Preeclampsia is a disorder of pregnancy that is characterized by hypertension (high blood pressure) and proteinuria (excessive protein in the urine); often including edema (swelling) and occasionally involving thrombocytopenia (low platelets) or liver function abnormalities.
Preeclampsia complicates 5 to 7 percent of pregnancies in otherwise healthy patients. Preeclampsia (toxemia in pregnancy) is characterized by increasing blood pressure, headaches, the presence of albumin (a blood protein) in the urine, and edema (accumulation of water) in the lower extremities.
If the condition is not properly treated, the patient may develop eclampsia, a potentially fatal condition involving coma and convulsions. Five percent of all patients with preeclampsia progress to eclampsia. Preeclampsia-eclampsia can occur any time after 20 weeks of gestation and up to six weeks postpartum (after delivery).
The cause of preeclampsia is not known, but may be related to immune factors. Preeclampsia may result from fetal antigens – elements of the fetus that trigger an immune response in the mother.
The risk of preeclampsia is highest in primagravidas (women in their first pregnancy) and in women with minimal exposure to sperm (having used barrier methods of contraception, e.g., condoms).
A person with mild preeclampsia may feel perfectly well. Therefore, it is important to attend all prenatal checkups to spot this condition early. The symptoms of severe preeclampsia, which can develop during the last weeks of pregnancy are headaches, blurred vision, intolerance for bright light, nausea and vomiting, and salt and water retention. It may progress to eclampsia, the symptoms of which are convulsions (seizures) and sometimes unconsciousness.
The diagnosis of preeclampsia is primarily, but not exclusively, made on the basis of proteinuria and edema in a hypertensive pregnant woman.
Other factors helpful in making the diagnosis are hemoconcentration, hyperreflexia, hypoalbuminemia, liver function abnormalities, thrombocytopenia, and hyperuricemia. Abnormal prostaglandin synthesis may be the pivotal defect causing increased peripheral vascular resistance, severe vasoconstriction, endothelial injury and secondary hypertension.
Management of preeclampsia has centered on aggressive maternal,fetal assessment and earliest safe delivery. Frequent monitoring of maternal blood pressure, urinary protein excretion, weight change, and symptoms is mandatory. Regular biophysiologic assessment of the fetus is also essential.
The backbone of management continues to be parenteral (intravenous) administration of magnesium sulfate and delivery as soon as the fetus is mature or when maternal risks outweigh any risks to the fetus. Parenteral management of preeclampsia focuses on the use of magnesium sulfate. The main purpose of this therapy is to inhibit progression to eclampsia. Magnesium may be given intramuscularly or intravenously.
Most patients with preeclampsia are treated on an inpatient basis. If the preeclampsia is mild and blood pressure is adequately controlled with no signs of impending seizure, patients may be managed at home with bedrest. In this situation, blood pressure should be monitored twice daily and fetal status should be assessed at least twice weekly with a non-stress test and a biophysiologic profile. Delivery at maturity is still mandatory in this group of patients, unless induction has been unsuccessful. In the latter case, cesarean section or a second trial of induction must be considered.
Is this condition harmful to the unborn child?
What medications, if any, will be prescribed to control this condition?
What, if any, are the side effects of the drug?
Will the unborn child experience the side effects also?
Should a specific diet be followed? What kind?
Will exercise help or enhance the condition?
What about intercourse?
If the condition worsens and eclampsia is present, what will the course of treatment be?
Will there be a complete recovery after the baby is born?