Archive for the 'Pregnancy Related Disorders' Category

December 5th 2007

Premature Rupture of The Membranes

What is this Condition?

Premature rupture of the membranes (”breaking water”) is a spontaneous break or tear in the amniochorial sac before onset of regular contractions, resulting in progressive cervical dilation. This condition occurs in nearly 10% of all pregnancies over 20 weeks’ gestation . Labor usually starts within 24 hours after the membranes rupture, and more than 80% of these infants are mature.

The latent period (between membrane rupture and onset of labor) is generally brief when the membranes rupture near term; when the infant is premature, this period is prolonged, which increases the risk of death from maternal infection and fetal infection.

What Causes it?

Although the cause of this condition is unknown, malpresentation and a contracted pelvis commonly accompany the rupture. Predisposing factors may include:

• poor nutrition and hygiene and lack of proper prenatal care

• incompetent cervix (perhaps as a result of abortions)

• increased intrauterine tension due to excessive amniotic fluid or multiple pregnancies

• defects in the amniochorial membranes’ tensile strength

• uterine infection.

What are its Symptoms?

Typically, premature rupture of the membranes causes blood-tinged amniotic fluid to leak or gush from the vagina. Maternal fever, fetal rapid heart rate, and a foul-smelling vaginal discharge indicate infection.

How is it Diagnosed?

Characteristic passage of amniotic fluid confirms this condition. A physical exam shows amniotic fluid in the vagina. Examination of this fluid helps determine appropriate management. The physical exam also determines the presence of multiple pregnancies, and helps determine fetal presentation and size.

How is it Treated?

Treatment of this condition depends on fetal age and the risk of infection. In a term pregnancy, if spontaneous labor and vaginal delivery don’t occur within a relatively short time (usually within 24 hours after the membranes rupture), the doctor usually tries to induce labor; if induction fails, cesarean delivery is usually necessary. Cesarean. hysterectomy is recommended for women with a severe uterine infection.

Management of a preterm pregnancy of less than 34 weeks is controversial. However, with advances in technology, a conservative approach has now proved effective. In a preterm pregnancy of 28 to 34 weeks, treatment includes hospitalization and observation of the mother and fetus for signs of infection while awaiting fetal maturation. If tests confirm infection, labor must be induced, followed be, intravenous administration of antibiotics. The newborn may also require antibiotics.

What can a Woman with Premature Rupture of the Membranes do?

If you think your membranes have ruptured, call your doctor right away. Don’t use a douche or have sexual intercourse.


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December 2nd 2007

Abnormal Vomiting During Pregnancy

What is this Condition?

Unlike the nausea and vomiting a woman may normally have between the 6th and 12th weeks of pregnancy, this condition involves severe, constant nausea and vomiting that persist after the first trimester. If untreated, it produces substantial weight loss, starvation, dehydration, and other problems.

This condition occurs in about 1 in 200 pregnancies. The prognosis is good with appropriate treatment.

What Causes it?

Although its cause is unknown, abnormal vomiting during pregnancy often affects women with conditions that produce high levels of a hormone called human chorionic gonadotropin. These conditions include cysts in the uterus or multiple pregnancy. Other possible causes include pancreatitis, bile duct disease, drug toxicity, inflammatory bowel disease, and vitamin deficiencies (especially of vitamin B G )·

What are its Symptoms?

The cardinal symptoms of this disorder are constant nausea and vomiting. The vomit initially contains undigested food, mucus, and small amounts of bile; later, only bile and mucus; and finally, blood and material that resembles coffee grounds. Persistent vomiting causes substantial weight loss and eventual emaciation.

How is it Diagnosed?

Diagnosis depends on a history of uncontrolled nausea and vomiting that persists beyond the first trimester, evidence of substantial weight loss, and other characteristic symptoms. Lab tests may also provide important evidence. Diagnosis must rule out other conditions with similar clinical effects.

How is it Treated?

The woman with this condition may require hospitalization to correct electrolyte imbalances and prevent starvation. Intravenous feedings maintain nutrition until her condition improves. She progresses slowly to a clear liquid diet, then a full liquid diet and, finally, small, frequent meals of high-protein solid foods. Snacks help stabilize blood sugar levels, and vitamin B supplements help correct vitamin deficiency.

