Hacker & Moore's Essentials of Obstetrics and Gynecology: With STUDENT CONSULT Online Access,5th ed.

Chapter 16

Common Medical and Surgical Conditions Complicating Pregnancy

Lony C. Castro, Dotun Ogunyemi

The more common medical, infectious, and surgical disorders that may complicate pregnancy are covered in this chapter. The pharmacologic agents recommended for these disorders have been classified by the Food and Drug Administration (FDA) for fetal risk (see Box 7-1 on page 73). Up to date information on these drugs can be found at www.FDA.gov/ by selecting “Drugs” from the menu and searching for a specific agent.

image Endocrine Disorders

Diabetes mellitus and thyroid disease are the two most common endocrine disorders complicating pregnancy.


Incidence and Classification

The prevalence of diabetes mellitus has greatly increased in the last 20 years. Reports show a rate of 3% to 8% of gestational diabetes mellitus (GDM). Pregestational diabetes is present in about 1% of pregnancies. Overall, 90% of diabetes in pregnant women is gestational and about 10% pregestational.

GDM is defined as glucose intolerance with onset or first recognition during pregnancy. Pregnancy is associated with progressive insulin resistance. Human placental lactogen, progesterone, prolactin, cortisol, and tumor necrosis factor are associated with increased insulin resistance during pregnancy. Studies suggest that women who develop GDM have chronic insulin resistance and that GDM is a “stress test” for the development of diabetes in later life. Most obstetricians use White’s classification of diabetes during pregnancy. This classification is helpful is assessing disease severity and the likelihood of complications (Table 16-1).






Gestational diabetes; glucose intolerance developing during pregnancy; fasting blood glucose and postprandial plasma glucose normal

Diet alone


Gestational diabetes with fasting plasma glucose >105 mg/dL; or 2-hr postprandial plasma glucose >120 mg/dL, or 1-hr postprandial plasma glucose >140 mg/dL

Diet and insulin


Overt diabetes developing after age 20 yr and duration < 10 yr

Diet and insulin


Overt diabetes developing between ages 10 and 19 yr or duration 10-19 yr

Diet and insulin


Overt diabetes developing before age 10 yr or duration 20 yr or more or background retinopathy

Diet and insulin


Overt diabetes at any age or duration with nephropathy

Diet and insulin


Overt diabetes at any age or duration with proliferative retinopathy

Diet and insulin


Overt diabetes at any age or duration with arteriosclerotic heart disease

Diet and insulin


Maternal and fetal complications of diabetes are listed in Table 16-2. Diabetes often coexists with the metabolic syndrome. Most fetal and neonatal effects are attributed to the consequences of maternal hyperglycemia, or, in the more advanced classes, to maternal vascular disease. Glucose crosses the placenta easily by facilitated diffusion, causing fetal hyperglycemia, which stimulates pancreatic β cells and results in fetal hyperinsulinism. Fetal hyperglycemia during the period of embryogenesis is teratogenic. There is a direct correlation between birth defects in diabetic pregnancies and increasing glycosylated hemoglobin levels (HbA1C) in the first trimester. Fetal hyperglycemia and hyperinsulinemia cause fetal overgrowth and macrosomia, which predisposes to birth trauma, including shoulder dystocia and Erb’s’ palsy. Fetal demise is most likely due to acidosis, hypotension from osmotic dieresis, or hypoxia from increased metabolism coupled with inadequate placental oxygen transfer.









Close prenatal surveillance; blood glucose monitoring, ultrasonography


Evaluation for signs and symptoms

Infections, e.g., urinary tract infection and candidiasis

Urine culture, wet mount, appropriate therapy

Cesarean delivery

Blood glucose monitoring, insulin and dietary adjustment to prevent fetal overgrowth

Genital trauma

Ultrasonography to detect macrosomia, cesarean delivery for macrosomia




Teach signs and symptoms; blood glucose monitoring; insulin and dietary adjustment; check for ketones, blood gases, and electrolytes if glucose > 300 mg/dL

Diabetic coma






Electrocardiogram first visit and as needed


Renal function studies, first visit and as needed


Funduscopic evaluation, first visit and as needed

Peripheral vascular

Check for ulcers, foot sores; noninvasive Doppler studies as needed



Peripheral neuropathy

Neurologic and gastrointestinal consultations as needed

Gastrointestinal disturbance




Type 2 diabetes

Postpartum glucose testing, lifestyle changes (diet and exercise)

Metabolic syndrome

Lifestyle changes (diet and exercise)


Lifestyle changes (diet and exercise)

Cardiovascular disease

Annual checkup by physician, lifestyle changes (diet and exercise)



Maintenance of maternal euglycemia will decrease most of these complications.

Macrosomia with traumatic delivery (shoulder dystocia, Erb’s palsy)

Ultrasonography for estimated fetal weight before delivery; consider cesarean delivery if estimated fetal weight > 4250-4500 g



Pulmonary, hepatic, neurologic, pituitary-thyroid axis; with respiratory distress syndrome, hypocalcemia

Avoid delivery before 39 weeks in the absence of maternal or fetal indications unless amniocentesis indicates lung maturity. Maintain euglycemia intrapartum.



Cardiovascular anomalies

Preconception counseling and glucose control, HbAlc in the first trimester

Neural tube defects

Maternal serum alpha-fetoprotein screening; fetal ultrasonography and fetal echocardiogram; amniocentesis and genetic counseling

Caudal regression syndrome


Other defects, e.g., renal




Intrauterine growth restriction

Serial ultrasonography for fetal growth and estimated fetal weight, serial fetal surveillance with nonstress test, amniotic fluid index, and fetal Doppler. Avoid postdates pregnancy.

Intrauterine fetal death

Abnormal fetal heart rate patterns

In pregestational diabetes, maternal complications include worsening nephropathy and retinopathy, a greater incidence of preterm preeclampsia and a higher likelihood of diabetic ketoacidosis. Hypoglycemia is much more common because of the tighter control attempted during pregnancy. Fetal complications include an increased rate of abortions, anatomic birth defects, fetal growth restriction, and prematurity.


Screening for gestational diabetes is generally performed between 24 and 28 weeks of gestation with a 50-g 1-hour oral glucose challenge test (GCT), given without regard to last oral intake. This timing will identify most gestational diabetic patients while providing several weeks of therapy to reduce potentially adverse consequences. Screening is advised at the first prenatal visit in pregnant women with risk factors such as maternal age greater than 25 years, previous macrosomic infant, previous unexplained fetal demise, previous pregnancy with GDM, family history of diabetes, history of polycystic ovarian disease, and obesity. If overt signs and symptoms of diabetes are present, a fetal scalp blood test should be undertaken first. If the first-trimester screen is negative, it should be repeated at 24 to 28 weeks. Glucose values above 130 to 140 mg/dL on a GCT are considered abnormal and have an 80% to 90% sensitivity in detecting GDM.

An abnormal screening GCT is followed with a diagnostic 3-hour 100-g oral glucose tolerance test. This involves checking the fasting blood glucose after an overnight fast, drinking a 100-g glucose drink, and checking glucose levels hourly for 3 hours. If there are two or more abnormal values on the 3-hour GTT, the patient is diagnosed with GDM (Table 16-3). If the 1-hour screening (50-g oral glucose) plasma glucose exceeds 200 mg/dL, a glucose tolerance test is not required and may dangerously elevate blood glucose values.



Maximal Normal Blood Glucose (mg/dL)



1 hr


2 hr


3 hr


From Carpenter and Coustan.



Management of gestational diabetes requires a team approach involving patient teaching and counseling, medical-nursing assessments and interventions, strategies to achieve maternal euglycemia, and avoidance of fetal-neonatal compromise. Ideally, this team should include the patient, obstetrician, maternal fetal medicine specialist, clinical nurse specialist, nutritionist, social worker, and neonatologist. The patient is included as an active participant in formulating management strategies.


The importance of strict metabolic control before and during pregnancy to decrease the incidence of congenital anomalies, perinatal morbidity, and perinatal mortality has been established. For optimal outcome, the fasting blood glucose should be less than 95 mg/dL, 1-hour postprandial glucose level less than 140 mg/dL, and 2-hour postprandial glucose level less than 120 mg/dL.


Caloric requirements are calculated on the basis of ideal body weight: 30 kcal/kg for those patients 80% to 120% of ideal body weight; 35 to 40 kcal/kg for those less than 80% of ideal body weight; and 24 kcal/kg for gravidas who are 120% to 150% of ideal body weight. The diet comprises about 50% carbohydrate, 20% protein, and 20% fat. The diet should also contain a generous amount of fiber. Caloric intake is divided into 25% at breakfast, 30% at lunch, 30% at dinner, and 15% at a bedtime snack.


Oral hypoglycemic agents have traditionally not been recommended for pregnant women because of the risks for teratogenesis and neonatal hypoglycemia. However, oral hypoglycemic agents (e.g., glyburide), which do not appear to enter the fetal circulation in appreciable quantities, have been used successfully to treat gestational diabetes after the first trimester.

Insulin use is the gold standard to maintain euglycemia in pregnancy. The peak action of lispro insulin is at 30 to 90 minutes, of regular insulin at 2 to 3 hours, and of NPH insulin at 6 to 10 hours. A combination of rapid-acting or short-acting (lispro or regular) and intermediate-acting (NPH) insulin is usually given in split morning and evening doses or more frequently to achieve euglycemia. A method for calculating insulin dosage is shown in Box 16-1.


BOX 16-1 Method for Calculation of Starting Dose of Insulin.

Insulin units = body weight (kg)

×0.6 (First trimester)

×0.7 (Second trimester)

×0.8 (Third trimester)

Dosage schedule: give 2/3 in AM and 1/3 in PM

Before breakfast: 2/3 NPH, 1/3 regular or lispro

Before dinner: 1/2 NPH, 1/2 regular or lispro (if on lispro, administer additional dose before bedtime snack)



Diabetic patients should be encouraged to engage in mild to moderate aerobic exercise (e.g., brisk walking) for about half an hour after meals.

Antepartum Obstetric Management

Aside from achieving euglycemia, adequate surveillance should be maintained during pregnancy to detect and possibly mitigate maternal and fetal complications. In pregestational diabetic patients, or in those with GDMs diagnosed before 20 weeks, a first-trimester dating ultrasound followed by a detailed obstetric ultrasonic study, fetal echocardiogram, and maternal serum alpha-fetoprotein level should be obtained at 16 to 20 weeks to check for congenital malformations. Maternal renal, cardiac, and ophthalmic functions must be closely monitored. The HbA1C should be obtained at the first prenatal visit, which is preferably scheduled early in the first trimester. Individuals with significantly elevated values (>8.5%) should be particularly targeted for careful ultrasonic assessment for congenital anomalies. Regular electronic, biochemical, and ultrasonographic fetal monitoring should be performed. For diabetic classes A, B, and C, fetal macrosomia is common and should be investigated, whereas for classes D, F and R, fetal growth restriction occurs more commonly.

Serial fetal testing should be performed in the third trimester. In patients with GDM on diet, fetal testing can be initiated at term; while in those on insulin, fetal testing should be initiated between 32 and 34 weeks of gestation or sooner if complications develop.

If the maternal state is stable, blood glucose is in the euglycemic range, and fetal studies indicate a healthy baby, spontaneous onset of labor at term may be awaited. Earlier intervention is indicated if these conditions are not met. For macrosomic babies, increased birth trauma to both mother and fetus should be kept in mind. Cesarean delivery may be elected for large fetuses (>4250 to 4500 g).

Intrapartum Management

Intrapartum management of a diabetic patient requires the establishment of maternal euglycemia during labor. This may be achieved by giving a continuous infusion of regular insulin. Plasma glucose levels are measured frequently, and insulin dosage is adjusted accordingly to maintain a plasma glucose level between 80 and 120 mg/dL. Not all insulin-dependent patients require exogenous insulin during labor. Continuous electronic fetal heart rate monitoring is recommended for all diabetic patients.

Postpartum Period

After delivery of the fetus and placenta, insulin requirements drop sharply because the placenta, which is the source of many insulin antagonists, has been removed. Many insulin-dependent diabetic patients may not require exogenous insulin for the first 48 to 72 hours after delivery. Plasma glucose levels should be monitored and lispro or regular insulin given when plasma glucose levels are elevated. Patients can be restarted on two thirds of the prepregnancy insulin dosage, with adjustments made as necessary. Gestational diabetic patients (with class A1 and A2 disease) frequently do not need insulin therapy postpartum. A fasting blood glucose or a 75-g oral glucose tolerance test should be performed at 6 to 12 weeks postpartum.

Patients should be counseled about changes in diet. The American Dietetic Association diet with the same distribution of carbohydrates, proteins, and fat should be maintained. If the mother is breastfeeding, 500 calories/day should be added to the prepregnant diet.

Sterilization should be discussed with patients who desire it and those with advanced vascular involvement.


Normal Thyroid Physiology during Pregnancy

With the increase in glomerular filtration rate that occurs during pregnancy, the renal excretion of iodine increases, and plasma inorganic iodine levels are nearly halved. Goiters due to iodine deficiency are not likely if plasma inorganic iodine levels are greater than 0.08 μg/dL. Inorganic iodine supplementation up to a total of 250 μg/day is sufficient to prevent goiter formation during pregnancy.


The free thyroxine (free T4) concentration is the only accurate method of estimating thyroid function that compensates for changes in thyroxine-binding globulin (TBG) capacity because serum levels of bound triiodothyronine (total T3) and total T4 are increased during pregnancy. Values of thyroid function tests during pregnancy are shown in Table 16-4.




Before 10 weeks’ gestation, no organic iodine is present in the fetal thyroid. By 11 to 12 weeks, the fetal thyroid is able to produce iodothyronines and T4, and by 12 to 14 weeks, it is able to concentrate iodine. Fetal thyroid-stimulating hormone (TSH), T4, and free T4 levels suggest that a mature, autonomous, thyroid-pituitary axis exists as early as 12 weeks’ gestation.


