 10mg STAT for 10mg
for 3 days for PT/INR problems; KIV FFP if PCC not available; KIV
discuss with haematologist on call
Standby blood products as per surgeon request
Obtain antidote for DOAC if patient on DOAC – idarucizumab for
dabigatran (each vial is about 1000 bucks, we have one vial in TTSH,
but we need two to reverse, with the other vial at SGH)

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KIV IV Mannitol (1g/kg, followed by infusions of 0.25 to 0.5g/kg
every 6h) – check with senior, NES surgeon; will need Q6H renal
panel, Osm, Urea, glucose to assess osmolar gap (stop if > 15)
KIV get urgent CT angiogram – check with NES surgeon
Anticonvulsants for seizure prophylaxis: Keppra 500mg BD x
1/52
GI prophylaxis - IV esomeprazole
II. SEIZURES
CTSP: jerking, seizures – ongoing, aborted
On the phone:
- Vitals, hypocount STAT, oxygen supplementation, do not put

anything in mouth
- Left lateral position
- Diazepam from crash cart – draw 5mg (ward has no PR benzos)
- Set plug and draw 4 tubes
- Tell nurses to keep time
Initial assessment and management:
- Airway, Breathing, Circulation, Disability (GCS), pupils equal or not

- Hypocount STAT if not yet done, correct any hypoglycemia STAT
- Neuro exam: reflexes, gaze deviation away from side of epileptic
focus
- NBM while seizing/drowsy, hypocount 6h, drip
- First line: IV Lorazepam 4mg (preferred BZD due to better
pharmacokinetic properties. May repeat in 5 min. KIV reduced
dose in geriatric patients
- Alternatives: IV diazepam 5-10mg per dose (0.15 mg/kg) / IV
Midazolam 5mg, watch for respiratory depression/ hypotension

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- History from witness regarding semiology of seizure, loss of
continence, tongue biting, duration, time of onset, LOC, associated
symptoms prior
- Check admitting diagnosis – any relation to seizure?
- Look for known epilepsy
- Evaluate for causes using history, NEHR, case notes:
o Known epilepsy: non-compliance, febrile illness, sleep
deprivation, change in meds, drug interactions, alcohol use
o Non-epileptic: central (trauma, haemorrhage, infection,
tumour, acute stroke with swelling); peripheral (electrolyte /
metabolic abnormalities e.g. uremia, drugs, alcohol – DT,
BZD/barbiturate withdrawal)
Investigations:
- Bloods: FBC, UECr, Ca/Mg/PO4, glucose, LFTs, ABG, AED levels,

CK +/- CRP
- Toxicology screen (Urine/ blood)
- ECG TRO cardiac cause of LOC; if history and ECG suggestive of
cardiac event, send Trop I
- KIV CT brain (e.g head trauma, focal deficits, hx of malignancy,
shunts, HIV, previous CVAs, anti-coagulant use), LP – check with
senior while escalating case.
Management after giving first IV diazepam:
- Hourly monitoring, fit chart (inform nurse of semiology of fit), CLC

(inform if GCS drops by >2)
- NBM with IV drip, hypocount monitoring 6h, aim euglycemia
- Escalate to senior and update
- IV thiamine 100mg for cirrhotics/alcoholics before giving dextrose if
required – prevention of Wernicke Encephalopathy

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- Standby rectal diazepam for nurses to use if patient seizes again
later on
- If status epilepticus i.e. >=5min of continuous seizure or two or
more seizures without recovering consciousness, KIV:
o Second IV lorazepam 2mg
o Escalate to seniors to intubate
o Consider loading with longer acting anti seizure drugs: IV
phenytoin 15-20mg/kg at maximum rate of 50mg/min infusion
with cardiac monitoring (then maintenance of 1V 100mg every
6-8hrs)
o Alternatives: load IV valproate 20mg/kg if liver function and
FBC ok, IV keppra if LFTs deranged (but efficacy not as good
as phenytoin)
o Refer to Neuro
III. GCS – CTSP: drop in GCS
- Check baseline GCS / mental status, ascertain if there has been a

true drop compared to previous assessments
- Check vitals, assess airway, breathing, circulation. (May need
intubation if GCS <8 for airway protection)
- Always check HYPOCOUNT (hypoglycaemia is easily reversible)
- Differential diagnosis
o Neurologica (localising signs but absence does not rule out)l:

e.g. stroke / seizure or post-ictal state /
ICH/encephalitis/meningitis
o Non-neurological (no localising signs): Cardiac(ACS),
Respi(T2RF), Metabolic (hypo/hyperglycemia, electrolyte
imbalances, hepatic encephalopathy / uremia,), delirium,
drugs/alcohol (e.g. antihistamines / AEDs / opioids), sepsis,
PSY issues
- Check PMHx / current medical issues:

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o If admitted for stroke / HI / ICH: consider raised ICP /
extension of stroke or haemorrhagic conversion / post-ictal
state / non-convulsive seizure (also consider non-convulsive
status epilepticus especially if there's a CNS infection, or if
subtle twitching or eye deviation observed)
o Dementia / delirium: look for cause of delirium e.g. ARU,
constipation (rule out emergencies: e.g. AMI)
o Liver cirrhosis / ESRF: hepatic encephalopathy / uremia
o Recent changes in medications
- Immediate management:
o Nursing: vitals Q1h, supplemental O2, CLC monitoring, H/C,
NBM if drowsy, ECG
o Bloods: ABG (CO2 narcosis), urea/electrolytes, Ca / Mg /
PO4, FBC, CRP, LFT, +/- ammonia, lactate, blood c/s
o Imaging: KIV plain CT brain STAT
o Inform senior if significant drop in GCS. Treat accordingly to
clinical diagnosis.
IV. MENINGITIS – CTSP: AMS, fever, headache, seizures
Clinical features:
- Fever, headache (usually severe and generalised), neck stiffness,

AMS, photophobia, vomiting from raised ICP
- Complications: seizures, focal neurological deficits,
- Full neurological exam looking for focal neurological signs.
- Signs of raised ICP: sluggish dilated pupil(s), papilledema,
abnormal level of consciousness)
- Look for meningococcal rash, especially purpura
- Check past history of CNS disease, immunocompromised state,
travel history, focal infection (e.g. septic emboli from infective
endocarditis, contiguous spread from ENT source e.g. mastoiditis)

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If there is clinical suspicion of meningitis, proceed with the following
orders:
- Vitals q1h, CLC monitoring, fit chart (if applicable)

- FBC, baseline UECr (IV acyclovir is nephrotoxic), CRP,
PT/PTT/INR (coagulation screen before LP), blood c/s, CXR
- CT brain should be done before LP if not done recently (check with
senior)
LP should be done emergently if CNS infection is suspected and

expertise is available (consult your MO). However, if CT brain has to
be done before LP or expertise is not available, blood c/s should be
done and empirical Abx started immediately. DO NOT delay
antibiotics because of LP or imaging; if there is clinical suspicion of
meningitis, start antibiotics immediately after blood culture.
Empirical antibiotic therapy:
- IV Ceftriaxone 2g STAT, then 12H

- IV Vancomycin 15mg/kg STAT, then dose adjust according to renal
function and vanco trough
- IV Acyclovir 10mg/kg STAT, then renal dose adjust
- Consider IV Ampicillin if Listeria monocytogenes is suspected: <1
month old, >50yo (renal dose adjust)
- If penicillin allergy (non- anaphylaxis) , consider: IV meropenem 2g
q8H with 10% test dose to look for cross reaction (renal dose
adjust)
- If an LP is performed, record opening and closing pressures,
appearance of CSF fluid. Send CSF for FEME, protein, glucose
(together with h/c STAT), bacterial gram stain and c/s, tetraplex
PCR (HSV, VZV, CMV, Toxoplasma), AFB smear and c/s, TB
PCR, +/- fungal smear and c/s, India ink stain and cryptococcal
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antigen, cytology. Memo lab to keep extra specimen for further
tests if indicated.
* consider use of steroids for tuberculosis meningitis
V. HEADACHE
- Determine if it is a primary headache syndrome

o Common primary headache includes: migraine , tension ,
trigeminal neuralgia and less common are other forms of
trigeminal cephalgia ( e.g. cluster headache)
- Identify red flags of headache ( SNOOPI)
o Systemic symptoms: fever , weight loss, cancer,
immunocompromised
o Neurologic symptoms / signs : focal deficits, obtundation of
sensorium, seizure, meningism
o Onset : new onset / thunderclap (pain maximal within seconds
to minutes).
o Others : head trauma , decrease in visual acuity (acute
glaucoma/temporal arteritis), illicit drug use, neurosurgical
procedures
o Previous headache history with progression or change in
headache character
o Intra- cranial pressure : features of raised ICP e.g. nausea or
vomiting , worsen with straining/sneezing/coughing, early
morning headache, blurring of vision, fundoscope for
papilloedema
- Management:
o Guided largely by clinical impression

o Tx of tension headache: Paracet or NSAIDs if no CI.
o Tx of acute migraine: Paracet/IV Maxolon (rmbr oculogyric
crisis)/NSAIDs if no CI (Ketorolac/Diclofenac)
o May consider Ergots (e.g cafergot) or Triptans in acute
treatment of migraine( to check with senior prior to giving).
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o Consider brain imaging if clinical suspicion is high for a space
occupying lesion / SAH
o Blood may not be seen in plain CT brain if patient presented
1-2 days after symptoms onset
o If brain imaging is negative but history is still suspicious of
SAH, consider LP. Collect 10 drops of CSF into yellow tube
covered with foil (to look for xanthochromia; obtain tube from
lab during office hours
PALLIATIVE MEDICINE
COMFORT MEASURES ≠ DO NOTHING! ALWAYS LOOK FOR

REVERSIBLE CAUSES.
APPROACH TO PALLIATIVE CARE PATIENTS

History pearls:
- Functional/ Social history

- Oncological history (when was it diagnosed, investigations leading
to diagnosis, treatments including surgeries/ chemotherapy/
radiotherapy)
- Drug history including analgesia regime, any recent change,
frequency of breakthrough doses taken. Pain history (Site, Onset,
Character, Duration, Temporal pattern and progression, Alleviating
and exacerbating factors, Severity/ Intensity, Associated symptoms
and signs, Response to previous/current analgesia, Impact on
patient)
- Put up EOL form after discussion with patient/ family (check
discharge summaries/ Advance Care Plans (ACP) for previous
EOL discussions)
- Service provider at home
Check homecare file for latest medications, symptom control

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Examination pearls:
- Remember to check for existing fentanyl patches on chest wall/

deltoids/ upper back, and due date (fentanyl patch is changed
Q72H)
- Look out for reversible causes that can reverse the patient’s
symptoms (e.g. constipation, ARU)
MANAGEMENT OF PAIN AND DYSPNEA
Existing palliative patients usually have breakthrough medications

that you can instruct nurses to serve first
However you MUST review patient to assess for symptom

severity that is not relieved by breakthrough medication, or pain
of a different nature!
Opioids are HIGH-ALERT medications.

