Hypertensive Disorders in Pregnancy

Ramu Kharel

Megan C. Henn

Michelle D. Lall

OVERVIEW

The primary causes of maternal mortality around the world are hemorrhage, hypertension, and infection.¹ In the United States, hypertensive disorders during pregnancy are increasing, with the prevalence of pregnancy-related hypertension rising at a substantially higher rate than chronic hypertension in pregnant women.² Hypertensive disorders are the most common medical complication of pregnancy and affect 5% to 10% of all pregnancies.³ The gestational age, time course in developing hypertension, and specific laboratory abnormalities are all used to identify the various types of hypertensive disorders in pregnancy. Four categories of hypertensive disorders occur during pregnancy: chronic hypertension; gestational hypertension; preeclampsia/eclampsia; and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. See Table 16.1. It is essential for emergency medicine providers to be able to recognize and manage these distinctive hypertensive conditions in pregnancy in order to reduce the associated maternofetal morbidity and mortality.

CHRONIC HYPERTENSION IN PREGNANCY

Background

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines define Stage 1 hypertension as a blood pressure (BP) of 130-139/80-89 mm Hg, and Stage 2 as any BP 140/90 mm Hg or more. These are accurate measurements of two or more readings on two or more separate occasions. Prehypertension (an older definition) has been replaced with “elevated BP” that is between 120 and 129/<80 mm Hg.⁴ Primary hypertension is responsible for the majority of hypertension in the United States. About 6% to 8% of hypertensive patients have identifiable secondary causes such as renal parenchymal disease (polycystic kidneys, glomerular disease, interstitial disease); renal vascular disease (renal artery stenosis, fibromuscular dysplasia); endocrine disorders (adrenocorticosteroid or mineralocorticoid excess, pheochromocytoma, hyperthyroidism or hypothyroidism, growth hormone excess, hyperparathyroidism); coarctation of the aorta; or oral contraceptive-induced hypertension.⁵ These rarer causes of hypertension are important to consider as they can have significant impact on maternal and fetal well-being, and most of them are treatable and/or curable.⁵

TABLE 16.1 Hypertensive Disorders of Pregnancy

Disorder	BP Measurements	Clinical Features	Laboratory Features	Treatment
Chronic HTN in Pregnancy	Stage 1: ≥ 130-139/80-89 Stage 2: ≥ 140/90 (measured <20 wk gestation or >12 wk postpartum on two separate occasions)	Symptomatic in hypertensive emergency; maternal mortality due to stroke and congestive heart failure	No laboratory abnormalities seen, but must obtain CBC, CMP, LFTs, UA, 24-h urine creatinine clearance, and protein excretion	For <140/90: Lifestyle modification For ≥ 160/100, labetalol, alpha-methyldopa, clonidine, nifedipine, hydrochlorothiazide, and hydralazine are options
Gestational HTN	BP ≥ 140/90 without proteinuria (measured >20 wk gestation or immediate postpartum period)	No proteinuria or lab abnormalities Risk factors: prior history of preeclampsia, primigravida status, age, family history of hypertension, obesity, multiple gestation	No abnormalities, but must obtain same labs as chronic hypertension of pregnancy to establish baseline	Labetalol, alpha-methyldopa, clonidine, nifedipine, hydrochlorothiazide, and hydralazine are options
Preeclampsia Without Severe Features	BP ≥ 140/90 (measured >20 weeks or immediate postpartum), with proteinuria	Proteinuria present, no other systemic signs or symptoms	Proteinuria only, >0.3 g in 24-h urine collection; no other lab abnormalities	Outpatient management with frequent follow-up; labetalol, alpha-methyldopa, clonidine, nifedipine, hydrochlorothiazide, and hydralazine are options
Preeclampsia With Severe Features	BP ≥ 160/110 (measured >20 weeks or immediate postpartum)	Severe BP with any of the following present: visual/mental disturbance; pulmonary edema or cyanosis; RUQ pain; epigastric pain; abnormal LFTs; thrombocytopenia; oliguria; or proteinuria ≥ 5 g in 24-h collection; or ≥ 3+ protein in two random urine samples	Abnormal LFTs, thrombocytopenia, increased creatinine, protein/creatinine increased, proteinuria ≥ 5 g in 24-h collection or ≥ 3+ protein in two random urine samples	First line: IV labetalol, hydralazine, and immediate release oral nifedipine; IV magnesium sulfate for seizure prophylaxis Alternatives: nicardipine, esmolol, sodium nitroprusside
Eclampsia	Same as mild preeclampsia (occasionally can occur in setting of normal BP or lack of proteinuria)	Development of new-onset seizure, coma, or encephalopathy in setting of preeclampsia	Any of the above laboratory abnormalities found in preeclampsia: Abnormal LFTs, thrombocytopenia, increased creatinine, protein/creatinine increased, proteinuria ≥ 5 g in 24-h collection or ≥ 3+ protein in two random urine samples	IV magnesium sulfate for seizure prophylaxis. Same antihypertensive as above for proper BP management
HELLP Syndrome	No BP criteria	Defined as hemolysis, elevated liver enzymes, and low platelet count	Schistocytes on peripheral smear, thrombocytopenia <100 K, increased total bilirubin >1.2 mg/dL, normal/increased BUN/creatinine, abnormal coagulation studies, increased LDH	IV magnesium sulfate for seizure prophylaxis; BP control similar to preeclampsia depending on the level of hypertension; correction of coagulopathy; admission for stabilization
BP, blood pressure; BUN, blood urea nitrogen; CBC, complete blood count; CMP, comprehensive metabolic panel; HTN, hypertension; LDH, lactate dehydrogenase; LFTs, liver function test; RUQ, right upper quadrant; UA, urinalysis.