Iodide freely crosses the placenta, but TSH does not. Limited transfer of T4 occurs across the placenta and appears to be important for fetal neural development in the first trimester before fetal thyroid function begins. Thyroid hormone analogues such as propylthiouracil and methimazole, with smaller molecular weights, cross the placental barrier and could potentially cause fetal hypothyroidism.

Thyroid-releasing hormone (TRH) can cross the placental barrier, but there is no significant placental transfer because of circulating low levels. Thyroid-stimulating antibodies also cross the placenta and can potentially cause fetal thyroid dysfunction.

Maternal Hyperthyroidism

The incidence of maternal thyrotoxicosis is about 1 per 500 pregnancies. It is accompanied by an increased incidence of prematurity, intrauterine growth restriction (IUGR), superimposed preeclampsia, stillbirth, and neonatal morbidity and mortality. Graves’ disease is an autoimmune disorder caused by thyroid-stimulating antibodies and is the most common cause of hyperthyroidism. Other causes of hyperthyroidism in pregnancy include hydatidiform mole and toxic nodular goiter. Patients with Graves’ disease tend to have a remission during pregnancy and an exacerbation during the postpartum period. The increased immunologic tolerance during pregnancy may lead to a decrease in thyroid antibodies to account for the remission.


The clinical diagnosis of hyperthyroidism in pregnancy is difficult because many of the signs and symptoms of the hyperdynamic circulation associated with hyperthyroidism are present in a normal euthyroid pregnant individual. A resting pulse rate greater than 100 beats/minute that fails to slow with a Valsalva maneuver, eye changes, loss of weight, failure to gain weight despite normal or increased food intake, and heat intolerance are all helpful in making the clinical diagnosis.


An elevated serum free T4 level and a suppressed TSH level establish the diagnosis of hyperthyroidism. Infrequently, a free T3 determination might be needed to diagnose T3 thyrotoxicosis.


Because radioactive iodine treatment is contraindicated during pregnancy, medical treatment is generally employed. Thioamides are the mainstay of antithyroid therapy. They block the synthesis but not the release of thyroid hormone. Propylthiouracil (PTU) and methimazole (Tapazole) have been used interchangeably, although PTU has the added advantage of blocking conversion of T4 to T3, and methimazole may cause fetal gastrointestinal defects. Because these drugs readily cross the placenta, a concern during maternal treatment is the development of fetal goiter and hypothyroidism.Although there is no conclusive evidence that PTU treatment leads to cretinism or abnormalities in physical or intellectual development, up to 1% to 5% of children exposed in utero will develop a goiter. For this reason antithyroid drugs are reduced to the lowest dose that results in free T4 levels within the upper range of normal. Levels should be checked every 2 to 4 weeks. Antithyroid therapy can often be discontinued after 30 weeks of gestation.

Propylthiouracil excretion in breast milk is minimal, and no changes occur in the thyroid function tests of breastfed neonates.

Surgical management of the hyperthyroid pregnant patient during the second trimester is recommended only if medical treatment fails.

Thyroid Storm

The major risk in a pregnant patient with thyrotoxicosis is the development of a thyroid storm. Precipitating factors include infection, labor, cesarean delivery, or noncompliance with medication.It is not uncommon to mistakenly attribute the signs and symptoms of severe hyperthyroidism to preeclampsia. In the former, significant proteinuria is usually absent. The maternal mortality of thyroid storm exceeds 25% despite good medical management. The signs and symptoms associated with a thyroid storm include hyperthermia, marked tachycardia, perspiration, and high output failure or severe dehydration.

Specific treatment is directed at (1) blocking β-adrenergic activity with propranolol, 20 to 80 mg every 6 hours; (2) blocking secretion of thyroid hormone with sodium iodide, 1 g intravenously; (3) blocking synthesis of thyroid hormone and conversion of T4 to T3 with 1200 to 1800 mg of PTU given in divided doses; (4) further blocking the deamination of T4 to T3 with 8 mg of dexamethasone per day; (5) replacing fluid losses; and (6) rapidly lowering the temperature with hypothermic techniques.

Neonatal Thyrotoxicosis

About 1% of pregnant women with a history of Graves’ disease give birth to children with thyrotoxicosis due to transplacental transfer of thyroid-stimulating antibodies. It is transient and lasts less than 2 to 3 months but is associated with a neonatal mortality rate of about 16%. Fetal thyrotoxicosis can be suspected if the baseline fetal heart rate consistently exceeds 160 beats/minute. A fetal goiter can often be identified by ultrasonography in such cases. This situation is associated with an increase in perinatal morbidity and mortality and should be treated prenatally and postnatally.


Pregnant women on appropriate thyroid replacement therapy can expect a normal pregnancy outcome, but untreated maternal hypothyroidism has been associated with an increased risk for spontaneous abortion, preeclampsia, abruption, low-birth-weight or stillborn infants, and lower intelligence levels in the offspring.

The most important laboratory finding to confirm the diagnosis of hypothyroidism is an elevated TSH level. Other findings include low levels of serum free T3 and free T4. Once diagnosed, therapy such as levothyroxine should be started and serum TSH levels performed monthly with appropriate adjustments in levothyroxine dosage.


Thyroid hormone deficiency during the fetal and early neonatal periods leads to generalized developmental retardation. The severity of symptoms depends on the time of onset and the severity of the deprivation.

The incidence of congenital hypothyroidism (cretinism) is about 1 in 4000 births. The etiologic factors include thyroid dysgenesis, inborn errors of thyroid function, and drug-induced endemic hypothyroidism. The most common cause of neonatal goiter is maternal ingestion of iodides present in cough syrup. The goiters associated with maternal iodine ingestion are large and obstructive, unlike those associated with maternal PTU treatment.

image Heart Disease

The categories of heart disease in pregnancy include rheumatic and congenital cardiac disease as well as arrhythmias, cardiomyopathies and other forms of acquired heart disease. Better treatment of rheumatic fever and improvements in medical and surgical management of congenital heart disease has meant that in a modern tertiary referral center, about 80% of patients with cardiac disease in pregnancy now have congenital heart disease.


The most common lesion associated with rheumatic heart disease is mitral stenosis. Regardless of the specific valvular lesion, patients are at higher risk for developing heart failure, subacute bacterial endocarditis, and thromboembolic disease. They also have a higher rate of fetal wastage.

Pure mitral stenosis is found in about 90% of patients with rheumatic heart disease. During pregnancy, the mechanical obstruction worsens as cardiac output increases. Asymptomatic patients may develop symptoms of cardiac decompensation or pulmonary edema as pregnancy progresses. Atrial fibrillation is more common in patients with severe mitral stenosis, and nearly all women who develop atrial fibrillation during pregnancy experience congestive heart failure. However, pulmonary congestion and heart failure develop in only half of women in whom atrial fibrillation predates pregnancy. Tachycardia can result in decompensation because cardiac output in patients with mitral stenosis depends on an adequate diastolic filling time.


Congenital heart disease includes atrial or ventricular septal defects, primary pulmonary hypertension (Eisenmenger’s syndrome), and cyanotic heart disease such as tetralogy of Fallot or transposition of the great arteries. If the anatomic defect has been corrected during childhood with no residual damage, the patient is expected go through pregnancy without complications. Patients with persistent atrial or ventricular septal defects and those with tetralogy of Fallot with complete surgical correction generally tolerate pregnancy well. However, patients with primary pulmonary hypertension or cyanotic heart disease with residual pulmonary hypertension are in danger of undergoing decompensation during pregnancy. Pulmonary hypertension from any cause is associated with an increased risk for maternal mortality during pregnancy or in the immediate postpartum period. In all these patients, care should be taken to avoid overloading the circulation and precipitating pulmonary congestion, heart failure, or hypotension with reversal of the left-right shunt, all of which may lead to hypoxia and sudden death. In general, significant pulmonary hypertension with Eisenmenger’s syndrome is a contraindication to pregnancy.


Supraventricular tachycardia is the most common cardiac arrhythmia. It is usually benign and occurs secondary to structural changes in the heart that have presumably been present since birth. Atrial fibrillation and atrial flutter are more serious and are usually associated with underlying cardiac disease.


This entity is rare but occurs exclusively during pregnancy. Patients have no underlying cardiac disease, and symptoms of cardiac decompensation appear during the last weeks of pregnancy or within 6 months postpartum. Pregnant women particularly at risk for developing cardiomyopathy are those with a history of preeclampsia or hypertension and those who are poorly nourished. It appears to be a dilational cardiomyopathy with decreased ejection fraction. Hypertensive cardiomyopathy, ischemic heart disease, viral myocarditis, and valvular heart disease must be excluded in patients with cardiac dysfunction before the diagnosis can be made. The mortality rate is at least 20%. About 30% to 50% of patients have persistent cardiac dysfunction, and recurrence occurs in about 20% to 50% of patients in a subsequent pregnancy.


The New York Heart Association’s functional classification of heart disease is of value in assessing the risk for pregnancy in a patient with acquired cardiac disease and in determining the optimal management during pregnancy, labor, and delivery (Table 16-5). In general, the maternal and fetal risks for patients with class I and II disease are small, whereas risks are greatly increased with class III and IV disease or if there is cyanosis. However, the type of defect is important as well. Mitral stenosis and aortic stenosis carry a higher risk for decompensation than do regurgitant lesions. Other patients at high risk include those with significant pulmonary hypertension, a left ventricular ejection fraction less than 40%, Marfan syndrome, a mechanical valve, or a previous history of a cardiac event or arrhythmia.


Class I

No signs or symptoms of cardiac decompensation

Class II

No symptoms at rest, but minor limitation of physical activity

Class III

No symptoms at rest, but marked limitation of physical activity

Class IV

Symptoms present at rest, discomfort increased with any kind of physical activity

Prenatal Management

As a general principle, all pregnant cardiac patients should be managed with the help of a cardiologist. A careful history and physical examination, along with an electrocardiogram and echocardiogram, should be performed. The patient should be counseled about risks associated with pregnancy and all options presented. Frequent prenatal visits are indicated, and frequent hospital admissions may be needed, especially for patients with class III and IV cardiac disease.

Avoidance of excessive weight gain and edema. Cardiac patients should be placed on a low-sodium diet (2 g/day) and encouraged to rest in the left lateral decubitus position for at least 1 hour every morning, afternoon, and evening to promote diuresis. Adequate sleep should be encouraged. If there is evidence of chronic left ventricular failure not adequately treated with sodium restriction, a loop diuretic and β blockers should be added. Aldosterone antagonists should be avoided because of their potential antiandrogen effects on the fetus.


Individuals with significant heart disease are unable to increase their cardiac output to the same extent as healthy individuals to meet the increased metabolic demands associated with exercise.


With anemia, the oxygen-carrying capacity of the blood decreases. Oxygen delivery to tissues is generally maintained by increased cardiac output. An increase in heart rate, especially with mitral stenosis, leads to a decrease in left ventricular filling time, resulting in pulmonary congestion and edema. Another factor that might lead to cardiac decompensation is the inability of the right ventricle to efficiently pump a percentage of the venous return.


Women with mechanical valves require full anticoagulation with heparin in pregnancy. Warfarin may be restarted post partum.

Management of Delivery and the Immediate Postpartum Period

Cardiac patients should be delivered vaginally unless obstetric indications for cesarean are present. They should be allowed to labor in the lateral decubitus position with frequent assessment of vital signs, urine output, and pulse oximetry. Adequate pain relief is important. Pushing should be avoided during the second stage of labor because the associated increase in intraabdominal pressure increases venous return and cardiac output and can lead to cardiac decompensation. The second stage of labor can be assisted by performing an outlet forceps delivery or by the use of a vacuum extractor.

The immediate postpartum period presents special risks to the cardiac patient. After delivery of the placenta, the uterus contracts, and about 500 mL of blood is added to the effective blood volume. Cardiac output increases up to 80% above prelabor values in the first few hours after a vaginal delivery and up to 50% after cesarean delivery. To minimize the risk for overloading the circulation, careful attention is paid to fluid balance and prevention of uterine atony. Methergine should be avoided owing to its vasoconstrictor effects.

Of particular concern is the risk for endocarditis. The 2007 guidelines from the American Heart Association state that delivery does not increase the risk for infectious endocarditis. Antibiotic prophylaxis is only recommended for high-risk patients (e.g., prosthetic valves, unrepaired or incompletely repaired congenital heart disease, congenital heart disease repaired with prosthetic material, previous history of bacterial endocarditis and valvulopathy in heart transplants) if bacteremia is suspected (such as in the setting of chorioamnionitis).

Acute cardiac decompensation with congestive heart failure should be managed as a medical emergency. Medical management may include administration of morphine sulfate, supplemental oxygen, and an intravenous loop diuretic (e.g., furosemide) to reduce fluid retention and preload. β Blockers should not be used in the setting of acute heart failure. Vasodilators such as hydralazine, nitroglycerin, and rarely nitroprusside are used to improve cardiac output by decreasing afterload. Some patients may require inotropic support with dobutamine or dopamine. The use of digitalis is controversial. Angiotensin-converting enzyme inhibitors are contraindicated in pregnancy. Calcium channel blockers such as nifedipine may accelerate the progression of congestive heart failure and should be avoided. Continuous pulse oximetry can be very helpful in managing these patients. Monitoring with a pulmonary artery catheter can provide a good index of left ventricular function but is discouraged in those with pulmonary hypertension.

image Autoimmune Disease in Pregnancy

An autoimmune disease is one in which antibodies are developed against the host’s own tissues. A summary of the interactions of primary immunologic disorders and pregnancy is shown in Table 16-6.




