This chapter examines the diagnosis and treatment of the most important maternal emergencies occurring after 20 weeks of pregnancy and during the postpartum period. The second half of pregnancy is often characterized as ≥20 weeks of gestation for simplicity, but until 24 weeks, the chances of fetal survival are less than 50%. The postpartum period is generally accepted as the 6 weeks after delivery. Vast physiologic shifts in maternal cardiovascular tone occur as pregnancy progresses, highlighting the need for maternal blood pressure recordings and fetal heart tones during any ED visit. Conditions discussed are thromboembolic disease; chest pain; disorders associated with elevated blood pressure (hypertension, preeclampsia and HELLP syndrome [hemolysis, elevated liver enzymes, and low platelet count], and eclampsia); vaginal bleeding in the second half of pregnancy; premature rupture of membranes; postpartum hemorrhage; amniotic fluid embolus; peripartum cardiomyopathy; and endometritis.

Venous thromboembolism includes deep venous thrombosis (DVT) and pulmonary embolism (PE) and is the leading cause of maternal morbidity and mortality in industrialized nations. Compared with nonpregnant women, the risk of venous thromboembolism increases fivefold during pregnancy and is increased by 60-fold in the first 3 months after delivery.^1,2

PATHOPHYSIOLOGY

Pregnancy-related hypercoagulability is due to increased levels of clotting factors, increased platelet and fibrin activation, and decreased fibrinolytic activity, all of which are adaptations to prevent maternal hemorrhage. Physiologic changes include venous stasis, decreased venous outflow, and uterine compression of the inferior vena cava and iliac veins (particularly the left common iliac and left leg veins). Clots tend to develop in the deep venous system of the legs and pelvis, which includes the internal iliac, femoral, greater saphenous, and popliteal veins. Up to 24% of DVTs are complicated by PE, so early DVT diagnosis is important.^1,2,3,4,5,6

RISK FACTORS AND CLINICAL FEATURES

Physiologic signs and symptoms of thromboembolic disease, such as tachycardia, tachypnea, lower extremity edema, and dyspnea are nonspecific and also occur during normal pregnancy. Predictive scoring criteria, such as Wells criteria, have not been validated in pregnant women, but left leg symptoms, calf circumference difference ≥2 cm, and leg symptoms in the first trimester are associated with DVT. Iliac vein thrombosis often presents with unilateral swelling of the entire leg and groin or back pain.

A personal or family history of thrombosis is an important risk factor. Other major risk factors include thrombophilias (not identifiable at the first presentation), obesity, maternal age >35, smoking, sickle cell disease, diabetes, hypertension, immobility, in vitro fertilization (greater risk for twins than for singleton), and preeclampsia. Cesarean delivery and postpartum complications further increase the risk.^1,4,5

DIAGNOSIS OF DEEP VENOUS THROMBOSIS

Compression or duplex US is the test of choice, with a reported sensitivity and specificity for detecting proximal DVT in nonpregnant patients of 89% to 96% and 94% to 99%, respectively.⁷ Compression US is less accurate for isolated calf and iliac vein thrombosis. MRI, either with or without contrast venography, is highly sensitive and specific for the diagnosis of pelvic and iliac vein thrombosis. MRI without contrast is preferred with the addition of contrast only if absolutely needed.^8,9 Impedance plethysmography and CT scan of the pelvis are alternatives to diagnose iliac vein thrombosis if MRI is not available. Impedance plethysmography is not widely available and requires operator expertise. CT exposes the fetus to radiation, and iodinated contrast media may affect fetal thyroid tissue.¹ If imaging resources are limited, venography with pelvic shielding is another option.¹⁰

d-dimers are not useful to include or exclude DVT or PE because levels progressively increase throughout pregnancy, and venous thromboembolism has been reported with negative d-dimers.¹¹ See chapter 56, Venous Thromboembolism, for a detailed discussion of d-dimers.

DIAGNOSIS OF PULMONARY EMBOLISM

Pregnant women with symptoms suggestive of PE and compression US results positive for DVT should receive anticoagulation without waiting for further confirmatory diagnostic studies.

Women with normal findings on US with suspicion of PE require further diagnostic imaging. The major options for definitive imaging are chest CT–pulmonary angiography and pulmonary perfusion scanning. As of this writing, the fetal and maternal radiation dose with either modality is felt to be within acceptable limits.^1,12 Typically, in most institutions, a consensus is obtained between emergency physicians, obstetricians, and radiologists in deciding the imaging steps. Table 100-1 lists advantages and disadvantages of different imaging modalities.

