Hypertension, pregnancy-induced
Hypertension, pregnancy-induced: Excerpt from Handbook of Diseases
Toxemia of pregnancy, or pregnancy-induced hypertension (PIH), usually develops late in the second trimester or in the third trimester. Preeclampsia, the nonconvulsive form of toxemia, develops in about 7% of pregnancies. It may be mild or severe, and the incidence is significantly higher in low socioeconomic groups.
Eclampsia is the convulsive form of toxemia. About 5% of women with preeclampsia develop eclampsia; of these, about 15% die of toxemia itself or its complications. Fetal mortality is high because of the increased incidence of premature delivery.
Causes
The cause of PIH is unknown, but it appears to be related to inadequate prenatal care (especially poor nutrition), parity (more prevalent in primigravidas), multiple pregnancies, preexisting diabetes mellitus, and hypertension.
Age is also a factor. Adolescents and primiparas over age 35 are at higher risk for preeclampsia. Other theories postulate a long list of potential toxic sources, such as autolysis of placental infarcts, autointoxication, uremia, maternal sensitization to total proteins, and pyelonephritis.
Signs and symptoms
❑ Mild preeclampsia generally produces the following signs: hypertension, proteinuria, generalized edema, and a sudden weight gain of more than 3 lb (1.4 kg) a 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, which eventually lead to the development of oliguria. Hemolysis, elevated liver enzyme levels, and a low platelet count (the HELLP syndrome) is commonly severe.
Clinical tip A daughter whose mother had toxemia is at high risk for developing HELLP syndrome with a new pregnancy.
Other symptoms that indicate worsening preeclampsia include blurred vision due to retinal arteriolar spasms, epigastric pain or heartburn, irritability, emotional tension, and severe frontal headache.
❑ In eclampsia, all the clinical manifestations of preeclampsia are magnified and associated with seizures and possibly coma, premature labor, stillbirth, renal failure, and liver damage.
Diagnosis
The following findings suggest mild preeclampsia:
❑ elevated blood pressure readings — 140 mm Hg systolic or a rise of 30 mm Hg or more above the patient’s normal systolic pressure measured on two occasions, 6 hours apart; 90 mm Hg diastolic or a rise of 15 mm Hg or more above the patient’s normal diastolic pressure measured on two occasions, 6 hours apart
❑ proteinuria — greater than 500 mg/24 hours.
The following findings suggest severe preeclampsia:
❑ much higher blood pressure readings — 160/110 mm Hg or higher on two occasions, 6 hours apart, while on bed rest
❑ increased proteinuria — 5 g or more/24 hours
❑ oliguria — urine output less than or equal to 400 ml/24 hours
❑ deep tendon reflexes — possibly hyperactive as central nervous system (CNS) irritability increases.
Typical clinical features — especially seizures — with typical findings for severe preeclampsia strongly suggest eclampsia. An ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.
Real-time ultrasonography and stress and nonstress tests evaluate fetal well-being. 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.
Treatment
Adequate nutrition, good prenatal care, and control of preexisting hypertension with hydralazine during pregnancy decrease the incidence and severity of preeclampsia. Early recognition and prompt treatment of preeclampsia can prevent progression to eclampsia.
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.
Conservative measures
Therapy may include sedatives, such as phenobarbital, along with complete bed rest to relieve anxiety, reduce hypertension, and evaluate response to therapy. If renal function remains adequate, a high-protein, low-sodium, low-carbohydrate diet with increased fluid intake is recommended.
If blood pressure fails to respond to bed rest and sedation and persistently rises above 160/100 mm Hg or if CNS irritability increases, magnesium sulfate may produce general sedation, promote diuresis, reduce blood pressure, and prevent seizures.
Cesarean delivery
If these measures fail to improve the patient’s condition or if fetal life is endangered (as determined by stress or nonstress tests), cesarean delivery or oxytocin induction may be required to terminate the pregnancy.
Treatment for seizures
Emergency treatment of eclamptic seizures consists of immediate administration of I.V. diazepam, followed by magnesium sulfate (I.V. drip), oxygen administration, and electronic fetal monitoring. After the patient’s condition stabilizes, a cesarean delivery may be performed.
Special considerations
❑ Monitor regularly for changes in blood pressure, pulse and respiratory rates, fetal heart tones, vision, level of consciousness, and deep tendon reflexes and for headache unrelieved by medication. 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 distress 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 (including diazepam and magnesium sulfate) available in case of seizures and cardiac or respiratory arrest. Also keep calcium gluconate at the bedside because it counteracts the toxic effects of magnesium sulfate.
❑ To protect the patient from injury, maintain seizure precautions. Don’t leave an unstable patient unattended.
❑ Give emergency treatment to the patient having seizures. Provide a quiet, darkened room until the patient’s condition stabilizes, and enforce absolute bed rest. Carefully monitor administration of magnesium sulfate; give oxygen. Don’t administer anything by mouth. Insert an indwelling urinary catheter for accurate measurement of intake and output.
❑ Provide emotional support for the patient and family.
Clinical tip If the patient’s condition necessitates premature delivery, point out that neonates of mothers with toxemia are usually small for gestational age but sometimes fare better than other premature babies of the same weight, possibly because they’ve developed adaptive responses to stress in utero.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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