This chapter reviews the most common comorbid conditions encountered in pregnant women in the ED environment: diabetes and hypoglycemia; thyroid disorders; hypertensive disorders; cardiac arrhythmias; thromboembolism; asthma; renal disease; urinary tract infections; sickle cell disease; headache; seizures; substance abuse; and intimate partner violence. Drug risk during pregnancy, lactation, and fetal effects of radiation are summarized based on currently available data. Resuscitation is covered in chapter 25, “Resuscitation in Pregnancy.”

Maternal diabetes affects >8% of the 4 million live births annually in the United States.¹ Three fourths of pregnant patients with diabetes have either gestational diabetes or type 2 diabetes diagnosed through prenatal screening. Of the remaining 25%, 1% have preexisting type 1 diabetes, and the remaining are type 2 diabetics. Pregnant diabetic women are at increased risk for spontaneous abortion, particularly patients with poor glycemic control early in pregnancy, preexisting vascular disease, and pre-eclampsia. Pregnant diabetics are also at increased risk for several pregnancy complications, including pregnancy-induced hypertension, preterm labor, spontaneous abortion, pyelonephritis, and diabetic ketoacidosis (DKA). The goal of treatment during pregnancy is to prevent spontaneous abortions, hyperglycemia-induced congenital abnormalities and ketoacidosis, and hypoglycemia.

Oral hypoglycemic agents, such as metformin and glyburide, are occasionally used in select patients with gestational diabetes.² A significant portion of gestational diabetics can be managed with diet alone if they can maintain glycemic goals with frequent glucose monitoring.

The American College of Obstetricians and Gynecologists recommends the following goals for maintaining euglycemia in pregnant diabetic patients: a fasting blood glucose concentration of ≤95 milligrams/dL and a 2-hour postprandial glucose concentration ≤120 milligrams/dL.³ Patients with gestational diabetes who are managed by diet alone rarely develop acute hyperglycemic complications because glucose values rarely reach levels consistent with DKA. Among patients with preexisting type 1 and type 2 diabetes, the need for insulin increases throughout the course of pregnancy. Historically, all type 2 diabetics were switched to insulin as soon as possible (even prior to conception) to ensure appropriate glycemic control and due to concerns over the safety of oral hypoglycemic agents in pregnancy. Recent studies in gestational diabetes have not shown metformin or glyburide to have any harmful fetal effects, but long-term studies are needed. Although metformin may be continued in select patients, there is no consensus on the use of these oral agents alone in the pregnant patient with type 2 diabetes.^2,3,4,5

In general, during the first trimester, the initial insulin requirement is 0.7 units/kg/day. By late pregnancy, patients generally require 1 unit/kg/day.⁶

Neutral protamine Hagedorn (NPH)/regular insulin combinations are still first-line insulin therapy, but the long-acting analog insulin detemir (Levemir) is approved by the U.S. Food and Drug Administration for use in pregnancy and is category B. Compared to NPH, insulin detemir improves fasting plasma glucose and decreases hypoglycemic events. There is a strong evidence base to recommend insulin detemir in pregnancy, but the lack of definitive fetal benefit means that there is no pressing need to switch a woman whose diabetes is well controlled by NPH insulin to insulin detemir.

Insulin glargine (Lantus) is still category C. It is generally not initiated during pregnancy. However, it seems reasonable to continue insulin glargine when it was successful maintaining excellent glycemic control in a woman who is now pregnant.⁷

HYPOGLYCEMIA

Women with type 1 diabetes have three to five times more hypoglycemic episodes than the period prior to pregnancy.⁸ Risk factors for severe hypoglycemia during pregnancy include a history of severe hypoglycemia in the year preceding pregnancy, impaired hypoglycemia awareness, long duration of diabetes, low HbA_1c in early pregnancy, fluctuating plasma glucose levels, and excessive use of insulin injections between meals.⁸ Hypoglycemia generally presents as sweating, tremors, blurred or double vision, weakness, hunger, confusion, paraesthesias, anxiety, palpitations, nausea, headache, or stupor. Moderate and infrequent hypoglycemic episodes are generally well tolerated by the fetus.⁴ Pregnant diabetic women should be educated about the symptoms and treatment of hypoglycemia. Treat mild hypoglycemia (i.e., a glucose level of <70 milligrams/dL in patients who are able to follow commands) by giving juice, glucose, or food by mouth. Provide standard treatment for more severe hypoglycemia, with IV glucose or PO glucose or glucagon 1 to 2 milligrams SC or IV (see chapters 223, “Type 1 Diabetes Mellitus” and 224, “Type 2 Diabetes Mellitus”).

