Preeclampsia and eclampsia

The exact nature of the primary event causing preeclampsia is not known. However, evidence accumulated in the past 20 years indicates that

¨1abnormal placentation is one of the initial events in this disease.

The main feature of abnormal placentation is inadequate trophoblastic invasion of the maternal spiral arterioles. In normal pregnancy the wall of the spiral arteries is invaded by trophoblastic cells and transformed into large, tortuous channels space and are resistant to the effects of vasomotor agents. These physiologic changes are restricted in patients with preeclampsia with resulting decreased uteroplacental perfusion. The anatomic and physiologic disruption of normal placentation is thought to lead to altered endothelial cell function and multiple organ damage by a mechanism that is unknown at the present time.

The evidence indicating that endothelial cell dysfunction is responsible for the most significant biochemical changes and the wide spectrum of clinical presentations that characterize preeclampsia is increasing rapidly.

Pathophysiology

There are several important pathophysiologic changes in preeclampsia

Hyperdynamic circulation

Recent studies suggest that an increase in maternal cardiac output, rather than increased peripheral vascular resistance, is the most common hemodynamic feature of preeclampsia.

The work of Easterling et al. (1990) demonstrated that cardiac output values significantly higher than those found in normotensive gravidas are a common feature in preeclamptic patients. This elevation in cardiac output is already apparent at 11 weeks and remains in the puerperium despite resolution of the hypertension. These investigators also found that the systemic vascular resistance of preeclamptic patients was always less than that of normotensive patients and remained lower in the postpartum period.

Clark et al. (1989) found that the findings of hyperdynamic left ventricular function and decreased peripheral vascular resistance in preeclampsia may have important consequences in selecting the best approach to the treatment of severe hypertension in these patients. Beta-adrenergic blockers, rather than vasodilators, may be the drugs of choice. Also, these observations open the possibility of screening patients at risk for developing preeclampsia by measuring the cardiac output early in gestation.

Changes in intravascular volume

It is known that the increase in intravascular volume that normally occurs during pregnancy is minimal or completely occurs during pregnancy is minimal or completely absent in patients with preeclampsia. This limited blood volume expansion is probably the result of generalized constriction of the capacitance vessels. However, it is also possible that the decrease in capacitance may be a result rather than the cause of the decreased intravascular volume The reduced volume is predominantly of plasma, and as a result, hemoconcentration results as the disease progresses.

After delivery the plasma volume increases, and the hemoglobin and hematocrit values will decrease.

Postpartum, a significant drop in and hematocrit almost always results from decreased vasospasm, excessive blood loss during delivery, or mobilization of extracellular fluids or from a combination of all of these phenomena.

Loss of resistance to angiotensin II and catecholamines

Women who remain normotensive during pregnancy show a progressive resistance to the pressor effect of catecholamines and angiotensin II throughout gestation. In contrast, patients destined to develop preeclampsia show a progressive loss of resistance to the pressor effects of these agents. For example, at 24 to 26 weeks’ gestation a woman that remains normotensive will require an infusion of 12 to 14 ng/kg/min of angiotensin II to raise the diastolic pressure by 20 mmHg. At the same gestational age, a patient likely to develop preeclampsia will need less than 8 to 9 ng/kg/min to have a similar pressure response.

Coagulation abnormalities

The work of Pritchard et al. (1976) demonstrated that overt coagulation abnormalities exist in only a minority of patients with severe preeclampsia. The most serious hematologic complication of preeclampsia has become well known since it designation as the HELLP syndrome (hemolytic anemia, elevated liver enzymes, low platelet count).

Prediction

Several tests have been proposed to identify women at risk of developing preeclampsia. Some of these tests, such as

¨ the cold pressor test,

¨ the isometric hand grip exercise, and

¨ the roll-over test, depend on the presence of some pathophysiologic changes that occur in preeclampsia.

Other tests, such as

¨ the measurement of urinary calcium or plasma fibronectin, are based on the presence of biochemical alterations peculiar to this disease.

Angiotensin sensitivity test

Roll-over test

The roll-over test was originally described as a noninvasive office procedure having excellent correlation with the angiotensin sensitivity test and an excellent predictor of the development of preeclampsia. A positive test is an elevation of 20 mmHg or more in blood pressure when the patients rolls over from the lateral decubitus to the supine position.

Second-trimester mean arterial pressure

Page and Christianson have emphasized the importance of the mean arterial pressure(MAP) during the second trimester as a predictor of the development of preeclampsia.

