Previously known as toxemia of pregnancy, pregnancy-induced hypertension is a potentially life-threatening disorder. It usually develops late in the second trimester or in the third trimester. Clinical manifestations of PIH include rapid weight gain, edema, high blood pressure, excretion of albumin in the urine, and convulsions.
PIH complicates about 5% of pregnancies and is among the leading causes of maternal deaths, prenatal deaths, and low birth-weight infants. It is categorized into two classifications:
1. Pre-eclampsia is the non-convulsive form of toxemia. It develops in about 7% of pregnancies and can either be mild or severe. It is characterized by hypertension with proteinuria (excretion of protein in the urine) and/or edema.
2. Eclampsia is the convulsive form of toxemia. About 5% of females with pre-eclampsia develop eclampsia. Of these, about 15% die from toxemia itself or its complications. This condition is characterized by convulsions or coma, both are usually associated with hypertension, proteinuria, and edema.
An unusually high incidence of pre-eclampsia seems to exist among socio-economically deprived groups. Epidemiologists interpret this as meaning that the high incidence is related more to the degree of nutritional deficiencies than to any other environmental factors. In fact, several studies have indicated that calcium and magnesium deficiency may play a role in the development of pre-eclampsia.
Therapy for pre-eclampsia is designed to halt the disorders progress, specifically the early effects of eclampsia such as convulsions, 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 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 the patient’s blood pressure fails to respond to bed rest and sedation and persistently rises above 160/110 mmHg, or if CNS (central nervous system) irritability increases, magnesium sulfate may produce general sedation, promote diuresis, reduce blood pressure, and prevent convulsions. If these measures fail to improve the patient’s condition, or if fetal life is endangered (as determined by stress or non-stress tests), cesarean section or oxytocin induction may be required to terminate the pregnancy.
Emergency treatment of eclamptic convulsions consists of immediate administration of Diazepam IV, followed by magnesium sulfate via IV drip, oxygen administration, and electronic fetal monitoring. After the patient’s condition stabilizes, a cesarean section may be performed.
Adequate nutrition, good prenatal care, and control of preexisting hypertension during pregnancy decrease the incidence and severity of pre-eclampsia.