Consult Palliative-on-call or a senior doctor who is familiar with
opioids before starting opioid/ opioid infusions/ escalating
doses of opioid!
Be cautious when starting opioids for the following groups of

patients
- Elderly
- Renal/ hepatic impairment
- Opioid naïve
- Conditions predisposing to respiratory failure (e.g.
COPD, neuromuscular diseases)

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Consider dose reduction or switch to fentanyl if renal /
hepatic impairment
Types of Opioids & other Analgesia
Morphine
- Short acting: mist morphine – syrup form; usually started in opioid

naïve patients, can be used as breakthrough, can be administered
through NGT
- Long acting: morphine SR (MST) – tablet form; DO NOT cut/ pound,
cannot be used as breakthrough
- Starting dose in normal adults: Mist morphine 2.5mg Q4-6H
Starting dose in elderly or above groups of pt labelled #: Mist
morphine 2.5mg Q6-8H
- Breakthrough dose: (1/6 total daily morphine) PRN up to Q2-4H for
pain/ SOB
Fentanyl
- Available in SC/ patch form

- Safe in renal/ hepatic impairment, useful in patients who are unable
to take orally

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- Minimum patch dose: 6mcg/h (patches come in 12/25/50mcg/h)
Onset 8-12hours, effect lasts 72hours
- SC/ transdermal fentanyl dose (mcg/h) = total daily PO mist
morphine requirement ÷ 2.4
- Breakthrough (SC fentanyl) = (1/10 total daily fentanyl requirement)
PRN up to Q2-4H for pain/ SOB
Oxycodone/ Oxycontin
Do not cut/pound
Pethidine should be AVOIDED as its active metabolites can

accumulate and result in seizures
Controlled-released opioids (including fentanyl patch,

oxycontin, morphine SR tablets) are NOT suitable for patients
whose symptoms are not well controlled
If unable to take orally/ very symptomatic patients with severe pain or

dyspnea, consider opioid infusion:
i) SC morphine mg/day= 1/3 total daily PO morphine or
ii) SC fentanyl (if renal / liver impairment)
Other dyspnea management
- Non-pharmacological: Oxygen supplement, blowing cold air into

patient’s face
- If anxious, consider benzodiazepines as second line to calm patient
e.g. lorazepam 0.25 -0.5 mg ON-TDS PRN/ alprazolam 0.125mg BD
PRN

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- In case of severe dyspnea, SC midazolam infusion can be
considered as adjunctive to opioid(but pls consult senior first)
Always consult palliative doctors / senior doctors who

are familiar with opioids before starting infusion
EMERGENCIES IN PALLIATIVE MEDICINE
Pain crisis
- Intolerable physical pain which distresses the patient

- Often scored ≥ 7/10 on NRS (numeric rating scale)
- Pain usually rapidly escalates, and not relieved by opioid
breakthrough doses
- Mainstay management is aggressive pain control with rapid
escalation of opioid doses by a trained personnel
- General principles: administer SC/IV breakthrough then review in
15 min. If no improvement, administer 2nd breakthrough. If no
response after 2 to 3 breakthroughs, start or increase infusion.
Repeat the process till symptom control achieved.
- Aim to reduce pain by >50% by verbal assessment or NRS
It is advisable to call an experienced Palliative Care

Clinician during a Pain Crisis
Opioid toxicity
Organ system Signs/ Symptoms
Central nervous Confusion, altered mental status
system Excessive drowsiness, lethargy, stupor

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Slurred speech (new onset)
Myoclonic jerks
Respiratory Apnea
Decreased respiratory rate (<8/minute) or
cyanosis
Cardiac Bradycardia, hypotension, or shock
If previously tolerating opioids well, look for precipitating factors –

dehydration, AKI, worsening hepatic function, sepsis, overdose.
Management
- Consult senior doctors/palliative care physician immediately

- Vitals Q1H, IV hydration (1-2L), strict IO charting
- Mild toxicity (no respiratory depression): decrease opioid dose by
50%, KIV put up low dose breakthrough to avoid patient
experiencing unnecessary pain
- Severe respiratory depression (RR<8/min, pinpoint pupils): discuss
with senior if naloxone is indicated. Administer IV naloxone 0.4 mg
Q2-3min(up to max 10mg), watch for rebound pain/ SOB
- Review patient (esp for patient with severe respiratory depression)
at close intervals(2-5 min) even after naloxone is given as naloxone
is short-acting and patient is still at risk of respiratory depression
Please contact senior doctors / palliative care physician

immediately when dealing with opioid toxicity especially
if naloxone is required
CARE OF DYING PATIENT

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Goals
- Good symptom control

- Patient’s emotional/ social/ spiritual reconciliation
- Keep family closely involved
Common terminal symptoms
- Increasingly dependent – loss of mobility and ADLs

- Reduced oral intake – loss of hunger/ thirst, unable to swallow pills
- Altered breathing pattern – mandibular breathing, cheyne-stokes
breathing
- Increased drowsiness, sleep-wake cycle reversal
- Terminal secretions (‘rattling’)
- Decreased BP, HR, urine output
Pain & Dyspnea
- Drowsy patients can still feel pain! Look for grimacing/ moaning/
furrowing of brows
- If patient is already on regular dose opioids, DO NOT stop it
Opioid naïve If patient is drowsy and unable to take orally, consider

SC route:
• SC morphine continuous infusion 0.2-1 mg/h,

titrate to symptom relief, AND
• Breakthrough dose: SC morphine 1- 2.5 mg
PRN up to q2-4h
OR In the presence of renal or liver impairment,

consider:
• SC fentanyl continuous infusion 10-20 mcg/h,
titrate to symptom relief, AND

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• Breakthrough dose: SC fentanyl 25 mcg PRN
up to q1-2h
Non-Opioid If patient is already on existing oral morphine and is

naive unable to swallow, consider SC route:
• SC morphine (mg/h) =1/3 of total basal daily

PO mist morphine required ÷ 24 AND
• Breakthrough SC morphine: 1/10 of total basal
morphine requirement per day
Eg if patient’s morphine infusion rate is at
1mg/hr, the breakthrough morphine dose is 2 –
2.5 mg
Eg if patient’s morphine infusion rate is
<1mg/hr, the breakthrough morphine dose is at
least 1 - 2.5mg PRN up q2-4h
OR In the presence of renal or liver impairment,
consider:
• SC fentanyl (mcg/h) = total basal daily PO mist
morphine required ÷ 2.4 AND
• Breakthrough SC fentanyl: 1/10 of total basal
fentanyl requirement per day
Eg if patient’s fentanyl infusion rate is at
25mcg/hr, the breakthrough fentanyl dose is
50-60 mcg PRN up q1-2h
** If the patient has an existing fentanyl patch,
be cautious as the effects would continue for 8-
10 hours after removal. Please consult
Palliative doctors or your senior doctors.
You are NOT expected to start opioid infusion yourself.
Always consult palliative doctors / senior doctors who are

familiar with opioid before starting infusion.

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Terminal delirium
- Always look for reversible causes! Eg ARU, constipation, pain

- Non-pharmacological: Reassurance, presence of familiar faces,
soothing music/ lighting, good sleep hygiene
- First line: antipsychotics
E.g. SC haloperidol 0.5-1.5mg Q4H PRN, if persistent start infusion
5-10mg/24hv OR SL olanzepine
- Second line: benzodiazepines E.g. SC Midazolam 1.5mg Q4H
PRN
Benzodiazepines SHOULD NOT be first line for delirium as it
may precipitate paradoxical agitation
You are NOT expected to start infusion yourself.
Always consult palliative doctors / senior doctors who are

familiar with before starting benzodiazepine infusion
Terminal rattling
- Noisy respiration caused by secretions in the airway of patients who

are too weak to cough effectively
- Non-pharmacological: Stop oral feeding, stop IV hydration, gentle
oral suctioning
- SC Buscopan (starting dose 40mg/day continuous infusion; max
120mg/day); or
- SC Glycopyrrolate (starting dose 1.2 mg/day continuous infusion;
max 2.4mg/day) for patients with arrhythmias; or
- Sublingual atropine drops (not useful if symptoms severe)
Seizures in patients with intracranial pathology / uremia

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- SC midazolam 2mg PRN
What else can I do for my dying patient?
- Oral care – oral-seven, sodium bicarbonate powder

- Eye drops
- Skin care – regular bed turning and repositioning
- Clearing of bowels, ensure no ARU
- Review IV hydration/ NG feeding
- Review non-essential medications and antibiotics (e.g. Vitamins!
Glucosamine!)
- Minimize unnecessary blood-taking/ hypocount/ vitals monitoring
- Communicate with family – establish shared goals of comfort care,
help family to be involved in care of patient, render emotional
support
- Consider transferring patient to an EOL room (located in levels 7-
12) to have privacy with their families
- If family is keen for terminal discharge, to inform palliative team and
to prepare the following documents: discharge summary, memos to
GP (CCOD)/ ambulance (to send patient home even if he passes
on)/ refer palliative home care team – more details on TTSH Intranet
PALLIATIVE RESOURCES
- Back of EOL form

- eIMR> Template > Template select > Palliative care infusion/
Palliative oral care
- TTSH intranet > Advance care planning & palliative care > Palliative
care> to assess information on how to convert opioids and start
infusion
- Palliative-on-call or seniors in your team who are experienced with
use of opioids

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REHABILITATION MEDICINE
Rehabilitation Medicine
Autonomic dysreflexia
Introduction
- Autonomic dysreflexia is an acute syndrome of excessive and

uncontrolled sympathetic discharge resulting from strong sensory
stimuli
- This can occur in patients who have had an injury to the spinal
cord at the thoracic level T6 or above
- AD is a medical emergency where prompt reduction of BP is
necessary
- Imbalanced sympathetic discharge can potentially cause life-
threatening hypertension
- If left untreated, it can cause seizures, retinal haemorrhage,
pulmonary oedema, renal failure, acute myocardial infarction,
cerebral haemorrhage and death
Pathophysiology
- Autonomic dysreflexia is triggered by a strong sensory (not

necessarily noxious) stimulus, usually from the bladder or bowel
- The stimulus is carried by intact sensory nerves below the level of
the lesion to the spinal cord and activates thoracolumbar
sympathetic nerves, causing massive vasoconstriction and
increased BP
- In particular, significant vasoconstriction takes place in the
splanchnic vascular bed, one of the body’s largest reserves of
circulatory volume

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- Increased BP is sensed by baroreceptors in the carotid and aortic
arch and activates parasympathetic nerves above the lesion to
counter the sympathetic response
- This parasympathetic response including descending inhibitory
signals which would normally counteract the rise in blood pressure
are blocked at the level of the spinal cord injury
- The T6 level is of particular importance in the pathogenesis of
autonomic dysreflexia
- Lesions to the spinal cord at or above T6 allow the strong
sympathetic tone to constrict the splanchnic vascular bed (supplied
by the greater splanchnic nerve, derived from T5-T9) uninhibited,
causing systemic hypertension
- Lesions below T6 generally allow enough descending inhibitory
parasympathetic control to modulate the splanchnic tone and
prevent hypertension
- Once the inciting stimulus is removed, the hypertension resolves
Causes – any strong/painful/irritating stimulus occurring below the

level of the SCI
- Bladder: distention (75-85% of cases), UTI, stones, instrumentation

- Lower GI: constipation/faecal impaction (13-19% of cases),
haemorrhoids, fissures, instrumentation, manual evacuation
- Upper GI: gastritis, reflux, gallstone disease
- Skin: pressure areas, ulcers, tight clothing, ingrown nails
- Genital: sexual stimulation, scrotal compression, testicular torsion,
menstruation, labour
- Others: DVT, PE, meds (nasal decongestants, misoprostol),
fractures

