Hypertensive Disorders of Pregnancy

Published on 10/03/2015 by admin

Filed under Obstetrics & Gynecology

Last modified 10/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 650 times

Chapter 14 Hypertensive Disorders of Pregnancy

The hypertensive disorders of pregnancy are major contributors to maternal and perinatal morbidity and mortality. In the mother, they can cause multiorgan system dysfunction including renal failure, hepatic failure, central nervous system (CNS) hemorrhage and stroke, pulmonary edema, placental abruption and disseminated intravascular coagulation (DIC). Fetal and neonatal complications include growth restriction, prematurity, and perinatal death. The Centers for Disease Control and Prevention (CDC) have reported that preeclampsia/eclampsia is the third leading cause of maternal mortality in the United States, primarily due to CNS hemorrhage. The combined incidence of hypertensive disorders in pregnancy varies depending on the population being studied and on the criteria used but is reported to range from 12% to 22%, whereas the preeclampsia/eclampsia syndrome occurs in about 5% to 8% of pregnancies.

image Classification and Definitions

The general classification of hypertensive disorders recommended by the Working Group Report on High Blood Pressure in Pregnancy (2000) and adopted by the American College of Obstetricians and Gynecologists (ACOG) in 2002 is listed in Box 14-1. Toxemia should not be used because it represents the entire spectrum of hypertensive disorders of pregnancy and may also refer to isolated proteinuria.

Blood pressure readings vary depending on maternal position and the gestational age of the pregnancy. Maternal blood pressure tends to be lower in the left lateral decubitus position and higher in the sitting position. In the supine position, some pregnant women have elevated pressures, whereas others have supine hypotension due to compression of the vena cava by the uterus. In addition to positional variations, arterial blood pressure normally declines during the first and second trimesters of pregnancy and rises to prepregnant levels in the third trimester.

The diagnosis of hypertension should be reserved for patients with a systolic blood pressure of greater than or equal to 140 mm Hg or a diastolic pressure of greater than or equal to 90 mm Hg. Blood pressure measurements should be taken in the sitting position after the woman has rested at least 10 minutes. Arterial pressures may also be taken in the lateral decubitus position, but the measurements should be corrected to the level of the right atrium. In the hospitalized patient, either sitting or lateral decubitus measurements may be used, but consistency is advised. The length of the blood pressure cuff should be at least 1.5 times the circumference of the upper arm, and the fifth Korotkoff sound (disappearance) should be used for determining diastolic pressure.


Preeclampsia is a syndrome unique to pregnancy, characterized by the new onset of hypertension and proteinuria in the latter half of gestation. Preeclampsia is classically considered to be a disease affecting the first pregnancy, but it also occurs in multiparas, especially if there are predisposing risk factors such as twins, diabetes mellitus, chronic hypertension, or a change in husband/partner. When it arises in the early second trimester (14 to 20 weeks), a hydatidiform mole or choriocarcinoma should be considered.

The following two criteria are essential for the diagnosis of preeclampsia: (1) the development of hypertension (systolic blood pressure ≥ 140 mm Hg or diastolic blood pressure ≥ 90 mm Hg), in a woman whose blood pressures were previously normal, after the 20th week of pregnancy; (2) the development of new-onset proteinuria after the 20th week of gestation. Proteinuria is defined as more than or equal to 0.3 g protein in a timed 24-hour urine collection. This usually correlates with a urinalysis report of 30 mg/dL (1+ on dipstick) or greater on a clean-catch urine sample.

In the past, a 30-mm Hg rise in systolic blood pressure or a 15-mm Hg rise in diastolic pressure was considered a sign of preeclampsia. Because of the previously described physiologic rise in blood pressure during the third trimester and the frequent lack of accurate prepregnant blood pressures for use as a baseline, this rise is no longer considered diagnostic if the blood pressure remains under 140/90 mm Hg. Despite this, rising blood pressures should be of concern because they may precede the development of the full preeclampsia syndrome. Similarly, preeclampsia is often preceded by, or associated with, the development of generalized edema. Dependent edema (edema of the lower extremities) is very common in normal pregnancies. Hand and facial edema are more likely to be associated with preeclampsia, but if unaccompanied by hypertension and proteinuria, they are not diagnostic of the preeclampsia syndrome.

