Williams Manual of Pregnancy Complications, 23 ed.

CHAPTER 30. Amnionic Fluid Embolism

Amnionic fluid embolism is a complex disorder classically characterized by the abrupt onset of maternal hypotension, hypoxia, and consumptive coagulopathy. There is great individual variation in its clinical manifestation, and women will be encountered in whom one of these three clinical hallmarks dominates, or is entirely absent. The syndrome is uncommon in an absolute sense (1 case per 20,000 deliveries); however, it accounts for approximately 10 percent of maternal deaths.

In obvious cases, the clinical picture frequently is dramatic. Classically, a woman in the late stages of labor or immediately following delivery begins gasping for air, and then rapidly suffers seizure or cardiorespiratory arrest complicated by disseminated intravascular coagulation, massive hemorrhage, and death. These are unquestionably the most dramatic cases. However, there appears to be variation in the clinical presentation of this condition. Amnionic fluid embolism is rare, unpredictable, and unpreventable, and maintaining a high index of suspicion is key in improving morbidity and mortality.

PATHOGENESIS

Amnionic fluid enters the circulation as a result of a breach in the physiological barrier that normally exists between the maternal and fetal compartments. Such events appear to be common, if not universal, with both squames of presumed fetal origin and trophoblasts being commonly found in the maternal vasculature. There may be maternal exposure to various fetal elements during pregnancy termination, following amniocentesis or trauma, or more commonly during labor or delivery as small lacerations develop in the lower uterine segment or cervix. Alternately, cesarean delivery affords ample opportunity for mixture of maternal blood and fetal tissue.

In most cases, these events are innocuous. In certain women, however, such exposure initiates a complex series of physiological reactions characterized by hypoxia from acute pulmonary hypertension and right ventricular failure, followed by hypotension and left ventricular dysfunction with cardiogenic pulmonary edema, bronco spasm, and often noncardiogenic pulmonary edema from pulmonary capillary endothelial damage. Thereafter, disseminated intravascular coagulation (DIC) ensues in up to 80 percent, often manifested by profuse hemorrhage.

DIAGNOSIS

Amnionic fluid embolism is a clinical diagnosis, essentially a diagnosis of exclusion. In the past, the detection of squamous cells or other debris of fetal origin in the maternal pulmonary circulation was felt to be pathognomonic for amnionic fluid embolism. Indeed, in fatal cases, histopathological findings may be dramatic, especially in those involving meconium-stained amnionic fluid. However, the diagnosis of amnionic fluid embolism is generally made by identifying clinically characteristic signs and symptoms (see Table 30-1).

TABLE 30-1. Clinical Findings in 84 Women with Amnionic Fluid Embolism

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MANAGEMENT

Initial therapy is directed at maintaining oxygenation and inotropic support of the failing myocardium. Lateral maternal positioning and circulatory support with blood and component replacement is paramount. Placement of central catheters can aid in monitoring ongoing resuscitation. In undelivered women suffering cardiac arrest, consideration should be given to emergency perimortem cesarean delivery within 3 minutes of arrest in an effort to improve fetal outcome. However, for the mother who is hemodynamically unstable, but who has not suffered arrest, such decision making becomes more complex. Women who survive the initial phase will need intensive care monitoring and consultation with cardiology and pulmonary specialists. Newer data has shown benefits from technology such as left ventricular assist device (LVAD), nitric oxide (NO), and extracorporeal membrane oxygenation (ECMO).

PROGNOSIS

The reports of maternal mortality rates associated with amnionic fluid embolism are wide ranging (25 to 90 percent). Of the women who survive, profound neurological damage from hypoxic insult is seen in up to 85 percent. Outcome is also poor for fetuses and is related to the maternal arrest-to-delivery interval. Overall neonatal survival is approximately 70 percent, but almost half of the infants suffer residual neurological impairment.


For further reading in Williams Obstetrics, 23rd ed.,

see Chapter 35, “Obstetrical Hemorrhage.”