To evaluate the etiology, management, and maternal and perinatal outcome in patients with septic shock during pregnancy. In 18 patients with septic shock during pregnancy, the criteria for the diagnosis were sepsis-induced hypotension unresponsive to adequate fluid resuscitation and requirement for vasopressors. Causes of shock were pyelonephritis (n = 6), chorioamnionitis (n = 3), postpartum endometritis (n = 2), toxic shock (n = 2), and one each of septic abortion, ruptured appendix, ruptured ovarian abscess, necrotizing fasciitis, and bacterial endocarditis. Five women (28%) died. Comparing medians of the initial laboratory data for the 13 survivors with those of the five nonsurvivors revealed significant differences for hematocrit (26 compared with 35%; Z = −2.267, P = .023), aspartate aminotransferase (30 compared with 287 U/L; Z = −2.068, P = .042), total bilirubin (1.6 compared with 5.8 mg/dL; Z = 2.046, P = .045), arterial carbon dioxide pressure (30 compared with 19 mmHg; Z = −2.384, P = .013), and arterial oxygen pressure (62 compared with 104 mmHg; Z = −2.004, P = .048). Comparing medians of the hemodynamic data showed differences in blood pressure (88 compared with 70 mmHg; Z = −2.439, P = .013), stroke volume (74 compared with 52 mL; Z = −2.041, P = .038), and left ventricular stroke work index (42 compared with 12 g · m · m2; Z = −1.929, P = .052). Sixty-four percent of survivors and 80% of nonsurvivors had depressed left ventricular function (Fisher exact test, P > .99). Locating the source of infection was difficult and delayed in eight patients. In women with septic shock, progression to death can be dramatically rapid. Because vascular permeability is increased, it may be appropriate to administer vasopressors early during resuscitation. An initial low cardiac output is a poor prognostic sign.