In this condition thrombocytopenia occurs when peripheral platelet destruction exceeds bone marrow production. Idiopathic thrombocytopenia (ITP) is considered to be an autoantibody disorder in which immunoglobulins attach to maternal platelets leading to platelet sequestration in the reticuloendothelial system. ITP may be confused with gestational thrombocytopenia. The latter is unlikely to have a platelet count less than 70,000/μL, is not associated with bleeding complications, occurs late in pregnancy, and resolves after delivery.


Therapy is usually not initiated unless platelet counts are less than 40,000/μL or petechial hemorrhages are present. Prednisone at a dose of 1 mg/kg per day is given initially, maintained for 2 to 3 weeks, then tapered slowly. Severe ITP can be treated with intravenous immunoglobulin (IVIG), or if the patient is Rh positive, anti-D antibody infusions, which can raise the platelet count within 12 to 48 hours. In patients with life-threatening hemorrhage, platelet transfusions, combined with high-dose steroids and IVIG, may be requiredSplenectomy is a last resort for patients who fail to respond to medical therapy. Platelet transfusions are also indicated if the maternal platelet count is less than 20,000 before vaginal delivery, or less than 40,000 before cesarean delivery.

The neonate should be monitored for thrombocytopenia because placental transfer of maternal antiplatelet antibodies can occur. Rarely, neonatal intracranial hemorrhage occurs once the neonatal platelet count reaches its nadir after the first 2 to 3 days of life. There is no correlation between fetal platelet counts and neonatal outcome; thus, monitoring fetal platelet counts is not done in pregnancy. Vaginal delivery is generally carried out because there is no good evidence that the fetal outcome is improved by cesarean delivery, and surgery carries additional maternal risks.


Lupus occurs mainly in women. Associated antibodies include antinuclear, anti-RNP and anti-SM antibodies; anti-dsDNA is associated with nephritis and lupus activity; anti-Ro (SS-A) and anti-La (SS-B) are present in Sjögren’s syndrome and neonatal lupus with heart block; while antihistone antibody is common in drug-induced lupus. The diagnosis of systemic lupus is made if 4 or more of the 11 revised criteria of the American Rheumatism Association are present, serially or simultaneously (Table 16-7).




Malar rash

Malar erythema

Discoid rash

Erythematous patches, scaling, follicular plugging



Oral ulcers

Usually painless


Nonerosive involving two or more peripheral joints


Pleuritis or pericarditis

Renal disorder

Proteinuria > 0.5 g/day or > 3+ dipstick, or cellular casts

Neurologic disorders

Seizures or psychosis without other cause

Hematologic disorders

Hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia

Immunologic disorders

Anti-dsDNA or anti-Sm antibodies, or false-positive VDRL, immunoglobulin M or G anticardiolipin antibodies, or lupus anticoagulant

Antinuclear antibodies

Abnormal titer of antinuclear antibodies

VDRL, Venereal Disease Research Laboratory.

 If four criteria are present at any time during course of disease, systemic lupus can be diagnosed with 98% specificity and 97% sensitivity.

From Hochberg MC: Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 40(9):1725, 1997. Copyright 1997 American College of Rheumatology. Reprinted with permission of John Wiley & Sons, Inc.

During pregnancy, lupus improves in one third of women, remains unchanged in one third, and worsens in the remaining third. A lupus flare can be life threatening, but it is difficult to differentiate a lupus flare from superimposed preeclampsia (and both may coexist). Often only a trial of therapy will distinguish between the two. Flares and active disease can generally be managed with steroids, such as prednisone, 1 mg/kg per day.

Fetal and neonatal complications include an increased rate of preterm delivery, fetal growth restriction, and stillbirth, especially when associated with antiphospholipid antibodies. These pregnancies require close monitoring, often with weekly maternal and fetal assessments once they reach the third trimester. There is about a 10% risk for neonatal lupus, which is characterized by skin lesions, hematologic manifestations such thrombocytopenia or hemolysis, systemic effects such as hepatic involvement, and occasionally congenital heart block.


Antiphospholipid antibodies are circulating antibodies to negatively charged phospholipids. They include lupus anticoagulant, anticardiolipin immunoglobulin G (IgG), or IgM antibodies and β2-glycoprotein I antibodies. They may occur alone or in association with lupus. Antiphospholipid antibody syndrome is defined as the presence of at least one antibody in association with arterial or venous thrombosis with or without one or more obstetric complication (unexplained fetal demise after 10 weeks’ gestation or severe preeclampsia or fetal growth restriction before 34 weeks’ gestation). Lupus anticoagulant can be screened for with an activated partial prothrombin time or the dilute Russell viper venom test (DRVVT); a sensitive and specific radioimmunoassay is available for the detection of anticardiolipin. In pregnancy, a history of antiphospholipid antibody syndrome is treated with intermediate-dose heparin or low-molecular-weight heparin and baby aspirin, unless there is a history of thrombosis, in which case full-dose anticoagulation is indicated.

image Renal Disorders


Acute renal failure during pregnancy or in the postpartum period may be due to deterioration of renal function secondary to a preexisting renal disease or to a pregnancy-induced disorder. The underlying causative factors may be prerenal, renal, or postrenal. With prerenal causes, a history of blood or fluid loss, such as occurs with obstetric hemorrhage, is usually apparent or can be elicitedRenal causes are usually suspected in a patient with a history of preexisting renal disease or with a hypercoagulable state, such as thrombotic thrombocytopenic purpura or hemolytic-uremic syndrome Prolonged hypotension can lead to acute cortical necrosis or acute tubular necrosis. Postrenal causes are less common but should be suspected in situations in which urologic obstructive lesions are present or in which there is a history of kidney stones.

Laboratory Studies

Laboratory tests are directed at assessing renal function, cardiovascular status, and the patency of the urologic tract.


Renal studies include urine output, blood urea nitrogen (BUN)-to-creatinine ratio, fractional excretion of sodium, and urine osmolality. Oliguria is defined as urine output of less than 25 mL/hour, whereas anuria is the cessation of urine output. Not infrequently, a decrease in urine output alerts the physician to an impending crisis. During pregnancy, the serum values of BUN and creatinine decrease, but the BUN-to-creatinine ratio remains about 20:1. A ratio greater than 20:1 suggests tubular hypoperfusion (prerenal failure).

Urine osmolality greater than 500 mOsm/L or a urine-to-plasma osmolality ratio greater than 1.5:1 is highly suggestive of renal hypoperfusion. Urine specific gravity is of limited value, especially when the urine contains protein or hemolyzed blood.


Acute blood and fluid losses are usually associated with orthostatic hypotension, tachycardia, decreased skin turgor, and reduced sweating. In a pregnant hypertensive or preeclamptic patient who is in labor, many of these signs are overlooked. If indicated, a Swan-Ganz catheter allows monitoring of right and left ventricular filling pressures, cardiac output, and pulmonary capillary wedge pressure. This can help to distinguish between congestive heart failure, cardiac tamponade, and volume depletion, any of which can lead to acute renal failure.


A Foley catheter and renal sonogram are usually sufficient to diagnose obstructive lesions. Rarely, a one-shot intravenous pyelogram is needed. It is important not to mistake the physiologic hydronephrosis of pregnancy for true obstruction.



Restoration of intravascular volume, cardiac output, and arterial pressure to normal values is sufficient to reverse oliguria. Careful attention should be given to electrolyte imbalance when large amounts of crystalloids are infused.


Acute tubular necrosis, acute cortical necrosis, or both, may be present. Because acute cortical necrosis is generally irreversible, treatment is directed toward preventing further damage. A trial of diuretic therapy to increase urinary output appears to decrease the duration and severity of acute tubular necrosis and increase survival rates. Furosemide (Lasix) is given initially and repeated every 4 to 6 hours for 48 hours in the presence of adequate urinary response. If the diuretic therapy fails to increase the urine output, an oliguric fluid regimen (<500 mL/24 hr) is initiated. Fluid intake should be limited to replacement of urine output and insensible water loss, and renal function studies should be monitored on a daily basis. For the first few days after the renal ischemic episode, renal function may worsen, but within 7 to 10 days, most patients with acute tubular necrosis show marked improvement. If renal function deteriorates rapidly or fails to recover, hemodialysis is recommended.

In some patients in whom acute renal failure is accompanied by oliguria, a diuretic phase coincides with the recovery period. The urine output may exceed 10 L/day, and if fluid and electrolyte losses are not replaced promptly, death ensues. About 50% of obstetric patients who develop acute renal failure during pregnancy or the postpartum period recover enough renal function during the first year to survive without dialysis.


In many instances, simple measures, such as turning the patient on the left side to displace the gravid uterus away from the ureters, or inserting a Foley catheter into the bladder to overcome urethral obstruction, will resolve the problem. In situations in which a ureteral or renal pelvic obstruction is present (e.g., stones), surgical intervention is indicated to relieve the obstruction.


The outcome of pregnancies complicated by chronic renal disease is less favorable. Good pregnancy outcome may be expected in mild renal disease. There is increased risk for adverse fetal outcome and loss of maternal renal function with increasing renal insufficiency severity. In general a serum creatinine greater than 1.5 to 2.0, especially if accompanied by hypertension or nephrotic syndrome, greatly worsens the prognosis for the mother and fetus. Management principles include serial monitoring of renal function by 24-hour urinary creatinine clearance and protein excretion, and screening for asymptomatic bacteruria. Diastolic pressure should be maintained at 90 mm Hg or less to prevent further renal damage. Superimposed preeclampsia is more difficult to diagnose because hypertension and proteinuria are already present. Fetal surveillance is important to assess fetal growth and well-being.


Pregnancy after renal transplantation should not be considered before a thorough assessment of maternal, fetal, and neonatal risk factors is undertaken. Hypertension (up to 70%) and preeclampsia are common in women with renal transplantation, and up to 14% experience significant loss of graft function or graft rejection. Fetal complications include steroid-induced adrenal and hepatic insufficiency, prematurity, and IUGR. In addition, the infant may inherit the primary disease of the mother or other family members. The mother and neonate are at increased risk for infection because of immunosuppressive therapy.

Patients who are good candidates for pregnancy are those who are 1 to 2 years posttransplantation, have stable renal function (serum creatinine < 1.5 and proteinuria < 500 mg/day), are not significantly hypertensive, and are on low doses of prednisone and stable doses of azathioprine and cyclosporine. These medications do not appear to have significant teratogenic effects, but long-term consequences on growth, immune function, and neurocognitive development are unknown. Cyclosporine may have adverse maternal consequences, including a rise in blood pressure, a decline in renal function, hyperkalemia, hyperuricemia, and less frequently, hemolytic-uremic syndrome.

image Gastrointestinal Disorders


About 60% to 80% of pregnant women complain of nausea and vomiting during the first 8 to 12 weeks of gestation. The symptoms are usually mild and disappear during the early part of the second trimester. The underlying causes of nausea and vomiting during pregnancy are not well understood.

Treatment is usually symptomatic. Patients are instructed to refrain from eating large and late meals, to avoid the recumbent position, especially after meals, and to use an extra pillow to elevate the head when sleeping. Many patients respond to pyridoxine (vitamin B6), whereas others may require antiemetics such as promethazine.


Hyperemesis gravidarum is defined as persistent nausea and vomiting in pregnancy that is associated with ketosis and weight loss (>5% of prepregnancy weight). Even though the exact cause is unknown, proposed theories include psychological abnormalities, hormonal changes such as high human chorionic gonadotropin (hCG) and estradiol levels, gastric dysrhythmias, hyperacuity of the olfactory system, subclinical vestibular disorders, and impairment of mitochondrial fatty acid oxidation. The overall incidence is about 1%. The disorder appears more frequently with first pregnancies, multiple pregnancies, and those with trophoblastic disease, but tends to recur with subsequent pregnancies. Pregnancy outcome is usually good.

A history of intractable vomiting beginning in the first trimester and inability to retain food and fluid is usually elicited. Physical findings of weight loss, dry and coated tongue, and decreased skin turgor are very suggestive. Significant abdominal pain and tenderness are generally absent. Laboratory workup includes urine tests for ketonuria and blood tests for electrolytes and acetone. Electrolyte disturbances may include hypokalemia, hyponatremia, and hypochloremic alkalosis. Amylase and lipase levels may be elevated.

Treatment is symptomatic, but if outpatient management fails, patients must be admitted for intravenous administration of fluids, electrolytes, glucose, vitamins, and medical therapy. Vitamin B6 (pyridoxine), doxylamine, antihistamines, antiemetics of the phenothiazine class, and promotility agents (e.g., metoclopramide), and droperidol are used. Acupressure and ginger have been shown to be beneficial. The few who do not respond to medical therapy may require nasogastric feeding or parenteral nutrition.


Reflux esophagitis or heartburn occurs in about 70% of pregnant women. The main symptoms include substernal discomfort aggravated by meals and the recumbent position and occasional hematemesis. An unusual symptom peculiar to reflux esophagitis is water brash, which is best described as the sudden filling of the mouth with clear, watery material that has a salty taste and produces a nauseous sensation.


Treatment is usually symptomatic. Patients are instructed to refrain from eating large and late meals, to avoid the recumbent position, especially after meals, and to use an extra pillow to elevate the head when sleeping. Antacids can be helpful and should be taken 1 to 3 hours after meals and at bedtime. A histamine-2 (H2) blocker (cimetidine) or proton pump blocker (omeprazole) is indicated if there is no response to the above measures.


Pregnancy conveys relative protection against the development of peptic ulceration and may ameliorate an already present ulcer. Gastric acid secretion is probably not altered during pregnancy, although some studies suggest modest suppression. The diagnosis of ulcer disease is mainly based on symptomatic improvement in response to conservative treatment. Endoscopy is reserved for patients who do not respond to treatment, have more severe gastrointestinal symptoms, or manifest significant gastrointestinal hemorrhage. Treatment involves avoiding caffeine, alcohol, tobacco, and spicy foods and administering antacids, proton pump inhibitors, or H2-receptor antagonists. Antibiotic therapy is indicated for patients with Helicobacter pylori infection.