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CTSP for:
- ‘I am having AD!’ (SCI patients generally know their own condition

quite well)
- BP elevated by 20-40mmHg above resting BP (Spinal Cord Injury
patients often have resting BP of about 90/60)
- Relative bradycardia despite elevated BP (increase
parasympathetic stimulation to the heart via the uninjured vagus
nerve to cause bradycardia)
- Any signs and symptoms of AD (see below)
- Blocked catheter
Signs and symptoms
- Related to HTN: Pounding headache, blurring of vision, dizziness,

chest pain
- Anxiety
- Parasympathetic stimulation above the level of lesion: Profuse
sweating, flushing of skin above the level of lesion (due to
parasympathetic stimulation causing vasodilation above the level
of lesion), nasal congestion
- Unopposed sympathetic stimulation below the level of lesion: Pale,
cold skin and piloerection below level of lesion
- May be asymptomatic despite a significantly elevated BP
Assessment and management:
- Full exam to look for underlying cause: CVM, respi, skin, abdo (esp
palpable/percussible bladder), genitalia, PR
- Sit patient up (to induce an orthostatic decrease in blood pressure)
- Loosen clothing/restraints
- Check BP and pulse every 2-5mins during the episode of AD
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- If no IDC is present, insert an IDC ASAP
- If IDC already in situ, check for blockage/kinks. If the catheter is
not draining, insert a new one
- If signs and symptoms of AD persist despite reliving the bladder
distension, perform a PR examination: check for faecal impaction
KIV gentle manual evacuation. Lubricate generously with
lignocaine gel.
- If symptoms persist, search for other causes
- ECG if bradycardia TRO cardiac event KIV bloods
- Antihypertensives (rapid onset and short duration) if SBP still
>150-170 after removal of the noxious stimuli
o Can use sublingual captopril 12.5-25mg, sublingual nifedipine
(immediate release) 5-10mg (alternative: PO via bite and
swallow method) or sublingual GTN
o NOTE: nitrates are contraindicated in patients taking sildenafil
(some men with SCI use this for erectile dysfunction)
- Consider IV labetalol/GTN/hydralazine (which will require ACA/high
dependency care) if patient remains in AD and is not responding to
oral/sublingual medication and after addressing the underlying
cause.
For patients at TTSH Rehab ward @ AMKCH:
- AMKCH does not have the manpower, expertise or equipment for

the care of sick patients. There are also no standby HD/ICU
resources
- After initial stabilisation, update Rehab Med consultant on-call KIV
for transfer back to TTSH ward or TTSH ED
- Prior to transfer back to TTSH, you will need to hand-over to the
previous or appropriate specialty team. Inform the on-call
SR/senior (if after working hours) for hand-over and approval

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RENAL/ELECTROLYTES
CLERKING NEW RENAL CASES
Things to note for ESRF patients:

- Etiology of ESRF: e.g. DM nephropathy, HTN, chronic GN
- Follow-up: Hospital, primary nephrologist if in TTSH
- RRT: initiated since when / type (HD, PD, transplant) &
complications e.g. access issues, infections
If HD:
- Which center, which days? E.g. NKF AMK (Ave 1) 1/3/5
- Vascular access: e.g. AVF, permanent catheter (PC), AVG; if PC –
date of insertion is important
- When was the last dialysis? Completed? (usually 4h)
- Problems with dialysis? (e.g. hypotension/ poor flow)
- Latest dry weight, able to hit dry weight during dialysis?
- HBV/HCV/HIV status (HBV/HCV Q3Monthly, HIV Q6Monthly)
- Call dialysis center to get flowsheets
o Any intradialytic issues? E.g. hypotension, poor blood flow (Qb)
o Fax flowsheets, med list, virology to ward
- Dialysis centers may change meds / give meds not reflected in
discharge prescription (e.g. IV calcijex (calcitriol), IV recormon),
usually in NKF IMR / dialysis IMR
- Non-urgent bloods can be taken pre-HD in next HD except PT/INR
- PT/INR should not be taken pre-HD if patient is on
catheter-based dialysis (PermCath, femoral cath or IJ
Cath) as dialysis catheters are usually heparin-locked
- PT/INR please take pre-HD peripherally before any
Heparin goes into system.
- Once given Heparin-dialysis, do not take PT/INR for 10
hours as result will be interfered by heparin
If PD:
- CAPD / APD? Regime?
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- Caregiver?
- Look for PD book – usual UF? Retention? Missed exchanges?
Outflow time (in CAPD)
- Previous peritonitis / problems with PD?
- Inform PD nurse for PD inpatient
If transplant:
- What kind – deceased, living related from whom, overseas from
where?
- Follow-up where/who?
- How long ago was the transplant?
- Medications – What immunosuppression?
- Transplant functioning, failed on dialysis / being planned for
dialysis / allograft dysfunction – previous renal function?
- Previous infectious complications?
- Previous rejections? Allograft biopsies?
- Complications from immunosuppression?
- Avoid nephrotoxins in a patient with functioning allograft
- common drug to avoid – NSAIDs
- Not sure? Ask senior and/or pharmacist
Common reasons for admission:

- Mechanical issues: Blocked PC / TK, AVF / AVG thrombosis
- Infection: fever / chills during dialysis - due to infected Perm Cath
or other systemic illness? PD peritonitis
- Hypotension / giddiness during dialysis: whether high intradialytic
weight gain / shortened dialysis time / problems with dialysis
o Presentation for SOB / BP if on hemodialysis – rule out
other causes (MI, sepsis) before blaming on over-UF
- Fluid overload, hyperkalemia: Assess if due to missed HD and
whether any indication for urgent dialysis (see below)
NOTE: Do not open Perm Cath dressing yourself. Do not take

cultures from Perm Cath yourself. The HD nurses will help you.
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Special care for ESRF patients:
- Fluid restrict < 1L/day or 800mls/day
- ESRF patients when kept NBM e.g. for op/procedures DO NOT
need IV drip
- DO NOT take BP / bloods on AVF arm
- Try to take blood / set IV plug below wrist of other arm to preserve
blood vessels for AVF creation
- Always assess fluid status of your patient (tongue, skin turgor,
JVP, crepitation, pedal oedema), and whether in uremia (Flap/Rub)
- If planned for Perm Cath insertion, please consult Reg/Consultant
regarding need to withhold antiplatets/clexane days before
procedure
- Medications:
- Avoid Pethidine/Morphine (renal excretion), phosphate fleet
(increases PO4 / K load - can use CENTA ENEMA if really
needed (Na fleet)), nephrotoxic agents (NSAIDS, check for TCM
use)
- Renal adjust all drugs e.g. antibiotics (Commonly used -
Cockcroft gault, if in doubt, consult pharmacist)
Indications for urgent dialysis

A- Metabolic acidosis (pH < 7.1)
E- Electrolyte disturbance (Refractory hyperkalaemia / rapidly
rising K levels / with ECG changes/ hyperK in ESRF or anuric
state
I- Intoxication (SLIME : S alicylates, L ithium, I sopropanol, M
ethanol, E thylene glycol – dialyzable toxins)
O- Overload (Refractory fluid overload )
U- Uremia (E.g. uraemic flap, pericarditis /pericardial rub,
encephalopathy /decline in mental status with no other obvious
reason)

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(I) HAEMATURIA
- Common causes: UTI, stones, tumour, renal pathology (e.g.

GN), bleeding diathesis, trauma from IDC (tugging / recent
insertion), others (APKD, trauma, procedures / surgery)
- Ask for:
1. Severity – Gross? With clots?
2. Symptoms of anaemia: SOB / chest pain / giddiness
3. LUTS (frequency, urgency, dysuria, hesitancy, poor stream,
dribbling)
4. abdominal pain / nausea or vomitting
5. Any proteinuria (frothy urine)
6. Constitutional symptoms: fever/chills/rigors
7. Bleeding diathesis: gum bleeding/easy bruising etc
8. Sore throat / rash / joint pains
9. LOA / LOW
10. FHx renal disease
11. Recent urological procedures
12. TRO other causes: e.g. gynaecological conditions / exercise
13. Systemic review: Cough, SOB, (Think vasculitis)
- Assess for hypertension, bruising / purpura, oedema, abdominal

mass / tenderness (renal punch), DRE (prostate), colour of urine
- Investigations:
o FBC (Hb), UECr, PT/PTT
o UFEME + urine PCr (do not order dipstick for proteinuria),
urine c/s, urine cytology
o CT KUB (hydronephrosis, stones, cystic kidney disease,
tumour)
o Flexible cystoscopy
If suspicious of renal cause / GN:

- UPCr (non-DM), UACr (DM), serum albumin
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- Urine phase contrast (>80% dysmorphic- glomerular, >80%
isomorphic- urological vs RPGN with brisk bleeding)
- ANA, anti-dsDNA, ANCA, hepatitis B / C, C3 / C4 (If suggestion of
systemic immune activation)
- US kidneys (if CT KUB ordered, no need for US)
- Trend UECr (Can’t assume Cr is normal if it falls into the normal
range – look at previous results)
- KIV renal biopsy - refer renal by then
Management:
1. Trend Hb, keep >9 esp if IHD
2. Correct coagulopathy
3. Severe haematuria: MBWO / start CBWO with 3-way IDC – if
blocked and/or clots present
4. Treat underlying cause
- UTI: antibiotics based on urine c/s OR empiric: cefazolin +
gentamicin STAT (non-catheterised); cefepime + amikacin STAT
+ CHANGE IDC (if catheter-related UTI)
- Stones: conservative (fluids >2L/day, analgesia, Harnal) if <
1cm; ESWL vs ureteroscopy vs laser lithotripsy if >1cm (refer
Uro)
(II) ACUTE KIDNEY INJURY

- Definition: Cr rises ≥1.5x from baseline (i.e.lowest Cr recorded in
last 3months), known/presumed to have occurred <1/52
(KDIGO) OR urine output <0.5ml/kg/h for >6 consecutive hours.
(AKIN)

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Causes: PRE-RENAL, RENAL, POST-RENAL
- Look for key reversible causes (HIDDO): Hypertension, Infection,
Dehydration (including hypotension), Drugs, Obstructive uropathy
Plans:
- Treat reversible causes (e.g. IV fluids for volume expansion)
- Review medications – stop nephrotoxic medications; hold
ACEI/ARB
- Strict I/O chart ( watch urine output!! earliest indicator of
deterioration/improvement in renal function ) , ± insert IDC

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- KIV FBC, UECr, Ca/PO4, PT/PTT, ABG, serial ECG ± CE, CXR,
UFEME, UPCR, urgent US KUB
- May need urgent dialysis (see above) – send PT/APTT early in
preparation for insertion of femoral dialysis catheter
(III) CONTRAST INDUCED NEPHROPATHY

- Risk factors: CKD, DM / HTN / metabolic syndrome, heart failure,
hypovolemia, multiple myeloma, hypoalbuminemia, ACEI/ARB
- Prevention:
**There is no role for prophylactic dialysis before contrast**
**If ESRF on regular dialysis, do NOT have to schedule
contrasted scans specifically prior to dialysis sessions / dialysis
days
1. Adequate hydration pre-procedure & post-procedure (this is the

only evidence-based practice)
2. No evidence for benefit for using acetylcysteine /fluimucil
3. Stop nephrotoxic drugs i.e ACEi/ARB and diuretics e.g. lasix
4. No evidence for sodium bicarbonate (Although disputed by
radiologists – PRESERVE trial, Feb 2018 NEJM)
(IV) LOW URINE OUTPUT / URINE CATHETERS

- If NPU >12h: ask for random bladder scan
- Assess fluid status, intake/output charts: low output may be due to
dehydration → fluid challenge, watch urine output
General Guide:
- If symptomatic (abdominal pain / discomfort), palpable bladder +
PVRU >250-300mls: insert IDC
- If PVRU 150-300ml: KIV insert IDC if symptomatic; otherwise, try
potting / repeat PVRU / CIC if recurrent
- If RU <150ml: watch / pot patient

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If difficult catheterization: try different sizes / Nelaton catheter; beware
not to create false passage and document procedure / difficulties
- Larger IDC for easier insertion (suspected BPH)
- Smaller IDC for strictures
Evaluate for common causes of ARU: UTI (UFEME/urine c/s),
constipation, BPH (DRE: prostate size / faecal loading)
If BNO: consider laxatives STAT usually dulcolax suppository
Do not attempt to change IDC post TURP (anatomy will have changed)
→ inform Urologist in charge! / call Uro team to insert
If NPU and IDC in situ:

