SHOCK IN

OBSTETRICS
PRESENTER- Dr.SHREYA(2nd yearPG)
MODERATOR-Dr.S.LAVANYA Prof & HOD Dept of
OBGY
“shock during pregnancy is one of the
most difficult problems faced by the
obstetricians and necessitates initiation
of management even before full
identification of its cause for better
survival”
DEFINITION
• It is a clinical condition arising out of an inability of the
circulatory system to provide adequate tissue perfusion
causing cellular hypoxia and organ damage
• It is a systemic disorder affecting multiple organ systems
• Perfusion may either be decreased throughout the body or
distributed poorly
• Incidence- it accounts for 0-3%
 Types and causes
Hemorrhagic shock Non-hemorrhagic shock
• Hemorrhagic shock due • Septic shock due to
to hypovolemia is the infections
most common cause of • Hypertensive disorders
shock in obstetrics • Anaesthesia
• </= 1000ml- • Cardiogenic
compensated
• Neurogenic
• 1000-1500ml-mild
• embolism
• 1500-2000ml-moderate
• >2000ml-severe
 Hypovolemic or hemorrhagic shock
Causes
Commonest of all is atonic PPH
Early pregnancy
• Abortion
• Ectopic pregnancy
• Gestational trophoblastic disease
Antepartum hemorrhage
• Placenta previa
• Abruptio placenta
• Rupture uterus
Post partum hemorrhage
• Traumatic PPH
• Atonic PPH
Clinical picture
• Pallor
• Rapid and thready pulse
• Low blood pressure
• Cold clammy extremities
• Air hunger
• Diminution of vision
• Oliguria
• Anuria
Phases of hemorrhagic shock
Phase of compensation Clinical picture
• Blood loss less than 15% • Pallor
• Postural hypotension is • Tachycardia
noted
• Normal blood pressure
• Sympathetic stimulation
is the initial response • Tachypnea
leading to peripheral • Sweating
vasoconstriction to • Hyperventilation
maintain blood supply to • At this phase, transfusion
vital organs resuscitation and control of
• ↓ venous return causes hemorrhage are usually
↓CO due to constriction effective in restoring the
of pre and post capillary normal circulation and
sphincters perfusion
 Phase of decompensation Clinical picture

• Blood loss is 20-35% • classic clinical picture of

• Blood loss exceeds 1000ml shock
in normal patient or less if • Cold and clammy skin
other adverse factors are
operating like severe • Tachycardia
anemia. • Tachypnea
• There is relaxation of • Low pulse pressure
precapillary sphincters and • Low systolic pressure
damage to the
microcirculatory bed due to • Adequate treatment at this
thromboxane A2 and phase improves
leukotriens. • If untreated it can become
irreversible by passing onto
the phase of cellular damage
Irreversible decompensated shock
• Blood loss is more than 40%
• Profound hypotension with only the carotid pulse being
palpable
• Oliguria and anuria are noted
Arterioles Anoxia

Capillary & dilate release of

proinflammatory
Venular walls mediators d/t tissue
damage

Progessive vasodilatation vascular permeability

Peripheral pooling of blood

Further in circulating Blood volume

 Progessive ↓ in BP
↓
Coronary insufficiency
↓
↓ CO& Blood flow→ ↑ tissue anoxia
↓ ↓ anaerobic glycolysis
pulmonary hypoperfusion Met. acidosis

Pulm. Oedema tachypnea ARDS

Hypercoagulability of blood
• Tissue damage→activates coagulation cascade
↓
slowing of blood stream &
vascular thrombosis
↓
hypercoagulability of blood