The pregnant patient in labor is at an increased risk for acid aspiration because of delayed gastric emptying. This is made worse when associated with increased anxiety or the use of sedatives, narcotics, and anticholinergic agents and increased intraabdominal and intragastric pressure, making regurgitation more likely. Damage to the pulmonary tissue is greatest when the pH of the aspirated fluid is less than 2.5 or the volume of the aspirate is greater than 25 mL. Acute gastric aspiration is a cause of adult respiratory distress syndrome (ARDS). Treatment consists of supplemental oxygen, measures to maintain the airway, and usual therapy for treatment of acute respiratory failure.

Preventive efforts are directed at decreasing the acid secretion by the stomach. Toward this end, women are usually not fed during labor. Liquid magnesium and aluminum antacids may be given during labor to decrease the gastric acidity, but they increase the volume of the gastric acid-antacid emulsion. If the patient is to undergo any surgical procedure that requires general anesthesia, a “full stomach” should be presumed and intubation performed.


The two entities described under this disorder are Crohn disease (regional enteritis) and ulcerative colitis. In about 25% of patients with inflammatory bowel disease, differentiation between these two disorders is difficult.

Patients with inflammatory bowel disease do well during pregnancy, provided there are no acute exacerbations. It seems unlikely that the natural history of the disease changes during pregnancy. If inflammatory bowel disease is active at the time of conception, the spontaneous abortion rate is doubled. If surgery is required for complications of inflammatory bowel disease, fetal survival is reduced.


Treatment of an acute exacerbation is the same for pregnant and nonpregnant patients, although some of the more experimental drugs should not be used during pregnancy. If diarrhea is the main complaint, dietary restriction of lactose, fruits, and vegetables is necessary. If a lactose-free diet is used, calcium supplementation is needed. Constipating agents, such as Pepto-Bismol and psyllium hydrophilic mucilloid (Metamucil), may be used daily and are quite effective. The use of diphenoxylate-atropine (Lomotil) or loperamide (Imodium) should be restricted to patients in whom conservative management fails. For those patients with mild to moderate symptoms, sulfasalazine may be beneficial. Recently, several antibiotic regimens have been used to treat Crohn disease.

image Hepatic Disorders

Liver disorders that are peculiar to pregnancy are discussed next.


Although the pathogenesis of this syndrome is not known, some distinctive features are present: (1) cholestasis and pruritus in the second half of pregnancy without other major liver dysfunction, (2) a tendency to recurrencewith each pregnancy, (3) an association with oral contraceptives and multiple gestations, (4) a benign course in that there are no maternal hepatic sequelae, and (5) an increased rate of meconium-stained amniotic fluid and fetal demise. There is a high prevalence in Latin America with rates of 4% to 22%. The highest rates occur in Chile in winter. The prevalence in the United States has been reported from between 0.001% and 0.32%, with a high prevalence of 5.6% reported in a Latina population in Los Angeles.

Most probably, genetic, geographic, or environmental factors are involved. A mutation in the MDR3 gene may be associated with up to 15% of cases.

The main symptom is itching, without abdominal pain or a rash, which may occur as early as 20 weeks of gestation. Jaundice is rarely observed. Laboratory tests show elevated levels of serum bile acids. Serum levels of bilirubin and liver enzymes (e.g., aspartate and alanine transaminase) are usually normal but may be mildly elevated. If liver enzymes and bilirubin levels are significantly elevated, abdominal ultrasonography should be performed to exclude gallbladder obstruction, a hepatitis screen should be done to exclude viral hepatitis, and an autoantibody screen for primary biliary cirrhosis should also be undertaken.


Local measures such as cold baths, bicarbonate washes, or phenol (0.5% to 1% in water-soluble creams) may be of some help. The best results have been obtained with ursodeoxycholic acid. It significantly ameliorates the pruritus and reduces serum levels of bile acids, aminotransferases, and bilirubin. Serial fetal surveillance is performed in the third trimester, with delivery at term if testing remains reassuring.


Acute fatty liver of pregnancy is a serious complication that is peculiar to pregnancy. It is associated with diffuse microvesicular fatty infiltration of the liver resulting in hepatic failure. The incidence is about 1 per 10,000 pregnancies. It most commonly occurs in the third trimester of pregnancy or the early postpartum period. Although the cause is unknown, it may in some instances result from an inborn error of metabolism, possibly a deficiency of long-chain 3-hydroxyl coenzyme A dehydrogenase. Presentation is variable, with abdominal pain, nausea and vomiting, jaundice, and increased irritability. Extreme polydipsia or pseudodiabetes insipidus may be present. Hypoglycemia is infrequently present. Hypertension and proteinuria are present in about half of patients, raising the issue of coexisting preeclampsia. Invariably, patients suffer hepatic coma and renal failure.


Laboratory findings include an increase in prothrombin time (PT) and partial thromboplastin time (PTT), hyperbilirubinemia, hyperammonemia, hyperuricemia, and a moderate elevation of the transaminase levels. Hematemesis and spontaneous bleeding become manifest as disseminated intravascular coagulation (DIC) develops. Liver failure is indicated by elevated blood ammonia levels.


Termination of pregnancy and intensive supportive care are indicated on diagnosis. Treatment is mainly directed at supportive measures, such as administration of intravenous fluids with 10% glucose to prevent dehydration and severe hypoglycemia. For the coagulopathy of hepatic failure, vitamin K supplementation is not effective, and fresh-frozen plasma or cryoprecipitate should be given.

With early recognition, immediate delivery, and advances in critical care management, maternal mortality is about 7% to 18%, and fetal mortality about 9% to 23%. In those who survive, recovery is complete, with no signs of chronic liver disease.

image Thromboembolic Disorders

Pregnancy is a hypercoagulable state and is associated with an increased risk for superficial thrombophlebitis, deep venous thrombosis (DVT), and pulmonary embolism. The risk increases postpartum and with cesarean delivery.


This is more common in patients with varicose veins, obesity, or limited physical activity. In most patients, superficial thrombophlebitis is limited to the calf area, and symptoms include swelling and tenderness of the involved extremity. On physical examination, there is erythema, tenderness, warmth, and a palpable cord over the course of the involved superficial veins.

Superficial thrombophlebitis does not lead to pulmonary embolization. Bed rest, pain medications, and local application of heat are often sufficient treatment. There is no need for anticoagulants, but antiinflammatory agents may be considered. When symptoms disappear, patients may gradually begin to ambulate. They should be instructed to wear support hose to help avoid a repeat episode.


The incidence of DVT is 1 in 2000 patients antepartum and 1 in 700 patients postpartum. Virchow’s triad of vascular injury, infection, and tissue trauma, coupled with the hypercoagulability and venous stasis of pregnancy, are the triggering factors for DVT.


The clinical diagnosis of DVT is difficult. Half of cases are asymptomatic. DVT is much more common in the left than the right leg. Pain in the calf in association with dorsiflexion of the foot (positive Homans’ sign) is a clinical sign of DVT in the calf veins. Dull ache, tingling, tightness, or pain in the calf or leg, especially when walking, may be present. Acute swelling and pain in the thigh area and tenderness in the femoral triangle are suggestive of iliofemoral thrombosis.


Compression ultrasonography with Doppler flow studies is a noninvasive technique that has high sensitivity and specificity and is currently the primary mode of diagnosis used for DVT. Magnetic resonance imaging (MRI) has been used to evaluate patients suspected of having pelvic thrombosis with a negative Doppler ultrasonic examination. D-Dimers can be used in nonpregnant women to screen for DVT, but their use in pregnancy is unproved. The most reliable test for deep venous (noniliac) thrombosis is a well-performed venogram, but this is not generally performed because of the 2% risk for dye-induced phlebitis and radiation exposure, the latter dosage being between 0.05 and 0.628 Gy (see Table 16-8 on page 216).


When a clinical diagnosis of DVT is made, anticoagulant therapy should be started pending the results of a diagnostic workup. If the workup fails to identify any iliofemoral or calf thrombosis, therapy may be discontinued.

Treatment of proven DVT during pregnancy is initiated with either intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin (enoxaparin sodium) to achieve full anticoagulation. The unfractionated heparin dose is adjusted to 1.5 to 2.5 times the control activated PTT (aPTT). Intravenous anticoagulation should be maintained for at least 5 to 7 days, after which treatment is converted to subcutaneous heparin, which must be continued for the duration of pregnancy and up to 6 weeks postpartum with weekly monitoring of the aPTT. Alternatively, enoxaparin can be administered at a dose of 1 mg/kg subcutaneously every 12 hours. Although anti–factor Xa levels can be used to monitor enoxaparin’s anticoagulant activity, they are not generally useful because of the long lag in receiving results. Both forms of heparin may be associated with thrombocytopenia and osteoporosis. Supplemental calcium and vitamin D are advised along with periodic platelet counts.

Warfarin is a vitamin K antagonist, which crosses the placenta, carries the risks for fetal hemorrhage and teratogenesis and, with few exceptions, should only be used in the postpartum period. The International Normalized Ratio (INR) is commonly used to measure the effects of warfarin, and the target INR is 2.5 (range, 2.0 to 3.0).


The incidence of pulmonary embolism during pregnancy is about 1 in 2500. The maternal mortality rate is less than 1% if treated early and greater than 80% if left untreated. It is one of the most common causes of pregnancy-related deaths in the United States. In about 70% of cases, DVT is the instigating factor.


Suggestive symptoms include pleuritic chest pain, shortness of breath, air hunger, palpitations, hemoptysis, and syncopal episodes. Suggestive signs include tachypnea, tachycardia, low-grade fever, a pleural friction rub, chest splinting, pulmonary rales, an accentuated pulmonic valve second heart sound, and even signs of right ventricular failure. In most obstetric patients, the signs and symptoms of a pulmonary embolus are subtle.


An electrocardiogram can show sinus tachycardia with or without premature heartbeats or right ventricular axis deviation. On chest film, atelectasis, pleural effusion, obliteration of arterial shadows, and elevation of the diaphragm may be present. Arterial blood gases obtained on room air may show an oxygen tension below 80 mm Hg. Pulmonary embolism is ultimately a radiologic diagnosis. Three algorithms may be used: (1) If bilateral compression ultrasonography of the lower extremities is positive for DVT, a pulmonary embolism may be assumed in a symptomatic patient. (2) A ventilation-perfusion scan has minimal risk to the fetus, but it cannot be used in patients with an abnormal chest x-ray or in patients with asthma or chronic obstructive pulmonary disease. (3) Helical computed tomography has the advantage that the presence of a thrombus can be visualized by a noninvasive technique. It has comparative sensitivity to conventional pulmonary angiography and has been shown to be a cost-effective technique in pregnancy. Pulmonary angiography is rarely required because it is invasive, expensive, employs a higher radiation dose, and has a significant mortality.

Treatment of acute episodes and follow-up during pregnancy, labor, delivery, and the postpartum period are the same as for DVT.


A thrombophilia workup should be considered in patients with a pulmonary embolus, especially those with recurrent thromboses or a positive family history. Tests to order include those for acquired (lupus anticoagulant, anticardiolipin antibody) and inherited thrombophilias (factor V Leiden mutation, protein C, protein S and antithrombin III deficiencies, and the prothrombin G20210A mutation).


In pregnant patients with a history of a pulmonary embolus or DVT during a previous pregnancy, prophylactic doses of heparin or low-molecular-weight heparin are given during pregnancy and the immediate postpartum period. Minidose heparin (10,000 to 15,000 U/day) or enoxaparin sodium (40 mg once daily) provides sufficient prophylaxis for most patients, although some pregnant women may require full anticoagulation.

image Obstructive Lung Disease


The incidence of bronchial asthma in pregnancy is about 5% to 9%. Status asthmaticus, the most severe form of asthma, complicates about 0.2% of pregnancies. Asthma is a chronic inflammatory airway disorder with a major hereditary component and usually an allergic stimulant. Asthma currently is classified according to severity as (1) mild intermittent, (2) mild persistent, (3) moderate persistent, and (4) severe persistent. The course during pregnancy is variable. About 33% of patients improve, and 33% deteriorate.

Pulmonary function studies done during an acute episode show (1) increased airway resistance; (2) increased residual volume, functional residual capacity, and total lung capacity; (3) decreased inspiratory and expiratory reserve volume; (4) decreased vital capacity; and (5) decreased 1-second forced expiratory volume (FEV1), peak expiratory flow rate, and maximal mid-expiratory flow rate. Severe asthma is associated with an increased rate of miscarriagepreeclampsia, intrauterine fetal death, fetal growth restriction, and preterm birth. These complications may occur as a result of intrauterine hypoxia.

Obstetric Management

Pregnant asthmatic patients should be followed closely during pregnancy. The avoidance of dehydration, early and aggressive treatment of respiratory infections, and the avoidance of hyperventilation, excessive physical activity, and allergens are important. Serial measurements of peak expiratory flow rates can provide useful information on respiratory status. For those with mild intermittent asthma, a short-acting inhaled β2 agonist can be used as needed. Patients with mild persistent asthma should be treated with a low-dose inhaled corticosteroid. The preferred treatment for moderate persistent asthma is a combination of a daily inhaled corticosteroid and a long-acting β2 agonist. Those with severe persistent asthma may require the addition of a systemic corticosteroid. Alternative therapies include inhaled cromolyn sodium, leukotriene receptor antagonists, or sustained-release theophylline. Acute severe exacerbations must be treated aggressively with oxygen therapy, intravenous fluids, intravenous corticosteroids, and administration of β2 agonists by nebulized aerosol and antibiotics if there is evidence of bacterial infection. A few patients may require endotracheal intubation and mechanical ventilation to maintain an adequate oxygen supply.