- Assess for blocked IDC / kinks in tubing
- ?palpable bladder, do bladder scan
- Flush IDC under aseptic technique (20-30ml of sterile NS flushed
with large tipped 50ml syringe, repeat until in/outflow both smooth,
- If unable to get smooth flow, change IDC (never reinsert same IDC
as it is no longer sterile) – IDC manipulation not advised
- If clots / sediments present and unable to get smooth flow: change
to 3-way catheter, perform manual bladder washout (MBWO) until
urine clear and flow smooth
- KIV continuous bladder washout (CBWO) if gross hematuria with
clots - call Urology
- If all else fails, refer Uro urgently, KIV suprapubic catheterisation
(V) HYPERKALAEMIA
- Vitals, ECG, CBG, hyperkalaemia protocol
- Exclude spurious result (e.g. hemolysis)
- Causes: drugs (ACEI/ARB/spironolactone), CKD, transcellular shift
- Make it a point to act on all cases of Hyperkalaemia, even if you
think it is spurious
K 6-6.5:
- IV calcium gluconate 10% 10mls over 10min
- IV actrapid 10units with IV dextrose 50% 40ml SLOW over 5 mins

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- If h/c >18: omit D50; if h/c <6 / risk of hypoglycaemia: KIV dextrose
drip
- PO 15-30g / PR 30g resonium STAT and TDS for 1 day
- Stop all medications that can increase K (e.g. ACEI/ARB, K-
containing drip)
- H/C q1h x 6h (12h if in renal failure)
- Vitals q1h until resolution
- Repeat K and ECG in 4h
- ESRD pts on regular HD will need dialysis to remove K
o Insulin / D50% may have already been given in ED, always (1)
check ED interventions (2) recheck K early (3) consider
informing registrar early if K is still elevated (5.5 – 6.0) post
correction for consideration of dialysis
K > 6.5 or IF THERE ARE ECG changes as long as K > 5 / high risk
patients (e.g. IHD): as above AND
- IV calcium gluconate 10% 10ml over 2-3 min (** check if patient is
on digoxin)
- Telemetry monitoring – Please speak to MO / Reg before calling
CVM for telemetry approval
- Repeat ECG in 10mins to check for resolution; if not, repeat IV
calcium gluconate
- Otherwise, repeat ECG in 1h and K in 2h
- If persistent, repeat above ± IV lasix / salbutamol nebs / dialysis
(urgent Renal referral)
- ESRD pts on regular HD will need dialysis to remove K
(VI) HYPOKALAEMIA
- Hypokalemia = K< 3.5, severe hypokalemia = K<2.5
- Look for symptoms and complications: constipation, muscle
weakness / cramps, rhabdomyolysis, arrhythmias **Beware
respiratory muscle weakness if severe
- Check ECG: U waves (V4-6), ST depression, T inversion, large /
wide P wave, prolonged QT interval, ectopics, arrhythmias
- Check Mg / bicarbonate / CK (if muscle aches, weakness)
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- Check medications: digoxin toxicity in hypokalaemic patients (keep
K ≥4)
- Look for source of loss: GI (e.g. diarrhoea) / renal (e.g. diuretics)
- Look for causes of intracellular shift: insulin, hyperthyroidism, beta-
2 agonist
- Check BP: if high, may need to consider 1) hypertension with
diuretic use, 2) Conn’s syndrome 3) RAS 4) hypercortisolic states
Hypokalemia Algorithm
- Exclude gastrointestinal losses:
- Spot urine K:Cr > 1.5 meq/mmol = renal loss (TTKG not used now
as may have false positives)
o Once K is being replaced, doing urine K/osm will not be useful
(difficult to interpret)
Potassium replacement
Preparation K (mmol)
Span K 0.6g 8
Mist KCL 10ml 13.4
Potassium citrate
28
10ml
Potassium citrate 1
10
tab
IV 7.45% KCl 10ml 10
IV KH2PO4 10ml 10
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Management:
** Review medication list - any new Omeprazole etc.
** Correct hypomagnesemia first
If symptomatic / K <2.5 / any ECG changes:

- Replace 3 cycles pre-mixed KCl (10 mmol of KCl in 100ml NS),
then recheck symptoms / ECG / K 2h post replacement
- **Rate of replacement should be ≤10mmol/h in peripheral lines
- Consider cardiac monitoring (telemetry/HD) for patients with critical
hypokalaemia (<2mmol/L) / ECG changes / needing rapid
replacement (>10mmol/h)
If asymptomatic / K >2.5:
(Check if pt has hx of persistent hypokalemia refractory to
replacement – may require more aggressive treatment)
- PO Span K 1-2 tabs OM to BD (large tablet, cannot be pound) or
mist KCl 5-10ml TDS (bitter) for a fixed duration (e.g. 2 days)
If hypokalemia noted pre-HD bloods, please replace across dialysis

with IV KCl as necessary
(VII) HYPERNATREMIA
- Deficit of water relative to Na
- Common causes to consider:
o Dehydration
o Increased losses
• Impaired thirst mechanism: central/nephrogenic DI
• Insensible: sweat, glucosuria
• Overt losses: GIT / vomiting, medications- diuretics
• Increased Na load: post citrate dialysis, post correction of
metabolic acidosis with Na bicarbonate

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- Approach:
Pocket Medicine 5th edition
Symptoms: increased thirst, AMS, coma, seizures
Management:
- Correct underlying cause
- Correct hyperosmolar and hypernatremic state
o Maximum rate: 0.5 mmol/L/h or 10 mmol/L/day prevent
cerebral oedema and convulsions
Calculation of infusate (for those with net water loss)

- Preferred route of administering fluids is PO/NG; IV fluids only if
enteral route not feasible
- Hypotonic fluids; NS only if there is significant hypotension from
dehydration
Infusate Na (mmol/L)
Dextrose 5% 0
0.45% NaCl 77
0.33% NaCl/Dextrose 5%/10mmol KCl 56
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Step 1: Decide on the infusate and estimate the effect of 1L of the
infusate on the serum sodium via Adrogue-Madias formula
Change in serum Na = (Infusate Na - Serum Na) / (Total Body Water
+ 1)
If using infusate with potassium: change in serum Na = ((Infusate Na

+ Infusate K) – Serum Na) / (Total Body Water + 1)
**TBW = F x Body Weight (where F = 0.6 in nonelderly men, 0.5 in

nonelderly women; 0.5 in elderly men and 0.45 in elderly women)
Step 2: Determine rate of infusion; usual target is to reduce serum

sodium by no more than 10 mmol/L over 24 hours
Volume of Infusate required =10 / Change in serum Na (determined
at step 1)
Step 3: Determine total volume of infusate to be given over 24 hours

Total volume to be administered over 24 hours = Volume of infusate
required (determined at step 2)
Monitor the serum sodium closely and adjust the volume and
rate of infusate accordingly (in the case of severe hypernatremia
(Na >160 mmol/L, serum Na should be checked more frequently,
e.g. q6-8h to prevent overcorrection)
Note: In hypotensive patients with hypernatremia, we should still

consider fluid challenging with NS. If patients are intravascularly
depleted, they need fluids that will stay within the intravascular
compartment. When a patient is hypotensive, correcting BP is of
greater importance.
(VIII) HYPONATREMIA
- Common principles to consider
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o Tonicity: Hypotonic (Osm<280), Isotonic (280-295), Hypertonic
(>295)
o ADH activity: reflected by Urine osm
• Urine osmolality is sensitive to activation of ADH
• Non ADH (Urine Osm <100), ADH not suppressed-
assumed to be activated (Urine Osm >130),
o Urine sodium: useful in intravascular volume depletion /
hypovolemic hypotonic hyponatremia
• Una <25: extra renal losses e.g. 3rd spacing (CCF /
cirrhosis), GIT (vomiting/diarrhoea)
• Una >40: renal losses e.g. (renal salt wasting- RTA,
recovery phase of AKI), CKD (tubules unable to
concentrate Na), cerebral salt wasting (stroke / ICH)
- Exclude
o Errors in collecting the blood sample, especially in a well
patient with an extremely low serum sodium
o Pseudohyponatremia: hyperproteinaemia, hyperlipidaemia
(triglycerides), hyperglycaemia (corrected Na = Measured Na
+ 0.3 (glucose/mmol - 5.5))
o Symptomatic?
o Determine the acuity/chronicity of the hyponatremia as this
affects severity of symptoms and how fast it should be
corrected
- At the bedside
o GCS, neurological status
o Volume status; I/O charts, clinical- skin turgor, tongue, JVP
o Check medications which can cause hyponatremia-
spironolactone, SSRI / carbamazepine
- Investigations / Management
o UECr, Plasma glucose
o Plasma osmolality, urine osmolality, urine sodium
o TFT, 8am cortisol evaluation for hypocortisolism (euvolaemic)
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o Inform MO / registrar if Na ≤125 – risk of seizures increased,
will need closer monitoring
Acute KIV hypertonic saline. (escalate to senior)

Symptomatic Goal: increase Na to abort symptoms e.g.
Hyponatremia seizures / >120mmol/L to avoid cerebral edema.
(<48h) Monitor frequently e.g. 2h then q4-6h
Chronic Increased risk of irreversible osmotic
Symptomatic demyelination.
Hyponatremia Rule out true volume depletion / dehydration.
(>48h) KIV hypertonic saline if severe. (escalate to
senior)
Calculate appropriate infusion rate and amount.
Monitor frequently: q4-6h
Chronic Most patients with serum Na >125 mmol/L /
Asymptomatic chronic hyponatremia do not have neurologic
Hyponatremia symptoms.
Use of hypertonic saline is not warranted.
Treat underlying cause after appropriate
investigations.
On a night call, do not presume the cause is
SIADH*.
1L of 3% NS contains 513 mmol of Na
1L of 0.9% NS contains 154 mmol of Na
Limits of therapy: increase serum Na < 6-8 mmol/L q24hours

- In patients with concomitant hypokalemia, aim <6mmol as each
molar increase in K translate to equimolar increase in Na – risk of
rapid overcorrection
*SIADH is a diagnosis of exclusion.

