Copyright © 2005, The European Society of Cardiology
Echocardiographically detected mass "in transit" in early amniotic fluid embolism
American University of Beirut – Medical Center, P.O. Box 11-0236 Beirut, Lebanon
Received 21 March 2005; received in revised form 16 June 2005; accepted after revision 30 June 2005.
* Corresponding author. Tel.: +961 3 384640; fax: +961 1 744464. dg00{at}aub.edu.lb
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Background Amniotic fluid embolism is a catastrophic illness related to the passage of fetal material into the pulmonary circulation causing cardiovascular collapse.
Case A 29-year-old female sustained cardiopulmonary arrest during delivery presumably due to amniotic fluid embolism. A right atrial mass "in transit" was detected by echocardiography. It had an appearance and pattern of motion that was suggestive of a gelatinous consistency and is likely to have been an amniotic fluid embolus. There was also evidence of acute right ventricular overload.
Conclusion We recommend that echocardiography be considered early on such conditions to gain more insight into the pathogenesis of this complication.
Keywords: Amniotic fluid embolism; Mass "in transit"
Amniotic fluid embolism is a devastating obstetric syndrome that constitutes the leading cause of mortality during labor and during the first few postpartum hours.1 It has been reported to occur in 1 in 8000 to 1 in 80,000 pregnancies causing 5–18% of all maternal deaths.1 Only 15% of those affected survive neurologically intact.2 While the majority of maternal deaths caused by amniotic fluid embolism are due to cardiopulmonary collapse, the mechanism of this collapse is still unclear. Echocardiography is one modality which when used early in the course of amniotic fluid embolism provides useful information pertaining to the pathophysiology of this syndrome. We report a case of amniotic fluid embolism in whom early transthoracic echocardiography showed a mass in the right atrium that resolved few minutes later when transesophageal echocardiography was attempted.
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A 35-year-old gravida 5, para 3, aborta 2, previously healthy except for allergic rhinitis and chronic sinusitis presented at 40 weeks of gestation to the delivery room with active labor. Her previous obstetrical history includes two normal vaginal deliveries at 40 and 39 weeks, one spontaneous abortion during the first trimester and a twin pregnancy delivered by C-section at 38 weeks resulting in one healthy baby and another with intrauterine fetal demise. During this pregnancy, the patient had a smooth prenatal course with adequate weight gain and normal anomaly scan done at 20 weeks of gestation. All through her pregnancy she had normal blood pressure around 110/70, and did not report pretibial edema nor any symptom suggestive of cardiac or pulmonary disease. The decision was to allow a trial of labor following her last C-section, given the history of her two previous successful normal vaginal deliveries.
On admission the patient was in severe pain reporting contractions and pelvic heaviness. There was a questionable history of a recent amniotic fluid leak. She was conscious and responsive. Fetal heart rate was appropriately reactive. The cervix was 3–4cm dilated, 100% effaced and very soft. The fetus was in a vertex presentation and the fetal head was at plus 1 station. Intravenous oxytocin was administered as this was judged necessary by her physician. The patient had precipitate labor and in 15min the cervix was already fully dilated with the fetal head at plus 3 station. After her first push, the patient suddenly stopped breathing and became cyanotic and unresponsive. At that time she was unconscious with undetectable pulses. Active cardiopulmonary resuscitation was started and endotracheal intubation was performed.
Meanwhile, a right mediolateral episiotomy was done and suprafundic pressure was applied. In few minutes, a live male weighing 4080g was delivered with an APGAR score of 7 at 1min and 9 at 5min. The placenta was delivered completely and the previous uterine scar was free of dehiscence upon manual inspection. Maternal cardiopulmonary resuscitation was continued and a normal pulse and blood pressure were restored in about 25min. A transthoracic echocardiogram was done at this time showing a mildly dilated and severely hypokinetic right ventricle. The left ventricle showed fair contractility. An elongated mass was seen in the right atrium projecting into the right ventricular inflow through the tricuspid valve and exhibiting motion with the cardiac cycle (Fig. 1A and B). Minutes later, a transesophageal probe was inserted at which time no masses could be visualized in the heart, the main pulmonary artery or its proximal branches. Repeat transthoracic imaging showed disappearance of this mass. Because pulmonary embolism was suspected at this stage, heparin was administered. The patient, however, developed profuse vaginal bleeding not responsive to uterine massage, oxytocin and protamine. Heparin was discontinued and blood transfusion was started. Laboratory values at this stage were compatible with disseminated intravascular coagulation (Hemoglobin 8.5g/dl, hematocrit 25%, D-dimer >32,000 ng/ml, PTT 47/28.5, fibrinogen 0.7g/l, INR 1.50, platelets 40,000/mm3).
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The patient was then transferred to the intensive care unit for further management. She was unconscious (Glasgow coma scale=3), with a borderline blood pressure on vasopressors. The next day, a repeat transthoracic echocardiography in the intensive care unit showed normal left ventricular systolic function, with a persistently dilated hypokinetic right ventricle. Tricuspid regurgitation allowed estimation of pulmonary artery pressure of 45mmHg. Again, no intracardiac masses were seen. She received multiple transfusions with packed red blood cells and fresh frozen plasma and was started on broad spectrum antibiotics. Her DIC started to resolve 24h later. Chest X-ray was initially clear but bilateral intra-alveolar edema and left lower lobe consolidation were noted on the fourth day. CT brain done on the day of delivery showed severe brain edema, multiple areas of infarcts with transtentorial herniation. Patient's condition continued to deteriorate and developed renal shutdown and cardiac arrest not responsive to resuscitation. Patient was declared dead four days after her delivery. An autopsy was declined by the patient's husband.