Serial fetal monitoring and ultrasonic assessment of fetal growth should be implemented. The timing of delivery is dependent on the status of both the mother and the fetus. If pregnancy is progressing well, there is no need for early intervention, and it is advisable to await the spontaneous onset of labor. Early delivery can be considered for fetal growth restriction or maternal deterioration.

Management of Labor and Delivery

Glucocorticoid therapy, including inhaled or high-potency topical use for more than 3 weeks, may suppress the hypothalamic-pituitary-adrenal axis. Delivery is probably associated with moderate surgical stress, and stress doses of steroids should be considered. A selective epidural block during labor reduces pain, anxiety, hyperventilation, and respiratory effort, all of which are known to aggravate the disease or precipitate an attack. Vaginal delivery should be anticipated. Cesarean delivery is performed only for obstetric reasons.


Because of improvements in diagnosis and treatment, most females with cystic fibrosis now survive to adulthood. Cystic fibrosis is due to mutations in cystic fibrosis conductance transmembrane regulator, or CFTR, which is the gene that regulates epithelial cell chloride channel function. It is the most severe form of obstructive lung disease observed during pregnancy, but there is no evidence that pregnancy increases the maternal risk. However, those with pulmonary hypertension should be counseled against pregnancy. There are risks for superimposed infections during pregnancy. Exocrine pancreatic insufficiency is present in about 90% of patients with cystic fibrosis. Women with malabsorption symptoms might become more emaciated during pregnancy. Preconception counseling is recommended. The fetus is at increased risk for IUGR and premature delivery.

For labor and delivery, epidural analgesia is recommended. Outlet forceps or vacuum-assisted delivery should also be considered. The Valsalva maneuver should be avoided because of the associated increase in maternal oxygen requirements. Breastfeeding is recommended unless the maternal condition does not allow it.

image Seizures

In most cases, seizure frequency does not change in pregnancy. Factors during pregnancy that may contribute to increased seizure frequency include nausea and vomiting leading to missed doses, decreased gastrointestinal motility, expanded intravascular volume lowering serum drug levels, induction of enzymes increasing drug metabolism, and increased glomerular filtration hastening drug clearance.


If patients have no seizure activity for at least 2 years, antiepileptic drug (AED) therapy can be discontinued before conception. If patients are pregnant and their seizures are well controlled, no change in therapy should be attempted. The AED that is effective should be used. Monotherapy should be attempted using the lowest drug dose that will control the seizures. There is no ideal anticonvulsant in pregnancy, and all AEDs should be considered potential teratogens. Valproate should probably not be used because it is has been shown to be more teratogenic when compared with other AEDs.

Historically, the two most commonly used drugs for seizure treatment have been phenytoin (Dilantin) and phenobarbital. Phenobarbital at a dose of 100 to 250 mg/day may be given in divided doses. The serum levels are monitored, and the dose is increased gradually until a therapeutic level (10 to 40 μg/mL) is reached. Phenytoin may be given at 300 to 500 mg/day, in single or divided doses, to achieve serum levels of 10 to 20 μg/mL (1 to 2 μg/mL free level). Other first-generation AEDs include trimethadione, clonazepam (Klonopin), and carbamazepine (Tegretol). Second-generation AEDs includelamotrigine, topiramate, and gabapentin.

Women on AEDs should take 1 mg/day of folate supplementation. Those on carbamazepine or valproate should take 4 mg per day of folate supplementation. Oral vitamin K supplementation, 10 mg/day, should be considered in the last month of pregnancy for women taking enzyme-inducing AEDs (e.g., phenobarbital, carbamazepine, phenytoin, topiramate, oxcarbazepine). Phenytoin interferes with intestinal calcium absorption, leading to maternal and fetal hypocalcemia. In patients taking phenobarbital, primidone, or phenytoin, vitamin D supplements may be taken starting at about 34 weeks. Antacids and antihistamines should be avoided in patients receiving phenytoin because they lower plasma levels of phenytoin and may precipitate a seizure attack.

For the treatment of status epilepticus, immediate hospitalization is required. Management is similar to that in the nonpregnant adult. Patency of the airway and adequate oxygenation should be insured. After blood is drawn for plasma levels of anticonvulsants, intravenous diazepam (or lorazepam) should be given slowly, followed by a loading dose of phenytoin (at a rate no faster than 25 to 50 mg/minute with continuous cardiac monitoring). If seizure patterns continue, pentobarbital may be added, and the patient should be intubated and mechanically ventilated.

The management of labor and delivery follows obstetric indications. During labor and in the immediate postpartum period, anticonvulsant drugs must be continued. Postpartum, the dose of the anticonvulsant drug may be lowered, provided that a therapeutic level is maintained. Although anticonvulsants are excreted in breast milk in small amounts, breastfeeding is not contraindicated.


Pregnant patients with epilepsy have a twofold increase in such maternal complications as preeclampsia, abruption, hyperemesis, and premature labor. Fetal hypoxia is a potential consequence of maternal seizures, and there is a high incidence of intrauterine fetal demise. In the neonate, higher rates of coagulopathy, drug withdrawal symptoms, and neonatal morbidity and mortality are reported. Congenital anomalies are more common in neonates exposed to AEDs in utero compared with offspring of untreated women with epilepsy and women without epilepsy. The overall risk for major malformations is 4% to 6%. Small retrospective studies have raised the possibility of impaired cognitive and neurologic function in the offspring that may manifest later in life. The risk for a seizure disorder is greater among the children of mothers with epilepsy.

image Human Immunodeficiency Virus and Other Infectious Diseases

Infections in pregnancy are a frequent cause of maternal and neonatal morbidity. In some cases (e.g., HIV and syphilis), treatment of the maternal infection will decrease the chance of fetal or neonatal infection.


About 16.4 million women have HIV worldwide; mother-to-child transmission is the primary cause of the annual HIV infection rate of 600,000 in children. Since 1994, significant progress has been made in reducing the vertical transmission rate.

The Virus

HIV is an RNA retrovirus that replicates in certain cell types, in particular in helper T4 lymphocytes in the hematopoietic system and in cells of the central nervous system. As with all retroviruses, HIV contains a reverse transcriptase in its core. HIV has specific surface proteins gp120 and gp41 and core proteins p18 and p24. HIV infects a cell by making contact with the gp120 protein. It then enters the cell, releases its core RNA, makes a DNA copy of itself with its reverse transcriptase, and inserts this DNA into the host genome. This viral gene then either enters into a latent state or begins making viral RNA and proteins with production of an infectious virus.

Laboratory Diagnosis

Indirect serologic methods that detect HIV antibody include the enzyme-linked immunosorbent assay (ELISA), Western blot, and immunofluorescence assay (IFA) tests. The sensitivity of the ELISA is 93% to 99%, and the specificity is 99%. Although rare, false-positive ELISA results can occur, so a confirmatory test is always needed. The Western blot test, which identifies the presence of HIV core and envelope antigens, is 99% sensitive and 98.5% specific. False-positive Western blot results are extremely uncommon. Indirect serology with the capture ELISA technique can also identify HIV antigen (e.g., p24 antigen test). The virus can also be identified by direct tissue culture or by HIV DNA polymerase chain reaction.

Disease Course

Infection with HIV results in a chronic progressive disease. Seroconversion typically occurs 3 to 14 weeks after exposure but may take 6 months or more. In 90% of cases, seroconversion is associated with a mononucleosis-like syndrome or aseptic meningitis. Once the virus has been acquired, the patient enters an asymptomatic period, but lifetime infection should be assumed. Because HIV has a predilection for helper (T4) cells, a gradual destruction of the patient’s cell-mediated immunity occurs, rendering the host susceptible to opportunistic infections. Eventual reversal of the T4-to-T8 ratio to less than 1 is seen on laboratory analysis.

Typically, the patient develops asymptomatic lymphadenopathy, followed by the onset of constitutional symptoms (anorexia, fever, weight loss, diarrhea, nausea, and vomiting). Eventually, opportunistic infections, secondary cancers (Kaposi’s sarcoma, non-Hodgkin’s lymphoma), or neurologic diseases (dementia, neuropathy) develop. Opportunistic infections that may be seen include the following: Pneumocystis carinii pneumonia (PCP), tuberculosis, cryptococcal meningitis, cytomegalovirus (CMV) retinitis, atypical mycobacterial disease, cerebral toxoplasmosis, severe herpes, and cryptosporidiosis. The average interval from initial infection to the onset of AIDS in adults not receiving potent antiviral therapy is 10 years.

Pregnancy does not appear to accelerate the course of HIV infection. Pregnant women may be at increased risk for developing infectious complications during pregnancy. These infections include opportunistic infections, postpartum infections, antepartum urinary tract infections, and sexually transmitted diseases. No direct detrimental effects on perinatal outcome have been documented. Studies in the United States have not shown an increased risk for growth restriction, preterm labor, or premature rupture of the membranes. In children, the disease progresses more rapidly. Of infants infected with HIV, half develop AIDS in the first year of life, and 85% develop AIDS by age 3 years. Children have an extremely poor prognosis, the average survival time from diagnosis being 3 years.

Vertical Transmission

The risk for vertical transmission of HIV from an infected mother to her infant is between 20% and 30%. Such transmission accounts for 99% of cases of HIV infection in children. Vertical transmission may occur antepartum (transplacental), intrapartum, and postpartum. It is suspected that more than 50% of transmissions occur near the time of or during labor and delivery. Maternal-fetal transmission as a result of invasive procedures such as amniocentesis, chorionic villus sampling, umbilical blood sampling, or scalp electrode placement is theoretically possible, but the exact risk is unknown. Breastfeeding may increase the risk for transmission by 10% to 20%. There is no confirmed evidence that fetal HIV infection can result in structural anomalies. It appears that women with advanced disease, recent HIV infection, or preterm delivery have an increased risk for vertical transmission to their infants.

In 1994, Pediatric AIDs Clinical Trial 076 showed that the administration of the nucleoside reverse-transcriptase inhibitor zidovudine to the mother during pregnancy and labor and to the infant for 6 weeks postpartum reduced the maternal transmission to the newborn from 25.5% to 8.3%, with a 68% reduction in vertical transmission. More recently, potent antiretroviral therapy, which reduces the maternal plasma HIV RNA levels to less than 1000 copies per milliliter, has been shown to reduce the vertical transmission rate to only 1% to 2%.

The current management for pregnant women involves the use of multiple agents to minimize the development of drug resistance, and unless contraindicated, all drug regimens should include zidovudine.Antiretroviral drug classes currently used in pregnancy include nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs); non-nucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors. A common regimen currently used is zidovudine plus lamivudine (Combivir) plus lopinavir and ritonavir (Kaletra). Pregnant women with HIV infection on nucleoside analogues should have liver enzymes and electrolytes monitored in the third trimester. Pregnant women on protease inhibitors should be screened for gestational diabetes at the initial visit in addition to the usual time at 24 to 28 weeks because these drugs can cause hyperglycemia. For women who are immunocompromised, with CD4 counts of 0.20 × 109/L (200/μL) or below, prophylaxis against PCP, Mycobacterium aviumcomplex infection, and others should be offered. Trimethoprim sulfamethoxazole is relatively safe for use in pregnancy and is the first choice for PCP prophylaxis.

Because the risk for vertical transmission increases with maternal plasma HIV RNA concentrations, the therapeutic goal is to keep the maternal viral load either undetectable or less than 1000 copies per milliliter.In general, pregnant women should be maintained on the same antiretroviral therapy they received in the nonpregnant state. Invasive fetal diagnostic procedures, such as amniocentesis and chorionic villus sampling, pose a theoretical risk for infecting the fetus and should probably be avoided.

Pregnant women should receive counseling on the risk for newborn infection and the delivery choices available. Women who have viral loads greater than 1000 should be offered a cesarean delivery, which may reduce vertical transmission under these conditions. Such cesarean deliveries should be scheduled at about 38 weeks of gestation to reduce the chance of labor or rupture of membranes. Women on antiretroviral therapy with viral loads less than 1000 HIV RNA copies per milliliter are at low risk (1% to 2%) of passing the virus on to the fetus or newborn. Vaginal delivery should be offered to such patients. All procedures should be avoided that may increase the risk for fetal HIV infection, including artificial rupture of membranes, invasive fetal heart rate monitoring, fetal blood sampling, assisted delivery (forceps or vacuum), or episiotomy. Once the membranes have ruptured, labor should be augmented with oxytocin to reduce the interval between membrane rupture and delivery.

Regardless of the mode of delivery, all women should continue to receive antiretroviral medications as prescribed. Zidovudine (2 mg/kg over 1 hour, followed by 1 mg/kg per hour) should be infused intravenously after the onset of labor or rupture of membranes until delivery or at least 3 hours before cesarean delivery.

In the United States, breastfeeding is not recommended and should be discouraged.

Screening for HIV Infection in Pregnancy

All pregnant women should be tested for HIV unless they refuse. When counseling an HIV-positive pregnant woman, it is necessary to discuss the risk for perinatal transmission. Counseling on disease prevention, including a discussion of safe sexual practices, information on zidovudine therapy, and avoidance of breastfeeding, is imperative. Reproductive options with respect to the present pregnancy and future family planning need to be addressed. Rapid HIV testing should be offered to pregnant women presenting intrapartum whose HIV status is unknown. If the rapid test is positive, zidovudine prophylaxis should be administered and confirmatory testing sent.


Rubella results from infection with a single-stranded RNA togavirus transmitted through the respiratory route, with highest attack rates occurring between March and May. It is highly contagious, with 75% of those infected becoming clinically ill. The incubation period is 14 to 21 days.