- True plasma hypoosmolality (< 275mOsm/kg H2O)
- Inappropriate urinary response to hypoosmolality (Uosm
>100mOsm/kg).
- Euvolemic, other causes of euvolemic hyponatremia ruled out
(hypothyroidism, hypocortisolism)
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- Causes: medications (e.g. TCA, SSRI, antipsychotics), CNS
disorders (e.g. bleed, SOL), pulmonary disorders (e.g. pneumonia,
TB, lung CA), transient causes (e.g. nausea, pain, stress,
endurance exercise, general anaesthesia)
Overcorrection
- Stop PO and IV sodium replacement
- Correct other electrolytes (e.g. potassium) in hypotonic solution
(0.45% saline, water)
- 6ml/kg D5% /2h (lowers Na by around 2mmol), recheck Na
- Q1h urine output
- Recheck paired urine Na / osm
Osmotic Demyelination Syndrome (ODS)

Sx Beginning 2-6 days after correction of Na+
Insidious onset
Symptoms: Dysarthria, Dysphagia, AMS, Seizures, Tetraparesis
Risk in: malnourished, alcoholic, hypokalaemia, liver cirrhosis
(IX) HYPERCALCEMIA
Corrected Ca = [(40-Alb) x 0.02] + Ca
Symptoms: “stones”, “groans”, “bones” and psychic “moans”,”
Causes:
- PTH dependent (PO4 usually low): hyperparathyroidism
(primary/tertiary), FHH, malignancy associated PTHrP secretion
- PTH independent (PO4 usually normal/high): dehydration,
immobilisation, multiple myeloma, lymphoma, sarcoidosis, vitamin
D excess, thyrotoxicosis, Paget’s, malignancy induced osteolytic
bone activity
Management:
- Assess ABCs, fluid and neurological status
- Check paired Ca panel and serum iPTH, ALP, UECr, Mg, FBC,
plasma glucose, CXR, ECG (look for short QT)
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- KEY: IV HYDRATION i.e. aim for total fluids ≥3L/day as tolerated
- If symptomatic/severe ≥3.5mmol/L, consider:
1. IM/SC/intranasal calcitonin 200-400 units/day in 2 divided doses
(tachyphylaxis develops in 48-72h) - Fast onset
2. IV bisphosphonates (CI: dehydrated patients with renal
impairment. Effect peaks in 5-6 days)
o IV Zoledronate 4mg over 15mins
o IV Pamidronate 60mg in 500mls NS slow infusion over 4h
(renal impairment is a contraindication)
3. Consider IV hydrocortisone 100mg 6H for hypervitaminosis D,
bone mets, sarcoidosis
- Treat underlying etiology
(X) ACID-BASE DISORDERS

1. Identify primary abnormality
- pH <7.35 and HCO3 <20mmol/L: metabolic acidosis **AG =
HAGMA even when pH and HCO3 is normal
- pH <7.35 and pCO2 >45mmHg: respi acidosis
- pH >7.35 and HCO3 >24mmol/L: metabolic alkalosis
- pH >7.35 and pCO2 <35 mmHg: respi alkalosis
2. Identify any secondary abnormality by checking the adequacy of
compensation
3. Identify the possible underlying cause
Metabolic Acidosis – CTSP: hyperglycemia, BP, AMS, renal

failure, drug OD
1. Identify HAGMA vs NAGMA
- AG = Na - HCO3 - Cl (HAGMA: AG>12)
- Correct for albumin: 2.5mmol fall in albumin = -1 in Anion gap
2. Identify concurrent respiratory acid-base abnormality
- Expected pCO2 = (1.5 x HCO3) + 8 ± 2

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- If pCO2 <expected, concurrent respi alkalosis; if pCO2 >
expected, concurrent respi acidosis
3. Identify concurrent metabolic acid-base abnormality
- Corrected HCO3 = (AG-12) + measured HCO3
- If >28, concurrent metab alkalosis; if <22, concurrent NAGMA
Causes
HAGMA (CATMUDPILES) NAGMA (USEDCARP)
C: CO, cyanide U: Ureterosigmoidostomy (K)
A: Alcoholic ketoacidosis S: Small bowel fistula (K)
T: Toluene E: Extra chloride (K)
M: Methanol, methemoglobin D: Diarrhoea (HCO3 > Cl loss)
U: Uremia (K)
D: DKA C: Carbonic anhydrase inhibitor
P: Paraldehyde (K)
I: INH/Iron A: Adrenal insufficiency (K)
L: Lactic acidosis (shock, R: RTA (I,II: K, IV: K)
hypoxia, metformin) P: Pancreatic fistula (K)
E: Ethylene Glycol Drugs: topiramate,
S: Salicylates, solvent acetazolamide
Other: paracet, lorazepam
Respiratory Acidosis – CTSP: respiratory distress, respiratory

failure, AMS
1. Identify the secondary abnormality
- Acute - Expected HCO3 1-2 mmol/L for every 10mmHg
PCO2
- Chronic – Expected HCO3 4-5mmol/L for every 10mmHg
PCO2
- If HCO3 >expected, concurrent metab alkalosis; if < expected,
concurrent metab acidosis
Causes - mainly CO2 retention from hypoventilation

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- Central: drugs (sedatives, opiates), HI, CNS lesions, metabolic
alkalosis, loss of hypoxic drive in chronic T2RF treated with O2
- Airway obstruction: COPD, asthma (low threshold of intubation if
normal or high CO2 with hypoxia )
- Thoracic cage abnormalities: kyphoscoliosis, obesity, chest
trauma
- Neuro/neuromuscular: myasthenia, GBS, cervical / high thoracic
spine injury
(If chronic type 2, good to find out baseline CO2 when well)
Management:
- Treat the underlying cause
- Ventilatory support; KIV intubate (if drowsy / upper airway
problem) / NIPPV (?Indications NIF values)
- Supplemental O2 for patients with known T2RF should be
delivered by low flow nasal prongs / fixed systems (Venturi
mask) to allow accurate titration and prevent suppression of
hypoxic drive
- Do not purely rely on SPO2 for pts with neuromuscular
weakness
- Low threshold for intubation if bedside pulmonary function test
are of these values: -> call RT for help to obtain the values
20/30/40 rule
- Vital capacity < 20ml/kg
- NIF < 30 cm h20
- Max expiratory pressure < 40
Useful Formulae:
Anion gap AG = Na – Cl – HCO3

Metab acidosis PaCO2 = 1.5 x HCO3 + 8 +2
(Winter’s formula)
Metab alkalosis ↑PaCO2 = 0.6 x ΔHCO3
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Acute respi acidosis ↑HCO3 = 0.1 x ΔPaCO2
Chronic respi acidosis ↑HCO3 = 0.4 x ΔPaCO2
Acute respi alkalosis ↓HCO3 = 0.2 x ΔPaCO2
Chronic respi alkalosis ↓HCO3 = 0.5 x ΔPaCO2
Serum osmolality 2 x Na + glucose + urea
(XI) HAEMODIALYSIS
Dialysis Prescription is ordered by Renal Team
i) Vascular Access- femoral catheter, tunnelled dialysis catheter,

AVF/AVG
ii) Duration
a. Conventional - usually 4 hours (newly initiated, 1st HD: 2hrs)
b. SLED (Sustained Low Efficacy Dialysis) – usually 6 hours
c. Isolated UF (For removal of excess fluid)– usually 3 hours
iii) Heparinization
a. Normal: 1000u bolus, then 500u/hr
b. Tight: 500u bolus, then 250u/hr
c. Heparin free - TBC with reg/ con; some indications: day of
surgery/ procedures e.g. scopes, angioplasty, catheter
insertion; coagulopathy/ thrombocytopenia; active bleeding
iv) Ultrafiltration
a. Max rate 1L/hr (ideally 10ml/kg/hr)
b. If chronic/stable pt, can order to DW
v) Calcium content of dialysate
a. Normal 1.5mmol/L (by default unless known hyperCa)
b. Low: 1.25mmmol/L- used in pt w tendency to hyperCa
vi) Glucose content of dialysate - glucose dialysate (by default)
a. Required for Diabetic and fasted patients – glucose can be
omitted if patient is having intradialytic parenteral nutrition
b. Glucose free dialysate can be considered in all other cases
vii) Blood flow (QB) ;

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a. Default for conventional: 250 ml/min
b. 150ml/min if newly initiated HD or unstable patients at risk of
dialysis disequilibrium syndrome (rapid removal of urea in
newly initiated HD cause hypo osmolar ECF → cerebral
edema)
viii) Dialysate flow (QD)
a. Default for conventional: 500ml/min
b. If newly initiated HD, start with 300ml/min if QB is
150ml/min
Example of conventional HD prescription:
- HD via R femoral cath; 4hours; QB 250ml/min, QD 500ml/min;

Heparin 1000u bolus, then 500u/hr; add glucose, and Ca
1.5mmol/L. UF to dry weight or maximum UF(determined with Reg)
- SLED: for patients at high risk of hemodynamic instability eg.
Recent NSTEMI (last 5/7), sepsis on inotropes, stroke/cerebral
oedema
- HD via R PermCath; 6hours, QB150, QD300, heparin 1000u bolus,
then 500u/hr; glucose and Ca 1.5mmol/L dialysate. UF to be
discussed with senior

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RESPIRATORY MEDICINE
(I) SHORTNESS OF BREATH/DESATURATION

Over the phone:
- Vitals including SpO2, respiratory rate + mental state. See STAT if
drowsy / SpO2 <90%
- Associated red flags e.g. chest pain / diaphoresis / stridor / usage
of accessory muscles / speaking in short words / drowsiness,
presence of clamped chest drain (to instruct nurse via phone to
unclamp immediately first)
- Admitting diagnosis
- Order: ECG, supplemental O2, CBG
- Check/Decide on resuscitation status / DIL – frequency of vitals
monitoring; update family if very sick / need to discuss extent of
care
Assessment:
ABC
1. Airway: GCS (ability to protect airway), stridor, secretions, tracheal
deviation, ability to talk
2. Breathing: Sitting in tripod position; increase or increasing work of
breathing – tachypnoea, accessory muscle use, recession VS tiring
out- drowsy, speaking in short sentences; nasal flaring, thoraco-
abdominal dyssynchrony; presence of crackles or rhonchi on
auscultation.
3. Circulation
- Tissue hypoperfusion: AMS, low urine output, cyanosis, cold
peripheries
- Sympathetic stimulation: tachycardia, sweating (hypotension and
bradycardia are late signs)
- CVS examination: JVP, arrhythmias, murmurs ± abdominal
examination / DRE (if pale / hypotensive)

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History
- To ask: duration, onset, progression, associated sx: CP/ nausea /
diaphoresis / orthopnea / PND / giddiness / calf pain / calf swelling
(suggestive of DVT)
- Review vitals, case notes (diagnosis, comorbids, current Tx),
investigations, eIMR
Ddx:
A. Airway obstruction (upper airway obstruction with stridor)
B. Cardiac: AMI with APO, CCF, arrhythmias, tamponade
C. Respi: pneumothorax, pulmonary embolism, pneumonia (Hx
prior dysphagia / vomiting – think aspiration), bronchospasm
(COPD / asthma exacerbation, anaphylaxis), effusion, ARDS
D. Metabolic: acidosis (e.g. DKA, lactic, uraemia), poisons (e.g.
salicylates)
E. Haem: severe anaemia
F. Neurological: GBS, myasthenia flare, MND
G. Others: ascites, anxiety, hyperventilation, pain. Stroke/drugs
(e.g. opioids) if desaturation w/o SOB.
Investigations
Depending on what you think may be the cause
- ECG + CE (x2 4-6h apart)
- h/c, BOHB, lactate if metabolic acidosis
- Septic w/u if febrile and localising s/s of infection (including FBC)
- Ca/Mg/PO4/TFT if arrhythmias or ECG changes
- BNP (or NT-BNP if patient on Entersto) if suspicious of cardiogenic
pulmonary oedema
- ABG (if SpO2 drops, drowsy, Hx of T2RF/ recent deranged ABGs)
- CXR
- ± CTPA if suspicious of pulmonary embolism

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Theory
Pulse oximetry – caveats:
- Useful in estimating arterial saturation
- But not 100% accurate – poor peripheral perfusion, poorly
adherent probe, excessive motion, nail varnish, bright light
- Remember the oxyhaemoglobin dissociation curve – SpO2/Hb
[O2] of 90% is a critical threshold. Below this level, small fall in
PaO2 results in a sharp fall in SpO2/Hb [O2]. Conversely,
increasing PaO2 has little effect on saturation.
Management:
- Escalate when in doubt / patient ill and may need HD /ICU
- ABCs first! (keep SpO2 ≥94%; for COPD, keep 88-92% – you
should still give O2 therapy as ultimately hypoxia kills)
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- NBM + IV drip if suspicious of aspiration / drowsy / too
tachypnoeic (risk of aspiration)
- Vitals Q1H
- ± strict I/O with indwelling urinary catheter if necessary.
- Regular suctioning if secretions ++, urgent chest PT
- Treat underlying cause
- Go back to review patient / trace what you have ordered – repeat
ABG as indicated
- Consider unclamping chest tube if left clamped and repeat a CXR
- If patient unwell/drowsy and likely requires intubation, can bag-
mask patient till help arrives
(II) HAEMOPTYSIS – CTSP: haemoptysis, blood-stained sputum