When vomiting stops and electrolyte balance has been restored, the pregnancy usually continues uneventfully, and most women feel better as they begin to regain normal weight. However, some continue to vomit throughout the pregnancy, requiring further treatment. If appropriate, some women may benefit from consultations with a clinical nurse specialist, a psychologist, or a psychiatrist.

What can a Pregnant Woman with Abnormal Vomiting do?

Eat dry foods if you have a poor appetite, and decrease your liquid intake during meals. To boost your appetite, try to have company and conversation at mealtimes. Stay upright for 45 minutes after eating to decrease the risk of vomiting.


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November 20th 2007

Cardiovascular Disease in Pregnancy

What is this Condition?

Cardiovascular disease ranks fourth (after infection, toxemia, and hemorrhage) among the leading causes of maternal death. The physiologic stress of pregnancy and delivery is often more than a compromised heart can tolerate and often leads to death of the mother and child.

Approximately 1 % to 2% of pregnant women have heart disease, but the incidence is rising because current medical treatment allows more women with rheumatic heart disease or congenital defects to reach childbearing age. With careful management, the prognosis for pregnant women with cardiovascular disease is good. Decompensation (the heart’s failure to maintain adequate circulation) is the leading cause of maternal death. Infant mortality increases with decompensation, because uterine congestion, insufficient oxygenation, and the elevated carbon dioxide content of the blood not only endanger the fetus, but also frequently cause premature labor and delivery.

What causes it?

More than 80% of pregnant women who develop cardiovascular complications have a history of rheumatic heart disease. In the rest, these complications stem from congenital defects (10% to 15%) or coronary artery disease (2%).

The diseased heart is sometimes unable to meet the normal increased demands of pregnancy, which include a 25% increase in cardiac output (the amount of blood pumped by the heart per minute), a 40% to 50% increase in plasma volume, increased oxygen requirements, retention of salt and water, weight gain, and alterations in hemodynamics during delivery. This physiologic stress often leads to decompensation. The degree of decompensation depends on the woman’s age, the duration of heart disease, and the functional capacity of her heart at the outset of pregnancy.

What are its Symptoms?

The woman with cardiovascular disease during pregnancy will have distended neck veins, diastolic murmurs, moist crackles heard at the base of the lungs, an enlarged heart, and irregular heartbeats. Other typical symptoms may include bluish skin discoloration, pericardial friction rub, and pulse irregularities.

Decompensation may develop suddenly or gradually. As it progresses, the woman may experience swelling, increasing shortness of breath on exertion, palpitations, a smothering sensation, and coughing up blood.

How is it Diagnosed?

Exam findings, including unusual heart sounds, irregular heartbeats, and an enlarged heart, suggest cardiovascular disease. To determine the extent and cause of the disease, an electrocardiogram, echocardiogram, or phonocardiogram may be performed. X-rays show heart enlargement and congestion in the lungs. Cardiac catheterization should be postponed until after delivery, unless surgery is necessary.

How is it Treated?

The goal of therapy is to prevent complications and minimize the strain on the mother’s heart, primarily through rest. This may require periodic hospitalization for women with moderate heart dysfunction or with symptoms of decompensation, toxemia, or infection. Older women or those with previous episodes of decompensation may require hospitalization and bed rest throughout the pregnancy.

Drug therapy, when necessary, will use the safest possible drugs in the lowest possible dosages to minimize harm to the fetus. Diuretics and drugs that increase blood pressure, blood volume, or cardiac output should be used with extreme caution. If an anticoagulant is needed, heparin is the drug of choice. Digoxin (also known as Lanoxin) and common antiarrhythmics, such as Cardioquin and Procan SR, are often required. The preventive use of antibiotics is reserved for women who are susceptible to endocarditis.

A therapeutic abortion may be considered for women with severe heart dysfunction, especially if decompensation occurs during the first trimester. Women hospitalized with heart failure usually follow a regimen of digoxin, oxygen, rest, sedation, diuretics, and restricted intake of sodium and fluids. If these measures fail to improve symptoms, heart surgery may be necessary. During labor, the woman may require oxygen and an analgesic for relief of pain and apprehension without adversely affecting the fetus or herself. Depending on which procedure would be less stressful for the woman’s heart, delivery may be vaginal or by cesarean section.

