Amniotic Fluid Embolism







‘Pulmonary embolism by the particulate matter contained in amniotic fluid which gained entrance to the maternal circulation has been demonstrated by us at autopsy in 8 cases in which it seemed to be the cause of death … Having gained entrance to the maternal venous system, the emboli would be carried to the first filter bed, in these instances the lungs, and would lodge in vessels corresponding to their size. Sudden showers of foreign particulate material lodging in the lungs may produce severe systemic reactions resembling shock or anaphylactoid reactions’.


C. C. Steiner and P. E. Lushbaugh


Maternal pulmonary embolism by amniotic fluid as a cause of obstetric shock and unexpected death in obstetrics. JAMA 1941; 117:1245–1254, 1340–1345

Amniotic fluid embolism (AFE) is rare (2−3.3/100 000 deliveries) but is a potentially catastrophic complication of pregnancy. Despite its rarity, it has such a high fatality rate that it accounts for 7–10% of direct maternal deaths in the developed world. However, more recent series show a reducing maternal mortality. This may be due to improving care or to milder cases being identified. Maternal mortality is 20−35% and perinatal mortality 13.5−32%.


Whilst individual cases have been reported in association with most interventions the larger series consistently show certain risk factors. Induction of labour is associated with a three- to fourfold increase in risk, multiple pregnancy with a 10-fold increase and older women also have an increased risk. Caesarean section is associated with an eightfold increased chance of an amniotic fluid embolism occurring after the birth of the baby, so the caesarean section is associated with the AFE rather than being performed as a result of the AFE. Ethnic minority groups may also be more vulnerable. Many cases present immediately postpartum but very rarely the manifestations may be delayed for 1–2 hours after delivery.


Pathophysiology


It is not uncommon for amniotic fluid and fetal squames to enter the maternal circulation without ill effect. In certain susceptible women, however, it seems that the presence of fetal cells and/or other components of amniotic fluid may trigger a complex pathophysiological cascade similar to that seen with anaphylaxis and septic shock. The initial pathophysiological mechanism is of acute pulmonary vascular obstruction and hypertension leading to cor pulmonale. This is quite transient and soon followed by left ventricular failure leading to profound hypotension and shock. An acute inflammatory response disrupts the pulmonary capillary endothelium and alveoli leading to a ventilation–perfusion imbalance – resulting in severe hypoxia, convulsions and coma. If the patient survives for more than 1 hour it is virtually inevitable that she will develop disseminated intravascular coagulation due to the activation of coagulation factors by the amniotic fluid (which contains tissue factor) and fetal cells, in addition to the profound shock.




Diagnosis


The clinical diagnosis is based on the sudden development of acute respiratory distress and cardiovascular collapse in a patient in labour or recently delivered. In some cases the signs and symptoms occur within minutes of the triggering event, such as amniotomy or caesarean section.


The current criteria for defining a case in the UK are:


Either


In the absence of any other clear cause, acute maternal collapse with one or more of the following features:




  • Acute fetal compromise



  • Cardiac arrhythmias or arrest



  • Coagulopathy



  • Convulsion



  • Hypotension



  • Maternal haemorrhage



  • Premonitory symptoms, e.g. restlessness, numbness, agitation, tingling



  • Shortness of breath

Excluding women with maternal haemorrhage as the first presenting feature in whom there was no evidence of early coagulopathy or cardiorespiratory compromise


Or


Women in whom the diagnosis was made at postmortem examination by finding fetal squames or hair in the lungs.


The differential diagnosis includes other acute catastrophies that may present with similar features. These would include cardiac causes (myocardial infarction, cardiomyopathy, heart failure secondary to volume overload, valvular disease), respiratory (pulmonary oedema secondary to volume overload, acute asthma, pulmonary embolus), infectious (severe sepsis, chest, chorioamnionitis, endocarditis), pregnancy complications (pre-eclampsia and eclampsia, HELLP (Haemolysis, Elevated Liver enzymes and Low Platelets) syndrome, ante- and postpartum haemorrhage) and others (anaphylaxis, air embolus, local anaesthetic toxicity).


The clinical features and context should help differentiate between these causes but, in any event, the initial management – cardiopulmonary resuscitation – may be required for all of these conditions. The initial clinical diagnosis of AFE, then, is really a combination of the above clinical features without any of the other obvious clinical causes.

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Jul 21, 2019 | Posted by in OBSTETRICS | Comments Off on Amniotic Fluid Embolism
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