The symptoms most often present at the time of labour and delivery but have been reported to occur, less frequently, with amniocentesis, abortions, miscarriages, caesarean deliveries, difficult and long labours, assisted vaginal deliveries and labour induction. Less frequently, disseminated intravascular coagulopathy (DIC) and/or refractory seizures can be associated with the cardiopulmonary collapse, but can also be the isolated initial presenting symptoms. This sudden collapse often is seen as a cardiopulmonary arrest either during labour and delivery or in the immediate post-partum period. 14, 15 Disseminated intravascular coagulopathy, very commonly seen in AFES, is most likely a result of activation of factor VII and platelets, and release of inflammatory and proinflammatory mediators that subsequently activate coagulation.ĪFES can present with a myriad of clinical signs and symptoms, although it most frequently presents precipitously, inexplicably and unpredictably with acute cardiopulmonary compromise and collapse, and haemodynamic instability and acute hypoxic respiratory failure ( Table 17.1). The proinflammatory responses seen in AFES are similar to those seen with the systemic inflammatory changes associated with sepsis and septic shock. 10– 13 These mechanisms probably result initially from a breach in the maternal–fetal interface, most likely at the level of the placenta or the uterus. Amniotic fluid in the maternal circulation can result in vasospastic, proinflammatory, humoral and/or immunologic mechanisms. 8, 9 However, amniotic fluid components are commonly found in the maternal circulation of women who do not demonstrate any evidence of AFES symptoms. 7 The clinical similarities with anaphylaxis have led to some experts proposing the alternate name ‘anaphylactoid syndrome of pregnancy’. The later presentation is characterized by acute left-heart failure with pulmonary oedema, but without pulmonary hypertension.Įarly researchers speculated that the mechanism was due to mechanical obstruction of pulmonary veins by intra-amniotic components such as fluid, fetal squames, fetal hair, etc., although it was later suggested that it may be a vasospastic disease process as a result of high concentrations of endothelin, proteolytic enzymes, histamine, serotonin, and leukotrienes in the composition of the amniotic fluid and debris. The early phase may manifest with acute right-heart failure and significant pulmonary hypertension within 15 to 20 minutes after the onset of AFES. 5, 6 Two phases of clinical presentation have been suggested.

Previous experimental animal models (usually the injection of amniotic fluid from a different non-human species into animal pulmonary vasculature) have not been very helpful in providing clinical information for pregnant women. Several hypotheses have been proposed, although none have been proven. It is unclear as to the exact aetiology of this disease process.

Ob gyn form 3 amniotic fluid embolism