Mabie W C, Barton J R, Sibai B
Department of Obstetrics and Gynecology, University of Tennessee-Memphis, Memphis, USA.
Obstet Gynecol. 1997 Oct;90(4 Pt 1):553-61. doi: 10.1016/s0029-7844(97)00352-9.
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.
评估妊娠期感染性休克患者的病因、治疗及母婴围产期结局。
18例妊娠期感染性休克患者，诊断标准为脓毒症诱导的低血压，对充分的液体复苏无反应且需要血管升压药。
休克原因包括肾盂肾炎（n = 6）、绒毛膜羊膜炎（n = 3）、产后子宫内膜炎（n = 2）、中毒性休克（n = 2），以及各1例的感染性流产、阑尾破裂、卵巢脓肿破裂、坏死性筋膜炎和细菌性心内膜炎。5名女性（28%）死亡。比较13名幸存者与5名非幸存者的初始实验室数据中位数，发现血细胞比容（26% 对比35%；Z = -2.267，P = .023）、天冬氨酸转氨酶（30对比287 U/L；Z = -2.068，P = .042）、总胆红素（1.6对比5.8 mg/dL；Z = 2.046，P = .045）、动脉二氧化碳分压（30对比19 mmHg；Z = -2.384，P = .013）和动脉氧分压（62对比104 mmHg；Z = -2.004，P = .048）存在显著差异。比较血流动力学数据中位数显示血压（88对比70 mmHg；Z = -2.439，P = .013）、每搏输出量（74对比52 mL；Z = -2.041，P = .038）和左心室每搏功指数（42对比12 g.m.m2；Z = -1.929，P = .052）存在差异。64%的幸存者和80%的非幸存者左心室功能降低（Fisher精确检验，P > .99）。8例患者难以定位且延迟了感染源。
感染性休克女性患者可迅速进展至死亡。由于血管通透性增加，在复苏早期给予血管升压药可能是合适的。初始心输出量低是预后不良的征象。