Bed rest and medications already instituted should continue for at least 1 week after delivery because of a high incidence of decompensation, cardiovascular collapse, and maternal death during the early puerperal period.

Breast-feeding is undesirable for women with severe cardiovascular disease because it increases fluid and metabolic demands on the heart.

What can a Pregnant Woman with Cardiovascular Disease do?

Get plenty of rest and control your weight to decrease the strain on your heart. To prevent vascular congestion, limit your fluid and sodium intake. Take supplementary folic acid and iron to prevent anemia.


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September 24th 2007

Pregnancy-Induced High Blood Pressure

What do Doctors call this Condition - Toxemia of pregnancy, preeclampsia, eclampsia

What is this Condition?

Pregnancy-induced high blood pressure, a potentially life-threatening disorder, usually develops late in the second or third trimester. Preeclampsia, the nonconvulsive form of the disorder, develops in about 7% of pregnancies. It may be mild or severe and is more common in low socioeconomic groups. Eclampsia, the convulsive form, affects about 5% of women with preeclampsia; of these, about 15% die from toxemia itself or its complications. The fetal mortality rate is high because of the increased incidence of premature delivery.

What Causes it?

The cause of pregnancy-induced high blood pressure is unknown, but it appears to be related to inadequate prenatal care (especially poor nutrition), first pregnancies, multiple pregnancies, and preexisting diabetes or high blood pressure. Age is also a factor: Adolescents and women having their first child over age 35 are at higher risk for preeclampsia.

What are its Symptoms?

Mild preeclampsia generally produces high blood pressure, excessive proteins in the urine, generalized swelling, and weight gain of more than 3 pounds (1.36 kilograms) per week during the second trimester or more than 1 pound (0.45 kilogram) per week during the third trimester.

Severe preeclampsia is marked by more pronounced high blood pressure and even higher levels of protein in the urine, eventually leading to decreased urine output. Hemolysis, elevated liver enzymes. and a low platelet count (the HELLP syndrome) are often present in severe preeclampsia. Other symptoms that may indicate worsening preeclampsia include blurred vision, stomach pain or heartburn, irritability, emotional tension, and a severe frontal headache.

In eclampsia, all the symptoms of preeclampsia are magnified and are associated with seizures and, possibly, coma, premature labor. stillbirth, kidney failure, and liver damage.

How is it Diagnosed?

The following findings suggest mild preeclampsia:

• high blood pressure (140 systolic, or an increase of 30 or mar: points above the woman’s normal systolic pressure, measured on two occasions 6 hours apart; 90 diastolic, or an increase of 15 or more points above the woman’s normal diastolic pressure, measured on two occasions 6 hours apart)

• urine protein levels higher than 500 milligrams per 24 hours.

These findings suggest severe preeclampsia:

• higher blood pressure readings (160/110 or higher on two occasions 6 hours apart) while the woman is on bed rest

• urine protein levels of 5 grams or more per 24 hours

• urine output less than or equal to 400 milliliters per 24 hours • possibly hyperactive deep tendon reflexes.

The presence of seizures along with typical symptoms of severe preeclampsia strongly suggests eclampsia.

During the crisis, real-time ultrasound and stress and nonstress tests evaluate the fetus’s well-being. Electronic monitoring reveals stable or increased fetal heart tones during periods of fetal activity.

How is it Treated?

Treatment of preeclampsia is designed to halt the disorder’s progress. to prevent the early effects of eclampsia - seizures, residual high blood pressure, and kidney shutdown - and to ensure the fetus’s survival. Some doctors induce labor promptly, especially if the woman is near term, whereas others follow a more conservative approach. Therapy may include sedatives and complete bed rest to relieve anxiety, lower blood pressure, and evaluate the woman’s response to therapy. If the kidneys are working normally, a high-protein, low-sodium, low-carbohydrate diet with increased fluids is recommended.

If the woman’s blood pressure persistently rises above 160/100 despite bed rest and sedatives, or if central nervous system irritability, increases, magnesium sulfate may be given to produce general sedation, promote urine excretion, reduce blood pressure, and prevent seizures. If the woman’s condition doesn’t improve, or if the fetus’s life is endangered, cesarean section or induction of labor may be required to terminate the pregnancy.