Consensus documents based on expert opinions of pulmonologists and radiologists recommend a plain chest radiograph first.¹³ If the chest radiograph is abnormal, or the patient has chronic pulmonary disease, asthma, or chronic obstructive pulmonary disease, chest CT–pulmonary angiography is preferred.¹³ If the chest radiograph is normal, a negative perfusion scan can be relied upon to exclude the diagnosis of PE, but an inconclusive perfusion scan will then require a chest CT.^1,12,13,14

Magnetic resonance angiography (MRA) can detect PE, but its use in pregnancy has not been well studied. Institutions in which MRA of the pulmonary vasculature is performed routinely have demonstrated a sensitivity of 78% and specificity of 99% when the study is qualified as technically adequate.¹⁵

TREATMENT OF DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLISM

Venous thromboembolism during pregnancy is treated with either unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) (Table 100-2).^1,16,17 UFH and LMWH do not cross the placental barrier. UFH is preferred over LMWH in patients in a hemodynamically unstable condition with PE, patients who are likely to bleed, patients with renal insufficiency, patients in labor, those receiving regional anesthesia, and patients undergoing cesarean delivery. Monitor activated partial thromboplastin times when using UFH.¹¹ Dosing requirements of UFH and LMWH increase due to the physiologic changes of pregnancy. Adverse effects of UFH include uteroplacental hemorrhage, heparin-induced thrombocytopenia, and heparin-induced osteopenia. LMWH has fewer adverse effects and fewer bleeding episodes than UFH, and monitoring with anti–factor Xa levels is needed only in special circumstances. See chapter 239, Thrombotics and Antithrombotics, for further discussion of heparins.

Fondaparinux is used in the United States for the prevention and treatment of venous thromboembolism in heparin-allergic or heparin-intolerant pregnant patients.¹ However, fondaparinux is transported across the placenta in low concentrations, and minimal data exist on maternal-fetal safety.^1,17

Do not prescribe warfarin (Coumadin^®) in pregnancy because it crosses the placental barrier, causes CNS abnormalities, and causes warfarin embryopathy (bone and cartilage abnormalities and nasal and limb hypoplasia). Warfarin increases the risk of maternal and fetal hemorrhage, especially during delivery. Warfarin is only considered for women with mechanical heart valves who demonstrate a continued risk of venous thromboembolism despite treatment with UFH or LMWH.¹

An inferior vena cava filter is indicated when anticoagulation is contraindicated, when an acute embolic event occurs despite anticoagulation, or when acute venous thromboembolism occurs with impending delivery of the fetus.¹⁸

Treatment of Life-Threatening Pulmonary Embolism

Treatment options include systemic thrombolysis, catheter-guided thrombolysis, and surgical or catheter-guided embolectomy.^19,20,21,22 Data regarding maternal-fetal outcomes in conditions of maternal extremis are limited to case reports, and catheter-guided thrombolysis and embolectomy require precious time for preparation. Recombinant tissue plasminogen activator (10-milligram bolus, 90-milligram infusion over 2 hours) does not cross the placenta and has a lower rate of hemorrhagic complications and lower mortality rate than do streptokinase and urokinase in the nonpregnant population. Streptokinase (250,000-unit bolus, 100,000 units/h infusion for 24 hours) is also used but with a higher rate of subchorionic hemorrhage, allergic complications, and longer infusion duration than recombinant tissue plasminogen activator. Catheter-directed thrombolysis allows for earlier reperfusion and likely improves long-term pulmonary function compared with systemic therapy.^1,19 Fetal loss subsequent to surgical embolectomy is higher than with thrombolysis.^20,22

The differential diagnosis of chest pain in pregnant women is similar to that of nonpregnant women, but disorders such as aortic dissection and cardiomyopathy are associated with pregnancy. Advances in reproductive technology resulting in pregnancies in older women may result in an increase in coronary artery disease in this population. Coronary artery dissection and coronary vasospasm are more likely in women who smoke and those with migraine. Coronary artery disease is more likely in those >35 years old, diabetics, and hypertensives.²³ Treat acute myocardial infarction with low-dose aspirin, heparin, and percutaneous coronary intervention rather than with thrombolytics.^24,25 Aortic dissection, although rare, is usually encountered in the third trimester and the postpartum period. Risk factors are pregnancy, bicuspid aortic valve, connective tissue disorders (e.g., Marfan’s syndrome), syncope, hypertension, and a family history of aneurysm.²⁶ Chest radiograph may not demonstrate a widened mediastinum, and diagnosis is made by MRI or CT scan.²³