Epidemiology

Chronic hypertension increases with age and has higher rates in African-Americans. The prevalence is from 0.6% to 4.6% for white women and 2% to 22.3% for African-American women.⁶ Chronic hypertension in pregnancy is defined as a BP 130/80 mm Hg or more measured on two separate occasions before 20 weeks’ gestation or persistent beyond 12 weeks postpartum.⁴^,⁷ Women with chronic hypertension have increased risk for placental abruption, preeclampsia, low birth weight, cesarean section delivery, premature birth, and fetal demise.⁷ The maternal-fetal risks of chronic hypertension are generally associated with complications in the second half of pregnancy and include preeclampsia, eclampsia, and HELLP syndrome. These acute processes can be superimposed on chronic hypertension, and up to 20% of patients with chronic hypertension develop preeclampsia during pregnancy.⁶ In severe hypertension, maternal mortality is associated with congestive heart failure (CHF) and stroke related to hypertension.

Treatment Goals

The recommendation for treatment of chronic hypertension in nonpregnant patients is to achieve a BP of less than 130/80 mm Hg, but in chronic hypertension in pregnancy, patients with Stage 1 hypertension (<140/90 mm Hg) can be managed with lifestyle modifications and observed unless renal disease is present.⁴^,⁷ A diastolic BP greater than 110 mm Hg has been associated with an increased risk of placental abruption and intrauterine growth restriction. A systolic BP greater than 160 mm Hg increases the risk of maternal intracerebral hemorrhage. Hence, patients with either a diastolic BP greater than 110 mm Hg or a systolic BP greater than 160 mm Hg should be promptly started on antihypertensive medications.

Diagnostic Considerations

The diagnostic workup for chronic hypertension in pregnancy includes a complete blood count (CBC), comprehensive metabolic panel (CMP; electrolyte panel including renal function and liver enzymes), urinalysis (UA), and a 24-hour urine collection for creatinine clearance and protein excretion to establish a baseline, which can be useful later in pregnancy when evaluating for the development of preeclampsia or HELLP syndrome.

Management

Treatment for chronic hypertension includes labetalol, alpha-methyldopa, clonidine, and nifedipine⁸ (Table 16.2). Labetalol is considered the first-line treatment option. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are both contraindicated in pregnancy as they cause damage to the fetal kidneys in the second and third trimesters. Hydralazine and hydrochlorothiazide can be added as adjuncts to existing treatment for refractory cases. In cases of hypertensive urgency or emergency before 20 weeks of gestation, hydralazine, labetalol, and nifedipine can be used⁸ (Table 16.3).

GESTATIONAL HYPERTENSION

Gestational hypertension is the most frequent cause of hypertension during pregnancy. The rates of gestational hypertension are 6% to 17% in healthy nulliparous women and 2% to 4% in multiparous women.³ Gestational hypertension is defined as uncomplicated hypertension with a BP of 140/90 mm Hg or more after 20 weeks’ gestation or in the immediate postpartum period in the absence of proteinuria. Risk factors for gestational hypertension include prior history of preeclampsia, primigravida status, age less than 20 or more than 40 years, family history of hypertension, obesity, and multiple gestation.⁹ The treatment for gestational hypertension is the same as for chronic hypertension. Labetalol is first line, with alpha-methyldopa or nifedipine added as needed for tighter BP control. Hydralazine can be used in hypertensive emergency. In the absence of preeclamptic features, the maternal-fetal complications of gestational hypertension are similar to those of chronic hypertension in pregnancy. Placental abruption and fetal growth restrictions are related to diastolic BPs greater than 110 mm Hg. All patients with gestational hypertension must be evaluated for preeclampsia and have baseline laboratory studies including CMP, CBC, UA, and 24-hour urine collection. Preeclampsia is rare before the third trimester; hence, gestational trophoblastic disease and molar pregnancy must be considered in the setting of severe hypertension or preeclampsia in the first or early second trimester.

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