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/pre·eclamp·sia/ (pre″e-klamp´se-ah) a toxemia of late pregnancy, characterized by hypertension, proteinuria, and edema.


A disorder occurring during late pregnancy or immediately following parturition, characterized by hypertension, edema, and proteinuria. Also called toxemia of pregnancy.

pre′e·clamp′tic (-tĭk) adj.


Also called toxemia, preeclampsia is a condition during pregnancy that results in high blood pressure, swelling that doesn't go away and large amounts of protein in the urine. Without treatment, it can progress to a dangerous condition called eclampsia, in which a woman goes into convulsions.


Etymology: L, prae + Gk, ek, out, lampein, to flash
an abnormal condition of pregnancy characterized by the onset of acute hypertension after the 24th week of gestation. The classic triad of preeclampsia is hypertension, proteinuria, and edema. The cause of the disease remains unknown despite 100 years of research by thousands of investigators. It occurs in 5% to 7% of pregnancies, most often in primigravidas, and is more common in some areas of the world than others. The incidence is particularly high in the southeastern part of the United States. The incidence increases with increasing gestational age, and it is more common in cases of multiple gestation, hydatidiform mole, or hydramnios. A typical lesion in the kidneys, glomeruloendotheliosis, is pathognomonic. Termination of the pregnancy results in resolution of the signs and symptoms of the disease and in healing of the renal lesion. Preeclampsia is classified as mild or severe. Mild preeclampsia is diagnosed if one or more of the following signs develop after the 24th week of gestation: systolic blood pressure of 140 mm Hg or more or a rise of 30 mm Hg or more above the woman's usual systolic blood pressure; diastolic blood pressure of 90 mm Hg or more or a rise of 15 mm Hg or more above the woman's usual diastolic blood pressure; proteinuria; and edema. Severe preeclampsia is diagnosed if one or more of the following is present: systolic blood pressure of 160 mm Hg or more or a diastolic blood pressure of 110 mm Hg or more on two occasions 6 hours apart with the woman at bed rest; proteinuria of 5 g or more in 24 hours; oliguria of less than 400 mL in 24 hours; ocular or cerebro vascular disorders; and cyanosis or pulmonary edema. Preeclampsia commonly causes abnormal metabolic function, including negative nitrogen balance, increased central nervous system irritability, hyperactive reflexes, compromised renal function, hemoconcentration, and alterations of fluid and electrolyte balance. Complications include premature separation of the placenta, hypofibrinogenemia, hemolysis, cerebral hemorrhage, ophthalmologic damage, pulmonary edema, hepatocellular changes, fetal malnutrition, and lowered birth weight. The most serious complication is eclampsia, which can result in maternal and fetal death. Healthy living conditions, including a diet high in protein, calories, and essential nutritional elements, and rest and exercise are associated with a decreased incidence of preeclampsia. Treatment includes rest, sedation, magnesium sulfate, and antihypertensives. Ultimately, if eclampsia threatens, delivery by induction of labor or cesarean section may be necessary. Formerly called toxemia of pregnancy. See also eclampsia.


a pathologic condition of late pregnancy characterized by edema, proteinuria, and hypertension; it is a precursor to eclampsia if not successfully treated. Called also toxemia of pregnancy and gestosis.
preeclampsia-eclampsia syndrome a group of symptoms associated with late pregnancy and encompassing both nonconvulsive and convulsive stages. Although the condition occurs in only 5 to 7 per cent of all pregnancies in the United States, it is the third most common cause of maternal mortality. Fetal mortality is also high because of the high incidence of premature delivery in these cases.
Etiologic Factors. This condition has sometimes been called toxemia of pregnancy because it was once believed that a toxin produced by the mother in response to a foreign protein from the fetus was responsible for the symptoms. This is not the case, although the cause of the syndrome is not known. Inadequate prenatal care and poor nutrition are suspected as contributing factors because the condition is more common in women who have a history of inadequate dietary intake, especially protein. It is also seen more often in primigravidas under the age of 20 or over 30, and in those who have had 5 or more pregnancies. Women who have a preexisting heart disease, diabetes mellitus with renal or vessel involvements, or essential hypertension are also at high risk for developing symptoms of hypertension, edema, and proteinuria.

Essentially, the pathology responsible for the elevation of blood pressure is spasm of the blood vessels. Normally, the blood vessels of a pregnant woman have a diminished response to the effects of such pressor substances as angiotensin and norepinephrine. In pregnancy-induced hypertension, resistance to vasospasm is somehow comprised and so blood pressure increases. It is not known whether the change in responsiveness to pressors is a cause or a result of vasospasm and elevated blood pressure.
Stages. For purposes of assessment and management, preeclampsia-eclampsia syndrome can be classified according to three stages: mild preeclampsia, severe preeclampsia, and eclampsia.
Mild Preeclampsia. This condition is characterized by a blood pressure reading of 140 mm Hg systolic, or an elevation of 30 mm Hg or more systolic or 15 mm Hg diastolic above the patient's prepregnancy level. The blood pressure readings are taken on two occasions 6 hours apart, with special attention to the diastolic pressure, which reflects peripheral vascular spasm.

Blood pressure can also be evaluated by determining the mean arterial pressure on two occasions at least 6 hours apart. A pregnant patient is considered hypertensive when her mean arterial pressure rises 15 mm Hg from her baseline or is over 100 mm Hg.