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Since the early report of Steiner and Lushbaugh in 19413 and despite all medical advances, amniotic fluid embolism is still lethal in about 86% of the cases.4 The majority of patients present during labor but before delivery.1 Several associations were identified including history of allergy or atopy, male fetal sex and partial abruptio placentae,1,5 most of which were present in our case. The diagnosis mainly depends on a typical clinical manifestation. Patients classically present with initial hemodynamic collapse were characterized by sudden dyspnea, hypotension and cardiopulmonary arrest followed by some degree of consumptive coagulopathy ranging from a transient rise in fibrin split products or fall in platelet count to overt disseminated intravascular coagulopathy.6 Seizure or seizure-like activity may precede the event in 10–20% of cases.6 If the patient survives the acute event, a secondary noncardiogenic pulmonary edema (ARDS) may occur in up to 70% of patients.6
Finding fetal squames in pulmonary artery aspirate which was thought by some to be pathognomonic of amniotic fluid embolism is currently considered of no diagnostic significance since fetal debris may be found in asymptomatic pregnant women.1 Animal studies taken as a whole have not yielded until now a uniform picture of the hemodynamic changes occurring in the acute phase of amniotic fluid embolism.6 Human data in the early course of this syndrome are still rare.2 Most studies were done at least 1h after the onset of clinical signs with some implicating left ventricular failure as the main hemodynamic alteration in amniotic fluid embolism.4,6,7 These studies showed an increase in pulmonary capillary wedge pressure paralleling the elevation in mean pulmonary artery pressure, and decrease in left ventricular stroke-work index.7 Systemic reaction to toxins similar to septic shock or anaphylaxis rather than an embolic phenomenon was proposed to explain the observed left ventricular depression.1 The few cases reporting hemodynamic findings in the hyperacute stage (within 10min of collapse) of amniotic fluid embolism, however, were consistent with early right ventricular dysfunction.2 These studies attributed the initial hemodynamic alteration to pulmonary vasoconstriction resulting in pulmonary hypertension with subsequent right ventricular failure.2 Treatment by cardiopulmonary bypass resulted in a successful outcome and resolving of right ventricular failure in some reported cases.2 Clark unified both findings by postulating a biphasic pattern whereby the initial alteration is transient pulmonary vasoconstriction and right ventricular failure followed by secondary depression of left ventricular function in eventual survivors.6
Our patient was diagnosed to have amniotic fluid embolism based on the typical clinical presentation including the sudden dyspnea, cardiovascular collapse and subsequent coagulopathy. Echocardiography within minutes of hemodynamic stabilization showed evidence of an elongated mass floating in the right atrium. The right ventricle appeared dilated and severely hypokinetic. The left ventricle was normal. No other masses were seen in the inferior vena cava or the proximal pulmonary arteries. A transesophageal echocardiogram done 10min later showed disappearance of this mass.
Previous reports of right atrial mass "in transit" are rare and were mostly described in cases of pulmonary embolism.8 This is the first report of echocardiographic findings in the hyperacute stage of amniotic fluid embolism consistent with a right atrial mass "in transit" occurring with right ventricular dysfunction. This mass had an appearance and pattern of motion suggestive of being of gelatinous composition. This visualized material could have played a role in the etiology of pulmonary hypertension and cardiopulmonary collapse either by a mechanical obstructive effect or by a biochemical vasoconstrictive reaction.
Further echocardiographic studies in the acute phase of amniotic fluid embolism are needed to help to understand more about the early pathophysiologic changes. If mechanical obstruction is the main putative factor emergency pulmonary embolectomy may be a reasonable option in this catastrophic condition.
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References |
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- Clark S.L., Hankins G.D.V., Dudley D.A., Dildy G.A., Porter T.F. Amniotic fluid embolism: analysis of the national registry. Am J Obstet Gynecol (1995) 172:1158–1169.[CrossRef][Web of Science][Medline]
- Stanten R.D., Iverson L.I.G., Daugharty T.M., Lovett S.M., Terry C., Blumenstock E. Amniotic fluid embolism causing catastrophic pulmonary vasoconstriction: diagnosis by transesophageal echocardiogram and treatment by cardiopulmonary bypass. Obstet Gynecol (2003) 102:496–498.[CrossRef][Web of Science][Medline]
- Steiner P.E., Lushbaugh C.C. Maternal pulmonary embolism by amniotic fluid. JAMA (1941) 117:1245–1254. 1340–5.
[Abstract/Free Full Text] - Girard P., Mal H., Laine J.F., Petitpretz P., Rain B., Duroux P. Left heart failure in amniotic fluid embolism. Anesthesiology (1986) 64:262–265.[Web of Science][Medline]
- Scully R.E., Mark E.J., Mc Neely W.F., Ebeling S.H., Phillips L.D. Case records of the Massachusetts general hospital. N Engl J Med (1998) 338:821–826.
[Free Full Text] - Clark S.L. New concepts of amniotic fluid embolism: a review. Obstet Gynecol Surv (1990) 45:360–368.[Medline]
- Clark S.L., Cotton D.B., Gonik B., Greenspoon J., Phelan J.P. Central hemodynamic alterations in amniotic fluid embolism. Am J Obstet Gynecol (1988) 158:1124–1126.[Web of Science][Medline]
- Pasierski T.J., Alton M.E., Van Frossen D.B., Pearson A.C. Right atrial mobile thrombus: improved visualization by transesophageal echocardiography. Am Heart J (1992) 123:802–803.[CrossRef][Web of Science][Medline]
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