Preeclampsia is divided into mild and severe forms, depending on the severity of the hypertension, the amount of proteinuria, and the degree to which other organ systems are affected. Box 14-2 lists specific criteria for the diagnosis of severe preeclampsia. If any of the symptoms, signs, or laboratory abnormalities listed in Box 14-2 is present in a woman with preeclampsia, it is very likely that she has severe disease, which is associated with much greater maternal and perinatal morbidity.

A variant of severe preeclampsia with particularly high morbidity is the HELLP syndrome. This syndrome occurs in preeclamptic women with evidence of hemolysis, elevated liver enzymes, and low platelets (thrombocytopenia). In contrast to more typical presentations of preeclampsia, the patient with HELLP syndrome is more likely to be multiparous, older than 25 years, and at less than 36 weeks’ gestation. Hypertension may be initially absent in 20% of the patients, whereas 30% will have mild elevations in blood pressure, and 50% will have severe elevations.

image Preeclampsia/Eclampsia


Preeclampsia is called a “disease of theories,” because genetic, immunologic, vascular, hormonal, nutritional, and behavioral factors have all been proposed as causes. No single, definitive “cause” has been identified, and the origins of the disease are considered to be multifactorial. Because of the resolution of the preeclampsia after delivery, most attention has been focused on the placenta and the uterine-placental-fetal interface.

Placental ischemia, or hypoxia, appears to be central to the development of the disease and has been attributed to failure of the cytotrophoblasts to adequately invade the uterine spiral arteries and establish the low-resistance uteroplacental circulation characteristic of normal pregnancy. Placental ischemia could also be due to underlying maternal vascular disease such as might occur in chronic hypertension, or to immunologically mediated placental vascular damage (see Chapter 6). Alternatively, ischemia could be caused by increased metabolic demand in the setting of a multiple gestation or a large singleton fetus.

It is postulated that uteroplacental ischemia results in oxidative stress leading to the production and release of toxins that enter the circulation and cause widespread inflammation, endothelial dysfunction, and activation of the coagulation system. The nature of these toxins has not yet been identified but may involve production of reactive oxygen and reactive nitrogen species. This is supported by the observation that preeclampsia is increased in pregnant women with underlying conditions such as obesity and diabetes that are associated with chronic inflammation and dyslipidemia. A hypoxic placenta may also shed microparticles derived from apoptosis of syncytiotrophoblasts, which can then lead to widespread endothelial injury. Antiangiogenic factors have also been shown to cause systemic hypertension, vascular injury, and activation of the coagulation system. Preeclamptic women have an imbalance in angiogenic and antiangiogenic proteins. Circulating levels of the proangiogenic proteins vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) are decreased, whereas levels of the antiangiogenic proteins soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin are markedly increased. In animal models, overexpression of sFlt1 results in a preeclampsia-like syndrome.

Endothelial dysfunction leads to an imbalance between different classes of locally produced vasoconstrictors and vasodilators. Preeclampsia is associated with a disturbance in prostaglandin production, with a decrease in the ratio of the vasodilators prostaglandin E2 (PGE2) and prostacyclin to the vasoconstrictor PGF series and thromboxanes. Endothelial changes also appear to involve a relative deficiency in the production of nitric oxide, a vasodilator and inhibitor of platelet aggregation, along with increased production of endothelin-I. Endothelin-I is an extremely potent vasoconstrictor and activator of platelets. This shift in the production of locally acting vasoactive substances could enhance vasoconstriction in response to circulating pressor hormones.

The net effect of these processes would be widespread vasoconstriction leading to hypoxic and ischemic damage in different vascular beds, systemic hypertension, the HELLP syndrome (see later) or DIC, and worsening placental ischemia. The relative severity of the signs and symptoms of preeclampsia in any given individual would vary on the basis of which specific organ systems were most affected.