The diagnosis of rubella is best made by serologic testing. The IgM response is a rapid one that begins at the onset of the rash and then declines and disappears by 4 to 8 weeks. IgG response also begins at the onset of the rash and remains elevated for life. The diagnosis can be made by the presence of a fourfold rise in the hemagglutination-inhibiting (HAI) antibody titer in paired sera obtained 2 weeks apart or by the presence of IgM. Rubella can also be diagnosed by culture and isolation of the virus during the acute phase of infection, although this technique is slow. The presence of IgM in cord blood or IgG in an infant after 6 months of age supports the diagnosis of perinatal rubella infection.

Impact on Pregnancy

Between 10% and 15% of adult women are susceptible to rubella. In a review of all cases of infants with congenital rubella syndrome (CRS) in the United States reported to the National Congenital Rubella Syndrome Registry from 1997 to 1999, 83% were born to Hispanic mothers and 91% were born to foreign-born mothers.

The disease course is unaltered by pregnancy, and the mother may or may not exhibit the full clinical disease. The severity of the mother’s illness does not have an impact on the risk for fetal infection.Rather, it is the trimester in which infection occurs that has the greatest impact on fetal risk. Infection in the first trimester carries up to 80% risk for development of CRS, whereas the risk for CRS drops to 30% to 50% later in pregnancy. CRS rarely occurs after 20 weeks of gestation. Components of CRS are outlined in Box 16-2.


BOX 16-2 Congenital Rubella Syndrome.

• Symmetrical IUGR

• Congenital deafness (detected after age 1 yr)

• Cardiac malformations

• Patent ductus arteriosus

• Pulmonary artery hypoplasia

• Eye lesions

• Cataracts

• Retinopathy

• Microphthalmia

• Hepatosplenomegaly

• Central nervous system involvement

• Microcephaly

• Panencephalitis

• Brain calcifications

• Psychomotor retardation

• Hepatitis

• Thrombocytopenic purpura


Routine rubella susceptibility testing should be performed in all pregnant women with a single IgG level. Those who are nonimmune should be vaccinated in the immediate postpartum period. It is recommended that women not become pregnant for at least 3 months after vaccination. Nonetheless, there are no reports of CRS after rubella immunization, and inadvertent immunization of a pregnant woman is not considered an indication for therapeutic abortion. Follow-up antibody titers should be obtained because up to 20% fail to develop an antibody response. Women should be screened for rubella susceptibility at each pregnancy, because immunity can wane.

Rubella is not a contraindication to breastfeeding. There is no specific treatment for rubella, and routine prophylaxis with γ-globulin after exposure is not recommended because it has not been shown to change the risk for fetal involvement.


CMV is a DNA virus and a member of the herpesvirus family and thus has the ability to establish latency. The virus is transmitted in a number of ways, including blood transfusion, organ transplantation, sexual contact, breast milk, urine, or saliva. It may also be transmitted transplacentally, or at delivery by direct contact. Between 30% and 60% of school-aged children are seropositive for CMV, as are 50% to 85% of all pregnant women. Infection may be expressed as a mononucleosis-like illness, although subclinical infection is more common. Viral excretion may continue for months, and the virus may establish latency in lymphocytes, salivary glands, renal tubules, and the endometrium. Reactivation may occur years after primary infection, and reinfection with a different strain of the virus is also possible.


The virus may be isolated on urine culture or by culture of other body secretions or tissues. Serologic testing is possible, with an elevation in IgM that peaks 3 to 6 months after infection and resolves by 1 to 2 years. IgG elevates rapidly and persists for life. Problems with serologic testing include (1) the prolonged elevation in levels of IgM, making delineation of timing of infection difficult, and (2) a 20% false-negative rate in IgM testing. In addition, the presence of IgG does not rule out the presence of persistent disease.

Impact on Pregnancy

CMV is the most common congenital viral infection in the United States, affecting 0.5% to 2.5% of all live-born infants per year, and it is postulated that each year about 40,000 infants are born with congenital CMV infection. Fetal infection can occur when the mother does not exhibit symptoms. There is a 40% to 50% maternal-infant transmission rate.

About 10% to 15% of infected infants are symptomatic at birth, exhibiting nonimmune hydrops, symmetrical IUGR, chorioretinitis, microcephaly, cerebral calcifications, hepatosplenomegaly, and hydrocephaly. About 80% to 90% are asymptomatic at birth but may later exhibit mental retardation, visual impairment, progressive hearing loss, and delayed psychomotor development(Box 16-3). Sensorineural hearing loss is the most frequent sequel of congenital CMV infection and is observed in 40% to 50% of symptomatic children. Recurrent CMV infection is associated with a much lower fetal risk, with a 0.15% to 1% maternal-fetal transmission rate. Few cases of severely affected infants have been reported.


BOX 16-3 Problems Associated with Congenital Cytomegalovirus Infection.

• Nonimmune hydrops

• Symmetrical growth restriction

• Chorioretinitis

• Microcephaly

• Cerebral calcifications

• Hepatosplenomegaly

• Hydrocephaly

• Later problems

• Visual impairment

• Hearing loss

• Delayed psychomotor development


Patients with a confirmed primary infection should have a detailed ultrasonic examination. Ultrasonic findings include fetal growth restriction, hydrocephaly, intracranial calcifications, microcephaly, echogenic bowel, hepatosplenomegaly, and nonimmune hydrops. If the ultrasound is normal, an amniocentesis should be performed to test for CMV by polymerase chain reaction (PCR). If the ultrasound shows signs of fetal anomalies, or the PCR test is positive, patients should be advised of options. Recently, hyperimmune anti-CMV globulin has been shown to be effective and can be offered. Ganciclovir has also been used in pregnancy with resolution of fetal CMV infection. The patient should also be advised of the option of termination.


Acute varicella infection, or chickenpox, is caused by the varicella-zoster virus, which is a DNA herpesvirus transmitted by direct contact or through the respiratory route. The attack rate in susceptible individuals is more than 90%. The incubation period is 10 to 21 days. Infection is believed to be more severe in adults, and potential complications include encephalitis and pneumonia. Because it is a herpesvirus, the varicella virus has the ability to establish latency in nerve ganglia. Reactivation of the virus results in herpes zoster (shingles).


The diagnosis of chickenpox is usually determined by the patient’s clinical presentation, although the virus may be cultured from vesicles during the first 4 days of the rash. On serologic testing, varicella-zoster IgM will rise in 2 weeks on ELISA or complement fixation. Paired sera for IgG obtained 2 weeks apart may also detect infection.

Impact on Pregnancy

Between 5% and 10% of adult women are susceptible to the varicella virus. Acute varicella infection complicates 1 in 7500 pregnancies. Potential maternal complications include preterm labor, encephalitis, and varicella pneumonia. Maternal management should be symptomatic, but a chest x-ray should be considered to rule out pneumonia. Varicella pneumonia complicates 16% of cases and carries a mortality rate of up to 40%. If pneumonia is confirmed or suspected, the patient requires immediate hospital admission and institution of antiviral therapy because rapid respiratory decompensation is not uncommon.

A congenital varicella syndrome has been described. Diagnosis of the syndrome is based on IgM-positive cord blood and clinical findings in the newborn, which include limb hypoplasia, cutaneous scars, chorioretinitis, cataracts, cortical atrophy, microcephaly, and symmetrical IUGR. The risk for this fetal syndrome is 2% if maternal infection occurred between 13 and 20 weeks and 0.4% if maternal infection occurred before 13 weeks of gestation. Only rarely have cases been identified as a result of maternal infection past 20 weeks’ gestation. In the presence of fetal infection, ultrasound may reveal hydrops, organ calcifications, limb deformities, microcephaly, or growth restriction. However, no reliable methods of definitive prenatal diagnosis are available.

If maternal infection occurs 5 to 21 days before delivery and the infant develops infection, it is typically mild and self-limited. However, if maternal infection occurs between 5 days before delivery and 2 days after delivery, transplacental transfer of maternal protective antibodies to the fetus has not occurred, and the infant is at great risk for developing a fulminant infection with a 30% mortality rate. Varicella-zoster immune globulin (VZIG) should be given to these infants at birth, and they should be placed in contact isolation. The placenta and fetal membranes should be considered infectious.

For the exposed gravid woman who has no knowledge of a prior infection, a varicella IgG titer should be obtained immediately. If the patient proves to be nonimmune, VZIG should be administered within 6 days of exposure, although it is unclear whether this therapy modifies the disease course and risk to the fetus. Administration of VZIG is also recommended after exposure to zoster.Alternatively, VariZIG may be administered up to 96 hours after exposure. Varicella vaccine is composed of a live attenuated virus and, therefore, is contraindicated in pregnancy. Herpes zoster does not occur more frequently in pregnancy. If it does occur, it poses no risk to the fetus. If zoster develops close to delivery, varicella may be transmitted through contact with a lesion, so this should be avoided.


The hepatitis B virus is a DNA virus that is transmitted through blood, saliva, vaginal secretions, semen, and breast milk and across the placenta. The population at greatest risk includes intravenous drug users, homosexuals, individuals of Asian descent, and health care workers. Infection with the virus is either asymptomatic or expressed as acute hepatitis. Ten percent of individuals go on to develop chronic active or persistent hepatitis.

Impact on Pregnancy

The course of acute hepatitis is unaltered in pregnancy. Fetal infection may occur and is most likely if maternal infection occurs in the third trimester. Chronic active hepatitis is associated with an increased risk for prematurity, low birth weight, and neonatal death. Maternal prognosis is very poor if the disease is complicated by cirrhosis, varices, or liver failure.

The incidence of hepatitis B surface antigen (HBsAg) positivity (chronic carrier state) in pregnancy in the United States is 6 to 10 per 1000 pregnancies. Women who are asymptomatic HBsAg carriers are at no higher risk for antepartum complications than are the general population. However, newborns delivered to mothers positive for HBsAg have a 10% risk for developing acute infection at birth. This is in contrast to those delivered to mothers positive for both HBsAg and hepatitis Be antigen (HBeAg), in which the infant’s risk increases to 70% to 90%. Infection in the infant may be fulminant and lethal. If the infant survives, it has an 85% to 90% chance of becoming a chronic hepatitis carrier and a 25% chance of developing liver cirrhosis, hepatocellular carcinoma, or both. Therefore, it is recommended that all pregnant women be screened for HBsAg carriage during pregnancy. Women in high-risk groups (Box 16-4) should be rescreened in the third trimester if the initial screen is negative.


BOX 16-4 High-Risk Groups for HBsAg Carriage.

• Birth in Haiti or Africa

• Asian, Pacific Island, or Eskimo descent (immigrant or born in the United States)

• Works or has been treated in a hemodialysis unit

• Works or resides in institutions for the mentally handicapped

• History of repeated transfusions

• Occupational exposure to blood

• Repetitive episodes of sexually transmitted diseases

• Intravenous drug abuse

• Prostitution

• Household contact with a hepatitis carrier

• Household contact with a hemodialysis patient


If a pregnant woman is found on screening to be HBsAg positive, liver function tests and a complete hepatitis panel should be performed. Household members and sexual contacts should be tested and offered vaccination if they are susceptible. Transmission to the infant is believed to occur by direct contact during delivery. Therefore, the newborn is given hepatitis immune globulin and hepatitis vaccine soon after delivery, which reduces the risk for infection to less than 10%. Pregnant women at high risk for becoming infected with hepatitis B who test negative for the HBsAg should be offered vaccination. Available vaccines are produced by recombinant DNA technology and are therefore safe for use in pregnancy. The Centers for Disease Control and Prevention (CDC) have recommended that all children receive vaccination against hepatitis B as well.

Hepatitis C virus (HCV) is the most common chronic blood-borne infection in the United States. Vertical transmission in HCV RNA–negative pregnant women is about 1% to 3% vs. about 4% to 6% in HCV RNA–positive women. Coinfection with HIV has been shown to increase the risk for vertical transmission of HCV. In HIV-negative women, route of delivery does not influence vertical transmission. Amniocentesis is a potential risk for transmission. There is no clear evidence demonstrating an increased risk for HCV transmission in HIV-negative women who breastfeed.

There is currently no safe treatment for HCV infection during pregnancy. Given the lack of measures to prevent transmission and to treat the infection efficiently, universal screening in pregnancy is currently not recommended. Women with high risk factors (such as blood transfusion or organ donation before 1992, HIV or hepatitis B positive, intravenous drug use, high-risk sexual behavior) should be offered anti-HCV testing during pregnancy.


Herpes simplex virus (HSV) is a member of the DNA herpes virus family and is transmitted by intimate mucocutaneous contact.

Impact on Pregnancy


Patients who acquire primary herpes in pregnancy have an increased risk for obstetric and neonatal complications. Maternal infection has been associated with an increased risk for spontaneous abortion, IUGR, and preterm labor. Fifty percent of infants born vaginally to mothers with a primary infection at delivery may develop HSV infection.


Complications from a recurrence in pregnancy are rare. However, 4% of infants born to mothers with recurrent infection at the time of delivery may have HSV infection.


The reported incidence of neonatal herpes ranges from 4 to 31.2 per 100,000 life births. Neonatal infection is acquired in three ways: intrauterine (5%), peripartum (85%), or postnatal (10%) transmission. Premature infants are at greatest risk for contracting infection, and they account for more than two thirds of reported cases. Symptoms typically present on day 2 to 3 of life, with rapid progression of disease thereafter. Neonatal infection can be classified as (1) disseminated disease with involvement of multiple major organs; (2) central nervous system disease with encephalitis; and (3) skin, eye, or mouth infection with localized involvement. Neonates with suspected neonatal herpes are treated with intravenous acyclovir, which has significantly reduced the mortality rate. Even with appropriate treatment, prognosis of neonatal encephalitis is still very poor. Between one third and one half of all treated neonates with disseminated disease die, and about two thirds of survivors have neurologic sequelae such as microcephaly, mental retardation, seizures, and microphthalmos.