• Clinically at this stage the patient has features of coma,

worsened heart function and progressive renal failure due
to acute tubular necrosis
 Management of hemorrhagic or
hypovolemic shock
“speed is vital and rapid restoration of the circulating
blood volume is the key to successful outcome”
• Establishment of airway and oxygen therapy at a
rate of 6-8 L per minute to maintain O2 saturation
of > 92% and PaO2 of 80-100 mm Hg
• ET intubation and mechanical ventilation are
required for severe hypoxia, severe tachypnea and
coma to maintain oxygen supply
• Establishment of two wide bore IV lines
• Elevation of legs to facilitate venous return
• Keep the woman warm
• Volume replacement should initially be done by crystalloid
solutions
• Plasma expanders, like, hemaccel may also improve the
microcirculation
• They will remain in circulation for 24hrs to 48hrs
• Plasma protein fraction or fresh frozen plasma and later, when
available, whole blood preferably packed cells should be
transfused quickly
• Insert a foleys catheter to measure urine output
• Positioning of the patient in the trendelenburg tilt may aid the
venous return
Drug therapy
• Analgesics- 10-15 ml morphine intravenously if, there is
pain, tissue damage or irritability
• Corticosteroids- hydrocortisone 1g or dexamethasone
20mg slowly (IV), It may reduce the perepheral
resistance and potentiate cardiac response to improve
tissue perfusion
• Sodium bicarbonate 100 mEq IV, if metabolic acidosis is
demonstrated
 • Vasopressors to increase the blood pressure so as to maintain
renal perfusion
a) Dopamine 2.5-10 micrograms/kg/min by IV infusion is the
drug of choice
b) Beta adrenergic stimulant isoprenaline 1mg in 500ml 5%
glucose slowly IV infusion
c) Digitalization may be carried out if inspite of volume
replacement the CVP remains high due to myocardial failure.
This is unlikely unless as a terminal event
d) Vasodilators – phenoxybenzamine an alpha receptor blocker
is given as 1mg/kg over 1 hr IV if it is felt that the
vasoconstriction is persisting inspite of adequate volume
replacement
• As this management is being done, simultaneously ultrasound
examination is carried out to find the cause of blood loss and
assess the fetus in antenatal patients and to rule out placental
bits in postpartum patients
• In addition to medical management, surgical intervention
depending upon the cause of hemorrhage like emergency
cesarean for antepartum hemorrhage, laparotomy, internal iliac
ligation or hysterectomy for severe postpartum hemorrhage
may be required
Monitoring is done by-
• Assessment of central venous pressure
• Pulse rate
• Blood pressure
• Urine output
• Pulmonary capillary wedge pressure
• By clinical improvement in
 pallor
 Cyanosis
 Air hunger
 Sweating
Non haemorrhagic
shock
Septic shock
• It refers to sepsis- related hypotension that persists in
spite of adequate fluid replacement
• Incidence 1 in 8000
• Maternal mortality can reach 13% in severe sepsis and up
to 30% in septic shock.
• Neonatal mortality can be as high as 40%
Predisposing factors
• Septicemia and septic shock usually occur following
maternal infection at one of the following sites:
pyelonephritis due to anatomic alterations in the renal
tract in pregnancy
Endometritis in the puerperium due to large area of
denuded maternal tissues exposed to bacteria
Septic abortion where inadequate evacuation of the
products provides a nidus for bacterial proliferation
Perforation of uterus with peritonitis
Infection of surgical wounds, where a breach in the skin
is liable for bacterial contamination
Clinical criteria for diagnosis of
sepsis
• Infection and bacteremia may lead to sepsis, which is
diagnosed by the presence of the following signs:
Fever or hypothermia
Tachycardia
Tachypnea
Leukocytosis or leukopenia
Thrombocytopenia
Hypoxemia
Oliguria
Increased serum creatinine
contd…….
 • As the sepsis worsens, severe sepsis is diagnosed by the
appearance of the following signs:
Hypotension
Worsening oliguria- urine output 30ml/hr for 2 hrs
Worsening renal failure- serum creatinine
> 2mg/dl
Acute lung injury
Serum bilirubin >2mg/dl
Platelets<1000000 mm3
Prothrombin time >1.5
 Lysis of gram –ve bacteria
↓
Endotoxin (LPS) in circulation + LPS protien
↓
CD14 molecule on surface of monocyte/ macrophage

