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Common Medical and Surgical Conditions Complicating Pregnancy
Clinical Keys for This Chapter
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Diabetes and thyroid disorders are among the most common and consequential medical conditions that occur during pregnancy, labor, and the postpartum period. Diabetes may precede pregnancy or may occur because of pregnancy, with a return to the prepregnancy state after delivery. Gestational diabetes mellitus (GDM) is defined as glucose intolerance with onset or first recognition during pregnancy. Pregestational diabetes mellitus may be type 1 (insulin-dependent) or type 2. Thyroid abnormalities occur in about 2% of pregnancies, and the presentation and course of the disease may be affected by the pregnancy.
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Other important medical conditions include heart, autoimmune, renal, gastrointestinal (GI), lung, and thromboembolic disorders. Preexisting cardiovascular disease and conditions such as asthma and cystic fibrosis are encountered more commonly because of modern medical management that has allowed more women than in the past to consider pregnancy. As a general rule, most pregnancies complicated by these medical conditions are considered “high risk” for maternal and fetal morbidity and mortality. Good outcomes often require frequent maternal and fetal assessment and the ability to respond in a timely fashion to changes in the clinical status of either the mother or her fetus.
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Elective delivery for medical and surgical conditions is indicated when deteriorating maternal or fetal status occurs in the presence of a term fetus or when there is evidence of fetal lung maturity. When a preterm delivery before 34 weeks' gestation is necessary, steroids (betamethasone) should be given to enhance fetal lung maturity and improve fetal outcomes. In some cases, cesarean delivery is indicated.
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Obstetricians and other providers should focus on the mitigation of the effects and prevention of medical conditions that may complicate pregnancy. The increased prevalence of obesity in pregnant women in the United States and elsewhere has resulted in metabolic dysregulation (metabolic syndrome) that increases inflammation and insulin resistance. The risk of some medical disorders, such as diabetes, hypertension, and heart disease, is increased due to excessive body weight during pregnancy. Women should be encouraged to lose weight before pregnancy and to limit weight gain during pregnancy. Physical activity and a healthy diet are very important before, during, and after pregnancy.
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Surgical conditions that may complicate pregnancy include appendicitis, cholecystitis and cholelithiasis, acute pancreatitis, bowel obstruction, abdominal trauma, or torsion of an adnexal structure such as an ovarian tumor. When trauma is evaluated during pregnancy, the possibility of intimate partner abuse must be ruled out, as in women who are not pregnant. Strongly indicated but nonemergent surgery is most safely performed in the second trimester. Laparoscopy is becoming more common during pregnancy, and guidelines have been published that should increase the safety for both the pregnant woman and her fetus.
Most of the conditions discussed in this chapter are not unique to pregnancy and understanding the causes, diagnosis, and management of them is based on the same principles that would apply in the nonpregnant woman. Important issues for the management of medical and surgical problems during pregnancy include how the physiologic changes of pregnancy may affect the diagnosis and clinical course of the disease, as well as how the disease may affect the pregnancy, with particular attention to the fetus.
The most common medical and surgical disorders that may complicate pregnancy are covered in this chapter. Common and important infectious diseases of both nonpregnant and pregnant women are covered in Chapter 22 , including perinatal infections (toxoplasmosis, others [syphilis, varicella zoster, parvovirus B19], rubella, cytomegalovirus [CMV], and herpes, referred to together as TORCH infections ), human immunodeficiency virus (HIV) infection, and acquired immunodeficiency syndrome (AIDS).
Endocrine Disorders
Diabetes mellitus and thyroid disease are the two most common endocrine disorders complicating pregnancy.
Diabetes Mellitus
Incidence and Classification
The prevalence of diabetes mellitus has greatly increased in the last 20 years. In the United States, rates appear to range from 6-12%, depending on the population studied and the diagnostic criteria used. Overall, 80-90% of diabetes in pregnant women is gestational, and about 10% is pregestational.
