HYPERTENSION IN PREGNANCY - DIAGNOSIS, PA THOPHYSIOLOGY AND TREATMENT

This review on hypertension in pregnancy focuses mainly on the pathoph ysiology and prevention of pregnancy induced hypertension which, when associated with proteinuria, is usually called preeclampsia. Rather th an a genuine hypertensive disease, preeclampsia is mainly a systemic e ndothelial disease causing activation of platelets and diffuse ischemi c disorders whose most obvious clinical manifestations involve the kid ney (hence the proteinuria, edema and hyperuricemia), the liver (hence the hemolytic elevated liver enzymes and low platelets, or HELLP synd rome), and the brain (hence eclamptic convulsions). Hypertension is ex plained by increased vascular reactivity rather than by an imbalance b etween vasoconstrictive and vasodilating circulating hormones. This in creased reactivity is due to endothelial dysfunction with imbalance be tween prostacyclin and thromboxane A2 and possibly dysfunction of NO a nd endothelin synthesis. The aggressive substances for endothelium are thought to be of placentar origin and the cause of their release is e xplained by placentar ischemia related to a defect of trophoblastic in vasion of the spiral arteries. The etiology of this latter defect is u nknown but involves immunologic mechanisms with genetic predisposition . The only effective treatment for PIH is extraction of the baby with the whole placenta. The decision for extraction is often a very delica te obstetric problem. Antihypertensive drugs are mainly indicated in s evere hypertension (> 160-100 mm Hg), with the aim of preventing cereb ral hemorrhage in the mother, but have not been shown to improve fetal morbidity or mortality. Eclamptic seizures can be prevented and treat ed more effectively with magnesium sulfate than with diazepam or pheny toin. Prevention of preeclampsia remains the main challenge. Whereas a ntihypertensive drugs are ineffective, calcium supplementation and low dose aspirin have proven effective but mainly in selected populations with a relatively high incidence of preeclampsia (>8-10%) In multipar as the selection of such a high risk population is relatively easy whe n at least 2 (or 1?) previous pregnancies were complicated with early preeclampsia and/or intrauterine growth retardation. In nulliparas the selection of the high-risk population is still a subject of research. The 2 most promising criteria are abnormal Doppler velocimetry of the uterine arteries at around 20 weeks of amenorrhea, and abnormally hig h plasma levels of beta HCG at 17 weeks of amenorrhea.