elaborates proinflammatory
Cytokines

TNF ᾳ & IL-1

↓
Promote vascular injury
Vasodilatation & hypotension
Activationof inflammatory
responses
• C5a and C3a → microemboli and endothelial damage
• mast cells → histamine release and increased capillary
permeability
• Coagulation system→enhances development of thrombi
• Kinin system→releases bradykinin, causes vasodilation
and increased vascular permeability
• The net result of above mechanisms is vasodilatation and
increased vascular permeability in septic shock
• Profound peripheral vasodilatation and pooling of blood
causes hyperdynamic circulation in septic shock, incontrast to
hypovolemic shock
• Increased vascular permeability causes development of
inflammatory oedema
• DIC is prone to develop in septic shock due to endothelial cell
injury by toxins
• Reduced blood flow produces hypotension, inadequate
perfusion of cells and tissues
Causative organisms and toxins
Causative organisms Toxins
• E.coli,
klebsiella,pseudomonas cause
Endotoxin
pyelonephritis and endo
metritis
Endotoxin
• Anaerobes and above
mentioned bacteria causes
pelvic infection and septic
abortion
• Group A Toxic shock syndrome like
hemolyticstreptococci staph
toxin
aureus TSST 1
methicillin resistant staph auerius
Super antigen
exotoxin
Clostridium perfringens
Causes wound infection
 Clinical features of septic shock
• Abrupt onset of fever, chills, and tachycardia
It has the following phases
• Warm phase- phase of perepheral vasodilatation
Tachycardia, Hypotension, Warm extremities, Low CVP due
tomarked decrease in intravascular fluid volume
• Cold phase- phase of peripheral vasoconstriction
Elevated CVP due to cardiac failure,Poor tissue perfusion and
lactic acidosis,Tachypnea, Adult respiratory distress
syndrome, Altered sensorium, DIC
• Multiorgan failure due to hypotension and DIC
Acute renal failure, Altered LFT, Respiratory failure, Cardiac
failure
Diagnosis of septic shock
• History
 Risk factors-
 Septic abortion
 Puerperal endometriosis
 Pyelonephritis
 Wound infection
• Symptoms and signs
 Fever, chills
 Hypotension
 Tachycardia, Tachypnea
• Evidence of multiorgan failureOliguria/anuria, Respiratory
distress, DIC, Cardiac failure, Altered sensorium
Management
• When sepsis is suspected, a three- pronged strategy is
instituted
• All the steps are undertaken concurrently to
• Initiate emergency goal-directed treatment
• Identify the organism and antibiotic therapy
• Find the source of infection
Emergency goal directed treatment
• Achieve hemodynamic stability
• The women should be admitted to ICU
• IV access should be established through a central vein
• The bladder is catheterized and urine sent for culture
• Rapid infusion of IV NS 2-4 L to get the CVP upto 8-12
cm and maintaining a urine output of 30-50ml/hr is
mandatory
• O2 administration through venturi mask to achieve a
saturation of >95% and PaO2 of >65%. If this is
unsuccessful, the patient may need to be intubated and
ventilated
• Patients in whom hypotension persists even after rapid IV
fluid administration, pressor agents like dopamine,
norepinephrine, dobutamine may have to be cosidered
Identification of organisms and antibiotic
therapy
Blood, urine, and pus are sent for culture
Pending culture reports, , antibiotics are started
Initial therapy
Ampicillin or augmentin and gentamicin, Meropenam and
aztreonam for gram- negative infections
Additional therapy- surgical wound infections
Cloxacillin - suspected staphylococcal infection
Vancomycin/linezolid-suspected MRSA
High dose benzyl penicillin 20,00,000 units 24hrly –suspected
group A beta hemolytic streptococci
Clindamycin- necrotizing fasciitis
High dose benzyl penicillin and clindamycin/ metronidazole-
suspected clostridial myositis
Identification of site of infection
• Unless the site of infection is identified and the pus or infected
tissue removed, it is not possible to eradicate the infection.
• Site of infection is identified by clinical examination,
ultrasonography, computerized tomography, and/ magnetic
resonance imaging when required
• If the uterus is found to be gangrenous, an emergency
hysterectomy may be lifesaving.
• Pelvic abscess should be drained by colpotomy.
• Laparotomy is indicated when there is intraabdominal
collection of pus
Neurogenic shock
• May be due to painful conditions like
Acute inversion
Rapid evacuation of uterine contents
Vasovagal stimulation
Spinal anaesthesia may cause serious hypotension due to
blockade of the normal sympathetic vasomotor tone
Management
General measures like fluid replacement
Correction of acidosis
Vasoactive drugs
Corticosteroids
Ventilation and elimination of the source of neurogenic
stimulus
Acute inversion