Gestational diabetes mellitus (GDM) is defined as glucose intolerance with onset or first recognition during pregnancy. Rising levels of human placental lactogen, progesterone, prolactin, and cortisol in pregnancy are some of the primary factors associated with progressive 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 later in life.
Pregestational diabetes mellitus refers to diabetes present before pregnancy and may be either type 1 or type 2 diabetes. Most obstetricians use the White classification of diabetes during pregnancy to further refine the categories for GDM and pregestational diabetes. This classification is helpful for assessing disease severity and the likelihood of complications ( Table 16-1 ).
TABLE 16-1
White Classification of Diabetes in Pregnancy
| Class | Description |
|---|---|
| A 1 | Gestational diabetes; diagnosed in pregnancy and controlled with diet alone |
| A 2 | Gestational diabetes; diagnosed in pregnancy and controlled with diet and glyburide or insulin |
| B | Pregestational diabetes developing after age 20 yr and duration <10 yr; controlled with diet and insulin |
| C | Pregestational diabetes developing between ages 10 and 19 yr or duration 10-19 yr and controlled with diet and insulin |
| D | Pregestational diabetes developing before age 10 yr or duration 20 yr or more or background retinopathy; controlled with diet and insulin |
| F | Pregestational diabetes at any age or duration with nephropathy; controlled with diet and insulin |
| R | Pregestational diabetes at any age or duration with proliferative retinopathy; controlled with diet and insulin |
| H | Pregestational diabetes at any age or duration with arteriosclerotic heart disease; controlled with diet and insulin |
Complications
Maternal and fetal complications of diabetes are listed in Table 16-2 . Diabetes often coexists with the metabolic syndrome. This syndrome consists of a group of risk factors for diabetes, coronary heart disease, and stroke that occur together (central obesity, insulin resistance, and hyperlipidemia). 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 that 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 A1C (HbA1C) levels in the first trimester. Fetal hyperglycemia and hyperinsulinemia later in pregnancy, especially in the third trimester, cause fetal overgrowth and macrosomia that predispose to birth trauma, including shoulder dystocia and Erb palsy. Fetal demise is most likely due to acidosis, hypotension from osmotic diuresis, or hypoxia from increased metabolism, coupled with inadequate placental oxygen transfer.
TABLE 16-2
Maternal and Fetal Complications of Diabetes Mellitus
| Entity | Monitoring |
|---|---|
| Maternal Complications | |
| Obstetric Complications | |
| Polyhydramnios | Close prenatal surveillance: blood glucose monitoring, ultrasonography |
| Preeclampsia | Evaluation for signs and symptoms |
| Infections (e.g., UTI and candidiasis) | Urine culture, wet mount, and 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 |
| Diabetic Emergencies | |
| Hypoglycemia | Teach signs and symptoms; blood glucose monitoring; insulin and dietary adjustment |
| Diabetic coma | Urgent medical management required |
| Ketoacidosis | Check for ketones if glucose >200 mg/dL |
| Vascular and End-Organ Involvement or Deterioration (in patients with pregestational diabetes mellitus) | |
| Cardiac | Electrocardiogram, first visit and as needed |
| Renal | Renal function studies, first visit and as needed |
| Ophthalmic | Funduscopic evaluation, first visit and as needed |
| Peripheral vascular | Check for ulcers, foot sores; noninvasive Doppler studies as needed |
| Gastrointestinal disturbance | Symptomatic treatment as needed |
| Neurologic | |
| Peripheral neuropathy | Neurologic and gastrointestinal consultations as needed |
| After Pregnancy | |
| Type 2 diabetes | Postpartum glucose testing of GDM, lifestyle changes (diet and exercise) |
| Metabolic syndrome | Lifestyle changes (diet and exercise) |
| Obesity | Lifestyle changes (diet and exercise) |
| Cardiovascular disease | Annual check-up by physician, lifestyle changes (diet and exercise) |
| Fetal and Neonatal Complications * | |
| Macrosomia with traumatic delivery | Ultrasonography for estimated fetal weight before delivery (shoulder dystocia, Erb palsy), offer cesarean delivery if EFW >4500 g |
| Delayed organ maturity (pulmonary, hepatic, neurologic) | Avoid delivery before 39 weeks in GDM in the absence of maternal-fetal respiratory distress syndrome indications, unless amniocentesis indicates lung maturity |
| Neonatal hypocalcemia, neonatal hypoglycemia | Maintain maternal euglycemia especially intrapartum |
| Congenital Defects | |
| Cardiovascular anomalies | Preconception counseling and glucose control |
| Neural tube defects | Maternal serum α-fetoprotein screening; fetal ultrasonography and fetal echocardiogram |
| Caudal regression syndrome | |
| Other defects (e.g., renal) | |
| Fetal Compromise | |
| Intrauterine growth restriction | Serial ultrasonography for fetal growth and estimated fetal weight, serial fetal antepartum surveillance; avoid postterm pregnancy |
| Intrauterine fetal death | Doppler |
| Abnormal FHR patterns | NST |
EFW, Estimated fetal weight; FHR, fetal heart rate; GDM, gestational diabetes mellitus; NST, nonstress test; UTI, urinary tract infection.
