Diseases of pregnancy

Keywords: hypertensive disorders of pregnancy, Abruptio placentae, Placental infarction, Gestational diabetes, Placenta accreta, Placental cysts and benign tumours, Trophoblastic disease, Anomalies of the umbilical cord

Part 2

Hypertensive disorders of pregnancy

The increase of blood pressure (hypertension) during pregnancy, which is often accompanied by accumulation of fluid in the tissues that causes swelling (edema) and proteinuria (protein in the urine), poses a serious threat to both the woman and the fetus. The maternal hazards include seizures, organ disturbances, and death; the fetal risks, premature delivery and death.

For many years, hypertensive disorders of pregnancy were referred to as toxemias of pregnancy. The basis for this terminology was the belief that circulatory toxins were responsible for the symptoms. These toxins were never discovered, and this terminology has been generally abandoned; however, in its wake, many different terms have been used to describe hypertensive disorders of pregnancy. To help clarify this situation, the Committee on Terminology of the American College of Obstetricians and Gynecologists prepared the following classification system, which has been recommended by the National Institutes of Health Working Group on High Blood Pressure in Pregnancy: (1) chronic hypertension, (2) preeclampsia and eclampsia, (3) preeclampsia superimposed on chronic hypertension, (4) transient hypertension, and (5) unclassified.

Chronic hypertension is defined as a systolic blood pressure of 140 millimetres of mercury (mm Hg) or higher and a diastolic blood pressure of 90 mm Hg or higher, which antedate pregnancy. (The systolic is the highest blood pressure after the heart has contracted; the diastolic, the lowest after the heart has expanded.) An elevated blood pressure that first develops during pregnancy and persists beyond the 42nd day postpartum also is classified as chronic hypertension.

Preeclampsia is diagnosed after 20 weeks' gestation and is categorized as either mild or severe, although both forms must be considered dangerous to the mother and fetus. Mild preeclampsia is typically characterized by the following symptoms: a rise in blood pressure from that prior to 20 weeks' gestation of at least 30 mm Hg systolic or 15 mm Hg diastolic (or, if the earlier blood pressure is unknown, a level of 140/90 mm Hg after 20 weeks' gestation) on two occasions at least six hours apart; excretion of 0.3 gram (0.01 ounce) of protein or more in the urine during a 24-hour period; and evident swelling or rapid weight gain resulting from fluid retention. Coagulation and disturbances of liver functions are less common but are extremely serious.

Severe preeclampsia is defined by any of the following symptoms occurring after the 20th week of pregnancy: a systolic blood pressure of 160 mm Hg or higher or a diastolic pressure of 110 mm Hg or higher on two or more occasions at least six hours apart, excretion of five grams or more of protein in the urine during a 24-hour period, a reduction in the amount of urine normally excreted (500 millilitres or less in 24 hours), cerebral or visual disturbances, epigastric pain, and pulmonary edema or cyanosis (bluish or purplish colour of the skin).

A patient with preeclampsia is always in danger of rapidly developing eclampsia, which is distinguished by convulsions that may lead to coma. Headache, epigastric pain, and facial twitching usually precede these seizures, although occasionally eclampsia can arise with no warning, sometimes developing in a woman who has only mild hypertension. Another type of preeclampsia that includes small variations in blood pressure, minor decreases in blood platelet count, and small elevations in liver enzymes can progress quickly from a benign state to a syndrome of life-threatening proportions. This condition is known as the HELLP syndrome and is denoted by hemolysis, elevated liver enzymes, and low platelet count. In this situation, delivery of the fetus must be induced, or pregnancy must be immediately terminated.

Preeclampsia can occur in women who have had hypertension prior to becoming pregnant, in which case the prognosis is much more serious for the mother and fetus than when either preeclampsia or chronic hypertension occurs alone. The diagnosis of preeclampsia superimposed on chronic hypertension is made based on increases of blood pressure of 30 mm Hg systolic and 15 mm Hg diastolic that are accompanied by the appearance of proteinuria or edema. A rise in blood pressure either during pregnancy or 24 hours postpartum, unaccompanied by other symptoms of preeclampsia or eclampsia, is categorized as transient hypertension.