Pathologic changes in the glomeruli of the kidney produce proteinuria, oliguria, and edema. Increased permeability of the glomerular membrane allows passage of serum proteins into the urine (proteinuria), diminished glomerular filtration lowers urine output, and increased reabsorption of sodium causes fluid retention and edema and weight gain.

Mild preeclampsia is said to be present when the patient has elevated blood pressure, proteinuria of 1+ or 2+ on a reagent test strip or 500 mg/24 hours or more, swelling in the upper part of her body rather than the usual ankle edema associated with pregnancy, and a weight gain of more than 1 kg (2 pounds) a week in the second trimester and 0.5 kg (1 pound) a week in the third trimester.

Mild preeclampsia is managed by bed rest to facilitate sodium excretion, which takes place more rapidly when the body is at rest. While resting in bed the patient is positioned on her left side to avoid pressure of the uterus against the vena cava and supine hypotension syndrome. Rest is often all that is needed to relieve the symptoms of mild preeclampsia. Some physicians also prescribe a high-protein diet to compensate for the protein lost in the urine and, perhaps, mild restriction of sodium intake. However, restriction of sodium can activate the angiotensin system and cause an undesirable elevation in blood pressure.

Diuretics are not used for control of edema because they can only aggravate the condition by increasing glomerular vessel permeability and stimulating angiotension activity.
Severe Preeclampsia. Preeclampsia becomes severe when systolic blood pressure is over 160 mm Hg or the diastolic pressure is over 110 mm Hg. To help establish the diagnosis two blood pressure readings are taken 6 hours apart after the woman has been on bed rest. Other symptoms are a marked increase in proteinuria, a 24-hour urinary output of 400 ml or less, visual disturbances, and marked hyperreflexia. Hospitalization is recommended to assure adequate rest, provide a quiet, nonstimulating environment, and monitor the progress of the mother and fetus. If more conservative measures fail, magnesium sulfate is given to promote excretion of fluid, reduce blood pressure, and forestall convulsive seizures. In addition to its cathartic properties, magnesium sulfate acts as a central nervous system depressant and therefore reduces the possibility of convulsions. The serum level of magnesium must be kept fairly constant between 4.0 and 7.5 mEq/L to achieve the desired anticonvulsant effect.

While magnesium sulfate is being administered, whether intravenously or intramuscularly, the patient must be monitored at frequent intervals to assess deep tendon reflexes and respiratory rate, which are indicators of its depressant effect. Urine output is measured every 4 hours or more often. If a patient excretes less than 100 ml of urine in four hours, she is likely to have a high level of serum magnesium because this mineral is excreted almost exclusively in the urine. In readiness for magnesium overdosage should it occur, a 10 per cent solution of calcium gluconate, the specific antidote for magnesium toxicity, should be on hand.

Other drugs that may be prescribed include hypotensive drugs to reduce blood pressure and sedatives such as phenobarbital to manage central nervous system irritability. Because of the high fetal and maternal morbidity and mortality associated with pre-eclampsia and eclampsia, the pregnancy is terminated as soon as feasible.
Eclampsia. If the patient's condition continues to deteriorate and edema worsens, she becomes eclamptic. Cerebral edema predisposes her to convulsions and coma. Signs and symptoms that may signal progression to eclampsia include elevated body temperature, sudden rise in blood pressure, gastrointestinal symptoms produced by congestion of portal circulation, and severe headache, blurred vision, and other signs of increased central nervous system irritability. The patient with eclampsia is critically ill. She is kept under constant surveillance, with her vital signs recorded at least every hour. All of the measures presented above for severe preeclampsia are instituted for management of eclampsia. Because of the potential for injury during convulsions, safety measures must be taken and preparations made for the possibility of a seizure. The comatose patient must be given the special care needed by anyone in a coma.

Maternal mortality from eclampsia is distressingly high. The cause of death can be cerebral hemorrhage, circulatory collapse, or renal failure. Mothers who survive eclampsia and the birth of their babies can continue to have hypertension for 10 to 14 days after delivery. Follow-up care is needed to evaluate residual or preexisting hypertension and renal disease and to initiate long-term management as indicated.

Infant mortality also is high when the mother is eclamptic. The status of the fetus is closely monitored before delivery to assure that hypoxia and life-threatening acidosis do not develop. When it is necessary to deliver the infant before term, problems of low birth weight and prematurity must be managed.


Obstetrics A hypertensive disorder occurring in the 3rd trimester in ± 5% of pregnancies Clinical HTN, proteinuria, dependent edema, vasospasm, coagulation defects Treatment Low-dose aspirin ↓ preeclampsia in nulliparas, especially with systolic HTN; aspirin ↑ risk of abruptio placentae, but does not ↓ perinatal mortality. See Eclampsia.


Development of hypertension with proteinuria or edema, or both, due to pregnancy or the influence of a recent pregnancy; it usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.
[pre- + G. eklampsis, a shining forth (eclampsia)]


(PE) (prē'ĕ-klamp'sē-ă)
Development of hypertension with proteinuria or edema, or both, due to pregnancy or the influence of a recent pregnancy; it usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.
[pre- + G. eklampsis, a shining forth (eclampsia)]

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References in periodicals archive ?
Estimation of glomerular filtration rate in preeclamptic patients.
The paradoxical effect of smoking in preeclamptic pregnancies: Smoking reduces the incidence but increases the rates of perinatal mortality, abruptio placentae, and intrauterine growth restriction.
research assistant professor of Obstetrics and Gynecology, demonstrate that elevated secretion of arginine vasopressin (AVP) can be a very early biomarker of a preeclamptic pregnancy.