• Acute inversion after delivery can be the cause of

neurogenic shock
• Causes-MC mismanaged 3rd stage of labor
 Diagnosis Prevention
• the classic triad of
• Proper training of all skilled
hemorrhage, shock and birth attendants in the
severe pelvic pain correct management of third
• due to traction on the stage of labor is essential to
ligaments supporting the prevent this complication
uterus causing para- • Early diagnosis, and
sympathetic stimulation or immediate reposition
due to hypovolaemia as a without removal of placenta
result of acute bloodloss if attached are important to
reduce the associated
• A bimanual examination morbidity and mortality
reveals cupped or the
missing fundus.
• Vaginally, there is a fleshy
reddish mass seen outside
the vulva.
Management
• Immediate resuscitation must be started simultaneously
with the efforts to reduce inversion
• Intravenous fluids must be infused with a wide bore
cannula pending the arrival of cross-matched blood for
transfusion.
• Ergometrine or oxytocin should not be given, as these
will only aggravate matters and make reduction or
replacement of the uterus more difficult
• Inversion should be immediately replaced without
attempting to remove the placenta from the inverted
fundus, which can be delivered later
Amniotic fluid embolism
• It is a rare obstetric emergency in which amniotic fluid,
fetal cells, hair or other debris enter the maternal
circulation, causing cardiorespiratory collapse
Risk factors
• Older maternal age
• Induction of labor using prostaglandins instead of
oxytocin
• Multiple pregnancy
• Polyhydramnios
• Placenta previa
• Placental abruption
• Operative deliveries
• Eclampsia
• Cervical lacerations and uterine rupture
Diagnosis
1. Sudden onset of cardiorespiratory arrest, or both
hypotension i.e. systolic blood pressure <90 mmHg and
respiratory compromise
2. DIC after appearance of the initial signs or symptoms.
Coagulopathy must be detected before loss of sufficient
blood to itself account for dilutional or shock-related
consumptive coagulopathy
3. Clinical onset during labor or within 30mins of delivery
of placenta
4. No fever during labor
Management
• Patient should be admitted to ICU
• Management is supportive as there is no specific therapy
for AFE
• Immediate administration of O2 and IV fluids are most
important measures to prevent further hypoxia and restore
circulation
• If hypotension does not respond to fluids alone,
vasopressors like dopamine or norepinephrine should be
infused
• Deranged coagulation parameters should be treated
by,cryoprecipitate or fibrinogen FFPs
• Plasmapheresis and haemofiltration have been shown to
be successful in arresting the progress of the disease ,
probably by clearing the plasma of cytokines
Pulmonary thromboembolism
• It occurs due to thrombus blocking pulmonary artery
• The symptoms depend on size of the artery obstructed
and there by the area of the lung which is not perfused
• Women are at higher risk of venous thromboembolic
disease in pregnancy due to the physiological changes in
pregnancy which promote venous stasis and
hypercoagulability of blood
• The risk increases further during the postpartum period
due to endothelial injury that occurs during delivery
Signs and symptoms
• Sudden onset dyspnoea
• Chest pain
• Features of collapse like tachycardia, cold clammy skin
and syncope
• Chest pain may occur anywhere in the chest and may
radiate to the shoulder, arm or jaw
• It is often associated with cough and haemoptysis
Diagnosis and treatment
• The diagnosis is easier in women with clinical suspicion
of deep vein thrombosis like redness, swelling and
tenderness over a vein in one of the legs
• Women with previous history of DVT should have a
thrombophilia screen, preferably before pregnancy,
because of the effect of pregnancy
• Low molecular weight heparin is as effective as
unfractionated heparin for the acute treatment of
pulmonary embolism
• Anti-coagulation must be continued for 3-6 months with
either LMWH, or alternatively warfarin, which can be
started once the acute phase is over
• Warfarin is not contraindicated during lactatiuon
Air embolism
• For an air embolus to enter the circulation, atleast part of
the placental site must be exposed
• Risk factors
Trendelenburg position
Abruptio placentae
Placenta previa
Exteriorization of the uterus
Manual extraction of placenta
Severe preeclampsia
APH
Hypovolemia
Symptoms and diagnosis
• A lethal embolism may follow a bolus of
3-5ml of air
• Tachypnoea
• Chest pain
• Gasping
• The diagnosis may be facilitated by pre-cordial doppler
monitoring, transoesophageal echocardiography
Management
• Unfortunately there is seldom time for effective treatment
• A useful immediate first aid procedure is to place the
patient in the head down, lateral position in the hope of
displacing the bolus of air towards the apex of the right
ventricle
• Management includes aspiration of air, discontinuation of
nitrous oxide, administration of 100% oxygen and
flooding the surgical site with saline to avoid further air
entry
Rupture uterus
• It is a condition that carries a very high mortality, if
neglected through failure to diagnose it
• The diagnosis is not easy, particularly in incomplete
rupture, but if shock persists inspite of adeqauate blood
transfusion to replace bloodloss, this possibility should be
excluded
DIC
• DEFINITION
Activation of coagulation in the microcirculation by entry of
large amounts of tissue thromboplastin or widespread
endothelial injury leading to activation of the intrinsic
pathway of coagulation and consumption of coagulation
factors with a resultant bleeding diathesis
Changes in normal pregnancy
• Pregnancy is considered to be a compensated
hypercoagulable state due to the changes that occur in the
coagulation pathways
• Platelet count marginally decreases, but platelet
aggregation increases
• There is an increase in fibrinogen and factors 7,8,9,10
• Thrombin activation is enhanced
• The fibrinolytic pathway as represented by plasmin
activity is partly suppressed
Causes of DIC in pregnancy
• Placental abruption- large amounts of thromboplastin at
the sites of abruption
• Amniotic fluid embolism- fetal squames, fetal antigens,
anaphylactic reaction
• Sepsis syndrome- endotoxins, exotoxins, SIRS,cytokine
storm, endothelial injury
• Eclampsia and HELLP syndrome- endothelial injury
• IUFD- release of thromboplastin from placenta
• Acute fatty liver of pregnancy- endothelial injury,
devcreased production of coagulation factors from liver
Clinical features
• Bleeding from venepuncture sites
• Ecchymoses
• Oozing/bleeding from incisions/lacerations/placental site
1. Episiotomy
2. Cesarean section incisions
3. Profuse vaginal bleeding
• Hypotension and shock
• Symptoms due to clotting in microvasculature
1. Tissue hypoxia and lactic acidosis
2. Decreased urine output
3. Metabolic acidosis
4. Acidotic breathing
5. Hypoxia and tachypnea, altered sensorium
Diagnosis
• A H/O predisposing obstetric events such as abruption,
sepsis, or amniotic fluid embolism is usually present
• Clinical features of bleeding, ecchymoses, or end-organ
failure are sufficient to make a clinical diagnosis
• Whole blood clotting time is markedly prolonged, a
bedside clot retraction test can be performed by collecting
a blood sample in a plain tube and observing the time
taken for formation of clot, in established DIC, clot may
not be formed for several hrs and even if a clot is formed,
it is soft and friable and does not retract