Approximately 7 percent of women whose pregnancies progress beyond the first trimester will develop preeclampsia. It is most common in women who are pregnant for the first time. A higher incidence of this condition occurs in family members of women who have a history of preeclampsia, which provides evidence for involvement of a single maternal gene. Medical disorders such as diabetes mellitus can predispose women to preeclampsia, and conditions such as twin pregnancies increase the risk of preeclampsia. A hydatidiform mole (an abnormal pregnancy caused by an abnormal ovum) is often responsible for a preeclamptic condition that develops before 24 weeks' gestation.

Although hypertension is an important diagnostic sign of preeclampsia, the disease is actually one of poor perfusion to the tissues, including the fetal-placental unit. This inadequate delivery of fluids to virtually all organs is attributed to the profound vasospasm (constriction of blood vessels that reduces calibre and blood flow) characteristic of preeclampsia that is also responsible for the associated blood-pressure elevation.

Certain organ systems are characteristically involved in preeclampsia, and their resultant abnormalities—alterations in renal function, endothelial cell injury, and cardiovascular changes—have provided insight into the mechanism of this complex disease. The normal immunologic changes that occur as a result of fetal-maternal interactions also have been postulated as having a pathogenetic role in the development of preeclampsia. The cause of the underlying vasoconstriction, however, still remains undefined.

Various approaches have been attempted to prevent preeclampsia in women at high risk for developing the condition. Dietary and sodium restrictions have been unsuccessful, but there is interest in the use of low-dose aspirin therapy and calcium supplementation as preventive measures. These methods are still under investigation.

Treatment of preeclampsia involves slowing the condition's progression to a more severe form to allow fetal growth to continue as long as possible. Bed rest is recommended in cases of mild preeclampsia, but, when more serious symptoms are involved, hospitalization is best. In cases of severe preeclampsia in which the fetus is beyond 30 weeks' gestation, delivery of the infant is thought to be the best course. Antihypertensive drugs are not used, because they mask the clinical signs by which worsening of the condition is recognized.

In the United States, magnesium sulfate is the drug of choice for preventing and treating eclamptic convulsions. European treatment differs—a variety of narcotics, barbiturates, and benzodiazepine derivatives are used. Because the preeclamptic process often accelerates during labour and the postpartum period, magnesium therapy is used during this time as well.

Gestational diabetes

Diabetes mellitus that has been diagnosed for the first time during pregnancy and resolves immediately after delivery is referred to as gestational diabetes. It occurs in between 1 and 4 percent of the total pregnant population, usually in the second or third trimester. Approximately 50 percent of women who develop gestational diabetes will, over the course of their lifetime, develop adult onset (type II) diabetes.

Effects that gestational diabetes can have on the fetus include high birth weight for gestational age, neonatal hypoglycemia, premature delivery with respiratory distress syndrome, difficult delivery, and a higher incidence of fetal-neonatal mortality.

Previously only women with recognizable risk factors for gestational diabetes were screened for glucose intolerance; these included obese women, women who had a family history of diabetes, and those older than 35 years. Because a significant proportion of cases of gestational diabetes—up to 50 percent—were missed in this way, it is now recommended that all women between the 24th and 28th week of gestation be screened for glucose intolerance; those at high risk should be screened during their first prenatal visit. Controversy exists concerning the best glucose-tolerance screening procedure to use.

Treatment of gestational diabetes varies according to the individual case. Controlling diet is the first, conservative approach; insulin therapy is instituted when glucose levels cannot be managed in this way. Fetal monitoring of growth development is necessary to measure the effectiveness of treatment and to anticipate and prevent complications. An early delivery by cesarean section (incision through the abdominal and uterine walls for fetal delivery) was frequently recommended in the past. Today the procedure, which has its own risks, is selected less often, as long as the disease has been well controlled and fetal development is normal.