Abstract
Amniotic fluid embolism occurs rarely but is a leading cause of maternal mortality. Regardless of emergent supportive medical treatment, it is associated with a very high mortality rate. Here, we present the case of a 33-year-old pregnant woman with amniotic fluid embolism, who sustained cardiac arrest and was rescued with early application of extracorporeal membrane oxygenation. The management of amniotic fluid embolism is to initially focus on rapid cardiopulmonary stabilization. Hemodynamic decompensation may be transient and recoverable within a few hours. Early application of extracorporeal membrane oxygenation should be considered in patients who are unresponsive to medical therapy before severe organ damage supervenes.
Keywords
embolism, amniotic fluid; extracorporeal membrane oxygenation; hemodynamics, decompensation; maternal mortality;
1. Introduction
Amniotic fluid embolism occurs under a variety of conditions such as cesarean section, seemingly uncomplicated pregnancy in the second trimester, abortion in the first or second trimester, abdominal trauma, and amniocentesis. It may also occur up to 48 hours postpartum.1 Amniotic fluid embolism is an extremely critical event and accounts for approximately 10% of all maternal deaths in the United States.2 The overall incidence of amniotic fluid embolism varies between 1 in 8000 to 1 in 80,000 live births, and the maternal mortality associated with amniotic fluid embolism is between 61% and 86%.3 The traditional management of amniotic fluid embolism is supportive; however, despite medical advances, the mortality rate remains high.
Here, we present a patient who sustained amniotic fluid embolism and developed cardiac arrest. She was successfully treated with early application of extracorporeal membrane oxygenation (ECMO).
2. Case Report
A 33-year-old pregnant woman, gravida 4, para 2, abortus 1, at 38 weeks of gestation, was admitted for labor with uterine contractions at term. Five months before this admission, placenta previa totalis had been diagnosed sonographically and elective cesarean delivery was planned. On admission, obstetric examination revealed cervical dilatation of 2 cm, and the fetal heart monitor revealed a normal cardiac tracing. Forty minutes after admission, a sudden episode of chest tightness and dyspnea was noted, which was followed by unexpected loss of consciousness in conjunction with fetal bradycardia. Since amniotic fluid embolism was highly suspected, the patient was immediately sent to the operating room with positive pressure ventilation by mask and bag en route.
Cyanosis and asystole were noted on arrival in the operating room, and the anesthesiologist immediately performed endotracheal intubation and started cardiopulmonary resuscitation. After initial resuscitation, her vital signs were heart rate of 130 beats/min and blood pressure of 55/30 mmHg. Instantaneous gas analysis with breathing 100% oxygen revealed pH of 7.1, PCO2 of 60.9 mmHg, PO2 of 44 mmHg and HCO3 of 10.7 mmol/L, suggestive of refractory hypoxemia and metabolic acidosis. Emergent cesarean delivery was performed and a live infant was delivered with Apgar scores of 3 at 1 minute and 5 at 5 minutes; the infant subsequently required intubation.
Postpartum, the patient developed arrhythmia, but the blood pressure could not be obtained with a noninvasive blood pressure device. Therefore, a central venous line and arterial line were established. During cardiopulmonary resuscitation cardiotonics, including epinephrine, dopamine and sodium bicarbonate, were infused; electroshock was attempted and blood was transfused. Cardiopulmonary resuscitation was continued for about 30 minutes but failed to maintain an ideal hemodynamic status.
At this juncture, a cardiologist was consulted. Ventricular-atrial mode ECMO was undertaken because of refractory cardiovascular collapse. An arterial line was established in the bifurcation of the iliac artery and a venous line was placed in the right atrium through a median sternotomy. Fifteen minutes after the administration of ECMO together with transfusion of blood components and vasopressors, the patient’s vital signs became stable. Abdominal total hysterectomy was performed due to placenta accreta and unrecognizable bleeders. The central venous blood sampled for cytologic analysis showed the presence of epithelial cells (Figure 1). The cytologic examination and clinical presentation strongly supported the diagnosis of amniotic fluid embolism.
The patient was weaned from ECMO after 4 hours and sent to the ICU. After a 2-week stay in the ICU for care of respiratory distress syndrome, she was returned to the ward with only minor sequelae. She had left-side muscle power weakness, which might have been due to hypoxic cerebral damage from the ischemic event, and she had to use walking aids after rehabilitation. The neonate was discharged without neurological dysfunction on the 3rd day of hospitalization.