* Maintenance of maternal euglycemia (normal glucose levels) will decrease most of these complications.
Pregestational diabetes is generally associated with a higher rate of maternal and fetal complications due to the greater difficulty in achieving glycemic control, the higher rate of congenital malformations, and the higher likelihood of vascular disease. Maternal complications include worsening nephropathy and retinopathy, a greater incidence of preterm preeclampsia, and a higher likelihood of diabetic ketoacidosis. Hypoglycemia is also much more common because of the need for insulin therapy and stricter glycemic control attempted during pregnancy. Fetal complications include an increased rate of abortions, anatomic birth defects, fetal growth restriction, and prematurity.
Diagnosis of Gestational Diabetes Mellitus
The American College of Obstetricians and Gynecologists (ACOG) recommends a two-step method to test for GDM. The first step involves universal screening for gestational diabetes between 24 and 28 weeks' gestation with a 50-g, 1-hour oral glucose challenge test (OGCT), given without regard to most recent oral intake. This timing recognizes the progressive nature of insulin resistance in pregnancy due to rising levels of hormones such as human placental lactogen, and the test will identify most women with gestational diabetes while allowing for several weeks of therapy to reduce potentially adverse consequences. Screening is advised at the first prenatal visit in women with risk factors such as a previous pregnancy with GDM, a history of polycystic ovarian disease, or obesity. If overt signs and symptoms of diabetes are present, the patient's fasting blood sugar should be checked first. If a first-trimester screen is done and is found to be negative, it should be repeated at 24 to 28 weeks. Glucose values above 130 to 140 mg/dL on an OGCT are considered abnormal and have an 80-90% sensitivity in detecting GDM.
The second step involves performing a diagnostic 3-hour, 100-g oral glucose tolerance test (OGTT) if the screening test is abnormal. This involves checking the patient's fasting blood glucose after an overnight fast, having the patient consume a 100-g glucose drink, and checking her glucose levels hourly for 3 hours. If there are two or more abnormal values on the 3-hour OGTT, the patient is diagnosed with GDM ( Table 16-3 ). If the 1-hour screening (50 g of oral glucose) plasma glucose exceeds 200 mg/dL, an OGTT is not required and may dangerously elevate blood glucose values.
TABLE 16-3
Three-Hour Oral Glucose Tolerance Test
From Berggren EK, Boggess KA, Stuebe AM, et al: National Diabetes Data Group vs Carpenter-Coustan criteria to diagnose gestational diabetes. Am J Obstet Gynecol 205:253.e1-e7, 2011.
| Test | Maximal Normal Blood Glucose (mg/dL) |
|---|---|
| Fasting | 95 |
| 1 hr | 180 |
| 2 hr | 155 |
| 3 hr | 140 |
Management
Team Approach
Management of gestational and pregestational diabetes requires a team approach involving patient education 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.
