Amniotic fluid embolism (AFE), a rare, often rapidly fatal complication of labor and delivery, occurs when fetal amniotic fluid enters the maternal circulation [1]. The hypothesized pathophysiology cites an anaphylactoid reaction to fetal antigens leading to a massive cytokine storm. The ensuing release of vasoactive and procoagulant mediators causes pulmonary hypertension, systemic hypotension, and subsequent cardiovascular collapse [1]. In developed countries, AFE comprises half of maternal deaths occurring in the first hour of delivery and 10% of all peri-partum maternal deaths [2],[3]. Successful treatment requires rapid recognition and intervention [1],[2],[3],[4]. Protocols for AFE management remain poorly studied. The A-OK protocol consists of atropine, ondansetron, and ketorolac [5], while the American Heart Association Advanced Cardiac Life Support (ACLS) protocols would employ epinephrine and hydrocortisone for circulatory support [6].

This report demonstrates how a novel combination of the A-OK protocol [5] and the ACLS pulseless electrical activity protocol [6], modified to avoid positive end-expiratory pressure (PEEP), can prevent the need for intubation and subsequent institution of extracorporeal membrane oxygenation (ECMO).

Written Health Insurance Portability and Accountability Act authorization has been obtained from the patient.

A 34-year-old G2P1 woman at 38 weeks gestation with twins underwent a planned, primary cesarean section due to breech-transverse presentation. The placentas were noted to be anterior. Following an adequate block with combined spinal–epidural anesthesia, the surgeons made a low transverse hysterotomy, delivering twin A in breech position and twin B in cephalic after internal version. Suddenly after delivery of twin A, the mother lost consciousness; her blood pressure (BP) decreased to 49/22 mmHg and oxygen saturation (SpO₂) to 60% (Table 1).

Suspecting either an air embolism or AFE, caregivers administered 0.3 mg IV epinephrine, resulting in a transient increase in BP to 187/117 mmHg. She then received IV hydrocortisone 100 mg, diphenhydramine 50 mg, and IV ondansetron 4 mg. The patient’s BP decreased to 84/52 mmHg (Table 1), necessitating a second dose of 0.3 mg IV epinephrine that yielded a peak BP of 221/132 mmHg. The BP remained above 140/80 mmHg thereafter. SpO₂ returned to 100% within 2–3 minutes of diagnosis, without intubation. The patient received only gentle mask ventilation without increased PEEP. Her immediate post-operative course included IV 30 mg ketorolac.

Placement of a radial arterial catheter 20 minutes after initial hypotension, and soon after circulatory stabilization, provided an arterial blood sample with the following values: pH 7.44, PCO₂ 31 mmHg, PO₂ 330 mmHg (15 L/min face mask oxygen), bicarbonate 21.1 mEq/L, base deficit 2.4 mEq/L, lactate 1.1 mEq/L, glucose 71 mg/dL, sodium 136 mEq/L, potassium 3.3 mEq/L, ionized calcium 0.98 mEq/L, hemoglobin 100 g/L, activated partial thromboplastin time 29 seconds, prothrombin time 13.7 seconds, international ionized ratio 1.1, and fibrinogen 354 mg/dL.

Amniotic fluid embolism is a catastrophic complication of delivery; its pathogenesis remains poorly understood. Initially, pulmonary congestion occurs, presumably from pulmonary vascular obstruction with contributions from cytokine-mediated pulmonary vasoconstriction, erythrocyte aggregation, and compression of the pulmonary vasculature [3],[7]. Cardiogenic shock and consumptive coagulopathy may follow. The initial pulmonary hypertension causes severe ventilation/perfusion mismatching and hypoxemia [7]. Damage to the endothelial-alveolar membrane and capillary leak result in pulmonary edema [7]. Circulatory collapse, hypoxemia, and sudden loss of consciousness, occurring in the reported case immediately following delivery of twin A, strongly suggested AFE.

Current treatment paradigms include chest compressions, intubation, positive pressure ventilation with PEEP, fluids, vasopressors, and ultimately ECMO. The sequence of actions presented in this report avoids positive pressure ventilation, PEEP, and fluid resuscitation to minimize compression of the pulmonary vasculature. Rather, this approach treats AFE as pulseless electrical activity, using epinephrine to increase peripheral resistance and decrease pulmonary resistance. This mitigates pulmonary edema and congestion and avoids increasing pulmonary vascular obstruction (Figure 1). Both hydrocortisone and ketorolac decrease thromboxane activity to minimize cytokine storm and platelet dysfunction [8]. The blockade of serotonin receptors from ondansetron helps to relieve pulmonary hypertension. This protocol omits atropine since epinephrine sufficiently increases heart rate.

The reported case demonstrates successful resuscitation from AFE using epinephrine, hydrocortisone, ondansetron, and diphenhydramine. This combination includes appropriate ACLS approaches, eliminating the potentially harmful aspects of intubation and PEEP on pulmonary vascular resistance, and avoiding ECMO. Additional evaluation is needed to determine its effectiveness in treating AFE.