(Ddx: haematemesis, epistaxis mimicking haemoptysis)
Causes
- Common: infection (pneumonia, TB, pyogenic), bronchogenic Ca,
bronchiectasis, pulmonary embolism
- Other causes: aspergilloma, emboli, coagulopathy, autoimmune
disorders, foreign body, AVM, alveolar haemorrhage, severe mitral
stenosis
Over the phone

- Vitals, mental status
- Amount (massive: >50ml/episode OR >150-200ml/day OR any
amount that can cause airway compromise)
- Differentiate from haematemesis and epistaxis (upper airway
bleed), frank blood / mixed with sputum (vessel vs parenchymal
bleed)
Initial evaluation and management

- ABCs – AIRWAY is of utmost importance (patients asphyxiate
rather than exsanguinate)
- Identify the site of bleed if possible: right / left sided position the
patient such that lung presumed to be bleeding is in the dependent
position. E.g. R lateral position if bleeding from R lung
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- Supplementary O2
Investigations
- FBC, PT/PTT, GXM, ECG (S1Q3T3)
- Sputum for AFB smear and c/s x2 sets with MTB PCR, gram stain
and c/s
- Check most recent CXR / CT thorax
- KIV CT thorax / CTPA / CT angiogram(consult senior first)
Further management
- If massive haemoptysis, keep NBM and consider intubation
- Treat underlying cause, if any
- Haemoptysis chart
- Correct low Hb, coagulopathy
- Cough suppressants (e.g. procodin), KIV antibiotics, consider
tranexamic acid (contraindicated in haematuric patient)
- Involve other specialties as required
o Nonsurgical: CT angiography / bronchial embolisation
(Interventional Radiologist), bronchoscopy (RM)
o Surgical: refer CTVS if non-surgical intervention not possible
(III) ACUTE COPD EXACERBATION

1. Know patient‘s resuscitation status
- Active management: potential need to escalate to ICU for
intubation
- Max general ward management with NIV: can escalate to
HD/NIVU
- End-stage with palliative support: symptom relief with
morphine
2. Confirm this is an exacerbation of COPD
- Quick Hx: staging / Hx intubation / chronic T2RF / need for
LTOT or NIV, cardiac risk
- Ask for symptoms
- DDx for dyspnea in COPD patients: CCF / AMI,
pneumothorax, infection or as above under section for SOB

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3. Assess severity of exacerbation (i.e. need to escalate to MO/Reg
emergently for NIV / intubation) – if assess to be other causes to
refer back to section (i)
- Vitals, mental status (drowsy), speech (can‘t speak /words /
phrases / short sentences)
- Signs of respiratory distress/CO2 retention (asterixis,
accessory muscle use, pursed-lip breathing, cyanosis)
- Respi: prolonged expiratory phase, rhonchi, decrease A/E
(severe bronchospasm, possible pneumothorax from ruptured
bullae)
4. Investigations:
- FBC, UECr, inflammatory markers
- CXR (pneumothorax / consolidation / effusion), ECG
- ± ABG (very helpful in deciding whether to escalate mx ie
BiPAP/ICU/HD)
- ± sputum gram stain and c/s, urine Strep or Legionella Ag,
influenza PCR, blood C/S if suspecting infective exacerbation
5. Management: aim to keep SpO2 88-92%
- ABC (controlled O2 therapy in chronic T2RF – SpO2 88-92%
acceptable)
- Neb salbutamol:N/S:ipratropium (1ml:2ml:1ml) q4-6h- for
patients just recovering from an exacerbation but with residual
wheeze/dyspnea, consider keeping on regular nebs overnight
(rather than PRN)
- Manage secretions:
o Oral suction q4-6h PRN
o Chest PT (there is a chest physiotherapist on call usually
located off-site at home, you may consider activating if
really indicated)
o Up to 2 stat salbutamol:ipratropium- > if clinically not
improved, to escalate to MO/ Reg
o Mucolytics (e.g. fluimucil / bromhexine)
- PO prednisolone 30mg OM / IV hydrocortisone 50-100mg q6-
8h (if unable to tolerate orally)
- ± Antibiotics
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i.
Sputum purulence + presence of SOB and/or sputum
volume
ii. Mechanical ventilation (NIV / IPPV)
- ± Oseltamivir 75mg q12h (require renal dose adjust) if history
suggestive of influenza (prominent rhinorrhoea / myalgia /
arthralgia, contact Hx, FBC shows viral picture)
- Assess need for NIV / intubation – watch response to initial
Mx, inform senior if patient unwell
(IV) ACUTE ASTHMA EXACERBATION

1. Confirm this is an exacerbation of asthma
- PMHx: assess risk (previous intubation/ICU admission)
- Ask for symptoms: chest tightness, wheezing, cough, dyspnea
- TRO DDX: CCF / AMI, pneumothorax, infection and other
causes of SOB as stated above
2. Assess severity of exacerbation
3. Investigations to consider:
- ECG
- FBC, RP, inflammatory markers
- ± ABG – PCO2: hypocarbia (due to hyperventilation)
expected. A normal PCO2 is NOT normal in asthma
exacerbation (red flag).
- CXR (consolidation / effusion)
- ± Septic w/u: sputum gram stain and c/s, urine Strep /
Legionella Ag, influenza PCR, blood C/S
4. Management: aim to keep SpO2 >92%
- Neb salbutamol:N/S (1ml:3ml), can up to Q15min if necessary
(need to monitor K and HR)
- PO prednisolone 30mg OM / IV hydrocortisone 50-100mg q6-
8h (if unable to tolerate orally)
- ± IV MgSO4 2g over 20min for refractory / severe attack
(usually given in ED)
- ± Abx
- KIV intubation if not responding to tx/signs of resp fatigue
(inform senior to review)
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- PEFR monitoring BD (pre-, post)
(V) PNEUMONIA – common cause of admission / desaturation /

deterioration
1. Assessment: fever, productive cough, URTI sx, SOB, contact /
travel Hx, swallowing impairment; breath sounds, dull percussion
note, crackles;
- CXR: consolidation; FBC, CRP, blood C/S, sputum C/S, Strep /
Legionella urinary Ag, influenza PCR
2. Treatment
- KIV NBM + IV drip if swallowing impaired/drowsy/tachypnoeic
- Empirical Abx? (can use ARUS-C / ASP guide on Intranet / eIMR
for help); Renal adjust doses as necessary
(A) Types of pneumonia

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(B) Previous culture results
(C) SEs of Abx – QTc (if prolonged, KIV doxycycline rather than
macrolides / quinolones), dose adjustment for renal impairment
- Disposition: KIV HD / ICU if CURB-65 >3, requiring FiO2 >50%,

haemodynamically unstable or rapid deterioration
(VI) ACUTE RESPIRATORY DISTRESS SYNDROME
Berlin Criteria:
1. Acute – <1/52 of a known clinical insult OR new /worsening
respiratory s/s
2. P/F ratio for severity: Mild >200 to ≤300 with PEEP/CPAP≥ 5;
Moderate>100 to ≤200 with PEEP≥5, Severe ≤100 with
PEEP≥5)
3. CXR – bilateral alveolar infiltrates / opacities consistent with
pulmonary oedema –not explained by effusion, collapse or
nodules and not fully explained by CCF / fluid overload (may
need TTE for objective assessment)
- Management: HD / ICU, usually requires mechanical ventilation
Sites for ABG-taking:

- Radial ABG – Always attempt radial first
- Femoral ABG – Surface marking: Mid-inguinal point (bisects line
joining ASIS and PS)
- DO NOT ATTEMPT Brachial ABG – Brachial artery is an end-
artery and thrombosis can lead to limb-threatening ischemia
(VII) ACUTE RESPIRATORY FAILURE

When respiratory system is no longer able to meet metabolic
demands of the body
- 2 types:
1. Type 1: Hypoxemic: PaO2 <60
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2. Type 2: Hypercapnic: PaO2 <60 + PaCO2 >50
- Acute / chronic (check baseline ABG for COPD pt)
- Pathophysiology for hypoxemic respiratory failure:
a) Shunting
b) Hypoventilation (failure to move gas in and out of lungs) – e.g.
neurological causes, decreased compliance of chest wall /
pleura / lung
c) V/Q mismatch e.g. COPD exacerbation, asthma exacerbation,
pulmonary embolism.
d) Diffusion defect (alveolar-capillary barrier) e.g. alveolar
fibrosis, severe oedema, ARDS
- Management: NIVU/HD/ICU, will usually require mechanical
ventilation for respiratory support
(VIII) MECHANICAL VENTILATION

- Invasive (intubation) or Non-invasive (CPAP/BiPAP; see next
section on ―NIVU)
- Indications:
1. Respiratory failure – hypoxic despite O2 therapy/AMS secondary
to hypercarbia
2. Compensation failure / tiring out – especially if poor
cardiopulmonary reserves / high ventilatory requirement due to
underlying disease (e.g. severe sepsis)
Criteria for NIVU admission (JCI-ACC-HAP-011 [Admission and

Discharge Policy of NIVU] on Intranet)
1. Acute respiratory distress (SOB, RR >24, accessory muscle use),
gas abnormalities (PaCO2 >45, pH 7.25- 7.35)
2. Specific conditions:
- Indications: COPD exacerbation with acute RF not requiring
intubation, mild RF from neuromuscular disease/chest wall
deformities, obesity hypoventilation syndrome/OSA
- Other indications (+/-): pneumonia in immunocompromised,
cardiogenic pulmonary oedema
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- Any other indications: please discuss with NIVU team (R4) if
continue to deteriorate.
Contraindications
1. Severe respiratory failure e.g. severe respiratory acidosis
(predictor of failure of NIV)
2. AMS – apnoea (no spontaneous breathing), inability to protect
airway, agitation
3. Unstable patient
4. Orofacial abnormalities, excessive secretions
5. Undrained pneumothorax (check CXR prior to initiating NIV)
6. Metabolic acidosis
NIV settings
The Respiratory Therapist (RT number: 81263648) should be
activated if you are unsure of NIV settings required.
1. Modes (NIV requires spontaneous breathing; if not, it is time to
intubate and send to ICU)
PACV: (Pressure Assist Control Ventilation)

- Machine provides inspiratory positive pressure, at a set
inspiratory rate and tidal volume.
- Provides more support than PSV mode, but sometimes less
comfortable for the awake patient
- Inspiration may be triggered by patient /machine. Inspiration is
cycled off (i.e.stopped) by machine
PSV: (Pressure Support Ventilation)

- Only provides pressure support, inspiration is both triggered and
cycled off by patient
2. Inspiratory / Expiratory Positive Airway Pressure

- Start IPAP at 10-12l; keep IPAP + PEEP <30mmH2O
- Start EPAP (/PEEP) at 5 (max 10-15; if low SpO2 despite EPAP
>10, escalate to MO / KIV intubation)

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3. FiO2 (on most NIV machines, this is O2 flow rate rather than
actual FiO2)
- Usually start with O2 flow of 2-4L/min, up to 10-15L/min based
on pulse oximetry (SpO2)
- Use the lowest possible FiO2 / flow rate to achieve SpO2 target
(88-92% in COPD)
- Increasing FiO2 requirement has to be attended to
4. Respiratory rate
- Minimum number of breaths that machine will deliver (in PACV
mode only), i.e. the “back-up respiratory rate”. Patient can give
additional spontaneous breaths above this number. Usually
preset at 12-16. In PSV, RR = 0.
5. Targeted tidal volume (TV):