Achieving Euglycemia
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. To achieve an optimal outcome, the patient's fasting blood glucose level should be less than 95 mg/dL, with the 1-hour postprandial glucose level less than 140 mg/dL and the 2-hour postprandial glucose level less than 120 mg/dL.
Diet
Caloric requirements are calculated on the basis of ideal body weight: 30 kcal/kg for those patients 80-120% of ideal body weight, 35 to 40 kcal/kg for those patients less than 80% of ideal body weight, and 24 kcal/kg for gravidas who are 120-150% of ideal body weight. The diet is composed of about 45-50% carbohydrate, 20-25% protein, and 20-25% fat. The diet should also contain a generous amount of fiber. Caloric intake is divided into 20% at breakfast, 30% at lunch, 30% at dinner, and 20% at a bedtime snack.
Exercise
Patients with diabetes should be encouraged to engage in mild to moderate aerobic exercise (e.g., brisk walking) for about half an hour after meals.
Pharmacologic Therapy
Patients with GDM are usually managed with diet and exercise alone, but if euglycemia cannot be achieved, an oral hypoglycemic agent (glyburide) or insulin should be added. Glyburide does not appear to enter the fetal circulation in appreciable quantities, and it has been used successfully to treat gestational diabetes after the first trimester.
Insulin is the medication of choice to maintain euglycemia in pregnancy and is the recommended therapy in women with pregestational diabetes. The peak action of insulin lispro occurs between 30 and 90 minutes after injection, that of regular insulin occurs between 2 and 3 hours after injection, and that of neutral protamine Hagedorn (NPH) insulin occurs between 6 and 10 hours after injection. A combination of rapid- 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 Calculating the Starting Dose of Insulin
Insulin Units = Body Weight (kg)
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×0.6 (first trimester)
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×0.7 (second trimester)
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×0.8 (third trimester)
Dosage Schedule: Give Two-Thirds in AM and One-Third in PM
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Before breakfast: two-thirds NPH, one-third regular or lispro
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Before dinner: one-half NPH, one-half regular or lispro (if on lispro, administer additional dose before bedtime snack)
NPH, Neutral protamine Hagedorn.
Antepartum Obstetric Management
Aside from achieving euglycemia, adequate surveillance should be maintained during pregnancy to detect and possibly mitigate maternal and fetal complications. In addition to routine prenatal screening tests for women with pregestational diabetes, a detailed obstetric ultrasonic study, fetal echocardiogram, and maternal serum α-fetoprotein should be obtained in the second trimester to check for congenital malformations. This is especially important if the first trimester HbA1C is significantly elevated (>8.5%). Maternal renal, cardiac, and ocular function must be closely monitored. In women with GDM as well as those with class B or C pregestational diabetes, fetal macrosomia is common and should be investigated, whereas for women with classes D, F, or R pregestational diabetes, fetal growth restriction occurs more commonly. Abnormalities of fetal growth are most likely to be present in the third trimester and can be confirmed by ultrasound.
Serial antepartum testing should be performed in the third trimester. This testing can usually be delayed until at or after 36 weeks, or later in women with well-controlled GDM. In patients with pregestational diabetes, fetal testing should be initiated between 32 and 34 weeks, or sooner if complications develop.
The timing of delivery depends on fetal and maternal status and the degree of glucose control. In general, in the setting of well-controlled GDM without other complications, 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 avoided. Cesarean delivery may be elected for large fetuses (>4500 g).
Intrapartum Management
Intrapartum management of a patient with diabetes requires the establishment of maternal euglycemia during labor. Plasma glucose levels are measured frequently, and, if elevated, a continuous infusion of regular insulin is given. Insulin dosage is adjusted as needed to maintain a plasma glucose level between 80 and 120 mg/dL. Many insulin-dependent patients will not require exogenous insulin during labor. Continuous electronic fetal heart rate monitoring is recommended for all patients with diabetes.
