Embolic Events of Pregnancy

Pulmonary Embolism

The symptoms of pulmonary embolism are listed in Box 141.1 . In cases of massive pulmonary embolism, hypotension, syncope, or sudden cardiovascular collapse may be the presenting features.

The diagnosis of pulmonary embolism in pregnancy is potentially difficult. Chest radiographs, electrocardiogram, and arterial blood gas analysis may assist but are generally not diagnostic. Plasma D-dimer measurements are already elevated in pregnancy and therefore interpretation can be difficult. The two main imaging modalities employed are ventilation perfusion scintigraphy and computed tomography (CT) pulmonary angiography. Ventilation perfusion scintigraphy is a potentially useful initial test, although the positive and negative predictive values are dependent on the pretest probability of a pulmonary embolism. CT pulmonary angiography can potentially diagnose other pathology in addition to a pulmonary embolism (e.g., aortic disease) but at the expense of higher radiation exposure, particularly to the maternal breast tissue.

Amniotic Fluid Embolism

The term amniotic fluid embolism is somewhat of a misnomer. Whereas traditionally the condition was thought to result from the embolization of amniotic fluid and debris into the pulmonary circulation, current thinking suggests that the condition is more likely to be immune mediated and that the presence of amniotic fluid in the maternal circulation is a relatively common occurrence. The term anaphylactoid syndrome of pregnancy has been suggested as an alternative name for the constellation of signs and symptoms; however, this term has not been widely employed.

The signs and symptoms of amniotic fluid embolism can range from subtle symptoms through to the sudden onset of cardiorespiratory collapse ( Box 141.2 ). The deterioration may be preceded by symptoms of anxiety and agitation, and electronic fetal monitoring may show decelerations, loss of variability, and prolonged bradycardia. Coagulation changes are prominent and may develop rapidly, and in rare circumstances they may be the presenting feature. The majority of cases occur in relation to labor and delivery.

The diagnosis of amniotic fluid embolism is clinical in nature and based on the presenting signs and symptoms while ruling out other potential causes of the presentation. There is no specific diagnostic test for the condition, although a mast cell tryptase may be useful to rule out anaphylaxis as a potential cause. The presence of amniotic fluid debris in the maternal pulmonary circulation at postmortem is potentially diagnostic but only if it is in keeping with the clinical presentation. Echocardiography, either transesophageal or transthoracic, may be useful for assisting with the diagnosis and for guiding therapy. Reported cases have shown findings including acute right ventricular failure, severe pulmonary hypertension, and left ventricular failure.

Venous Air Embolism

The symptoms and signs of venous air embolism are listed in Box 141.3 . The presentation of venous air embolism is variable and depends on the volume and speed that the air is entrained, the end location of the air embolism, and the underlying condition of the parturient. Air that becomes entrapped in the right ventricular outflow tract may result in an “air lock” and subsequently a rapid onset of hypotension and cardiac arrest. Air that embolizes into the coronary circulation may cause signs and symptoms consistent with acute myocardial infarction, including chest pain and arrhythmias. Cerebral air embolism may occur in conjunction with a persistent right-to-left shunt (e.g., a patent foramen ovale) and lead to visual disturbances, altered level of consciousness, seizures, and visual disturbances. Later changes may result from the interaction of the entrained air and endothelial and platelet surfaces, resulting in activation of the coagulation cascade, vasospasm, and microthrombi.

The detection of significant venous air embolism may be difficult. For parturients under general anesthesia, capnography is likely the most readily available and sensitive test. A sudden, sharp decline in end-tidal carbon dioxide concentration in conjunction with a decrease in oxygen saturation should alert the clinician to the potential diagnosis. Transesophageal echocardiography is likely to be even more sensitive, although it is unlikely to be in place at the onset of deterioration. Clinical signs that may assist with the diagnosis include the presence of a “wheel-mill” murmur, described as a splashing auscultatory murmur from intracardiac air. Blanching of arteriole segments in the nail beds and pallor of mucous membranes may also be seen.