- Usually only in PACV mode.
- If desired, can set a target tidal volume to ensure adequate tidal
volume delivery. The machine will deliver this set volume within
the pressure range limit (where minimum pressure is the
pressure support, and maximum pressure has to be set). E.g. if
PSV 12/5, target volume 400ml, max P 15 – a volume of 400ml
will be delivered per breath unless pressure hits 15
- Aim 6-8ml/kg of expected BW
Interpretation of ABGs while pts on NIV (in GW):

ABGs are usually taken:
1. Before putting on NIV (usually 9pm in nocturnal NIV)
2. 1h after NIV has been first initiated / settings have been changed
3. 1h before removal (usually 6 am in nocturnal NIV)
4. If and when patient desaturates
Notes: “NIV cycling” = when patients get on/off NIV time, e.g. 4
hours of NIV, 4 hours off NIV (on nasal prongs), then cycled again
Meal breaks – usually means that patients can be trialled off NIV
during meals (for 30 min-1h) with O2 given via nasal prongs

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Key points:
- If called to interpret ABG, do so in conjunction with the patient‘s
clinical condition and NIV setting
- ABG interpretation in the following order:
1. pH (homeostasis/cellular function depends on this, any pH <7.2
must be urgently corrected!)
2. Check if problem is respiratory (↑PCO2 with ↓HCO3 in
respiratory acidosis), metabolic (↑HCO3 with ↓PCO2). Most
common in pt on NIV: respiratory acidosis with T2RF
3. Compensated?
4. If metabolic acidosis: calculate anion gap
5. If HAGMA: calculate delta gap TRO concomitant NAGMA /
metabolic alkalosis (if delta gap 1-2 = pure AG met acidosis; if
<1: simultaneous non-AG acidosis; if >2: simultaneous non-AG
alkalosis)
- Always compare latest ABG to previous one, and note if any
settings were changed between the 2 results
Troubleshooting while on NIV

1. Check mask fit – adjust mask / KIV intubation
2. Any new contraindications to NIV?
3. Adjust NIV to increase oxygenation or PCO2 (see below)
Adjusting NIV:

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Note that if patient has underlying primary metabolic acidosis, the
cause of the metabolic acidosis should be treated. Discuss with
someone senior before adjusting the NIV settings.
When to Escalate:
1. Severe respiratory distress, desaturation / collapse, drop in GCS
2. ABG shows severe respiratory / metabolic acidosis: pH <7.1, pCO2
>70-75, pO2 <55, RR> 30, HCO3 <10, SpO2 <85%
4. NIV settings already very high (i.e IPAP >20, PEEP >10, FiO2
100% or O2 flow rate 15/min)
5. Worsening pH / acidosis despite adequate NIV settings tweak
6. Intra-arterial (IA) line falls out
7. Air leak noted in NIV circuit
8. If you are unsure of any of the above: check patients
resuscitation status - may have a “Do Not Intubate” order

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RHEUMATOLOGY, ALLERGY & IMMUNOLOGY
A. CLERKING RAI ADMISSIONS

● General
○ Check recent RAI clinic notes/ discharge summaries for
recent events.
○ CDOC may also contain additional instructions for elective
admissions.
○ Confirm allergy/ADR on CMIS and with patient.
● Medications
○ Obtain a complete medication list (patients may obtain
medications from different sources; include those from
GP/OPS). Take note of recent dose adjustments.
○ Use NEHR to review both prescribed and dispensed
medications.
○ Beware of step doses (esp. Prednisolone)
○ Some medications are taken weekly not daily – ensure they
are ordered correctly (e.g. Methotrexate, Alendronate).
Confirm day of administration with patient.
○ Folic acid/ Folinic acid is usually prescribed together with
Methotrexate (1 day apart).
○ Discontinue immunosuppressants (except
Hydroxychloroquine and Sulfasalazine) if patient is
admitted for a severe infection. Simple infections like UTI,
URTIs - do not need interrupt patient’s treatment by
stopping immunosuppresants. When in doubt, no harm to
withhold overnigh.
○ If a patient has AKI, medications should be dose adjusted/
withheld as necessary.
○ Do not discontinue anticoagulation for patients with
Antiphospholipid Syndrome unless instructed without first
consulting a senior/ primary Rheumatologist
○ Do not discontinue long term steroid therapy abruptly.
○ If patient is unwell due to infection and has been on long
term steroids, consider stress dose.
● Investigations
○ Order UFEME with dipstick (includes screening for
proteinuria) for patients with connective tissue disease.
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○ FBC, RP, ALT, AST – usually useful to look for side-effects
of most DMARDs.
○ Serologies/ special investigations do not need to be
ordered overnight (will not change management).
○ X-rays are generally not useful for acute joint pain unless
you suspect trauma / fracture.
B. ACUTE MONOARTHRITIS
● CAUSES:
○ Always rule out septic arthritis, which is an emergency and
requires you to recognise it early and initiate treatment
ASAP.
○ Mechanical (OA) vs Inflammatory/ crystal (RA, Gout,
Pseudogout, Psoriatic arthritis, AS etc)
● SYMPTOMS
○ Screen for symptoms to exclude septic arthritis: fever, chills,
immunocompromised state, recent surgery/procedure
involving joint, sexual history, IVDA, trauma or penetrating
injury
○ Differentiating symptoms: Small vs large joints,
Symmetrical vs Asymmetrical, tempo of illness, previous
history of inflammatory joint pain
● Investigations
○ Blood cultures prior to antibiotics if suspecting septic
arthritis.
○ Joint aspirate prior to antibiotics ideally but this is not
feasible most of the times when on call. Send for FEME,
cultures, microscopy (this includes crystal analysis). If
suspecting atypical infections/ TB, then to send for AFB
smear and cultures, though is very rare.
○ Presence of crystals does not exclude diagnosis of septic
arthritis, if diagnosis is not clear, wait for cultures before
taking off antibiotics.
○ For all diagnostic joint aspirations, label specimen bottles –
i.e. synovial fluid from the right or left knee.

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○ Evaluations if reactive arthritis is suspected: UFEME, urine
culture, urine PCR and genital swab for Chlamydia, stool
culture.
● Management
○ If septic arthritis is suspected, start empiric antibiotics (after
joint aspiration). IV cefazolin ( septic arthritis), IV
ceftriaxone/doxycycline (gonococcal, chlamydia)
○ As a rule, do not give more than 10mg/day Prednisolone for
inflammatory arthritis.
○ Patients should be on calcium/ Vitamin D if on long term
steroids.
○ Higher doses of Prednisolone will be needed in gout if
Colchicine/ NSAIDs are contraindicated.
○ Use Colchicine in gout only if patient presents within 48h of
onset of attack. Remember renal dose adjustment for
Colchicine.
○ Do not discontinue Allopurinol during a flare if patient is
already on Allopurinol– stopping may worsen the flare.
○ Steroid dose equivalents: Prednisolone: Hydrocortisone ~
1:4
C. CONNECTIVE TISSUE DISEASES

1) General
Patients are generally admitted for:
● Flare/ activity or complications of underlying condition (e.g. lupus

nephritis).
● Elective admissions for biologic treatment
● Non-rheumatological conditions in a rheumatological patient (e.g. sepsis
with bacteraemia – ED’s impression was flare of CTD).
● Newly diagnosed CTDs
2) Investigations/ Management

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● Patients with SLE – Think about disease manifestations in systems (skin,
blood, kidneys etc) and ask about symptoms from each system. This will
also help you in ordering appropriate investigations. The pneumonic
SOAP BRAIN MD helps you remember possible manifestations of the
disease!
● SLE presents differently in each patient. Patients tend to flare in the same
pattern as they present, so check old records to see how each patient’s
SLE usually manifests.
● You can also trace what is usually monitored at each follow-up. This will
also guide you in ordering investigations as markers of disease activity.
● C3/C4 and dsDNA may be markers of disease activity.
● Think about gut vasculitis in patients with lupus/vasculitis presenting with
diarrhoea– if bowel sounds are sluggish or abdomen tender, keep them
NBM, escalate to seniors and consider IV Hydrocortisone or CT
abdo/pelvis.
● Immunosuppressed patients may not mount high fevers; err on the side of
caution – do septic workup and cover with antibiotics if infection suspected.
D. ALLERGY
1) History/ examination
Clinical features Common culprits
Type I (IgE Urticarial rash 1. Drugs (Beta-lactams, anaesthetic agents,

mediated/ Pruritus biologics, NSAIDs, ACEi, radiocontrast) **
immediate onset) Angioedema previous exposure
● Onset Bronchospasm (Wheeze/ 2. Food (shellfish, molluscs, eggs, nuts, storage
typically < breathlessness) mites)
1 hour Anaphylaxis 3. Insect venom
Maculopapular rash
Type IV (T-cell Bullous eruptions Anticonvulsants (Phenytoin, Phenobarbital,
mediated/ delayed SJS/TEN/DRESS (ask for Carbamazepine) Antibiotics
onset) mucositis, ocular NSAIDs
involvement, systemic Allopurinol
symptoms.

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● Detailed description of reaction: symptom sequence and duration followed
by any treatment provided and outcome. Witness’ description will be useful
so will photos of reaction (if any).
● If food suspected, detailed food history in chronological order including
ingredients used.
● If drugs suspected:
● Previous use of suspected drug/ reactions.
● Timing of symptoms in relation to drug administration.
● Effects of discontinuing drug.
● Include over the counter meds, alternative remedies and
health supplements.
● Personal history of allergies/ adverse drug reactions
● Refer CMIS, previous clinic/ discharge summaries for
previous adverse drug reactions/ contrast use.
● A previous drug desensitisation does not mean the patient
is no longer allergic. The patient will have a reaction if the
drug is discontinued and reintroduced.
● Personal/ family history of atopy.
● If pure angioedema, consider HAE
● Personal/ family history of hereditary angioedema (HAE).
● If known HAE, document previous treatments (whether on
Danazol, C1 inhibitor given previously).
● Enquire about potential triggers (trauma, surgery, dental
work).
● Documentation of “rash” alone is not adequate, describe type of rash.
● Depending on type of rash, remember to look for other organ involvement
(e.g. bronchospasm and hypotension in Type I reactions or fever,
mucositis, nephritis/hepatitis in Type IV reactions).
● If SJS/TEN is suspected, look carefully for erosions, Nikolsky’s sign or
areas of potential skin denudation
● Red flags: hypotension, stridor, bronchospasm, bullous eruptions,
cutaneous vasculitis, mucositis, skin denudation.
2) Investigations:
● Laboratory investigations: FBC (lack of eosinophilia does not exclude a

drug allergy), UECr, LFTs, UFEME + dipstick if Type IV.
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3) Management:
● Prompt withdrawal of culprit agent

● Treatment for anaphylaxis: 0.3-0.5ml IM Adrenaline 1:1000 (i.e. neat), IV
Diphenhydramine, IV Hydrocortisone
● Supportive: Oxygen, nebulisations, IV fluids
● Most allergic reactions only require anti-histamines and symptomatic
treatment.
● Systemic steroids may be used in SJS, DRESS and AGEP, please consult
allergist.
● In SJS/ TEN patients: (consider urgent allergy referral) or Dernatology
referral
● IV Fluids and monitor electrolytes.
● Symptomatic management (analgesia, antipyretics).
● Wound care (use appropriate non adhesive dressings), monitor for
superimposed infections.
● Refer to Ophthalmology early for assessment if there is ocular involvement.
● May require HD care if severe or with multi-organ involvement and transfer
to Burns Unit if high BSA involved or high SCORTEN.
● Patients with severe cutaneous allergic reactions can be very ill
therefore always escalate to a senior early.
● PLEASE LEARN HOW TO REPORT DRUG ALLERGIES ON CMIS.
Ensure that you do a thorough and accurate job in reporting the
symptoms that manifests and when it did in relation to drug intake.
Remember that once you wrongly label a patient as having drug
allergy, you can potentially limit them from being able to used a wide
class/ classes of drugs which may be very useful for them - ie
Antibiotics in infections, Aspirin for IHD/ AMI patients, NSAIDs for
pain. ALWAYS CLARIFY what patients mean by them ‘ being allergic’
to certain medications.

