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Pregnancy-Induced Hypertension

Pregnancy-induced hypertension is a potentially life-threatening disorder that usually develops after the 20th week of pregnancy. It most often occurs in nulliparous women and may be nonconvulsive or convulsive.

Preeclampsia, the nonconvulsive form of the disorder, is marked by the onset of hypertension after 20 weeks of gestation. It develops in about 7 % of pregnancies and may be mild or severe. The incidence is significantly higher in low socioeconomic groups.

Eclampsia, the convulsive form, occurs between 24 weeks' gestation and the end of the first postpartum week. The incidence increases among women who are pregnant for the first time, have multiple fetuses, and have a history of vascular disease.

About 5% of women with preeclampsia develop eclampsia; of these, about 15% die of eclampsia or its complications. Fetal mortality is high because of the increased incidence of premature delivery.

Pregnancy-induced hypertension and its complications are the current most common cause of maternal death in developed countries.

Causes

No one understands what is the trigger for the development of this condition. However, it seems to strike most often in first pregnancies and becomes less common with subsequent pregnancies.

Signs and Symptoms

A patient with mild preeclampsia typically reports a sudden weight gain of more than 3 lb (1.4 kg) a week in the second trimester or more than 1 lb (0.5 kg) a week during the third trimester.

The patient's history reveals hypertension, as evidenced by elevated blood pressure readings: 140 mm Hg or more systolic, or an increase of 30 mm Hg or more above the patient's normal systolic pressure, measured on two occasions, 6 hours apart; and 90 mm Hg or more diastolic, or an increase of 15 mm Hg or more above the patient's normal diastolic pressure, measured on two occasions, 6 hours apart.

Inspection reveals generalized edema, especially of the face. Palpation may reveal pitting edema of the legs and feet. Deep tendon reflexes may indicate hyperreflexia.

As preeclampsia worsens, the patient may demonstrate oliguria (urine output of 400 ml/day or less), blurred vision caused by retinal arteriolar spasms, epigastric pain or heartburn, irritability, and emotional tension. She may complain of a severe frontal headache.

In severe preeclampsia, blood pressure readings increase to 160/110 mm Hg or higher on two occasions, 6 hours apart, during bed rest. Also, ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.

Preeclampsia can suddenly progress to eclampsia with the onset of seizures. The patient with eclampsia may appear to cease breathing, then suddenly take a deep, stertorous breath and resume breathing. The patient may then lapse into a coma, lasting a few minutes to several hours. Awakening from the coma, the patient may have no memory of the seizure. Mild eclampsia may involve more than one seizure; severe eclampsia up to 20 seizures.

In eclampsia, physical examination findings are similar to those in preeclampsia but more severe. Systolic blood pressure may increase to 180 mm Hg and even to 200 mm Hg. Inspection may reveal marked edema, but some patients exhibit no visible edema.

Diagnostic tests

Laboratory test findings reveal proteinuria (more than 300 mg/24 hours [1 + ] with preeclampsia, and 5 g/24 hours [5 +] or more with severe eclampsia). Test results may suggest HELLP syndrome.

Ultrasonography, stress and nonstress tests, and biophysical profiles aid evaluation of fetal well-being.

Differential diagnosis is used to distinguish we disorder from viral hepatitis, idiopathic thrombocytopenia, cholecystitis, hemolytic uremic syndrome peptic ulcer, neuroangiopathic syndrome, appendicitis, kidney stones, pyelonephritis, and gastroenteritis.

Treatment

Therapy for patients with preeclampsia is intended to halt the progress of the disorder - specifically, the early effects of eclampsia, such as seizures, residual hypertension, and renal shutdown - and to ensure fetal survival. Some doctors advocate the prompt inducement of labor, especially if the patient is near term; others follow a more conservative approach. Therapy may include:

  • complete bed rest in the preferred left lateral lying position to enhance venous return
  • antihypertensive drugs, such as methyldopa and hydralazine
  • magnesium sulfate to promote diuresis, reduce blood pressure, and prevent seizures if the patient's blood pressure fails to respond to bed rest and antihypertensives and persistently rises above 160/100 mm Hg or if central nervous system irritability increases.

If these measures fail to improve the patient's condition, or if fetal life is endangered (as determined by stress or nonstress tests and biophysical profiles), cesarean section or oxytocin inducement may be required to terminate the pregnancy.

Emergency treatment of eclamptic seizures consists of immediate administration of magnesium sulfate (I.V. drip), oxygen administration, and electronic fetal monitoring. After the patient's condition Stabilizes, cesarean section may be performed.

Adequate nutrition, good prenatal care, and control of preexisting hypertension during pregnancy decrease the incidence and severity of preeclampsia. Early recognition and prompt treatment of preeclampsia can prevent progression to eclampsia.

Prevention

Early identification of women at risk for pregnancy-induced hypertension may help prevent some complications of the disease. Education about the warning symptoms is also important because early recognition may help women receive treatment and prevent worsening of the disease.



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