Pregnancy-induced hypertension
Pregnancy-induced hypertension: Excerpt from Professional Guide to Diseases (Eighth Edition)
Pregnancy-induced hypertension (PIH), also known as gestational hypertension, is a potentially life-threatening disorder that usually develops late in the second trimester or in the third trimester. Preeclampsia, the nonconvulsive form of PIH, may be mild or severe. Eclampsia is the convulsive form of PIH.
Causes and incidence
The cause of pregnancy-induced hypertension is unknown, but geographic, ethnic, racial, nutritional, immunologic, and familial factors and pre-existing vascular disease may contribute to its development. Age is also a factor. Primiparas who are older than age 35 are at higher risk for preeclampsia.
Preeclampsia develops in about 7% of pregnancies. Incidence is significantly higher in low socioeconomic groups. About 5% of females with preeclampsia develop eclampsia; of these, about 15% die from PIH itself or its complications. Fetal mortality is high due to the increased incidence of premature delivery and uteroplacental insufficiency.
Signs and symptoms
Mild preeclampsia generally produces the following clinical effects: hypertension, proteinuria (less than 5 g/24 hours), generalized edema, and sudden weight gain of more than 3 lb (1.4 kg) per week during the second trimester or more than 1 lb (0.5 kg) a week during the third trimester.
Severe preeclampsia is marked by increased hypertension and proteinuria, eventually leading to the development of oliguria. Hemolysis, elevated liver enzymes, and low platelets (the HELLP syndrome) is a severe variant. Other symptoms that may indicate worsening preeclampsia include blurred vision due to retinal arteriolar spasms, epigastric pain or heartburn, and severe frontal headache.
In eclampsia, all the clinical manifestations of preeclampsia are magnified and are associated with seizures and, possibly, coma, premature labor, stillbirth, renal failure, and hepatic damage.
Diagnosis
The following findings suggest preeclampsia:
❑ elevated blood pressure readings: 140 systolic, measured on two occasions, 6 hours apart; 90 diastolic, measured on two occasions, 6 hours apart
❑ proteinuria: at least 300 mg/24 hours.
The following findings suggest severe preeclampsia:
❑ higher blood pressure readings: 160/110 mm Hg or higher on two occasions, 6 hours apart, on bed rest
❑ increased proteinuria: 5 g/24 hours or more
❑ presence of pulmonary edema
❑ ultrasound: may reveal oligohydraminos
❑ oliguria: urine output less than or equal to 400 ml/24 hours.
Seizures strongly suggest eclampsia. Rarely, ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.
Real-time ultrasonography, stress and nonstress tests, and biophysical profiles evaluate fetal status. In the stress test, oxytocin stimulates contractions; fetal heart tones are then monitored electronically. In the nonstress test, fetal heart tones are monitored electronically during periods of fetal activity, without oxytocin stimulation. Electronic monitoring reveals stable or increased fetal heart tones during periods of fetal activity.
Ultrasonography aids evaluation of fetal health by assessing fetal breathing movements, gross body movements, fetal tone, reactive fetal heart rate, and qualitative amniotic fluid volume.
Treatment
Therapy for preeclampsia is designed to halt the disorder’s progress — specifically, the early effects of eclampsia, such as seizures, residual hypertension, and renal shutdown — and to ensure fetal survival. Some physicians advocate the prompt induction of labor, especially if the patient is near term; others follow a more conservative approach. Therapy may include complete bed rest to increase placental perfusion, reduce hypertension, and evaluate response to therapy. Antihypertensive therapy doesn’t alter the potential for developing eclampsia. Diuretics aren’t appropriate during pregnancy.
If the patient’s blood pressure fails to respond to bed rest and sedation and persistently rises above 160/100 mm Hg, or if central nervous system irritability increases, magnesium sulfate may produce general sedation, promote diuresis, and prevent seizures. Cesarean birth or oxytocin induction 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 seizures subside and the patient’s condition stabilizes, delivery should proceed with induction of labor or cesarean birth, depending upon the circumstances.
Adequate nutrition, good prenatal care, and control of pre-existing hypertension during pregnancy decrease the incidence and severity of preeclampsia. Early recognition and prompt treatment of preeclampsia can prevent progression to eclampsia.
Special considerations
❑ Monitor regularly for changes in blood pressure, pulse rate, respiration, fetal heart tones, vision, level of consciousness, and deep tendon reflexes and for headache unrelieved by medication. Report changes immediately. Assess these signs before administering medications. Absence of patellar reflexes may indicate magnesium sulfate toxicity.
❑ Assess fluid balance by measuring intake and output and by checking daily weight.
❑ Observe for signs of fetal hypoxemia by closely monitoring the results of stress and nonstress tests.
❑ Instruct the patient to lie in a left lateral position to increase venous return, cardiac output, and renal blood flow.
❑ Keep emergency resuscitative equipment and drugs available in case of seizures and cardiac or respiratory arrest. Also keep calcium gluconate at the bedside because it counteracts magnesium sulfate’s toxic effects.
❑ To protect the patient from injury, maintain seizure precautions. Don’t leave an unstable patient unattended.
❑ Assist with emergency medical treatment for the convulsive patient. Provide a quiet, darkened room until the patient’s condition stabilizes, and enforce absolute bed rest. Carefully monitor administration of magnesium sulfate; give oxygen as ordered. Don’t administer anything by mouth. Insert an indwelling urinary catheter for accurate measurement of intake and output.
❑ Inform the patient about the tests that are done to evaluate fetal status. The baby’s welfare is of prime concern to the parents.
❑ Provide emotional support for the patient and her family. If the patient’s condition necessitates premature delivery, point out that infants of mothers with PIH are usually small for gestational age but sometimes fare better than other premature babies of the same weight, possibly because they have developed adaptive responses to stress in utero.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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