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 patients with insulin-dependent diabetes 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. Women with pregestational diabetes can be restarted on two-thirds of the prepregnancy insulin dosage, with adjustments made as necessary. Women with GDM treated with insulin or oral hypoglycemic agents during pregnancy frequently do not need treatment postpartum. Women with GDM should undergo a 75-g OGTT at 6 to 12 weeks postpartum.
Patients should be counseled about changes in diet. The American Diabetes 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 prepregnancy diet.
Contraception counseling should involve advising the patient that estrogen-containing oral contraceptives are not recommended for women with advanced-stage diabetes with vascular disease.
Thyroid Diseases
Thyroid diseases are relatively common disorders in pregnancy, complicating up to 2% of pregnancies. Pregnancy can alter the presentation, diagnosis, and course of thyroid disease. If inadequately treated, these disorders can lead to major maternal, fetal, and neonatal morbidity.
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 caused by iodine deficiency are not likely if plasma inorganic iodine levels are greater than 0.08 µg/dL but they do occur ( Figure 16-1 ). An inorganic iodine intake of 250 µg/day is sufficient to prevent goiter formation during pregnancy. Prenatal vitamins typically contain 150 µg of iodine.
Thyroid Function Tests
The estrogen-mediated increase in thyroid-binding globulin during pregnancy results in a pronounced rise in serum total thyroxine (T 4 ) and total triiodothyronine (T 3 ) levels. Total T 4 levels in a pregnant woman can be up to 50% greater than the upper limit of normal for nonpregnant women. Serum free thyroxine (free T 4 ) and free triiodothyronine (free T 3 ) levels usually remain in the normal range. Human chorionic gonadotropin (hCG) levels peak in the first trimester and can cause transient, subclinical hyperthyroidism. In the setting of a molar pregnancy, the extremely high hCG levels can result in thyrotoxicosis. When interpreting serum levels of thyroid-stimulating hormone (TSH) and free T 4 and T 3 , it is best to use a laboratory that has trimester-specific values. Generally accepted TSH ranges for nonpregnant and pregnant women by trimester are shown in Table 16-4 .
TABLE 16-4
Median Values of Thyroid-Stimulating Hormone
| Pregnancy Stage | Median Value * |
|---|---|
| Nonpregnant | 0.3-4.2 U/mL |
| First trimester | 0.5-5.0 U/mL |
| Second trimester | 0.5-3.5 U/mL |
| Third trimester | 0.5-4.0 U/mL |
Fetal Thyroid Function
Before 10 weeks' gestation, no organic iodine is present in the fetal thyroid. By the end of the first trimester (11 to 12 weeks), the fetal thyroid is able to produce iodothyronines and T 4 , and by 12 to 14 weeks, it is able to concentrate iodine. Levels of these hormones remain low even at term, but they increase rapidly in the neonate within 48 hours of birth.
Placental Transfer of Thyroid Hormone
Iodide freely crosses the placenta, but TSH does not. Limited transfer of T 4 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 methimazole and propylthiouracil (PTU), with smaller molecular weights, cross the placental barrier and can potentially cause fetal hypothyroidism. Thyroid-releasing hormone can cross the placental barrier, but there is no significant placental transfer because of circulating low levels. Thyroid-stimulating antibodies (TSH receptor antibodies) also cross the placenta and can potentially cause fetal and neonatal 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. It is the most common cause of hyperthyroidism. Other causes of hyperthyroidism in pregnancy include hCG-mediated hyperthyroidism, such as that seen in association with a hydatidiform mole, and toxic nodular goiter. Patients with Graves disease tend to have a remission during the third trimester of pregnancy and an exacerbation during the postpartum period. The increased immunologic tolerance during pregnancy may lead to a decrease in thyroid antibodies, which may account for the remission.
Clinical Features
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 woman. A resting pulse rate greater than 100 beats per minute, a wide pulse pressure, tremor, eye changes (exophthalmos), failure to gain weight despite normal or increased food intake, and heat intolerance, when present, are all helpful in making the clinical diagnosis.