DIABETIC KETOACIDOSIS IN PREGNANCY

A pregnant diabetic who is ill appearing, has persistent nausea and vomiting, and/or has a blood glucose level ≥180 milligrams/dL should be screened for DKA with serum or urine ketones and a serum chemistry panel. Management guidelines for pregnant women with DKA are the same as for nonpregnant patients⁹ (see chapter 225, “Diabetic Ketoacidosis”). In addition to the usual care, obtain fetal heart tones, administer oxygen, and for third-trimester patients, place in the left lateral decubitus position to displace the uterus and improve uterine blood flow. Most fetal heart rate abnormalities subside after correction of maternal hypovolemia and acidosis. Consult with the patient’s physician, and admit the patient to the hospital.

The incidence of DKA in pregnancy decreases with early diagnosis of insulin-dependent diabetes, improved prenatal counseling, and care with an identifiable primary care provider.^10,11 DKA most commonly affects women in the second or third trimester or pregnant women with new-onset type 1 diabetes.^10,12

Women who use continuous SC insulin infusions (the insulin pump) can develop DKA whether they are pregnant or not. DKA can develop very quickly and unexpectedly, especially in patients who have recently started using the pump.^13,14 Use of continuous insulin pumps during pregnancy is equivalent, but not superior, to scheduled injections. Management of DKA in a pregnant woman with an insulin pump is the same as the nonpregnant patient.

DKA is not an indication for delivery. Although fetal heart rate monitoring in maternal DKA may initially demonstrate a nonreassuring pattern, patterns usually improve as maternal ketoacidosis is corrected, and mother will tolerate delivery or cesarean section better once acidosis resolves.^10,15

TRANSIENT HYPERTHYROIDISM OF HYPEREMESIS GRAVIDARUM

Women in the first trimester with weight loss, tachycardia, and vomiting consistent with hyperemesis gravidarum may also demonstrate laboratory evidence of hyperthyroidism, or biochemical or transient hyperthyroidism. The most likely cause is thyrotropin receptor stimulation from high human chorionic gonadotropin serum concentrations. Women with transient hyperthyroidism have no previous history of thyroid disease, no palpable goiter, and except for tachycardia, no other symptoms or signs of hyperthyroidism. Test results for thyroid antibodies are negative. With transient hyperthyroidism of hyperemesis gravidarum, thyroid-stimulating hormone (TSH) may be suppressed and free thyroxine (T₄) elevated, but triiodothyronine (T₃) is lower than in true hyperthyroidism. With true hyperthyroidism, both free T₄ and T₃ are usually elevated. Only symptomatic treatment is suggested for transient hyperthyroidism, and antithyroid medication is not recommended.¹⁶

HYPERTHYROIDISM

True hyperthyroidism in pregnancy increases the risk of pre-eclampsia, low birth weight, and possibly congenital malformations. Symptoms of hyperthyroidism can mimic symptoms of normal pregnancy and may consist of nervousness, palpitations, heat intolerance, and inability to gain weight despite a good appetite. Methimazole and propylthiouracil (PTU) are equally efficacious in the treatment of pregnant women. However, methimazole has a possible association with congenital abnormalities during first-trimester organogenesis, and PTU can cause hepatotoxicity. Therefore, during the first trimester, hyperthyroidism in pregnancy is treated with PTU followed by methimazole during the second and third trimesters.^17,18,19 Agranulocytosis and aplastic anemia are rare but serious complications in patients treated with antithyroid drugs. If this occurs, immediately discontinue the medication and obtain obstetrical consultation.

THYROID STORM

Patients with thyroid storm develop fever, volume depletion, or high-output heart failure. Labor, cesarean section, and infection all may precipitate thyroid storm in a woman with a history of hyperthyroidism. Thyroid storm has been associated with a mortality rate of up to 25%. The principles of treatment are summarized in Table 99–1 and are similar to those for nonpregnant patients (see chapter 229, “Hyperthyroidism”).

Hypertensive disorders are the most common medical complication of pregnancy. Hypertension in pregnancy can be divided into five categories: chronic hypertension in pregnancy, gestational hypertension, pre-eclampsia, HELLP syndrome, and eclampsia. Chronic hypertension is discussed below, and the other disorders are discussed in detail in chapter 100, “Emergencies after 20 Weeks of Pregnancy and the Postpartum Period.”

