The multiple clinical presentations support the hypothesis that the early deaths are caused by the direct and “toxic” effects of a bolus of fetal material or amniotic fluid; the women who survive that initial event then become exposed to the cascade of related problems that follow. Most deaths now occur in this acute phase of collapse.1
Older women (i.e., over 25 years of age) appear to be at highest risk. In the past 15 years, only 1 woman under 25 has died of AFE in the UK, and only 2 women under 25 have been reported to the UK national registry.1 In a nonspecific way, intervention or complications at any stage of pregnancy seem more common in women who go on to have an AFE, though no distinct trigger has been found. Multiparity has been suggested as a risk factor, but neither the UK nor US registries have corroborated this.5 Eight of the 25 women reported to the UK registry were primiparas, and 1 had experienced 2 miscarriages but no other pregnancies. While labor is important in the etiology of AFE, cases have been reported under other circumstances, particularly after cesarean section, blunt abdominal trauma, amniocentesis, a ruptured uterus, and amnioinfusion in labor.9-13
The most useful diagnostic test to rule out a large segment of the differential diagnosis is a clotting screen.
The diagnosis of AFE is often one of exclusion—or else it is made postmortem. The differential diagnosis includes an exhaustive list of the causes of maternal collapse in the peripartum period. These include thrombotic embolus, air embolus, septic shock, acute myocardial infarction, peripartum cardiomyopathy, anaphylaxis, aspiration, placental abruption, transfusion reactions, local anesthetic toxicity, preeclampsia or eclampsia, uterine rupture, and postpartum hemorrhage (uterine atony).8,12
Initial management is supportive rather than specific. Basic resuscitation must be started immediately. Maximal initial oxygenation is required and, usually, early intubation and ventilation. An important step to consider is prompt delivery by cesarean section if the woman does not respond to cardiopulmonary resuscitation after 5 minutes. Prompt transfusion of fluids is necessary to replace blood loss. Vasopressors such as phenylephrine may help restore aortic perfusion pressure.12
As with any collapse, the early involvement of senior, experienced staff is critical, since the technical and practical aspects of resuscitation are more likely to be expertly performed by people who practice them regularly. A multidisciplinary approach—involving obstetricians, anesthesiologists, intensivists, and hematologists—carries the best prospect of the woman’s survival.
While the patient is being resuscitated, the team will have to investigate other causes of the collapse. The most useful diagnostic test to rule out a large segment of the differential diagnosis is a clotting screen. Clotting is often extremely abnormal even before the hemorrhage becomes apparent. If the patient is already hemorrhaging, abnormal clotting secondary to the hemorrhage needs to be considered. However, hemorrhage will not usually by itself cause a coagulopathy, unless there is considerable blood loss and blood replacement.
Because there is some “toxic” element to the effects of amniotic fluid, a number of reports have suggested that hemofiltration or plasma exchange may be effective.
If there are any signs of coagulopathy, such as blood in the urine or bleeding from the gums, the team should consider replacing clotting factor with fresh frozen plasma, cryoprecipitate, and platelets—even before massive blood loss is apparent and certainly before receiving the laboratory confirmation of coagulopathy. Indeed, cryoprecipitate may be of intrinsic value beyond its clotting-factor components because it contains fibronectin, which helps the reticuloendothelial system filter antigenic and toxic particulates.12
It also is important to perform an electrocardiogram to look for signs of myocardial damage. Be aware, however, that AFE can cause bizarre cardiac rhythms, which may need specific treatment and can make interpretation difficult. Because myocardial suppression is more common, dopamine or other inotropes may be helpful. Early pulmonary-artery catheterization is recommended to guide therapy.3,8,12 In fact, this step may be vital, helping prevent fluid overload that can worsen pulmonary edema and lead to adult respiratory distress syndrome. Arterial blood gases also may be of value, in addition to pulse oximetry, but will not differentiate causes specifically. In a patient who becomes stable, a ventilation-perfusion scan of the lungs may demonstrate defects. However, AFE can occlude the pulmonary vessels, so defects do not exclude it as a diagnosis.
If the fetal condition deteriorates suddenly, the team should consider coagulation studies and pulse oximetry. These will be more appropriate if the fetus is unexpectedly severely acidotic. Abnormalities detected by these investigations warrant earlier invasive monitoring, which may improve outcome.