FRCA Notes

Amniotic Fluid Embolism

The September 2019 joint CRQ/SAQ paper featured amniotic fluid embolism in the form of an SAQ (52% pass rate).

Examiner feedback criticised an "inability to differentiate between obstetric and non-obstetric causes of amniotic fluid embolism" - non-obstetric AFE seems oxymoronic to me...

Resources

  • Amniotic fluid embolism a rare but potentially devastating complication of pregnancy
  • Its rarity makes it difficult to study, although the UK Obstetric Surveillance System (UKOSS) has collected data on all cases of AFE since 2005
  • Non-uniform diagnostic criteria make establishing the incidence of, and mortality from, AFE difficult
Data Source Incidence (per 100,000) Mortality (%)
UKOSS (2005 - 2014) 1.7 19
Sytematic review (2014) 5.5 25
  • It is the fifth commonest direct cause of maternal mortality (after VTE, haemorrhage, suicide and sepsis)
  • Estimates for maternal mortality range wildly - as high as 86%
  • True maternal mortality may be closer to the realm of 19 - 30%
  • Death is usually rapid (within 4hrs)
  • 15% of cases have long-term neurological or respiratory morbidity

  • Neonatal mortality may be as high as 40%


Non-modifiable Iatrogenic
↑ maternal age Induction of labour
↑ parity ARM
Multiple gestation Uterine stimulants
Assisted delivery or LSCS


Trigger

  • The initial trigger is not understood
  • Animal models of autologous amniotic fluid injection do not necessarily cause an AFE syndrome
  • Women without AFE will have foetal squames within their circulation, so their mere presence isn't necessarily causative

  • Trauma to the uterus, cervix or uterine-placental unit may cause exposure of the vasculature to amniotic fluid and thus precipitate the event
    • It would be in keeping with the multiple iatrogenic risk factors (see above)

  • It's postulated the syndrome arises due to an abnormal factor within amniotic fluid which triggers the event
  • E.g. amniotic fluid is known to contain prostaglandins and arachidonic acid metabolites, which could trigger the initial vasospastic response

Theories of mechanism

  • Mechanical theory
    • Mechanical disruption of the cardiovascular system occurs
    • Caused by a large bolus of amniotic fluid (containing foetal squamous cells, vernix, lanugo, trophoblasts, foetal gut mucin or meconium)

  • Immune theory
    • An abnormal maternal immune response to foetal antigens in amniotic fluid occurs i.e. an anaphylaxis-like reaction
    • Supported by animal models which demonstrate prophylactic anti-histamines reduce symptoms and repeat exposure increases the response magnitude

Clark's biphasic model

  • Clark's model describes the biphasic pathophysiological response seen
  1. Initial phase (~30mins)
    • Pulmonary vasospasm causes acute, severe pulmonary hypertension
    • Pulmonary obstruction may be exacerbated by microthrombi formation

    • Consequent acute RV failure, with markedly decreased cardiac output and associated hypoxia
    • Can cause early death from AFE

  2. Secondary phase
    • There is relative recovery of the RV failure and normalisation of systolic BP, although pulmonary artery pressure remains high

    • LV dysfunction occurs due to:
      • Hypoxia
      • Reduced coronary blood flow
      • Direct myocardial depression

    • Endocapillary leak occurs with consequential pulmonary oedema and further reduced cardiac output

    • Procoagulant factors within amniotic fluid and/or trophoblasts entering maternal circulation can cause DIC and/or massive fibrinolysis

  • Should be suspected in ay pregnant woman with sudden and/or unexplained respiratory, cardiovascular or neurological difficulties
  • Timing typically:
    • During labour (70%)
    • During LSCS (19%)
    • Immediately post-vaginal delivery (11%)
Respiratory Cardiovascular Neurological Haematological Utero-foetal
Sudden respiratory distress (60%) Hypotension (100%) Confusion Coagulopathy (83%) Acute foetal compromise (100%)
Pulmonary oedema or ARDS (93%) Cardiovascular collapse / cardiac arrest (87%) Agitation DIC & hypofibrinogenaemia Uterine atony
Hypoxia and cyanosis (83%) Chest pain (2%) Numbness or paraesthesiae Massive fibrinolysis
Dyspnoea (49%) LV failure Headache (7%) Abnormal haemorrhage
Bronchospasm (15%) Seizures (48%)


Other embolic phenomenon

  • Pulmonary embolism
  • Venous air embolism
  • Fat embolism

Other obstetric emergencies

  • Eclampsia
  • Placental abruption
  • Uterine rupture
  • Major haemorrhage
  • Uterine inversion

Other aberrant reactions

  • Sepsis
  • Anaphylaxis

Iatrogenic issues

  • High or total neuraxial block
  • Local anaesthetic toxicity

Other

  • Acute cardiac failure e.g. from ischaemia or peripartum cardiomyopathy

  • Bloods:
    • Maternal blood show foetal tissue detected via immunohistochemistry
    • Coagulation profile will show
      • ↓ fibrongen
      • ↓ platelets
      • ↑ fibrin degradation products e.g. D-dimer
      • ↑ APTTr and INR

  • ECG: signs of RV strain
  • CXR: pulmonary oedema, cardiomegaly
  • TTE (/TOE): RV strain, pulmonary HTN

UKOSS Diagnostic Criteria

  • Either a clinical diagnosis of AFE (acute hypotension or cardiac arrest, acute hypoxia or coagulopathy in the absence of any other potential explanation for the symptoms and signs observed)

  • Or a pathological diagnosis at post-mortem (presence of fetal squames or hair in the lungs)

  • Management is largely supportive, targeted at normalising the physiological aberrancies in the respiratory, cardiovascular and haemtological systems

Airway and breathing

  • Oxygen supplementation
  • Low threshold for intubation to ensure adequate oxygenation

Cardiovascular

  • Large-bore IV access and blood for FBC | clotting | VHA | G&XM
  • Early use of CVP and cardiac output monitoring for goal-directed IV fluid resuscitation in view of ventricular dysfunction
  • Inotropic support
  • Management of maternal cardiac arrest

Haematological

  • Frequent laboratory testing and use of VHA to guide product use
  • Hypofibrinogenaemia is a common finding
    • Cryoprecipitate and/or fibrinogen concentrates should be used
    • TXA may play a role in preventing excessive fibrinolysis and reducing mortality from PPH