CHRONIC HYPERTENSION IN PREGNANCY

Chronic hypertension is sustained elevation of blood pressure to >140/90 mm Hg, measured on two separate occasions before 20 weeks of gestation or persistent beyond 12 weeks postpartum.^21,22 Patients with mild hypertension (140/90 mm Hg) and no evidence of renal disease should be counseled on lifestyle modifications and observed. Because there is no consensus that antihypertensives can reduce the risk of fetal death, growth restriction, abruption, or eclampsia, treatment with antihypertensive medication is not usually necessary unless renal disease develops.²³ Despite the lack of evidence supporting the benefit of antihypertensive therapy in women with blood pressure <180/110 mm Hg, there is a general consensus that pregnant women with hypertension in the blood pressure range of 150 to 160/100 to 110 mm Hg should be treated with antihypertensive therapy.^22,23,24 There is insufficient evidence to support or refute the theory that bed rest, either in the hospital or at home, improves outcomes.²⁵

Maternal mortality in patients with chronic hypertension results from severe hypertension and associated congestive heart failure or stroke. Fetal perinatal outcome is associated most closely with pre-eclampsia or placental abruption.

Commonly used agents for the treatment of chronic hypertension in pregnancy are listed in Table 99–2 and include labetalol, α-methyldopa (Aldomet), clonidine, and nifedipine. Based on the overall low rate of adverse effects and good efficacy, labetalol is a good option for first-line treatment of chronic hypertension in pregnancy.²² Thiazide diuretics can be continued during pregnancy.²² Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are the only class of antihypertensive medications contraindicated in pregnancy.²²

Pregnancy can precipitate cardiac arrhythmias not previously present in seemingly well individuals. The risk of arrhythmias rises during labor and delivery. Factors that promote arrhythmias in pregnancy include the direct cardiac electrophysiologic effects of hormones, changes in hemodynamics or autonomic tone, hypokalemia, and underlying heart disease. Reduction of uterine blood flow during prolonged tachyarrhythmic episodes may adversely affect the fetus. The incidence of arrhythmias in pregnancy is rising due to increasing maternal age and pregnancies in women successfully treated for congenital heart disease.²⁶ Just as in a nonpregnant patient, treat any hemodynamically unstable arrhythmia in pregnancy with direct-current cardioversion (50–200 J).^27,28 Treat hemodynamically stable arrhythmias medically. The chronic use of β-blockers in pregnancy can influence fetal and newborn size, but only atenolol is singled out as being a Food and Drug Administration class D drug in this regard (some evidence for harm to the fetus). Other β-blockers are Food and Drug Administration class B (sotalol) or C. Digoxin, verapamil, diltiazem, and adenosine have their usual efficacy without adverse fetal affects.²⁶

CARDIAC ARRHYTHMIA TREATMENT

Paroxysmal supraventricular tachycardia is the most common nonsinus tachycardia in women of childbearing age. The treatment of supraventricular tachycardia in pregnant women is the same as for nonpregnant women.²⁶ If vagal maneuvers are ineffective, give adenosine. Case reports show both efficacy and a lack of any direct adverse or teratogenic side effects to the fetus.²⁹ Additionally, acute treatment with β-blockers, verapamil, and diltiazem is safe in pregnancy when used in standard dosage.

The goal of management of atrial fibrillation in pregnancy is rate control or conversion to sinus rhythm. Use diltiazem, β-blockers, and/or digoxin, all of which are safe in pregnancy and with unchanged dosages.²⁹ Anticoagulation with unfractionated or low-molecular-weight heparin is safe in pregnancy and should be used if the patient meets criteria for anticoagulation described for nonpregnant patients.

Ventricular arrhythmias may occur during pregnancy, particularly in patients with congenital heart disease, cardiomyopathy, or valvular disease. Amiodarone is categorized as class D because its main metabolite (desethylamiodarone) and iodine cross the placenta. Chronic fetal exposure to amiodarone and its subsequent iodine overload are associated with neurotoxicity, fetal/neonatal hypothyroidism, and less frequently, goiter. Therefore, the use of amiodarone in pregnancy is limited to maternal/fetal tachyarrhythmias that are resistant to other drugs or are life threatening, because short-term use has not been linked to any harmful effects.²⁹

The presence of an artificial pacemaker or implantable cardiac defibrillator does not affect the course of pregnancy.³⁰

A detailed discussion of clinical features, diagnosis, and treatment of thromboembolism in pregnancy is found in chapter 100.

The pregnancy-related changes that increase the risk of thromboembolism include physiologic alterations in coagulation and reduced venous return from the legs, with venous pooling and endothelial injury. The clinical assessment is difficult because many of the typical clinical signs and symptoms are seen in normal pregnancy, including leg edema, shortness of breath, and tachycardia. The Wells Score for deep venous thrombosis (see Table 56–4), the most validated clinical decision rule in the diagnosis of deep vein thrombosis, has not been validated in pregnant women.^31,32

Obtain Doppler compression ultrasonography for diagnosis.³³ d-Dimer levels normally increase throughout pregnancy, and thromboembolism has been reported with normal d-Dimer levels.^34,35 Imaging modalities for diagnosis are provided in Table 100–1.