Investigations
An elevated serum free T 4 level and a suppressed TSH level establish the diagnosis of hyperthyroidism. Infrequently, a free T 3 determination might be needed to diagnose T 3 thyrotoxicosis. In cases where there is significant discordance between the clinical findings and TSH and free thyroid hormone levels, it is appropriate to measure the total T 4 level, accepting as normal up to 1.5 times the upper range in nonpregnant women.
Therapy
Because radioactive iodine treatment is contraindicated during pregnancy, medical treatment is generally given. When there is significant maternal tachycardia, β-blockers such as atenolol or propranolol may be used for short-term treatment, with longer-term treatment increasing the risk of fetal growth restriction. Thioamides are the mainstay of antithyroid therapy. They block the synthesis, but not the release, of thyroid hormone. PTU and methimazole (Tapazole) are both effective, but they have different safety profiles. Both cross the placenta, and methimazole has been associated with aplasia cutis congenita (absence of a portion of skin at birth) and fetal gastrointestinal (GI) defects to a greater degree than PTU. For the mother, methimazole appears safer because there is less risk of liver toxicity. These drugs readily cross the placenta, and 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, 1-5% of children exposed in utero will develop a goiter ( Figure 16-2 ). For these reasons , PTU should be used to treat overt hyperthyroidism in the first trimester, and methimazole should be used in the second and third trimesters. Importantly, antithyroid drugs should be reduced to the lowest dose that results in free T 4 levels within the upper range of normal. Free T 4 levels should be checked at least every 4 weeks. Antithyroid therapy can often be discontinued after 30 weeks' gestation, but the patient should be followed for recurrent disease postpartum.
Methimazole and PTU are excreted in breast milk, but no changes occur in the thyroid function tests of breastfed neonates. Methimazole is preferred over PTU in breastfeeding mothers because of the lower risk of liver toxicity.
Surgical management of a pregnant patient with hyperthyroidism during the second trimester is recommended only when medical treatment fails.
Thyroid Storm
The major risk for a pregnant patient with thyrotoxicosis is the development of a thyroid storm. Precipitating factors include infection, labor, cesarean delivery, or noncompliance with the medication regimen. It is not uncommon to mistakenly attribute the signs and symptoms of severe hyperthyroidism to preeclampsia. In the former, significant proteinuria is usually absent, but both may be present in the same patient. Thyroid storm in a pregnant woman is a life-threatening medical emergency and should be treated in an intensive care setting. The signs and symptoms associated with a thyroid storm include hyperthermia, marked maternal tachycardia, perspiration, and high-output renal failure or severe dehydration. Fetal tachycardia can also be present.
Specific treatment involves (1) blocking β-adrenergic activity and controlling maternal heart rate with propranolol, (2) blocking synthesis of thyroid hormone and conversion of T 4 to T 3 with PTU, (3) administering potassium iodide 1 to 2 hours after starting PTU to block secretion of thyroid hormone, (4) additional blocking of the deamination of T 4 to T 3 with glucocorticoids (dexamethasone), (5) replacing fluid losses, and (6) rapidly lowering the patient's body temperature with hypothermic techniques. Management also involves intensive maternal and fetal monitoring and correction of precipitating factors. It is important to stabilize the patient before attempting delivery if that is being considered. Once the patient is stabilized and no longer acutely ill, methimazole should be substituted for PTU to avoid hepatotoxicity.
Neonatal Thyrotoxicosis
About 5% of pregnant women with a history of Graves disease give birth to children with thyrotoxicosis due to transplacental transfer of TSH receptor antibodies. It is transient and lasts less than 2 to 3 months, but if clinically significant and untreated, it is associated with neonatal morbidity and mortality. Fetal thyrotoxicosis can be suspected if the baseline fetal heart rate consistently exceeds 160 beats per minute. A fetal goiter can often be identified by ultrasonography in such cases, and fetal growth restriction may be present. This situation is associated with an increase in perinatal morbidity and mortality and should be treated pre- and postnatally.