Peripartum cardiomyopathy is a dilated cardiomyopathy that can occur at any stage of gestation, but is classically defined as occurring in the last month of gestation or within the first 5 months after delivery, without an apparent cause or preexisting history of cardiac disease. The cause is unknown. Risk factors include cardiomyopathy during prior pregnancies, multiparity, maternal age >40 years old, chronic hypertension before pregnancy, gestational hypertension, preeclampsia, and HELLP syndrome. Symptoms and signs of peripartum cardiomyopathy are dyspnea, orthopnea, cough, palpitations, chest pain, edema, rales, and jugular venous distention. Diagnose and treat congestive heart failure and pulmonary edema with standard modalities (see chapter 53, Acute Heart Failure) except that nitroprusside is relatively contraindicated in pregnancy because it can cause thiocyanate and cyanide accumulation in the fetus. In the postpartum patient, angiotensin-converting enzyme inhibitors may be given. Anticoagulate with heparins because of increased risk of thromboembolism. Do not use warfarin during pregnancy. Warfarin can be given in the postpartum period.^27,28

CHRONIC AND GESTATIONAL HYPERTENSION

The decrease in systemic vascular resistance results in a decrease in maternal blood pressure, and blood pressure reaches its nadir at 16 to 18 weeks of pregnancy. Blood pressure returns to prepregnancy values near the end of the second trimester.

Chronic hypertension in pregnancy is defined as a systolic blood pressure of ≥140 mm Hg or a diastolic blood pressure of ≥90 mm Hg that existed prior to pregnancy, is diagnosed before the 20th week of gestation, or persists longer than 12 weeks after delivery. Severe chronic hypertension is systolic blood pressure >160 mm Hg or diastolic pressure >110 mm Hg. Women with chronic hypertension are at increased risk for placental abruption, preeclampsia, low birth weight, cesarean delivery, premature birth, and fetal demise.²⁹

Gestational hypertension is hypertension present only after the 20th week of pregnancy or in the immediate postpartum period but without proteinuria.

Safe treatment options for hypertensive women who are pregnant are labetalol and methyldopa.³⁰ All antihypertensive drugs cross the placenta. Labetalol is the first-line agent for chronic hypertension in pregnancy.²⁹ The starting dose is 100 milligrams PO twice a day, and the usual maintenance dose is 200 to 400 milligrams PO twice a day. Methyldopa, used safely in pregnancy for decades, is started at 250 milligrams every 6 hours PO and titrated to achieve the desired blood pressure. The usual daily dose is 500 milligrams to 3 grams divided in two to four doses per day, with a maximum of 3 grams per day.

Long-acting nifedipine may be added if blood pressure is not controlled with methyldopa or labetalol. Long-acting nifedipine is started at 30 milligrams PO once a day and can be increased up to 120 milligrams per day slowly if needed. For acute management of hypertensive emergencies, hydralazine 5 milligrams IV or IM, labetalol 20 milligrams IV, or nifedipine 10 to 30 milligrams PO (not a Food and Drug Administration–approved indication) may be used during pregnancy.^29,30,31 Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated because of their teratogenic effects on fetal scalp, lungs, and kidneys.²⁹

PREECLAMPSIA

Preeclampsia, or gestational hypertension with proteinuria, is characterized by hypertension before 20 weeks of gestation with either new-onset proteinuria, sudden increase in proteinuria, or development of HELLP syndrome.

The cause of preeclampsia is unknown. The histologic hallmark lesion of preeclampsia is acute atherosis of decidual arteries. Atherosis and thrombosis are thought to lead to placental ischemia and infarctions. Poor placental perfusion is presumed to lead to the formation of free radicals, to oxidative stress, and to inflammatory responses that may influence the mechanistic development of preeclampsia.³⁰

Preeclampsia is associated with intrauterine growth retardation, premature labor, low birth weight, abruptio placentae, and future risk of maternal cardiovascular disease.^30,32

Preeclampsia during an initial pregnancy increases the chances of recurrence in future pregnancies. Other important risk factors for preeclampsia include maternal age >40 years old, hypertension, diabetes, renal disease, collagen vascular disease, and multiple gestation. Low-dose aspirin therapy can prevent preeclampsia and its complications.^33,34

Diagnosis of Preeclampsia

Diagnostic criteria for preeclampsia are listed in Table 100-3, and laboratory evaluation is outlined in Table 100-4.³⁵

HELLP Syndrome

The HELLP syndrome (Table 100-5) is an important clinical variant of preeclampsia. HELLP is more common in the multigravid patient than in the primigravida. Hypertension may not be present initially or at all. This fact, combined with the usual complaint of epigastric or right upper quadrant pain, makes it easy to misdiagnose HELLP syndrome for other causes of abdominal pain, such as gastroenteritis, cholecystitis, hepatitis, pancreatitis, or pyelonephritis. A pregnant woman at >20 weeks gestation or up to 7 days postpartum with abdominal pain should be evaluated for HELLP syndrome.