Emergency treatment of eclamptic seizures consists of immediate intravenous administration of Valium followed by magnesium sulfate, oxygen administration, and electronic fetal monitoring. After the woman’s condition stabilizes, a cesarean section may be performed.


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August 6th 2007

TBlood Incompatibility Between Mother And Fetus

What do Doctors call this Condition - Erythroblastosis fetalis

What is this Condition?

When the fetus’s blood is incompatible with the mother’s, the mother produces antibodies against the fetus’s red blood cells. Intrauterine transfusions with human Rh(D) immune human globulin can save 40% of fetuses with this disorder. However, in severe, untreated blood incompatibility, the prognosis is poor, especially if kernicterus (infiltration of parts of the brain and spinal cord with bilirubin) develops. About 70% of these infants die, usually within the first week of life; survivors inevitably develop severe nervous system damage.

What Causes it?

Blood incompatibility between mother and fetus usually results from Rh isoimmunization - a condition that develops in approximately 7% of all pregnancies in the United States. Until treatment with human Rh(D) immune human globulin became available, this condition was an important cause of kernicterus and neonatal death.

During her first pregnancy, a woman with Rh-negative blood factors becomes sensitized (during delivery or abortion) by exposure to Rh-positive fetal blood factors inherited from the father. In the next pregnancy that produces an Rh-positive fetus, increasing amounts of maternal anti-Rh-positive antibodies cross the placental barrier, attach to Rh-positive cells in the fetal blood, and destroy them.

To compensate for this, the fetus steps up the production of new red blood cells, which are attacked in their turn. Escalating red cell destruction releases large amounts of unconjugated bilirubin (a red cell component), which the fetal liver cannot properly process and excrete.

ABO incompatibility, another form of blood incompatibility between mother and fetus, is less severe.

What are its Symptoms?

An infant with this incompatibility disorder has liver problems. Jaundice (resulting from the fetal liver’s failure to process bilirubin from the destroyed red cells) doesn’t usually appear at birth but may occur 30 minutes to 24 hours later. A mildly affected infant is pale and has a mildly to moderately enlarged liver and spleen. Severely affected infants who survive birth usually have pallor, swelling, small reddish skin spots, an enlarged liver and spleen, grunting respirations, abnormal breath sounds, poor muscle tone, nervous system unresponsiveness, possible heart murmurs, a bile-stained umbilical cord, and yellow or meconium-stained amniotic fluid.

How is it Diagnosed?

Diagnostic evaluation considers both prenatal and neonatal findings.

Important factors to consider are:

• maternal history (for blood incompatibility-related stillbirths, abortions, previously affected children, or previous anti-Rh blood levels)

• blood typing and screening

• father’s blood test results

• history of blood transfusion.

Other diagnostic tests that provide important information include amniotic fluid analysis and X-ray studies.

How is it Treated?

Treatment depends on the degree of maternal sensitization and the effects of hemolytic disease on the fetus or newborn .

• Intrauterine-intraperitoneal blood transfusion is performed when amniotic fluid analysis suggests that the fetus is severely affected and that delivery is inappropriate because the fetus will be premature. A transabdominal puncture under fluoroscopy into the fetal peritoneal cavity allows infusion of group 0, Rh-negative blood. This may be repeated every 2 weeks until the fetus is mature enough for delivery.

• Planned delivery is usually done 2 to 4 weeks before term date, depending on maternal history, serologic tests, and amniocentesis results; labor may be induced from the 34th to 38th week of gestation. During labor, the fetus should be monitored electronically; capillary blood scalp sampling determines acid-base balance. Any indication of fetal distress calls for an immediate cesarean delivery .

• The newborn’s serum bilirubin levels are brought down by phenobarbital administered during the last 5 to 6 weeks of pregnancy; or by an albumin infusion, which helps bind bilirubin; or by phototherapy with ultraviolet light .

• Administration of human Rh(D) immune globulin can provide passive immunization, which prevents maternal Rh isoimmunization in Rh-negative women. However, it’s ineffective if sensitization has already resulted from a previous pregnancy, abortion, or transfusion.


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