(776) Intra-Amniotic Infection Leading to Uterine Ischemia: A Cause of Refractory Shock

Introduction: Intraamniotic infection and inflammation is a known cause of maternal morbidity. Several changes in obstetric physiology complicate the care of the septic parturient, including airway edema, reliance of the uterine muscle on increased blood flow, and ease of bacterial transmission across placental vasculature.

Description: A 29 year-old G1 with a history of class III obesity (BMI 64) underwent induction of labor complicated by multiple diarrheal episodes and intraamniotic infection and inflammation. She delivered via cesarean for fetal distress and received antibiotics for chorioamnionitis. She developed septic shock, which was identified 12 hours postoperatively. Upon transfer to an intensive care unit (ICU), antibiotic coverage was broadened. Her vasopressor requirements escalated rapidly in the setting of refractory lactic acidosis. Blood cultures were negative. She developed acute respiratory distress with pulmonary edema. Intubation was unsuccessful due to tracheal obstruction, necessitating emergent cricothyroidotomy. She underwent exploratory laparotomy, which was notable for uterine blanching, concerning for ischemia; a hysterectomy and bilateral salpingectomy were performed. Intra-operative ascites cultures were positive for E. coli. Continuous renal replacement therapy was initiated for acidosis and acute renal failure. Vasopressor support was weaned postoperatively, however escalated the following morning as her hemoglobin dropped from 10 to 4 mg/dL and massive transfusion was initiated. The patient returned to the operating room, where bleeding bilateral ovarian arteries were ligated. Over the next three weeks, she had renal recovery and was discharged home with home health. Uterine pathology was consistent with acute endometritis.

Discussion: Our experience demonstrates a dangerous cycle of prolonged hypotension and intensive vasopressor support leading to uterine ischemia, resulting in significant lactic acidosis and refractory shock in the immediate postpartum period. It is rare to require hysterectomy to resolve postpartum shock in the absence of acute bleeding, necrotizing infection, or bacteremia. This case illustrates the importance of considering uterine ischemia in the setting of refractory lactic acidosis and distributive shock in the postpartum period.