B52-48 Beyond the Golden Hour: When Emboli Lay Waiting

Abstract Amniotic fluid embolism (AFE) is a rare, life-threatening obstetric emergency that typically occurs during labor, cesarean section, or immediately afterward. Population studies suggest higher incidence with cesarean delivery than with vaginal birth. It usually develops within minutes postpartum, with the longest previously reported delay of approximately four hours. The condition is thought to result from amniotic fluid or fetal debris entering maternal circulation, triggering acute respiratory distress, cardiovascular collapse, coagulopathy, and multiorgan dysfunction. Typical symptoms include sudden onset dyspnea, hypoxemia, hypotension, chest pain, arrhythmia, and pulmonary hypertension. We report the first known case of delayed AFE presenting 36 hours after an otherwise uncomplicated cesarean delivery. 36-year-old woman with no prior medical history of smoking, lung disease, or allergies underwent a routine cesarean section without complications. She remained stable postoperatively on room air. At 36 hours post-procedure, she developed sudden diffuse chest pain, myalgia, hypotension, tachycardia, and hypoxemia requiring high-flow nasal cannula. Laboratory evaluation showed D-dimer of 13 μg/mL. CT abdomen and pelvis demonstrated mild free fluid and blood products but no active hemorrhage, while CT chest angiography excluded pulmonary embolism. Echocardiography showed a left ventricular ejection fraction of 50 % and right ventricular systolic pressure of 34 mm Hg. She was treated with high-flow oxygen, heparin infusion, and patient-controlled hydromorphone. After delayed AFE was suspected, she continued supportive care until recovery. She was discharged on 1 L/min supplemental oxygen and instructed to receive intravenous iron therapy for acute blood loss anemia. AFE remains a clinical diagnosis, as no definitive imaging or biomarker exists. CT angiography is essential to rule out pulmonary embolism, while laboratory abnormalities may reflect hemodynamic compromise and coagulopathy. In this case, imaging excluded alternative causes, while labs pointed to hemoconcentration and cardiac strain. Pathophysiology suggests amniotic fluid breaching the maternal-fetal interface, leading to pulmonary vasospasm, inflammation, and impaired gas exchange. Management is supportive, including oxygen therapy or mechanical ventilation, fluid resuscitation, vasopressors, correction of coagulopathy, and analgesia. Delayed AFE, as in this patient, is virtually absent from literature and often not considered in the initial diagnosis, which can delay recognition and treatment. This case represents the first reported instance of AFE occurring more than 24 hours postpartum. Clinicians should recognize that AFE can manifest well beyond the expected timeframe and maintain suspicion in postpartum patients with sudden cardiopulmonary decompensation. Early recognition and rapid supportive care remain critical to prevent maternal morbidity and mortality. This abstract is funded by: None