Download full-size image
3. Discussion
Amniotic fluid embolism is a rare but catastrophic complication of pregnancy. The classical clinical features are sudden onset of dyspnea, cyanosis and hypotension disproportionate to the blood loss, followed quickly by cardiopulmonary arrest. The mortality rate associated with amniotic fluid embolism is high, with 50% of deaths occurring within the first hour after diagnosis and 25−50% of deaths occurring in the ensuing 4−5 hours.4 Sixty-five percent of cases of amniotic fluid embolism have symptoms before delivery. As a result of the high mortality rate, immediate cesarean section is therefore needed to prevent hypoxic damage to the fetus and to facilitate cardiopulmonary resuscitative efforts. The main role of the anesthesiologist is to provide supportive management and focus on maternal cardiopulmonary stabilization (Table 1).5 In 1995, Clark et al analyzed the clinical course and investigated possible pathophysiologic mechanisms of amniotic fluid embolism.6 They found that the factors causing amniotic fluid embolism are likely fetal elements and/or other mediators such as histamine, bradykinin, cytokines, prostaglandins, leukotrienes, and thromboxane. Their findings demonstrated that amniotic fluid embolism is not only caused by innumerable emboli in small pulmonary vessels,5 but is also more consistent with septic shock and anaphylactic shock.7,8 Thus, it has been proposed that the term “amniotic fluid embolism” be changed to “anaphylactoid syndrome of pregnancy”.9
When amniotic fluid or fetal cells enter the maternal circulation, it will produce a biphasic hemodynamic response.6 In the first stage, the spasm of pulmonary vessels results in pulmonary hypertension and increases the right ventricular pressure. Hypoxemia soon follows a secondary decrease in left ventricular function, resulting from myocardial ischemia. Then, the patient suffers from massive bleeding with uterine dystonia and disseminated intravascular coagulation. The consumptive coagulopathy is often the earliest sign of amniotic fluid embolism. The hemodynamic decompensation may be transient and recoverable within a few hours. The canine model of anaphylaxis has also shown the temporal sequence of hemodynamic decompensation and recovery.10 In the initial situation, ECMO can play an important role in supporting cardiovascular status and decrease further neurologic deficit with amniotic fluid embolism (Table 2).11,12
ECMO has been used mainly in the management of resuscitating patients suffering from refractory shock. It is a complex technique for providing life support in severe but potentially reversible respiratory failure. The technique oxygenates the blood outside the body, obviating the need for gas exchange in the lungs and, if necessary, provides cardiovascular support.13
There are a few case reports on the use of ECMO to treat amniotic fluid embolism.14,15 The goal is to achieve rapid maternal cardiopulmonary stabilization during anaphylactic shock. Hsieh et al14 and Reyftmann et al15 successfully managed the critical conditions with ECMO, and their patients were weaned from ECMO after 40 hours and 150 hours, respectively. In our case, we immediately decided to use ECMO due to previous experience and set up the instrumentation some 50 minutes after the onset of symptoms. Our patient, after meeting the criteria for weaning, was weaned from ECMO after only 4 hours, which is quite different from the previously reported cases. This difference may be due to the timely use of ECMO before massive damage to myocardial cells supervened. Complications such as hemolysis, renal function impairment, intracranial hemorrhage, sepsis, and limb ischemia are directly related to the duration of extracorporeal life support.16,17 To avoid these complications, patients should be weaned from ECMO as soon as possible.
Because encephalopathy, supposedly due to hypoxia and impaired oxygen delivery to the brain, is one of the gravest outcomes in patients with amniotic fluid embolism, early application of ECMO was seriously considered and effectively carried out in our case. Early application of ECMO also protects brain function and prevents vegetative state or brain death. We successfully rescued the patient and she gradually regained consciousness with intensive care.
Disseminated intravascular coagulation may develop early as a result of toxic substances in the amniotic fluid entering the circulation, or later as a result of systemic inflammatory insult. However, heparin infusion during ECMO may induce thrombocytopenia and other coagulopathy. Even when precoating accessories with heparin (including the mechanical pump, oxygenator and tubes), care should be taken to keep the activated clotting time within 130−150 seconds to prevent thrombotic formation.18 It is suggested that decreasing heparin dosage and early weaning from ECMO on the first day after the occurrence of amniotic fluid embolism can prevent compromised coagulopathy.14
Management of amniotic fluid embolism is supportive and focused initially on rapid maternal cardiopulmonary stabilization. The most important goal of therapy is to prevent hypoxia and subsequent end-organ failure. ECMO can quickly provide a short period of cardiopulmonary support and the supervening complications can thus be minimized.
In conclusion, early application of ECMO can be considered for the treatment of patients with amniotic fluid embolism who are unresponsive to aggressive medical therapy before organ damage occurs. For the best prognosis with regard to reducing mortality, a team of specialists, including an obstetrician, anesthesiologist and cardiac surgeon, should be involved in the management of amniotic fluid embolism and to decrease ECMO-associated complications.