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E. RAI PASSIVES
● RAI patients especially those on immunosuppressants can deteriorate

very quickly. Having said that, perform an assessment just as would on
any other general medicine patient and you will be okay.
● Escalate all patients with desaturation, hypotension, rashes and worsening
symptoms to a senior early if unsure of management.
● If called to see any fever – please assess clinically and do septic workup
early. RAI patients usually are immunocompromised and may not manifest
all the sepsis symptoms.
● Scleroderma renal crisis (very very rare but when it does manifest, very
important to pick up on it and act immediately) – aggressively bring down
BP, if no contraindications choose Captopril initially as drug of choice.
● If called to see haemoptysis/ desaturation in patients with vasculitis/active
lupus – be alert of possible DAH. Do GXM, FBC, PT/APTT and CXR at
least.

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ACKNOWLEDGEMENTS
Our mentors for helping to edit this book – Dr Ng Wee Khoon, Dr Faith Chia,
Dr Chia Yew Woon, Dr Lim Yen Loo, Dr Yeo Pei Shan, Dr Chew Wei Da,
Dr Huang Wenhui, Dr Lim Jun Pei, Dr Ong Kiat Hoe, Dr Mucheli Sharavan
Sadasiv, Dr Eileen Poon, Dr Koh Pei Xuan, Dr Poi Choo Hwee, Dr Matthew
Tay, Dr Lui Wen Li, Dr Bairy Manohar Giliyar, Dr Puah Ser Hon
Our Program Coordinators – Yap Yin Yin, Mohammad Hadi, Noor Arinah,
Shermaine Lim, Lisa Pok, Nur Mardiana Alias
And many others who have come together to make this book possible.
With contributions by:

R1s 2010/11 – Jacqueline Foo, Goh Wen Yang, Ho Quan Yao, Violet Hoon,
Raphael Lee, Joel Lee, Andrew Leong, Raymond Liang, Joel Lim, Brenda
Lim, Lin Huiyu, Mahaboob Shariff, Mogilan, Mok Kwang How, Ivy Ng, Quek
Zhihan, Emily Tan, Tan Seng Kiong, Kenny Tan, Valliammai, Daniel Yap,
Yeo Chong Ming, Zeng Shanyong
R1s 2011/12 – Boh Toon Li, Chiam Zi Yan, Eunice Chua, Koh Pei Xuan,
Joycelyn Lee, Cliff Li, Lim Xin Rong, Lydia Seetoh, Tai Yinxia, Tan Chong
Keat, Grace Tan, Daryl Tan, Tan Yan Ru, Teh Yi Lin, Yeo Pei Shan
R1s 2012/13 – Aw Chia Hui, Angela Chan, Abel Chen, Chia Po Ying,
Brenda Chiang, Jeremy Hoe, Jasmine Koh, June Koh, Samuel Lee, Xin
Rong, Jonathan Ong, Shen Jia Yi, Andrea Tan, Glorijoy Tan
R1s 2013/14 – Chow Min Yang, Elise Vong, Elizabeth Seitoh, Jeremy Choo,
Kalpana, Felicia Law, Andrew Fong, Benjamin Ho, Choy Chiaw Yee, Ong
Chin Ee, Tay Jun Yang, Teoh Xu Hui, Chin Han Xin, Vanessa Lim, Jennifer
Guan, Brandon Nah, Melvin Lee, Renuka, Caroline Choong
R1s 2014/15 – Charlene Tang, Lim Weiling, Michelle Tham, Ng Zhiguang,

Prathika, Joanne Xie, Odelia Koh, Chuang Dingfang, Shonda Ng, Loh
Zhiwen, Ho Chwin, Chee Ying Jie, Sean Ong, Derek Lim, Sabrina Lau,
Huang Yufang, Lee Khar Suan, Daphne Yang
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R1s & R2s 2015/16 – Alyssa Sim, Andrea Ang, Calvin Loh, Chang Fang-
Yu, Chen Zepeng, Chiew Yi Rong, Vanessa Chong, Chong Lip Leong,
Chuang Ding Fang, Ei Mon Aung, Ethan Goh, Felix Kho, Ho Sharlene,
Jason Martin D’ Souza, Joanne Xie, Juanita Lestari, Lavenia Kulendran, Lee
Ci Han, Derek Lim, Ng Kah Yan, Ng Shonda, Ong Poo Lee, Ooi Xi Yan,
Sabrina Lau, Pauline Seah, Shereen Ng, Stephanie Sutjipto, Tan Chee
Hian, Tay Poh Peng, Tham Ye Ni, Terence Tong, Ivy Wong, Yam Kai Feng,
Daphne Yang
R1s & R2s 2016/17 – Amanda Chong, Andalib Hossain, Nicole Chen, Jaryl
Cheng, Cheong Kah Wai, Cheryl Lie, Benita Chiang, Chua Jia Min, Heng
Xiao Wei, Ho Peiyan, Hong Liyue, Khoo Bo Yan, Kevin Kwek, Jonathan Lai,
Samuel Lam, Sandra Lau, Joshua Lee, Lim Yu Rui, Celestine Lim, Nicole
Lin, Kristabella Low, Muhammad Alimi B Ahmad Hatib, Jessica Ng, Deborah
Seow, Eran Sim, Elaine Tan, Wilnard Tan, Shirley Teo, Teoh Xuyan, Toh
Boon Chuan, Natalie Wee, Charlene Wee, Kenneth Yong
R1s & R2s 2017/18 – Bao Minfang, Chua Min Jia, Foo Hui Ling, Gan Sheng
Song, Erneda Reyes Gatdula, Edric Hee, Hong Liyue, Khin Hnin Su Wai,
Khoo Bo Yan, Lee Siew Fen, Lee Yin Yee, Lim Eilyn, Lim Ki Hui, Low Yee
Hong, Mah Yun Yuan, Muhammad Alimi B Ahmad Hatib, Gabrielle Cheryl
Ng Xin Han, Jeffer Pang, Pang Rui Yi, Mervyn Poh, Ren Dongdong, Justin
Seah, Alfred Seng, Tan Hui Li, Shauntel Tan, Gabriel Tan, Keefe Tan, Teo
Wee Shen, Thang Kim Wang, Sasha Thrumurthy, Charlene Wee, Xu
Chuanhui, Kenneth Yong
R1s & R2s 2018/19 – Shiane Lim, Cao Ruoxi, Tan Lip Hong, Wu Xiao Tian,
Crystal Phuan, Lai Yi Wye, Chiam Kunhan, Yeo Pei Ming, Ei Ei Thazin Win,
Cui Can, Soong Su-lin, Katrielle Joy Fu, Lee Shi Teng, Lee Yin Yee,
Llewelyn Tan, Tan Wei Liang, Xie Weilin, Dong Qinyun, Koay Leping,
Jonathan Paul Chong, Ruth Yap, Gareth Lim, Ravi Kartik, Lee Si Min,
Mathew Sachin Philip, Jan Lee, Jonathan Wong, Joshua Liew, Kalaiselvan
Karthigaiyan, Li Tingfang, Geraldine Ong, Rita Lai

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IMPORTANT CONTACT NUMBERS
TTSH prefix = 6357 + ____ (see below)
Lab Misc
Biochem 8938/9 BTS MO 91864133
Haemato 8955 Drug Info 2016
MicroB 8968/9 TTSH prefix 6357xxxx
Histo 8976 Operator 0/63571000
Immuno 8464 ITD help desk 1800 4834
357
Patho 8976 P’cist on call 98208023
Coroner 62221712 MSW 8222
Imaging Surgical
Duty Radio 8131 Main OT 1492/94
Interv Radio/ 8154/57 EOT 1485/92/95
Angio Suite
CT Room 3747 OT Fax 1478
US Room 8145 Endo Center 8484/85/88
2D Echo 2400 Day Surgery 1461
MRI 8163/8164 HD 2063
NNI (MRI) 7053/7055 SICU 2032/1446
NNI (CT 7047/7056 Stoma nurse 97703621
Brain)
EMG/EEG 7070 Anaesthesia 7771
secretary
Barium 8137 PACE 2218/19/20
Bone scan 7050 PACE MO 2238
Wards
E.g. 5A – 2051, 5B – 2052, 10C – 2103, 10D – 2104

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KTPH
KTPH prefix = 6602 + ____ (see below)
Lab main 2322 Radiology

MicroB 2335 On call radiographer
Biochem 2322/2325 91371751
Hemato 2338 Counter (appt) 2700/01/2698
Blood bank 2321 CT room 2699
Angio room 2669
MSW 2588/2599 US room 2693/94/95
MRI room 2709 /2679
MOT 2760/2770 Snr SN (Carol) Angio - 2669
MRO 2466/2464
ITD helpdesk 1800 587 Inpt Pharm 2633/34/35
4478 On call Pharm 98550620
Drug Info 2629

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CTSP

Our patients, who are our greatest teachers;

It brings me great pleasure as the Internal Medicine Programme

I am sure we can recall the helplessness, insecurity and anxiety on our

In response to these needs, our residents have come together to write

This booklet serves as a brief guide to the management of acute

Click here to return to Page 2

TTSH General Medicine HO Call Advice

You will cover patients from the following departments:

Active cases = New admissions

- Please do not remotely order investigations/medications without

Common types of cases encountered:

Clerking new cases

Click here to return to Page 7

Plan – have a system, order everything you can on Aurora

Click here to return to Page 8

(I) CHEST PAIN

Click here to return to Page 11

Click here to return to Page 12

Click here to return to Page 13

Click here to return to Page 14

(III) ACUTE DECOMPENSATED HEART FAILURE

- Over the phone: manual BP, BP trend, other vitals (tachycardic

(VI) APPROACH TO TELEMETRY

Treat underlying cause, e.g. dehydration / distress / pain /fever

- Ventricular Bigeminy/ trigeminy: May be associated with cardiac

- Non-sustained VT: (defined as VT <30 s), ensure BP stable.

- VT / VF / asystole: Get crash trolley to patient STAT, review

Management of AF with rapid ventricular response / atrial flutter

Consult senior before proceeding

If not in overt heart failure:

- Rhythm control (TRO thrombus, anticoagulate 3 weeks before /

(VII) POST CICU REVIEW

(VIII) POST COROS REVIEW

Specific to coronary angiogram

Guidelines for plans overnight

*** ESCALATE TO CARDIO MO/REG IF YOU ARE UNSURE***

* Probability ≥3 – high, 1-2 – moderate, ≤0 – low

Investigations: FBC, PT/PTT, D-dimer (TRO if low risk) ±

Wells Score for PE

*Probability: ≥7 – high; 2-6 – mod; ≤1 – low

Investigations: FBC, ABG, UECr, D-dimer (TRO if low risk

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Existing NSC patients’ dermatological histories (clinic consultation,

If patients have been admitted from NSC to TTSH Main Building,

1. Describe the rash

NB: Early referral to dermatologists should be done for these

Skin biopsy to be done by the Dermatology Senior Resident.

Parameters Scores SCORTEN Predicted

2. Malignancy Yes=1, 0-1 3.2%

3. Tachycardia Yes=1, 2 12.1%

4. Initial BSA of Yes=1, 3 35.3%

5. Serum urea Yes=1, 4 58.3%

6. Serum glucose Yes=1, 5 90%

On call, general supportive treatment will suffice as first line

Fluid and electrolyte replacement (consider electrolyte solution

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* ESCALATE TO CARDIO MO/REG IF YOU ARE UNSURE*