cont……….
• All bleeding parameters such as bleeding time, clotting time,
prothrombin time, partial thromboplastin time, and thrombin
time are prolonged
• Perepheral smear shows thrombocytopenia and schistocytes
• Plasma fibrinogen is markedly decreased. High levels of
fibrinogen and fibrin split products are present in the
perepheral blood, these products inturn inhibit formation of
fibrin and cause a vicious cycle
Management
• Control of hemorrhage, replacement of blood and blood
products, and treatment of the underlying cause
• Packed cells are used for correction of anemia
• Platelet concentrates for treating thrombocytopenia
• Fresh frozen plasma or cryoprecipitate to replenish
deficient factors
• Recombinant factor 7a can be used in uncontrollable
bleeding, but its use may be associated with increased
risk of stroke or pulmonary embolism
• Concurrently the underlying obstetric condition should be
promptly managed.
Cardiogenic shock
• Circulatory collapse caused by failure of the heart to
pump blood adequately
• Etiology
Failure of left ventricular ejection due to
Cardiac arrest
Myocardial infarction
Failure of ventricular filling
Cardiac tamponade
Pulmonary embolism
Any cause of obstetric shock can result in cardiac arrest
Cardiac arrest
• A variety of conditions, pregnancy related and non-
pregnancy related can cause cardiac arrest
• Most frequent reasons for cardiac arrest in pregnancy and
postpartum are obstetric hemorrhage (38.1%) followed
byAFE(13.3%), acute coronary syndrome (10%) and
venous thromboembolism in 4%
• Anaesthesia
• Bleeding
• Cardiovascular disorders
• Drugs
• Embolism
• Sepsis
• General causes like metabolic and electrolyte imbalance
• Hypertensive disorders including stroke
Management
• It is same as in non pregnant woman
• Epinephrine is vasopressor of choice and should be
administered by intravenous or intraosseous access above
the diaphragm
• Prompt resuscitation of the mother provided on the spot
can save both maternal and fetal life
• However resuscitation is difficult in pregnant patients due
to the physiological changes of pregnancy
System Changes in pregnancy Effects on resuscitation
Cardiovascular • Increased blood volume 40-50% • Dilutional anaemia
• RBC volume- 20% • Decreased O2 carrying
• Cardiac output increases by 40% capacity
• Increased oxygen consumption by • Increased circulation
20% demand
Respiratory Increased oxygen consumption by 20% Rapid decrease in PaO2 in
hypoxia
GIT • Delayed gastric emptying Aspiration of gastric
• Relaxed gastro-oesophageal contents
sphincter
uteroplacental Aortocaval compression Decreased cardiac output,
supine hypotension