Treatment is low-molecular-weight heparin (Table 100–2).³⁶ Do not use warfarin in pregnancy because it crosses the placenta and is associated with embryopathy in the first trimester; in the second and third trimesters, it may lead to CNS and ophthalmologic abnormalities. Protamine sulfate may be used safely in pregnancy for patients who require rapid reversal of heparin anticoagulation. Thrombolytics are not contraindicated and have been used successfully in multiple cases. Reported rates of maternal bleeding complications are between 1% and 6% with no maternal deaths, and rates of fetal loss are between 2% and 5%.^37,38,39,40

Asthma is the most common medical disease in pregnancy and complicates between 3.7% and 8.4% of all pregnancies.⁴¹ The clinical course may improve, remain unchanged, or worsen during pregnancy. Women with asthma have higher odds of pre-eclampsia, gestational diabetes, placental abruption, placenta previa, preterm delivery, low birth weight, maternal hemorrhage, pulmonary embolism, and intensive care unit admission.⁴²

Symptoms of cough, wheezing, and dyspnea are the same as in nonpregnant patients. Initial assessment should include history of asthma exacerbations and intubation, peak expiratory flow rate measurements or forced expiratory volume in 1 second, physical examination, assessment of oxygen saturation, and a fetal assessment (if >20 weeks’ gestation). Peak expiratory flow rate is not altered in pregnancy, with normal rates ranging between 380 and 550 L/min. Use peak expiratory flow rate as a guide to therapy. If the pregnancy has reached viability, apply continuous electronic fetal monitoring.

Treat rapidly and aggressively to reduce re-admission rates and improve fetal outcomes.⁴³ The principles of management are the same as in nonpregnant patients. Maintain oxygen saturation >95%, administer repetitive or continuous inhaled β₂-agonist (albuterol/salbutamol); give inhaled ipratropium and systemic corticosteroids; monitor maternal response to therapy; and monitor the fetus for signs of distress.⁴⁴ Terbutaline sulfate, 0.25 milligrams every 20 minutes, administered SC, may be used if needed. Avoid epinephrine because concerns exist about epinephrine vasoconstriction of the uteroplacental circulation.

Admission and discharge criteria are the same as in the nonasthmatic patient. For discharged women, prescribe oral prednisone, 40 to 60 milligrams per day (or equivalent), for 5 to 10 days, and a short-acting rescue β-agonist. Inhaled corticosteroids reduce recurrence during pregnancy and decrease re-admission rates following a hospitalization for asthma.⁴⁵ Anticipate maternal hyperglycemia when systemic corticosteroids are given.

Maternal risks associated with renal disease are linked to the patient’s degree of renal compromise. Patients with mild renal insufficiency and no hypertension tend to have good outcomes and preserved renal function. Patients with moderate or severe renal insufficiency are more prone to further decline in renal function and pre-eclampsia and preterm delivery. Patients with lupus nephropathy are at greatly increased risk for disease exacerbation and superimposed pre-eclampsia.

Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, which are frequently used in patients with chronic renal failure, are teratogenic and should be stopped at the first indication of pregnancy.

Hormonal and mechanical changes of pregnancy increase the risk of urinary stasis and subsequent urinary tract infection. After mid-pregnancy, mild right-sided hydronephrosis is found in 75% of women, and mild left-sided hydronephrosis is found in 33%.

Asymptomatic bacteriuria is diagnosed by urine culture, demonstrating the presence of bacteria in the urine in the absence of maternal symptoms of urinary tract infection. Reagent strips have limited sensitivity, and use in screening depends on resources available, but in general, a positive leukocyte esterase or urinary nitrite should be treated and a negative specimen should be cultured.^46,47 Treatment reduces the incidence of pyelonephritis and low birth weight.⁴⁸

Causative organisms of symptomatic cystitis and pyelonephritis are similar to those in the general population and include Escherichia coli (75%), Klebsiella pneumoniae, Proteus, and gram-positive organisms such as group B Streptococcus. Obtain a urinalysis and culture with drug sensitivities in pregnant women with urinary tract symptoms and also in those with hyperemesis. Urinary tract infections need prompt treatment because acute pyelonephritis can precipitate preterm labor, bacteremia, or septic shock.

Recurrent infections can occur as a result of bacteriuria, glycosuria, and mechanical compression of the ureter in the third trimester. Reflux nephropathy increases the risk of sudden escalating hypertension and worsening renal function.⁴⁹ Urolithiasis is associated with recurrent urinary tract infections.