Preeclampsia: pathophysiology, diagnosis, and management.
Preeclampsia: pathophysiology, diagnosis, and management.
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DOI：
10.1146/annurev.me.40.020189.001313
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发表时间：
1989
影响因子：
10.5
通讯作者：
Marshall D. Lindheimer;A. Katz
中科院分区：
文献类型：
--
作者：
Marshall D. Lindheimer;A. Katz
子痫前期是导致胎儿和产妇发病和死亡的主要原因，在临床上可能难以与其他妊娠高血压疾病区分。有助于诊断的体征包括妊娠后期出现的无孕伴水肿和蛋白尿，以及以下一项或多项：血浓缩、低白蛋白血症、肝功能和/或凝血功能异常、尿酸水平升高。鉴别子痫前期与危险性较低的高血压的有效措施是抗凝血酶III水平降低，血清铁和碳氧血红蛋白升高，尿钙降低。子痫前期的主要病理生理特征是心排血量、肺毛细血管楔压和血浆量减少；外周血管阻力明显增加，内源性血管紧张素II和儿茶酚胺的升压反应加剧。肾血流动力学降低，部分原因是肾小球特征性形态学病变（“内皮增生”），血管通透性增加，导致血管内白蛋白流失。当妊娠晚期，终止妊娠是治疗的选择；当需要延迟时，有几种抗高血压药物，其安全性和有效性已在孕妇中进行了测试。硫酸镁仍然是治疗即将发生的惊厥（该病的子痫期）的首选药物。最后，子痫前期的病因尚不清楚，但一种流行的理论认为，前列腺素代谢的改变可能是导致高血压和凝血功能障碍的原因。在这方面，低剂量阿司匹林的预防性治疗可以减少血小板血栓素的产生，但减少内皮细胞前列环素的释放，可能会降低“高危”人群先兆子痫的发生率。
Preeclampsia, a major cause of fetal and maternal morbidity and mortality, may be difficult to distinguish clinically from other hypertensive disorders of pregnancy. Signs helpful in its diagnosis include presentation during late gestation in a nullipara with edema and proteinuria, and one or more of the following: hemoconcentration, hypoalbuminemia, liver function and/or coagulation abnormalities, and increased urate levels. Measures that may prove useful in differentiating preeclampsia from less dangerous forms of hypertension are decreased antithrombin III levels, increments in serum iron and carboxyhemoglobin, and decreases in urinary calcium. Major pathophysiological features of preeclampsia are decreased cardiac output, pulmonary capillary wedge pressure, and plasma volume; and marked increases in peripheral vascular resistance, as well as exaggerated pressor responses to endogenous angiotensin II and catecholamines. Renal hemodynamics decrease, in part as a result of a characteristic morphological lesion in glomeruli ("endotheliosis"), and there may be increased vascular permeability leading to albumin loss from the intravascular space. When gestation is advanced, termination is the treatment of choice; when temporization is required, several antihypertensive medications whose safety and efficacy have been tested in pregnant women are available. Magnesium sulfate remains the drug of choice for impending convulsions (the eclamptic phase of the disease). Finally, the etiology of preeclampsia remains unknown, but a popular theory suggests that alterations in prostaglandin metabolism may be responsible for the hypertension and coagulopathy in this disorder. In this respect, prophylactic treatment with low doses of aspirin, which decrease platelet thromboxane production but spare endothelial prostacyclin release, may decrease the incidence of preeclampsia in "high-risk" populations.