Management in Pregnancy

Antenatal antiviral prophylaxis (valacyclovir and acyclovir) from 36 weeks until delivery is safe and has been shown to decrease asymptomatic viral shedding, decrease herpes outbreak at delivery, and reduce the need for cesarean delivery for genital herpes. Women with a prior history of herpes should be allowed to deliver vaginally if no genital lesions are present at the time of labor. Patients with active lesions, either recurrent or primary, at the time of labor should be delivered by cesarean birth. Those with active lesions at sites distant from the genital area may be delivered vaginally if the lesions are covered. Once delivered, isolation of the mother from her infant is not necessary as long as direct contact with lesions is avoided. Mothers may breastfeed so long as no lesions are present on the breasts.

image Bacterial Infections


Urinary tract infections occur more frequently in pregnancy and the puerperium and are among the most common medical complications of pregnancy. This increased incidence appears to be a result of both hormonal (progesterone) and mechanical factors that increase urinary stasis.

Urinary tract infections in pregnancy may be either asymptomatic or symptomatic (e.g., cystitis, pyelonephritis). By definition, asymptomatic bacteriuria is the presence of at least 100,000 organisms/mL in a clean urine specimen from an asymptomatic patient. The incidence of asymptomatic bacteriuria in pregnancy is the same as in the nonpregnant sexually active population, ranging from 2% to 10%. Highest rates are found in inner city populations and in patients with sickle cell disease or trait. Escherichia coli is the organism most frequently isolated (60%). Other organisms encountered are Proteus mirabilis, enterococci, Klebsiella pneumoniae, and group B streptococci. If the condition is left untreated, roughly 20% of pregnant women develop either acute cystitis or pyelonephritis later in pregnancy. Initial therapy consists of either nitrofurantoin, ampicillin or a cephalosporin. After treatment, it is wise to follow with urine cultures because up to 25% of patients have a recurrence later in the pregnancy.

Acute cystitis complicates 1% to 2% of pregnancies and is characterized by dysuria, frequency, urgency, and hematuria. Systemic signs and symptoms, such as flank pain or fever, are absent. Urinalysis reveals bacteriuria, pyuria, and often hematuria. As in patients with asymptomatic bacteriuria, treatment is instituted on an outpatient basis while awaiting the results of sensitivity tests. Follow-up surveillance cultures are indicated.

Acute pyelonephritis occurs in about 2% to 4% of pregnancies, most frequently in the second trimester. It is characterized by flank pain, fever, rigors, and the urinary complaints of cystitis. It is a leading cause of septic shock and ARDS in pregnancy. Often, nausea and vomiting are present, and the patient may be markedly dehydrated. Physical examination reveals fever and costovertebral angle tenderness. As a result of sepsis, premature uterine contractions are frequent. Urinalysis reveals the same findings as are found with acute cystitis, and blood cultures are positive in 10% of cases. Organisms responsible are the same as those causing asymptomatic bacteriuria and cystitis.

Hospitalization, blood and urine cultures, intravenous antibiotic therapy, monitoring for preterm labor, and close observation of fluid status and pulse oximetry are indicated when a diagnosis of pyelonephritis is made. Usually, ampicillin or cefazolin therapy is initiated, with cefazolin or gentamycin gaining a great deal of popularity in areas in which resistance to ampicillin is prominent. Most patients (>80%) become asymptomatic and afebrile within 48 hours of initiation of antibiotic therapy and may be discharged at this point, continuing oral antibiotics for a 10-day course. Serial urine cultures are indicated because 10% to 25% of patients have a recurrence later in the pregnancy. Those with recurrent pyelonephritis should receive chronic antibiotic suppression and have an intravenous pyelogram performed 6 weeks postpartum to rule out urinary tract abnormalities.


Group B streptococci (GBS) are considered part of the normal flora of humans. The gastrointestinal tract is the major reservoir, although the organism has been isolated from the vagina, cervix, throat, skin, urethra, and urine of healthy individuals. GBS may be transmitted to the genital tract by fecal contamination or sexual transmission from a colonized partner. Vaginal carriage rates vary from 15% to 40%, but they are the same in pregnant women as in sexually active nonpregnant women. Two thirds of pregnant women who carry GBS do so intermittently or transiently, and only one third of all pregnant GBS carriers have the organism chronically.


GBS grow readily on routine bacteriologic media and are easy to isolate from clinical specimens. A number of specific rapid assays for the detection of GBS have been developed, but none is sensitive enough for widespread use.

Impact on Pregnancy

GBS may be transferred from a colonized mother to her infant by vertical transmission at delivery. Transmission rates of 35% to 70% have been reported, with the highest transmission rates occurring in women with heavy vaginal colonization. Other risk factors for transmission are preterm labor or delivery, preterm rupture of membranes, low birth weight, prolonged rupture of membranes (>12 to 18 hours before delivery), intrapartum fever, and a history of previously delivering an infected infant.

GBS sepsis is the most common cause of neonatal sepsis in the United States, with 1 to 2 cases per 1000 live births per year reported. Neonatal infection with GBS is of two clinically distinct types: early-onset and late-onset disease. Late-onset GBS infection has been linked to a nosocomial source in the nursery, occurs after the first week of life (mean onset, 4 weeks), and usually is exhibited as meningitis (80%) or another type of focal infection. Early-onset GBS infection is characterized by its rapid onset and fulminant course, with presentation typically within the first 48 hours of life. Pathogenesis of this form of GBS sepsis is best explained by direct maternal-infant transmission at delivery. The infant presents with respiratory distress and pneumonia, and 30% of infants develop meningitis. Septicemia, shock, and death may result even when antibiotics are begun expediently. The overall infant mortality rate from early-onset disease is 50%. Preterm infants account for more than 90% of deaths. The risk for sepsis developing in a full-term infant with bacterial colonization is 1% to 2%, compared with 8% to 10% in the preterm infant.

GBS is the second most common cause of bacteriuria in pregnancy and is a major cause of puerperal infection. Infection with GBS accounts for 20% of cases of endomyometritis and is unique in its acute onset (within the first 48 hours postpartum) and typically fulminant course.

Treating carriers in labor will reduce the rate of transmission to the infant. Both the CDC and the Committee on Obstetric Practice of the American College of Obstetricians and Gynecologists support a screening program in which vaginal and rectal group B streptococci cultures are obtained at 35 to 37 weeks for all gravidas except those who have GBS bacteriuria during the current pregnancy or a previous infant with invasive GBS disease. Intrapartum antibiotic prophylaxis would be indicated for pregnant women with (1) a previous infant with invasive GBS disease, (2) GBS bacteruria during the current pregnancy, (3) positive GBS screening culture during the current pregnancy, or (4) unknown GBS status with one of the high-risk factors such as intrapartum fever (≥38°C), preterm delivery (<37 weeks of gestation), or prolonged membrane rupture (≥18 hours). Antibiotic prophylaxis is not indicated for those undergoing a scheduled cesarean delivery in the absence of labor or amniotic membrane rupture. Antibiotic prophylaxis is also not indicated for those who have risk factors but are GBS culture negative in the current pregnancy.


Although the incidence of active tuberculosis (TB) in the United States is very low (0.6% to 1%), about 10% of all women of childbearing age test positive on purified protein derivative (PPD) testing.A positive PPD test indicates that the patient has been infected with tuberculosis in the past. Tuberculin skin testing is not a routine component of prenatal screening but should be performed in minority women of lower socioeconomic status and in women who live in areas in which large numbers of immigrants from Southeast Asia, Central America, or South America reside. HIV-positive patients should also have a PPD test.

Pregnancy does not alter the course of active tuberculosis, nor does it place the known PPD-positive woman at greater risk for disease reactivation. Tuberculosis can, however, be passed to the fetus by a hematogenous route across the placenta or as a result of the fetus’s swallowing infected amniotic fluid. The risk for pregnancy wastage is increased, and congenital tuberculosis may be evident at birth. An affected infant exhibits low birth weight, failure to thrive, fever, respiratory distress, adenopathy, and hepatosplenomegaly and is at high risk for dying without rapid treatment. Treatment of the mother with active disease during pregnancy eliminates the fetal risks.

The pregnant patient who tests positive for tuberculosis should have a chest x-ray (with abdominal shielding) to rule out active disease. If the chest x-ray is suspicious for active disease, three sets of sputum culturesshould be obtained. If the cultures are positive, therapy should be instituted without delay. If the chest x-ray is normal, no further treatment is required, but the patient should be followed with an annual chest x-ray. Prophylactic treatment with single-agent therapy is recommended for patients who are recent PPD converters, those who live with someone with active TB, and those who are immunosuppressed and PPD positive (e.g., AIDS sufferers).

Several drugs are available for therapy. All have potential risks, but untreated TB is believed to be of greater risk to both the mother and infant. Isoniazid (INH) is the safest drug for use in pregnancy.Fetal risks include potential central nervous system toxicity, but treating the mother with vitamin B6 supplements eliminates this risk. The main risk to the mother is hepatitis, so monthly liver function tests should be performed. Rifampin has been linked to limb reduction defects in the fetus and hepatitis in the mother. Ethambutol is safer than rifampin but is not as effective, and it has been associated with a reversible maternal optic neuritis in 6% of patients. Streptomycin is to be avoided in pregnancy because of the risk for nephrotoxicity and permanent cranial nerve VIII damage in the fetus. For women with active disease, current recommendations are for 9 months of therapy with INH and rifampin. After delivery, newborns should be isolated from their mothers with active disease until the mothers are culture negative. INH prophylaxis of the infant is recommended because 50% of infants develop active TB by 1 year of age without it. Once the mother is culture-negative, she may breastfeed because only small concentrations of the drugs pass into the milk.


All pregnant women should be screened for syphilis at the first prenatal visit with either a Venereal Disease Research Laboratory (VDRL) test or a rapid plasma reagin (RPR) test. These tests carry a false-positive rate of between 0.5% and 14% because they are nonspecific for treponemes. Common causes of false-positive results are drug addiction, autoimmune disease, recent viral infection or immunization, and pregnancy. False-positive titers are usually 1:4 or less. Specific treponemal tests, such as the fluorescent treponemal antibody absorption test (FTA-ABS), are performed to confirm the diagnosis.

Impact on Pregnancy

Maternal infection can result in transplacental transmission to the fetus at any gestational age. Mothers with primary and secondary syphilis are more likely to transmit the infection, with more severe manifestations occurring in the fetus. Transmission rates for primary and secondary disease are between 50% and 80%. There is a wide range of fetal responses to infection.

Components of early congenital syphilitic infection include nonimmune hydrops, hepatosplenomegaly, profound anemia and thrombocytopenia, skin lesions, rash, osteitis and periostitis, pneumonia, and hepatitis. The perinatal mortality rate from congenital syphilis is roughly 50%.

Late congenital syphilis (diagnosed after 2 years of age) is a multisystem disease characterized by dental abnormalities (Hutchinson’s teeth, mulberry molars); saber shins; saddle nose deformity; interstitial keratitis; eighth nerve deafness; and failure to thrive.


Treatment of the condition in pregnancy is the same as that in the nonpregnant state. Penicillin G is the therapy of choice. Patients with primary, secondary, or latent syphilis of less than 12 months’ duration are treated with a single dose of benzathine penicillin, 2.4 million U given intramuscularly. Those with syphilis of undetermined length or with latent infection for longer than 1 year receive this therapy weekly for 3 weeks. For patients with penicillin allergy, desensitization and use of penicillin is recommended. Patients with neurosyphilis require admission and prolonged intravenous penicillin therapy.

Women treated for syphilis during their pregnancy require careful follow-up with monthly VDRL or RPR titers to ensure that the treatment is successful. Patients with syphilis remain positive on FTA-ABS testing for the remainder of their lives. Sexual contacts should be referred for treatment and neonates evaluated and treated as indicated.

image Parasitic Infections


Toxoplasmosis is a systemic disease caused by the protozoan Toxoplasma gondii. Between 15% and 40% of women of reproductive age have antibodies (IgG) to toxoplasmosis and therefore are immune to future infection. The organism is acquired by ingesting undercooked meat or unpasteurized goat’s milk, drinking contaminated water, exposure to feces from an infected cat, or rarely by tachyzoites from blood transfusion. In about 10% of maternal infections, toxoplasmosis presents as a mononucleosis-like syndrome, but most infections are subclinical.

Impact on Pregnancy

The incidence of primary infection in pregnancy is 1 in 1000. In immunocompromised women such as those with AIDS, a reactivation of toxoplasmosis could occur that would potentially be associated with a risk for fetal infection. The risk for transmission to the fetus is 15% in the first trimester, 25% in the second trimester, and 65% in the third trimester. However, the severity of fetal infection is greatest with first-trimester infection, and congenital defects are rarely seen if the infection occurs after 20 weeks of gestation. About 15% of infants with congenital infection are symptomatic at birth. A classic triad of hydrocephalus, intracranial calcifications, and chorioretinitis is described. Of the asymptomatic infants, 25% and 50% exhibit later sequelae (Box 16-5).


BOX 16-5 Manifestations of Congenital Toxoplasmosis Infection.

• Hydrocephalus

• Chorioretinitis

• Microcephaly

• Microphthalmia

• Hepatosplenomegaly

• Cerebral calcifications

• Adenopathy

• Convulsions

• Delayed mental development

• Rash

• Pneumonia

• Fever

• Anemia

• Later problems

• Visual impairment

• Hearing loss

• Delayed psychomotor development

• Seizure disorders

• Spasticity, palsies

• Mental retardation



Maternal infection is usually suspected if toxoplasmosis IgM antibodies are detected on routine screening. Occasionally pregnant women may be tested because of mononucleosis-like symptoms. A reference laboratory is used to confirm primary toxoplasmosis infection. At about 18 to 20 weeks of gestation, amniocentesis for toxoplasmosis PCR should be offered to women with a confirmed diagnosis of primary toxoplasmosis to detect fetal infection.


