Diagnosis. Proposed criteria for diagnosis of amnionic luid embolism are shown in Table 41-7. he classic example is dramatic, and a woman in the late stages of labor or immediately postpartum begins gasping for air. Seizures or cardiorespiratory arrest rapidly follows accompanied by massive hemorrhage from consumptive coagulopathy. Clinical manifestations are variable. For example, we and others have managed several women in whom otherwise uncomplicated vaginal or cesarean delivery was followed by severe acute consumptive coagulopathy without overt cardiorespiratory diiculties. In those women, consumptive coagulopathy appears to be the orme ruste of amnionic luid embolism (Kramer, 2012; Porter, 1996).
Because of this clinical variability, other sources of acute cardiac or respiratory failure should be considered. These include myocardial infarction, pulmonary or air embolism, high spinal blockade, eclampsia, and anaphylactic shock. In some cases, the temporal relationship of events aids diagnosis. Unortunatey, no
FIGURE 41 -31 Fatal amnionic fluid embolism. A.Autopsy
TABLE 41 -7. Diagnostic Criteria for Amnionic Fluid Embolism
Abrupt onset of cardiorespiratory arrest, or both hypotension and respiratory compromise.
Documentation of overt disseminated intravascular coagulation. Coagulopathy must be detected prior to loss of sufficient blood to cause dilutional or shock-related consumptive coagulopathy.
Clinical onset during labor or within 30 minutes of placental delivery. No fever �38°C.
Adapted from Clark, 201n6.
specic diagnostic laboratoy test conirms or refutes the diagnosis Management. The initial period of systemic and pulmonary of amnionic luid embolism, and it remains a clinical diagnosis. hypertension with amnionic fluid embolism is transient. Thus, Importantly, women sufering from excessive blood loss and immediate high-quality cardiopulmonary resuscitation and resulting coagulopathy may be misdiagnosed with amnionic advanced cardiac life support must be initiated without delay fluid embolism, when the true culprit is unrecognized or under(Society for Maternal-Fetal 1edicine, 2016). These are disappreciated hemorrhage (Clark, 2016). In either event, a woman cussed in detail in Chapter 47 (p. 931). with cardiopulmonary compromise should receive immediate If resuscitation is successful, hemodynamic instability is resuscitation (Society for Maternal-Fetal Medicine, 2016). common in survivors. Both fever and hyperoxia will worsen ischemia-reperfusion injury to the brain, and thus both are Pathophysiology.
The mechanism of injury from amnionic avoided. A suitable goal for temperature is 36°C and for mean luid embolism has evolved. Early theories proposed that amniarterial pressure is 65 mm Hg (Society for Maternal-Fetal onic fluid and debris entered maternal circulation and obstructed pulmonary artery flow, which led to hypoxia, right heart failure, and death. However, during normal delivery, amnionic fluid commonly enters the maternal circulation through venous channels at the placental implantation site or from small lacerations. Accordingly, squames, fetal cells, and trophoblasts can oten be identiied in maternal peripheral blood at delivery (Clark, 1986; Lee, 1986). And, infused amnionic luid is generally innocuous, even in large amounts (Adamsons, 1971; Stolte, 1967).