Hypothyroidism
Hypothyroidism (overt or subclinical) complicates up to 3% of pregnancies. The value of universal screening is still being debated, and ACOG is currently not recommending routine screening. However, pregnant women with symptoms consistent with low thyroid hormone levels (fatigue, intolerance to cold, excessive weight gain) or with risk factors (e.g., obesity, type 1 diabetes or history of thyroid disease) should be screened.
The most important laboratory finding of hypothyroidism is an elevated TSH level. If the TSH level is elevated, the diagnosis of overt vs. subclinical hypothyroidism can be made based on whether free T 4 levels are decreased. Once diagnosed, therapy such as levothyroxine should be started, and serum TSH levels should be measured monthly with appropriate adjustments in levothyroxine dosage. Pregnant women on appropriate thyroid replacement therapy can expect a normal pregnancy outcome, but untreated maternal hypothyroidism has been associated with an increased risk of spontaneous abortion, preeclampsia, abruption, low-birth-weight or stillborn infants, and lower cognitive function in offspring.
Congenital Hypothyroidism
Thyroid hormone deficiency during the fetal and early neonatal periods leads to generalized cognitive impairment. The severity of symptoms depends on the time of onset and the severity of the deprivation. The incidence of congenital hypothyroidism is about 1 in 2000 to 4000 births. The etiologic factors include thyroid dysgenesis, inborn errors of thyroid function, and iodine deficiency. Maternal and neonatal exposure to excess iodine (e.g., amiodorone, iodine-containing contrast dyes or disinfectants, and supplements) is another potentially preventable cause. Newborn screening programs can identify many cases of congenital hypothyroidism, and with early administration of thyroid hormone replacement, the impairment can be minimized.
Heart Disease
Less than 5% of pregnancies in the United States are complicated by maternal cardiac disease, but it is an important cause of maternal mortality. The cardiovascular adaptations to pregnancy, delivery, and the early puerperium can trigger acute cardiovascular decompensation in women with high-risk lesions. The physiologic changes discussed in Chapter 6 , including the rise in preload, decrease in afterload, and increase in cardiac output, begin in the first trimester and peak toward the end of the second or early third trimester. The corresponding physical findings of a new systolic flow murmur, an S 3 gallop, an increase in resting heart rate, a decline in diastolic blood pressure, and dependent edema can further complicate the clinical diagnosis and management of these pregnancies.
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, such as coronary artery disease. Better treatment of rheumatic fever and improvements in medical and surgical management of congenital heart disease have meant that in a modern tertiary referral center, about 80% of patients with cardiac disease in pregnancy now have congenital heart disease.
Rheumatic Heart Disease
The most common lesion associated with rheumatic heart disease is mitral stenosis, followed by mitral regurgitation. Patients with mitral stenosis, especially those with a valve area less than 1.5 cm 2 , are at high risk of developing heart failure, subacute bacterial endocarditis, and thromboembolic disease. They also have a higher rate of fetal wastage.
During pregnancy, the mechanical obstruction associated with mitral stenosis 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. Tachycardia can result in decompensation because cardiac output in patients with mitral stenosis depends on an adequate diastolic filling time.
Congenital Heart Disease
Congenital heart disease includes atrial or ventricular septal defects, valvular defects, primary pulmonary hypertension (Eisenmenger syndrome), and cyanotic heart diseases such as tetralogy of Fallot and transposition of the great arteries. If the anatomic defect has been corrected during childhood with no residual damage, the patient is expected to 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 experiencing decompensation during pregnancy. Pulmonary hypertension from any cause is associated with an increased risk of maternal mortality during pregnancy or in the immediate postpartum period. In all of these patients, care should be taken to avoid overloading the circulation and precipitating pulmonary congestion, heart failure, or hypotension, all of which may lead to hypoxia and sudden death. In general, significant pulmonary hypertension with Eisenmenger syndrome is a contraindication to pregnancy due to the high maternal mortality that accompanies this condition.
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