Preeclampsia-Eclampsia

Preeclampsia

  • Blood pressure of = 140 mm Hg systolic or = 90 mm Hg diastolic after 20 weeks of gestation.
  • Proteinuria of = 0.3 g in 24 hours.

Severe Preeclampsia

  • Blood pressure of = 160 mm Hg systolic or = 110 mm Hg diastolic.
  • Proteinuria = 5 g in 24 hours or 4+ on dipstick.
  • Oliguria of < 500 mL in 24 hours.
  • Thrombocytopenia.
  • Hemolysis, elevated liver enzymes, low platelets (HELLP).
  • Pulmonary edema.
  • Fetal growth restriction.

General Considerations

Preeclampsia is defined as the presence of elevated blood pressure and proteinuria during pregnancy. Eclampsia occurs with the addition of seizures. Classically, the presence of three elements was required for the diagnosis of preeclampsia-eclampsia: hypertension, proteinuria, and edema. Edema was difficult to objectively quantify and is no longer a required element.

Preeclampsia-eclampsia can occur any time after 20 weeks of gestation and up to 6 weeks postpartum. It is a disease unique to pregnancy, with the only cure being delivery of the fetus and placenta. Approximately 7% of pregnant women in the United States develop preeclampsia-eclampsia. Primiparas are most frequently affected; however, the incidence of preeclampsia-eclampsia is increased with multiple pregnancies, chronic hypertension, diabetes, renal disease, collagen-vascular and autoimmune disorders, and gestational trophoblastic disease. Five percent of women with preeclampsia progress to eclampsia. Uncontrolled eclampsia is a significant cause of maternal death.

The basic cause of preeclampsia-eclampsia is not known. Epidemiologic studies suggest an immunologic cause for preeclampsia, since it occurs predominantly in women who have had minimal exposure to sperm (having used barrier methods of contraception) or have new consorts, in primigravidas, and in women both of whose parents have similar HLA antigens. Preeclampsia is an endothelial disorder resulting from poor placental perfusion, which releases a factor that injures the endothelium, causing activation of coagulation and an increased sensitivity to pressors. Before the syndrome becomes clinically manifest in the second half of pregnancy, there has been vasospasm in various small vessel beds, accounting for the pathologic changes in maternal organs and the placenta with consequent adverse effects on the fetus.

The use of diuretics, dietary restriction or enhancement, sodium restriction, aspirin, and vitamin-mineral supplements such as calcium or vitamin C and E have not yet been shown to be useful in clinical studies. The only cure is termination of the pregnancy at a time as favorable as possible for fetal survival.

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Clinical Findings

Clinically, the severity of preeclampsia-eclampsia can be measured with reference to the six major sites in which it exerts its effects: the central nervous system, the kidneys, the liver, the hematologic and vascular systems, and the fetal-placental unit. By evaluating each of these areas for the presence of mild to moderate versus severe preeclampsia-eclampsia, the degree of involvement can be assessed, and an appropriate management plan can be formulated that is integrated with gestational age assessment (Table 18-2).

A. Preeclampsia
1. Mild to moderate
Precise differentiation between mild and moderate preeclampsia is difficult because the abnormalities that define the disease are quite variable and fail to accurately predict progression to more severe disease. Symptoms are generally minimal or mild. With mild preeclampsia, patients usually have few complaints, and the diastolic blood pressure is less than 90-100 mm Hg. Edema is usually more pronounced with moderate disease, and diastolic blood pressures are in the range of 90-110 mm Hg. The platelet count is over 100,000/uL, antepartum fetal testing is reassuring, central nervous system irritability is minimal, epigastric pain is not present, and liver enzymes are not elevated.

2. Severe
Symptoms are more dramatic and persistent. The blood pressure is often quite high, with readings over 160/110 mm Hg. Thrombocytopenia (platelet counts < 100,000/uL) may be present and progress to disseminated intravascular coagulation. Severe epigastric pain may be present from hepatic subcapsular hemorrhage with significant stretch or rupture of the liver capsule. The HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) is a form of severe preeclampsia.

B. Eclampsia
The occurrence of seizures defines eclampsia. It is a manifestation of severe central nervous system involvement. The other abnormal findings of severe preeclampsia are also observed with eclampsia.

Differential Diagnosis

Preeclampsia-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic renal disease, primary seizure disorders, gallbladder and pancreatic disease, immune or thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome. It must always be considered a possibility in any pregnant woman beyond 20 weeks of gestation. It is particularly difficult to diagnose when preexisting disease such as hypertension is present. Uric acid values can be quite helpful in such situations, since hyperuricemia is uncommon in pregnancy except with gout, renal failure, or preeclampsia-eclampsia.

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Treatment

A. Preeclampsia
Early recognition is the key to treatment. This requires careful attention to the details of prenatal care - especially subtle changes in blood pressure and weight. The objectives are to prolong pregnancy if possible, to allow fetal lung maturity while preventing progression to severe disease and eclampsia. The critical factors are the gestational age of the fetus, fetal pulmonary maturity status, and the severity of maternal disease. Preeclampsia-eclampsia at 36 weeks or more of gestation is managed by delivery regardless of how mild the disease is judged to be. Prior to 36 weeks, severe preeclampsia-eclampsia requires delivery except in unusual circumstances associated with extreme fetal prematurity, in which case prolongation of pregnancy may be attempted. Epigastric pain, thrombocytopenia, and visual disturbances are strong indications for delivery of the fetus. For mild to moderate preeclampsia-eclampsia, bed rest is the cornerstone of therapy. This increases central blood flow to the kidneys, heart, brain, liver, and placenta and may stabilize or even improve the degree of preeclampsia-eclampsia for a period of time.