Urinary calcium

Several recent studies Sanchez-Ramos L (1990), have demonstrated that preeclampsia is associated with hypocalciuria. Demonstrated of the calcium/creatinine ratio in a randomly obtained single voided urine sample seems to be as accurate as 24 hour collections.

Fibronectin

Patients with preeclampsia have elevated levels of plasma fibronectin, a glycoprotein that has an important role in cellular adhesions and is a component of connective tissue and basement membranes. There are studies Lockwood (1990) indicating that increased plasma levels of endothelium-originated fibronectin precede the clinical signs of preeclampsia and may be useful for prediction of the disease.

Doppler ultrasound

Some investigators Campbell (1986) have suggested that Doppler velocimetry may be useful at early gestational age, 18 to 24 weeks, to detect those patients destined to develop preeclampsia. Unfortunately, abnormal Doppler waveforms at this gestational age have a low sensitivity and low positive predictive value.

Diagnosis

Blood pressure elevation

Hypertension is the most important sign of preeclampsia because it reflects the severity of the disease. Unfortunately, mistakes are frequently made because of lack of consistency in the measurement of blood pressure.

¨One common error is taking the blood pressure of an obese patient with a regular-size cuff. This cause abnormally high readings and generates unnecessary alarm, testing, and consultation.

¨Another common error is not using the same maternal position when taking repeated measurements.

¨A common mistake is that if an abnormally high reading is obtained, the measurement is repeated with the patient in the lateral recumbent position. In the majority of patients, the second blood pressure reading will be lower because in the pregnant woman the lateral recumbent values are always lower than those taken in the sitting position. To avoid this error, repeated blood pressure measurement should be taken with the patient in the sitting position.

¨A third error is the use of different end points to measure the diastolic blood pressure. The experts in the field, as well as multiple professional organizational organizations, recommend that the Korotkoff IV sound, the point of muffling, is the best marker of the diastolic pressure and should always be used.

Proteinuria

Proteinuria is a sign of preeclampsia that usually follows, or appears simultaneously with, hypertension.

Proteinuria is extremely valuable as a prognostic sign in preeclampsia. Frequent monitoring of the amount of protein excreted in the urine must be apart of the evaluation of these patients. A significant increase in proteinuria indicates that the disease has worsened.

Vasospasm

Clinical evidence of vasospasm may be obtained by ophthalmologic examination, which must be a part of the initial evaluation of the patient with preeclampsia. The most common finding in patients with moderate or severe preeclampsia are an increase in the vein-to-artery ratio (normal is 4:3) and segmental vasospasm. Patients with mild preeclampsia usually have a normal funduscopic examination.

Excessive body weight gain and edema

Excessive weight gain and edema are no longer considered signs of preeclampsia. Large increases in body weight as well as edema of hands, face, or both are common in normal pregnancy, and the incidence of preeclampsia is similar in patients with or without generalized edema.

Other signs and symptoms of preeclampsia

Headaches are usually present in moderate-to-severe forms of preeclampsia. The pain may frontal or occipital, may be pulsatile or dull, may occur simultaneously with visual symptoms, and may frequently be intense, especially when preceding the onset of convulsions.

Epigastric or right upper quadrant pain is also common in patients with severe forms of the disease but may also occur before the onset of obvious signs or symptoms of preeclampsia.

The most common visual symptoms appearing in patients who are going to develop preeclampsia is scotoma, a transient perception of bright or black spots. This may progress to sudden inability to focus, to blurred vision, and in severe cases, to complete blindness.

Brisk deep tendon reflexes are also common and result from central nervous system irritability.

Laboratory findings in preeclampsia

The laboratory values are usually unrevealing in cases of mild preeclampsia, but there are multiple findings in severe forms of the disease.

The laboratory changes reflect the effects of the disease on the kidney, liver, fetoplacental unit, and in some cases, the hematologic elements.

Altered renal function. In severe preeclampsia there are elevations in serum creatinine, blood urea nitrogen (BUN), and uric acid levels, as well as decreases in creatinine clearance, proteinuria, and changes in the urinary sediment.

Changes in liver function tests.

Patients with mild preeclampsia show little or no alteration in hepatic enzyme levels, but in severe preeclampsia marked increases in serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), and lactic dehydrogenase (LDH) are commonly found.

Hematologic abnormalities.

The only hematologic change that may be observed in patients with mild preeclampsia is an elevation of hemoglobin and hematocrit caused by the characteristic decrease in plasma volume.

