Amniotic fluid embolism is an uncommon, but potentially lethal, complication of pregnancy. Because amniotic fluid embolism usually is seen with cardiac arrest, the initial immediate response should be to provide high-quality cardiopulmonary resuscitation. We describe key features of initial treatment of patients with amniotic fluid embolism. Where available, we recommend performing transthoracic or transesophageal echocardiography as soon as possible because this is an easy and reliable method of identifying a failing right ventricle. If such failure is identified, treatment that is tailored at improving right ventricular performance should be initiated with the use of inotropic agents and pulmonary vasodilators. Blood pressure support with vasopressors is preferred over fluid infusion in the setting of severe right ventricular compromise. Amniotic fluid embolism–related coagulopathy should be managed with hemostatic resuscitation with the use of a 1:1:1 ratio of packed red cells, fresh frozen plasma, and platelets (with cryoprecipitate as needed to maintain a serum fibrinogen of >150–200 mg/dL). In cases that require prolonged cardiopulmonary resuscitation or, after arrest, severe ventricular dysfunction refractory to medical management, consideration for venoarterial extracorporeal membrane oxygenation should be given.
Amniotic fluid embolism (AFE) is a rare and potentially lethal complication of pregnancy, with a reported frequency of 1.9–6.1 per 100,000 births and a mortality rate as high as 60%. Similar to other uncommon medical diseases, few clinicians will ever have extensive experience with this condition, because most will never even witness an episode of AFE. Because AFE may sometimes mimic other obstetric conditions, specific criteria have been proposed and validated for the research reporting of AFE cases. Such criteria facilitate the collection of case series for research purposes that are uncontaminated by the inclusion of unrelated conditions that have been classified mistakenly as AFE but exclude a small number of atypical cases of this condition. Unfortunately, AFE remains an unpredictable event; as such, no prophylactic intervention has been or will be (in the near future) effective at preventing it.
The syndrome of AFE is believed to represent a pathologic maternal response to the introduction of foreign antigenic material of fetal or infectious origin to the maternal central circulation and appears to involve the release of endogenous inflammatory mediators with secondary effects of cardiovascular and pulmonary function and activation of the clotting cascade. Early management that targets various evolving pathophysiologic phases that have been described in cases of AFE may provide the best chance at improved maternal and fetal outcomes. Although no data exist to document improved survival of such women with any specific treatment regimen, we describe here 1 organized, logical approach to the initial acute management of AFE that is recommended by the authors who have extensive experience in critical care obstetrics.
Cardiac arrest
Because AFE often presents with cardiac arrest, the initial immediate response should be to provide high-quality cardiopulmonary resuscitation (CPR). Without delay, chest compressions should be started, with the heel of the hand placed in the lower half of the sternum and a compression depth of 5 cm. Compared with nonpregnant individuals, no difference exists in the technique to provide chest compressions. If no airway is in place, the compression rate should be 30:2 (30 compressions with 2 ventilations provided with the use of a bag mask device). If an airway is in place (endotracheal tube or a supraglottic airway device), the clinician should provide 100–120 compressions/minute and 1 ventilation every 6 seconds (10/minute). Ventilations should not be vigorous, and the minimal amount of air needed to cause a rise in the chest wall should be used. Excessive ventilation leads to air trapping, increased intrathoracic pressure, decreased preload, and increased afterload, with a consequent reduction in cardiac output.
At all times, manual left-lateral displacement of the uterus should be provided when the uterus is palpated at or above the umbilicus to avoid inferior vena cava compression. Defibrillator pads should be placed as soon as possible (without interrupting compressions). If the rhythm is shockable (ventricular fibrillation or pulseless ventricular tachycardia), a nonsynchronized shock (120–200 Joules for biphasic defibrillators and 360 for monophasic) should be delivered, followed immediately by 2 minutes of CPR. After 2 minutes of CPR, a short pause of <10 seconds should be used to check for a pulse, analyze the current rhythm, and switch providers so that no one person gives compressions for >2 minutes because fatigue is inevitable. If after this pause a shockable rhythm is still present, a second shock is indicated, and the previous described sequence is followed again. If no intravenous access is available, early placement of an intraosseous line should be accomplished in the humeral head ideally (if placed in the tibia in patients with pelvic bleeding, administered products may not reach the central circulation). Placement of an intraosseous line is a straightforward and potentially life-saving intervention that provides a noncollapsible access point into the venous system. Interosseous drug administration appears to be superior to intramuscular but similar to intravenous administration of these agents. Several automatic intraosseous devices are available to facilitate access for fluid and medication administration.
If the rhythm persists after 2 shocks, epinephrine 1 mg intravenously or intraosseously every 3–5 minutes is started. If 3 shocks are required, amiodarone 300 mg intravenously is indicated, as the first-line antiarrhythmic therapy for refractory ventricular tachycardia or fibrillation.
If the initial rhythm is not shockable (asystole or pulseless electrical activity), CPR is started, and epinephrine is given 1 mg intravenously/intraosseously every 3–5 minutes. At all times, clinicians should think about reversible causes, such as hypovolemia, hypoxemia, hypothermia, acidosis, hyperkalemia, cardiac tamponade, tension pneumothorax, myocardial infarction, and pulmonary embolism. Because most AFE cases occur during the third trimester of pregnancy, once cardiac arrest is diagnosed, immediate preparations for delivery should be made either by operative vaginal delivery, if indicated, or perimortem cesarean delivery if no return of spontaneous circulation is achieved within a few minutes (classically 4 minutes, but, depending on the clinical scenario, this operation may be undertaken earlier). We recommend consideration for perimortem cesarean delivery during cardiac arrest when the fetus has reached a point of potential extra uterine survival (23 weeks gestation). If the gestational age is unknown, such intervention may be indicated if the uterus is palpated above the umbilicus. During the periviable period, the decision to perform a perimortem cesarean is driven mainly by maternal indications rather than expected survival of the neonate.
Assessment and management of pulmonary hypertension and cardiac failure
Once spontaneous circulation returns, many AFE survivors will have an acute phase characterized by right ventricular failure (acute cor pulmonale) because of a sudden increase in pulmonary vascular resistance that is induced by systemic vasoconstrictors, such as endothelin-1. Early identification and management of acute right ventricular failure is fundamental.
Where available, we recommend performing a transthoracic echocardiography (TTE) as soon as possible because it is an easy and reliable method of the identification of a failing right ventricle ( Figure 1 ). Transesophageal echocardiography would be a potential alternative, but it requires more training for appropriate use. If such failure is identified, management tailored at improving right ventricular performance should be initiated. Ventilator management should be adjusted to always avoid hypoxemia and/or hypercarbia with acidemia because any of the latter usually leads to further pulmonary vasoconstriction, aggravating the already compromised function of the right ventricle. Excessive fluid administration should be avoided because fluid overload will result in further right ventricular dilation (because the ventricle cannot empty because of the acute increase in pulmonary vascular resistances) with left-sided displacement of the interventricular septum, which leads to compression of the left ventricle and a decrease in cardiac output. Similarly, distention of the right ventricular free wall against the pericardium results in coronary compression and right ventricular ischemia with further right ventricular failure. Rather than relying on fluid therapy, blood pressure should be maintained with the use of norepinephrine (0.05–3.3 μg/kg/min). Simultaneously, inotropic support to improve right ventricular contractility should be provided with the use of either dobutamine and/or milrinone, a potent selective inhibitor of phosphodiesterase 3, an enzyme that degrades cyclic adenosine monophosphate. The latter 2 agents provide the additional benefit of dilation of the pulmonary vasculature with a beneficial reduction in right ventricular afterload.