Bed rest may be attempted at home or in the hospital. Prior to making this decision, the provider should evaluate the six sites of involvement listed in Table 18-2 and make an assessment about the severity of disease.

1. Home management
Home management with bed rest may be attempted for patients with mild preeclampsia and a stable home situation. This requires homemaking assistance, rapid access to the hospital, a reliable patient, and the ability to obtain frequent blood pressure readings. A home health nurse can often provide frequent home visits and assessment.

2. Hospital care
Hospitalization is required for women with moderate or severe preeclampsia or those with unreliable home situations. Regular assessment of blood pressure, reflexes, urine protein, and fetal heart tones and activity are required. A complete blood count, platelet count, and electrolyte panel including liver enzymes should be checked every 1 or 2 days. A 24-hour Urine collection for creatinine clearance and total protein should be obtained on admission and repeated as indicated. Sedatives and opioids should be avoided because the fetal central nervous system depressant effects interfere with fetal testing. Magnesium sulfate is not used until the diagnosis of severe preeclampsia-eclampsia is made or until labor occurs.

Fetal evaluation should be obtained as part of the workup. If the patient is being admitted to the hospital, fetal testing must be performed on the same day to make certain that the fetus is safe. This may be done by fetal heart rate testing with nonstress or stress testing or by biophysical profile. A regular schedule of fetal surveillance must then be followed. Daily fetal kick counts can be recorded by the patient herself. Consideration should be given to amniocentesis to evaluate fetal lung maturity status if hospitalization occurs at 30-37 weeks of gestation. If immaturity is present, steroids (betamethasone 12 mg or dexamethasone 16 mg, two doses intramuscularly 12-24 hours apart) can be administered to the mother. Fetuses between 26 and 30 weeks of gestation can be presumed to be immature, and steroids should be given.

The method of delivery is determined by the maternal and fetal status. Cesarean section is reserved for the usual fetal indications.

B. Eclampsia
1. Emergency care
If the patient is convulsing, she is turned on her side to prevent aspiration and to improve blood flow to the placenta. Fluid or food is aspirated from the glottis or trachea. The seizure may be stopped by giving an intravenous bolus of either magnesium sulfate, 4 g, or diazepam, 5-10 mg, over 4 minutes or until the seizure stops. A continuous intravenous infusion of magnesium sulfate is then started at a rate of 2-3 g/h unless the patient is known to have significantly reduced renal function. Magnesium blood levels are then checked every 4-6 hours and the infusion rate adjusted to maintain a therapeutic blood level (4-6 meq/L). Urinary output is checked hourly and the patient assessed for signs of possible magnesium toxicity such as loss of deep tendon reflexes or decrease in respiratory rate and depth, which can be reversed with calcium gluconate.

2. General care
The occurrence of eclampsia necessitates delivery once the patient is stabilized. It is important, however, that assessment of the status of the patient and fetus take place first. Continuous fetal monitoring must be performed and blood typed and cross-matched quickly. A urinary catheter is inserted to monitor urinary output, and blood is sent for complete blood count, platelets, liver enzymes, uric acid, creatinine or urea nitrogen, and electrolytes. If hypertension is present with diastolic values over 110 mm Hg, antihypertensive medications should be administered to reduce the diastolic blood pressure to 90-100 mm Hg. Lower blood pressures than this may induce placental insufficiency through reduced perfusion. Hydralazine given in 5- to 10-mg increments intravenously every 20 minutes is frequently used to lower blood pressure. Nifedipine, 10 mg sublingually or orally, or labetalol, 10-20 mg intravenously, both every 20 minutes, can also be used.

3. Delivery
Except in unusual circumstances, delivery is mandated once eclampsia has occurred. Vaginal delivery may be attempted if the patient has already been in active labor or the cervix is quite favorable and the patient is clinically stable. The rapidity with which delivery must be achieved depends on the fetal and maternal status following the seizure and the availability of laboratory data on the patient. Oxytocin may be used to induce or augment labor. Regional analgesia or anesthesia is acceptable. Cesarean section is used for the usual obstetric indications or when rapid delivery is necessary for maternal or fetal indications.

4. Postpartum
Magnesium sulfate infusion (2-3 g/h) should be continued until preeclampsia-eclampsia has begun to resolve postpartum, but in any case for at least 24 hours. This may take 1-7 days. The most reliable indicator of this resolution is the onset of diuresis with urinary output of over 100-200 mL/h. When this occurs, magnesium sulfate can be discontinued. Late-onset preeclampsia-eclampsia can occur during the postpartum period. It is usually manifested by either hypertension or seizures. Treatment is the same as prior to delivery - ie, with magnesium sulfate - though other antiseizure medications can be used since the fetus is no longer present.

Diagnosis and management of pre-eclampsia and eclampsia. ACOG Practice Bulletin No. 33, 2002. Int J Gynaecol Obstet 2002;77:67.

Lain KY et al: Contemporary concepts of the pathogenesis and management of preeclampsia. JAMA 2002;287:3183.

Provided by ArmMed Media
Revision date: July 9, 2011
Last revised: by Andrew G. Epstein, M.D.