With more severe disease other hematologic abnormalities, commonly thrombocytopenia, may be present. The thrombin time may also be altered in preeclamptic patients.

Abnormal fetoplacental function

A common finding in women with moderate or severe preeclampsia is fetal measurements showing growth of 2 to 4 weeks less than expected for their gestational age, suggesting the presence of intrauterine growth retardation. The head-to-abdomen and femur-to-abdomen ratios frequently are abnormally elevated in these cases.

The nonstess (NST) and contraction stress test (CST) are useful when a quick evaluation of the fetal status is necessary.

According to Ducey et al., (1987) hypertensive pregnant patients with normal umbilical and uterine velocimetry have fetal outcomes that are similar to those of normotensive patients. In contrast, patients with abnormal umbilical and uterine Doppler waveforms have poor outcomes: 51 % deliver small-for-gestational age infants, 62 % require cesarean section for fetal distress, 89 % are delivered preterm.

Management and Nursing Care

Once a diagnosis of preeclampsia is established, the patient must be admitted to the hospital.

When confronted with the management of a patient with preeclampsia, the clinician must first determine the severity of the disease.

Severe cases

If the patient has severe preeclampsia, the management will consist of

1) prevention of seizures,

2) control of hypertension, and

3) delivery.

Nursing process

Prevention

Because the etiology of the disease is unknown, it is difficult to outline a protocol for prevention. Based on scientific studies, there are some general principles, that appear to decrease the incidence of this disease.

Adequate Nutrition:

All pregnant patients should receive instructions regarding the benefits of eating a nutritious, balanced diet containing at least 60 to 70 g of protein; 1200mg of calcium; and an adequate intake of zinc, magnesium, sodium (salt), and vitamins every day. Drinking 6 to 8 glasses of water or fluid per day should be included in the instructions.

Adequate Rest:

Bed rest facilities venous return, increasing the circulatory volume, enhancing renal and placental perfusion and lowering blood pressure. Therefore high risk patients may benefit from 8 to 12 hours of sleep each night with a rest period in the middle of the day.

Early and Appropriate Care

Early, appropriate treatment is effective in preventing the severe form of preeclampsia or eclampsia.

Therefore early detection of its development is effective in lowering the high maternal and fetal mortality associated with the disease. Detection should begin on the first prenatal visit early in pregnancy.

The nurse should obtain an in-depth patient history that includes age, parity, and a medical history of such things as diabetes, persistent hypertensive disorders, and familial history of preeclampsia or eclampsia.

On each prenatal visit the patient should be weighed, an accurate blood pressure reading obtained, and an early-morning urine, it should be checked for protein. If protein is noted in the urine, it should be checked for bacteria and another specimen obtained by clean-catch midstream, because bacteria, vaginal discharge, blood, and amniotic fluid can give a false-positive result.

Prevention of seizures

Magnesium sulfate

Magnesium sulfate is the most commonly used medication for the treatment or prevention of seizure activity in patients with preeclampsia and eclampsia. There is a great deal of controversy over the mechanism of seizure control by magnesium sulfate. The evidence in the literature, however, indicates that magnesium sulfate is the ideal anticonvulsant in preeclampsia.

An intravenous dose of 4 g of magnesium sulfate causes an immediate elevation of the normal Mg⁺⁺ level, 1.6 to 2.1 mEq/L, to about 7 to 9 mEq/L.

It is necessary to monitor those patients who are receiving the medication to prevent serious side effects. The clinical variables to monitor are:

· Urinary output

· patellar reflex, and

· respiratory rate.

· Because Mg ⁺⁺ is eliminated by the kidneys monitoring of the urinary output is extremely important.

*Variable*	*Mild*	*Moderate*	*Severe*
Diastolic blood pressure	90-100 mmHg	100-110 mmHg	> 110 mmHg
Convulsions	Absent	Absent	Present
Blindness	Absent	Absent	Present
Headaches	Minimal	Mild	Marked, persistent
Visual symptoms	Minimal	Mild	Marked, persistent
Oliguria	Absent	Absent	Present
Upper abdominal pain	Absent	Absent	Present
Fetal distress	Absent	Absent	Present
Fetal growth retardation	Absent	Absent	Present
Intravascular hemolysis	Absent	Absent	Present
Thrombocytopenia	Absent	Absent	Present
Blood urea nitrogen (BUN,) creatinine, uric acid levels	Normal	Mildly elevated	Markedly elevated
Serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), lactate dehydrogenase (LDH)	Normal	Mildly elevated	Markedly elevated