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Paradoxical Embolization by Amniotic Fluid Seen on the Transesophageal Echocardiography

Vellayappan, Usha, MD; Attias, Miguel D., MD; Shulman, Mark S., MD

doi: 10.1213/ane.0b013e318195b4e3
Cardiovascular Anesthesiology: Echo Rounds
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CME
Video 1
Video 2

From the Department of Anesthesiology and Pain Medicine, Caritas St. Elizabeth’s Medical Center and Tufts University School of Medicine, Boston, Massachusetts.

This article has supplementary material on the Web site: www.anesthesia-analgesia.org.

Accepted for publication October 15, 2008.

Supported by the Department of Anesthesiology and Pain Medicine, Caritas St. Elizabeth’s Medical Center.

Reprints will not be available from the author.

Address correspondence to Mark Shulman, MD, Department of Anesthesiology and Pain Medicine, Caritas St. Elizabeth’s Medical Center, 736 Cambridge St., Boston, MA 02135. Address e-mail to mark.shulman@caritaschristi.org.

A 34-yr-old woman was admitted for delivery. Five minutes after her membranes were ruptured, she had a cardiac arrest. An Advanced Cardiac Life Support Protocol was started, the patient regained consciousness and an arterial blood pressure was obtained. The patient was taken emergently to the operating room for cesarean delivery. Anesthesia was induced with ketamine and succinylcholine to facilitate intubation. Fifteen minutes after the cardiac arrest, the infant was delivered. It was suspected that the patient’s cardiac arrest was due to an amniotic fluid embolism (AFE), but the patient remained hemodynamically stable with the use of minimal vasopressors and did not become hypoxic.

Since the clinical picture did not exactly fit the usual finding of hypoxia and severe hypotension of an AFE, a transesophageal echocardiogram (TEE) probe was placed to exclude any other cardiac pathology that may have caused the initial cardiac arrest. The TEE examination was performed about 90 min after the initial cardiac arrest and revealed an enlargement of the right ventricle and moderate hypokinesis of the right ventricle. The right atrium was moderately enlarged (width 6.5 cm), and there was a large mobile mass extending from the right atrium through a patent foramen ovale (PFO) into the left atrium (Figs. 1A and B; Video clips 1 and 2; please see video clips available at www.anesthesia-analgesia.org). The tricuspid annulus was dilated with trace-to-mild tricuspid regurgitation. Pulsed wave Doppler demonstrated a normal pattern of blood flow in the hepatic veins. There was no marked bulging of the interatrial and interventricular septum. The pulmonary arteries were dilated, and there were no visible masses. Pulmonary artery systolic pressure was not measured due to the very small amount of tricuspid regurgitation. Pulse wave Doppler measured a Qp/Qs shunt ratio of 2:1, indicating a left-to-right shunt through the PFO. The mitral and aortic valves were essentially normal, and there was no evidence of hypertrophic cardiomyopathy. There was a hyperdynamic left ventricular systolic function with an ejection fraction of 70%.

Figure 1.

Figure 1.

Because of the high risk of systemic emboli from the interatrial mass, it was determined that the patient should be transferred for immediate cardiac surgery at the conclusion of the cesarean delivery. The TEE findings prebypass (3.5 h after the initial cardiac arrest) were essentially the same as during the cesarean delivery. The patient was placed on cardiopulmonary bypass and underwent right atriotomy with the extraction of the embolus (Fig. 2) from both atria. The PFO was surgically closed and documented by an intact interatrial septum using color flow Doppler. In addition, agitated saline injected while viewing the TEE demonstrated that no contrast bubbles entered the left atrium for five cardiac cycles. Subsequent inspection of the proximal pulmonary arteries did not reveal any masses or thrombotic material. Pathologic examination revealed squamous cell epithelium in the interatrial mass consistent with a diagnosis of AFE. The patient’s recovery was uneventful, without neurologic sequelae, and with complete normalization of cardiac function.

Figure 2.

Figure 2.

The pathophysiology of AFE may resemble anaphylaxis or septic shock. Typically, hypotension, hypoxia, disseminated intravascular coagulation and neurologic symptoms are observed. The limited reports of TEE performed shortly after diagnosis or the early phase syndrome of AFE report normal left ventricular contraction and enlargement of the right ventricle with right ventricular failure.1–3 In our case, there are a number of reasons why the right ventricular function was only moderately impaired and better than expected. The TEE study was performed about 90 min after the initial event occurred. The right ventricular function may have dramatically improved over this time period due to our therapeutic interventions. There was no thrombotic material found in the pulmonary arteries that could have caused increased pulmonary artery pressures and acute right heart failure. Finally, a portion of the AFE may have bypassed the pulmonary circulation and, instead, formed a mass that was located in the PFO channel on both sides of the interatrial septum.

Since there was clearly a left-to-right shunt demonstrated by color-flow Doppler, an attempt was made to quantitate it by determining Qp/Qs ratio. The flow ratio between the pulmonary (Qp) and systemic (Qs) circulations indicates the magnitude of the interatrial shunt.4 Qp/Qs is calculated using the formula shown in Figure 3. The Qp/Qs ratio of 2:1 may not have been entirely precise because it can be difficult to determine the right-sided flow by measuring the right ventricular outflow tract diameter accurately. The shunt may have been right to left at the time of the initial event, but improvements to the patient’s oxygenation and hemodynamic status at the time of the TEE study clearly showed the shunt was now left to right.

Figure 3.

Figure 3.

Echocardiographic masses from an AFE have been found using a TEE,5,6 but a transeptal paradoxical AFE has never been described. The embolus pictured in Figure 2 appears more like a thrombus than a liquid embolism. The reason is that amniotic fluid has procoagulant activity which can cause a thrombus to form that incorporates the amniotic fluid. Paradoxical embolism is a well-known phenomenon, usually diagnosed by TEE based on its sequelae. An example of this is the case of a patient with an aneurysmal interatrial septum and an intracardiac thrombus traversing a PFO which was recently published in Echo Rounds.7 In our case, the transseptal paradoxical AFE was found by TEE performed to find the etiology of an unexpected cardiac arrest.

AFE has been described as a clinical diagnosis of exclusion. The use of TEE in this case for a suspected AFE not only helped make a definitive diagnosis, but allowed the proper therapeutic intervention that prevented a possible cerebral embolic event. We feel that, in any suspected case of AFE, a TEE study should be done as part of the standard of care for this clinical syndrome.

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