Physiological changes in pregnancy and cardiopulomonary resuscitation

• The implication of these hemodynamic changes in a bleeding
pregnant patient may lose up to 30-35% of her blood volume
before manifesting signs like tachycardia and hypotension,
although the fetal circulation suffers severely due to this loss
• An abnormal fetal heart pattern may be the first sign of
signinificant maternal blood loss
• oxygen demand of the pregnant mother increases and the
functional residual capacity of the lungs decreases due to
elevation and splinting of the diaphragm by the enlarging
uterus, intubation and ventilation may be difficult in obese
women.
• Gastroesophageal sphincter is less competent due to the
hormonal effects of the pregnancy which increase the risk of
regurgitation of gastric contents and aspiration pneumonitis,
H2 receptor antagonists can be given to reduce gastric acidity
• Patient should be placed in left lateral position to releive
aortocaval compression.
Basic life support
• Must be instituted immediately while preparations are
being made to gain an intravenous access to correct
hypovelemia
Airway and breathing
Head tilt, chin lift manouver after ruling out head and
neck injuries, jaw thrust manouver in case of head and
neck trauma are recommended to open the airway
Suction can be used to clear the airway
100% oxygen should be provided by a reservoir bag
Carotid pressure should be maintained to prevent gastric
contents regurgitation
Circulation-
Chest compressions are given by applying rhythmic pressure
over the sternum, which initiates circulation by increasing the
intrathoracic pressure and directly stimulates the heart
Patient should be placed in supine position with the uterus
displaced manually to left side if patient is >20 weeks POG in
order to prevent aortocaval compression
Advanced life support
• Inhalation – with a cuffed endotracheal tube
• Vasopressor- epinephrine should be administered to
patients with cardiac arrest in a dose of 1mg every 3-5
mins during CPR
• Defibrillation
Mendelson syndrome
• Gastric contents that are highly irritant may be inhaled
during induction of anasthesia
• Chemical pnemonitis is more likely following aspiration
of gastric contents
• Factors that increase risk-
o Emergency surgical procedures
o Inadequate depth of anaethesia
o Obesity
o Concomittant opioid administration
o Impaired concsiousness
o Lithotomy position
o Difficult airway or intubation
o Gastro intestinal reflux ,Hiatal hernia
Clinical features and prevention
• May appear between 2-5 hrs after anaesthesia
• Cyanosis
• Tachycardia
• Dyspnea
• Wheeze
• Crepitant rales
• Decreased arterial oxygen tension
Prevention
Solid foods should be avoided in labouring patients and those at
additional risk factors including diabetes, morbid obesity and a
difficult airway
Antacids decrease the risk of aspiration by increasing the pH of
gastric contents
• Treatment
• Patient should be placed in trendelenberg position and
oropharynx suctioned
• If signs of hypoxia present- patient should be intubated
• Bronchoscopy or pulmonary lavage should be done to remove
particulate matter from the lungs
• Mechanical ventilation may be required depending on the
patients condition