Toxoplasmosis is a self-limiting infection. Owing to the fetal risk, spiramycin is used for treatment of maternal primary infection, but it is obtainable in the United States only through special permission from the U.S. Food and Drug Administration. If fetal infection is identified, therapy with pyrimethamine and sulfadiazine plus folinic acid should be given and has been shown to reduce the severity of fetal damage. Most infected infants have no apparent physical abnormalities at birth, but without treatment, most of the infected infants develop morbidity related to chorioretinitis, hydrocephalus, or neurologic damage by the end of adolescence. Therefore treatment of infected infants in the first year of life is recommended. To prevent infection, pregnant women should be advised to avoid contact with cat litter or feces, to wear gloves while gardening, and to avoid ingestion of undercooked meat or unpasteurized goat’s milk and drink filtered water.

image Surgical Conditions during Pregnancy

Pregnancy substantially enhances the problems associated with surgery. Physiologic changes and the altered immunologic responses of pregnancy change the diagnostic parameters of surgical diseases. Surgery (especially abdominal surgery) can increase the rate of fetal loss. Reluctance to operate on a pregnant woman with an acute surgical condition may add to critical delays and increase the morbidity for both the fetus and the mother.


Elective surgery should be avoided in pregnancy. If surgery must be done, but not emergently (e.g., an ovarian neoplasm), the second trimester is the safest time. During this period, the risks for teratogenesis and miscarriage are much lower than in the first trimester, and the risk for preterm labor is lower than in the third trimester. Regional analgesia is preferred because it has lower mortality and morbidity than general anesthesia. There is little evidence of teratogenicity from commonly used anesthetics. Pulmonary aspiration is more common. All pregnant women should be treated as if they have a full stomach and premedicated with citrate and H2-receptor blockers. Precautions must be taken to avoid maternal hypotension and hypoxia, which have adverse effects on uteroplacental blood flow.If possible, the patient should be in the left lateral decubitus position. Preoperative and postoperative fetal and uterine monitoring are indicated in the third trimester. If significant blood loss is anticipated and the patient is anemic, it is advisable to transfuse the patient preoperatively.


The general approach to acute surgical emergencies during pregnancy is to manage the problem regardless of the pregnancy. Acute nonobstetric surgical emergencies occur in all three trimesters of pregnancy. The overall incidence is about 1 in 500 pregnancies. The more common acute conditions are discussed next.


Appendectomy for presumed acute appendicitis is the most common surgical emergency during pregnancy. The incidence of acute appendicitis in pregnancy is about 0.05% to 0.1%, and it is constant throughout the three trimesters. The usual symptoms of acute appendicitis, such as epigastric pain, nausea, vomiting, and lower abdominal pain, may be less apparent during pregnancy, although right lower quadrant pain is still the most common presentation. The differential diagnosis may be especially confusing (Box 16-6). The enlarging uterus displaces the appendix superiorly and laterally as pregnancy progresses (Figure 16-1). Tenderness and guarding are elicited more laterally than expected. The increased white blood cell count seen in normal pregnancy further confuses the issue. Surgery may be delayed, resulting in an increased rate of rupture, premature labor, infant morbidity, and, rarely, maternal death.


BOX 16-6 Differential Diagnosis of Acute Appendicitis in Pregnancy.

• Ruptured corpus luteum

• Torsion of an adnexal mass

• Pyelonephritis

• Nephrolithiasis

• Ectopic pregnancy

• Hyperemesis gravidarum

• Acute mesenteric lymphadenitis

• Inflammatory bowel disease

• Salpingo-ovarian abscess

• Acute mesenteric thrombosis

• Cholecystitis, cholelithiasis

• Concealed abruption



FIGURE 16-1 The changing position of the right colon and appendix as pregnancy progresses and the uterus enlarges.

Imaging studies can increase the accuracy of the diagnosis of appendicitis. The American College of Radiology recommends nonionizing radiation techniques such as ultrasonography and MRI for imaging in pregnant women. On ultrasound, the abnormal appendix can be visualized as a noncompressible tubular structure measuring 6 mm or greater in the region of the patient’s pain. Helical computed tomography has the disadvantage of radiation exposure, but appendicitis is suspected if right lower quadrant inflammation, an enlarged nonfilling tubular structure, or a fecalith is noted. The estimated fetal radiation exposure is about 250 mrad. Exposure to less than 5 rad (0.05 Gy) has not been associated with an increase in fetal anomalies or pregnancy loss. Table 16-8 shows the dose of ionizing radiation to the fetus from common diagnostic radiologic procedures.



Fetal Exposure

Chest radiograph (two views)

0.02-0.07 mrad

Abdominal film (single view)

100 mrad

Intravenous pyelography

>1 rad

Hip film (single view)

200 mrad


7-20 mrad

Barium enema or small bowel series

2-4 rad

CT scan of head or chest

<1 rad

CT scan of abdomen and lumbar spine

3.5 rad

CT pelvimetry

250 mrad

 1 rad = 0.01 gray (Gy).

 Exposure depends on the number of films.

Data from American College of Obstetricians and Gynecologists: Guidelines for diagnostic imaging during pregnancy. ACOG Committee Opinion No. 299. Obstet Gynecol 104:649, 2004.

If acute appendicitis is diagnosed, laparotomy with appendectomy should be carried out. A McBurney, transverse, or Rockey-Davis incision can be employed. Laparoscopic appendectomy may increase the risk for fetal loss. A potential concern is that carbon dioxide used for insufflation can be absorbed across the peritoneum into the maternal bloodstream and across the placenta, leading to fetal respiratory acidosis and hypercapnia. As gestation progresses, the likelihood increases that the pneumoperitoneum will decrease venous return, cardiac output, and uteroplacental blood flow. Laparoscopic appendectomy may be considered if specific recommendations are met (Table 16-9).


SAGES Guidelines

Moreno-Sanz’s Proposed Guidelines

Pneumatic compression devices

Same recommendation

Open abdominal access (Hasson)

Same recommendation

Pneumoperitoneum pressure ≤12 mm Hg

Same recommendation

No routine prophylactic tocolytic therapy

Same recommendation

Obstetric consultation should be obtained preoperatively

Preoperative and postoperative obstetric consultation should be obtained

Continuous intraoperative fetal monitoring

Preoperative and postoperative ultrasonographic examination and cardiotocography

Maternal end-tidal CO2 and/or arterial blood gases should be monitored

Maternal intraoperative end-tidal CO2 monitoring (30-40 mm Hg)


Routine venous thrombosis prophylaxis with low-molecular-weight heparin


Use of harmonic scissors

SAGES, Society of American Gastrointestinal and Endoscopic Surgeons.

 Proposed guideline change.

 Proposed guideline.

From Moreno-Sanz CJ: Laparoscopic appendectomy during pregnancy: Between personal experiences and scientific evidence. Am Coll Surg 205:37-42, 2007.

Acute Cholecystitis and Cholelithiasis

An increase in serum cholesterol and lipid levels in pregnancy, along with biliary stasis, leads to a higher incidence of cholelithiasis, biliary obstruction, and cholecystitis. High levels of estrogens in pregnancy increase the saturation of cholesterol in the bile. Virtually all of the gallstones associated with pregnancy are composed of crystallized cholesterol. Ultrasonography has revealed a fairly high incidence of cholelithiasis in pregnancy (4%). The incidence of hospitalization for cholecystitis in pregnancy is 1% to 2%, but only 1 in 2000 pregnant women require cholecystectomy.

Nausea and vomiting, along with right upper quadrant tenderness and guarding, generally suggest biliary tract disease. An increasing white blood cell count with elevated alkaline phosphatase and bilirubin levels, jaundice in the presence of stones, or increased thickness of the gallbladder wall on ultrasonography serves to authenticate the diagnosis. Viral hepatitis must be considered in the differential diagnosis. Markedly elevated aspartate transaminase and alanine transaminase levels (>200 U/L), especially without leukocytosis, should suggest viral hepatitis.

Generally, cholecystitis can be managed medically in pregnancy. Parenteral fluids, gastric decompression, and dietary measures should be the primary approach. Endoscopic retrograde cholangiopancreatography (ERCP) can be safely performed in pregnancy with little ionizing radiation exposure to the fetus if the patient has cholangitis or pancreatitis due to a common bile duct stone. If symptoms and signs persist with progressive peritonitis despite medical management or ERCP, cholecystectomy is indicated. Laparoscopic cholecystectomy has been performed in pregnancy.

Acute Pancreatitis

Generally, pancreatitis is associated with cholecystitis, cholelithiasis, or alcoholism. It has also been associated with viral infections and drugs such as thiazide diuretics, furosemide, acetaminophen, clonidine, isoniazid, rifampin, tetracycline, propoxyphene, and steroids. It is less common in pregnancy, and the incidence in pregnancy varies from 1:1000 to 1:4000, increasing somewhat in the third trimester. However, the mortality rate associated with pancreatitis is significantly higher when it does occur in pregnancy.

The prime symptom of pancreatitis is severe, noncolicky epigastric pain radiating to the high back, which is relieved somewhat by leaning forward. Nausea and vomiting generally are present. Upper abdominal guarding may be difficult to assess in late pregnancy. Elevated serum amylase (>200 U/dL) and lipase levels generally confirm the diagnosis, although cholecystitis, peptic ulcer, diabetic ketoacidosis, and hyperemesis gravidarum may also be associated with elevations of serum amylase

Generally, the disease is self-limited and responds within 1 to 10 days to bed rest, parenteral fluids, pain relief, and nasogastric suction. Occasionally the disease becomes severe and protracted, with extensive pancreatic edema and autodigestion, massive ascites, hemoperitoneum, fever, and paralytic ileus. In such cases, maternal and fetal mortality is high, and peritoneal lavage, operative drainage, partial pancreatic resection, or some combination of these procedures may be required.

Bowel Obstruction

Bowel obstruction in pregnancy is usually associated with postoperative adhesions, although volvulus and intussusception are rare causes. It generally occurs in late pregnancy and is associated with traction on adhesions as the uterus enlarges. An upright x-ray of the abdomen showing characteristic dilated loops of bowel and air-fluid levels serves to confirm the obstruction.

Management does not differ from that in the nonpregnant patient. Nasogastric suction should be instituted and fluid and electrolyte balance carefully monitored. If the obstruction does not resolve after 48 to 96 hours, an exploratory laparotomy should be carried out through an appropriate vertical incision. If uterine contractions occur postoperatively, tocolytics may be employed.

Adnexal Torsion

Torsion of the uterine adnexa occurs somewhat more commonly in pregnancy, possibly because the supporting ligaments elongate as the gestation progresses. Ovarian tumors (e.g., cystic teratomas, corpus luteum cysts) may become ischemic if their vascular pedicles undergo torsion. Such ischemic events are usually heralded by the sudden onset of severe, intermittent abdominal pain, which may radiate to the flank and down the anterior thigh.

During the first and early second trimesters, a mass is usually felt on pelvic examination or is visualized by ultrasonography. Later in the pregnancy it may be impossible to palpate a mass clinically. Low-grade fever and leukocytosis may be present, and serum creatine phosphokinase levels may be elevated, depending on the extent of the infarction. In the first trimester, the differential diagnosis includes ectopic pregnancy and hemorrhagic corpus luteum; later in pregnancy, a degenerating myoma should be considered.

Although the pain may diminish somewhat after 24 hours, removal of the infarcted organ is indicated. If the excised ovary contains the corpus luteum, progesterone supplementation is generally necessary before 8 weeks’ gestation.

Abdominal Trauma

By far, the most common abdominal trauma in pregnancy occurs in automobile accidents. Abruptio placentae, uterine contusions, and fetal skull fractures may result. Abruptio placentae is treated expectantly unless fetal monitoring indicates fetal distress, in which case immediate abdominal delivery is in order if the fetus is at a gestational age that is considered “viable” (23 to 24 weeks or greater). Abdominal exploration may be necessary to stop bleeding and repair uterine lacerations. Lap-shoulder harness seat belts, rather than lap belts, are advisable for pregnant women after 12 weeks’ gestation.

Gunshot wounds of the abdomen are treated as in nonpregnant patients, with measures taken to stop bleeding and repair visceral or uterine injuries. So long as the pregnancy is intact, the uterus should not be disturbed. Careful monitoring of fetal well-being should be maintained before and after the operation.

Ovarian Tumors

Adnexal masses are not uncommon and are usually identified by pelvic examination or ultrasonography early in the pregnancy. Paraovarian cysts, corpus luteum cysts, and mature teratomas are the most common. About 50% to 70% are functional cysts (e.g., corpus luteum cysts) and spontaneously resolve as the gonadotropin levels fall during the second trimester. The risk for malignancy is about 3% to 7%, with germ cell and epithelial tumors both occurring. Abdominal and transvaginal ultrasonography should be used for initial diagnosis, and any complex mass that persists, or simple cyst that continues to enlarge, should be removed in the second trimester.


Abalovich M., Amino N., Barbour L.A., et al. Management of thyroid dysfunction during pregnancy and postpartum: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2007;92:s1-s47.

McKay D.B., Josephson M.A. Pregnancy in recipients of solid organs—effects on mother and child. N Engl J Med. 2006;354:1281-1293.

Perkins J., Dunn J., Jagasia S. Perspectives in gestational diabetes mellitus: A review of screening, diagnosis and treatment. Clin Diabetes. 2007;25:57-62.

Saleh M.M., Abdo K.R. Intrahepatic cholestasis of pregnancy: Review of the literature and evaluation of current evidence. J Womens Health. 2007;16:833-841.

Sulenik-Halevy R., Ellis M., Fejgin S. Management of immune thrombocytopenic purpura in pregnancy. Obstet Gynecol Surv. 2008;63:182-188.