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Home :: Pregnancy Induced Hypertension

Pregnancy Induced Hypertension

Alternative names :- Toxemia, Preeclampsia

Pregnancy-induced hypertension (PIH), also known - although incorrectly - as toxemia of pregnancy, is a potentially life-threatening disorder that usually develops late in the second trimester or in the third trimester. Preeclampsia, the non convulsive form of PIH, develops in about 7% of pregnancies. Preeclampsia may be mild or severe, and the incidence is significantly higher in low socioeconomic groups. Eclampsia is the convulsive form of PIH. About 5 % of females with preeclampsia develop eclampsia; of these, about 15 % die from PIH itself or its complications. I Fetal mortality is high due to the increased incidence of premature delivery and uteroplacental insufficiency.

Causes of Pregnancy Induced Hypertension

The cause of PIH is unknown; however, geographic, ethnic, racial, nutritional, inmtunologic, and familial factors as well as preexisting cardiovascular disease (such as diabetes mellitus, hypertension, and hyperlipidemia) may contribute to its development. Age is also a risk factor for PIH. Printiparas over age 35 and those women with large placentas from multiple pregnancies are at higher risk for preeclampsia.

Signs and symptoms of Pregnancy Induced Hypertension

Mild preeclampsia generally produces:

  • hypertension
  • proteinuria (less than 5 g/24 hours)
  • generalized edema
  • sudden weight gain of more than 3 lb (1.4 kg) per week during the 2nd trimester or more than 1Ib (0.5 kg) per week during the third trimester.

Severe preeclampsia is marked by increased hypertension and proteinuria, eventually leading to the devel. opment of oliguria. HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) is a severe variant of preeclampsia. 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 of Pregnancy Induced Hypertension includes:

The following findings suggest mild preeclampsia:

  • elevated blood pressure reading 140 systolic, or a rise of 30 mm Hg or greater above the patient's normal systolic pressure, measured on two occasions, 6 hours apart; 90 diastolic, or a rise of 15 mm Hg or greater above the patient's normal diastolic pressure, measured on two occasions, 6 hours apart
  • proteinuria - more than 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
  • 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. 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 is administered to stimulate contractions and then fetal heart tones are monitored electronically. In the non stress 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.

Pregnancy Induced Hypertension 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 ensure fetal survival. Some physicians advocate the prompt induction of labor, especially if the patient is near term; others may take a more conservative approach. Therapy may include anticonvulsants (such as magnesium sulfate), along with complete bed rest, to relieve anxiety, 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 CNS 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., oxygen administration, and continuous electronic fetal monitoring. After the seizures subside and the patient's condition stabilizes, delivery should proceed with induction of labor or cesarean birth, depending on the circumstances.

Pregnancy Induced Hypertension Complications

Pregnancy induced hypertension may develop into eclampsia , the occurrence of seizures. Fetal complications may occur because of prematurity at time of delivery.

Special considerations

  • Monitor the patient regularly for changes in blood pressure, pulse rate, respiration, fetal heart tones, vision, level of consciousness, 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 hypoxentia by closely monitoring the results of stress and non stress 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 readily available 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.
  • 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 and 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 tests that evaluate fetal status because the baby's welfare is of prime concern.
  • Provide emotional support for the patient and 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.

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