Adult respiratory distress syndrome in pregnancy William C. Mabie, MD,John R. Barton, MD, and Baha M. Sibai, MD Memphis, Tennessee OBJECTIVE: Our objective was to determine the causes of adult respiratory distress syndrome in pregnancy, the treatment required, and maternal and perinatal outcomes. STUDY DESIGN: We examined a case series of 16 patients with adult respiratory distress syndrome initially treated in an obstetric intensive care unit. Criteria for the diagnosis were respiratory distress requiring mechanical ventilation and a lung injury score >2.5. RESULTS: The incidence of adult respiratory distress syndrome in pregnancy was 1 per 2893 deliveries, occurring primarily in the third trimester. The causes were infection (n = 8), preeclampsia/eclampsia (n = 4), hemorrhage (n = 2), thrombotic thrombocytopenic purpura (n = 1), and smoke inhalation (n = 1). Most patients (69%) were delivered before or soon after admission to our hospital. Multiple organ failure developed in 12 patients (75%). Complications of mechanical ventilation occurred in 81% of cases. Other complications of intensive care unit support were endocarditis, superior vena cava thrombosis, line sepsis, and bacteremia. Maternal mortality was 44%; perinatal mortality was 20%. CONCLUSIONS: Adult respiratory distress syndrome in pregnancy is associated with a maternal mortality similar to that of studies in the nonpregnant patient. The main causes in pregnancy are hemorrhage, infection, and toxemia. All maternal deaths occurred in patients with multiorgan failure. (AM J OBSTET GVNECOL 1992;167:950-7.)

Key words: Adult respiratory distress syndrome, pregnancy The adult respiratory distress syndrome (ARDS) is an acute lung injury that results in diffuse bilateral radiographic infiltrates, marked intrapulmonary shunting, and decreased lung compliance. The lung can respond in only a limited number of ways to injury. Therefore the causes of ARDS are many. The clinical course is variable, ranging from rapid reversal in a few days (e.g., fat embolism, drug reaction) to delayed reversal requiring weeks of mechanical ventilation (e.g., sepsis with multiple organ failure). Pathologic changes progress from an exudative phase characterized by type 1 cell destruction, atelectasis, neutrophil infiltration (days 0 to 4) to a proliferative phase with type II cell proliferation, hyaline membranes, capillary loss, and mononuclear cell infiltration (days 3 to 10) to a late phase with capillary loss and fibrosis (days 7 to 14).'·3 Overall mortality is 50% to 70%.