Acute hypertension in pregnancy is a severe obstetric complication that requires immediate evaluation and treatment. It can occur in the context of a variety of disorders of pregnancy and is associated with significant maternal and fetal morbidity and potential mortality. Hypertension in pregnancy can occur along a spectrum as noted in Table 17.1.

The spectrum of pregnancy-related hypertensive disorders frequently presenting with acute changes in blood pressure control will be presented. The common presenting symptomatology, the initial steps in maternal/fetal evaluation (history, physical examination, and laboratory evaluation), and management in the obstetric triage setting will be covered. In addition, other possible etiologies of acute hypertension, preeclampsia with severe features, and possible imitators of HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome will be discussed.

DEFINITIONS

Hypertension in pregnancy, otherwise known as gestational hypertension (GHTN), is defined as a systolic blood pressure level of 140 mmHg or greater and a diastolic blood pressure level of 90 mmHg or greater (National High Blood Pressure Education Program Working Group, 2000). Severe hypertension is defined as persistent systolic blood pressure of 160 mmHg or greater or diastolic blood pressure of 110 mmHg or greater. Severe hypertension is associated with a significantly higher rate of potentially catastrophic maternal and fetal events, including maternal stroke or other central nervous complications, and placental abruption with subsequent fetal compromise (Magee & von Dadelszen, 2009). Of note, elevated systolic blood pressure has been more strongly associated with maternal cerebral vascular accident than diastolic blood pressure (Martin et al., 2005).

As many as 25% of women with GHTN will go on to develop preeclampsia (Saudan, Brown, Buddle, & Jones, 1998), which is defined as persistent hypertension diagnosed after 20 weeks gestation with the addition of proteinuria or evidence of end-organ damage, or both. Preeclampsia occurs in 3% to 10% of all pregnancies (Haddad & Sibai, 2009) and is a disorder of largely unknown etiology that is likely associated with abnormal placentation and subsequent wide-reaching 182vascular and endothelial dysfunction (American College of Obstetricians and Gynecologists [ACOG], 2013). Preeclampsia is noted to have severe features if a variety of signs or symptoms indicating evolving endothelial dysfunction are present (see Exhibit 17.1; ACOG, 2013). Potential fetal effects of hypertensive disorders in pregnancy include placental dysfunction manifested as poor fetal growth, oligohydramnios, nonreactive fetal heart rate testing, abruption, and intrauterine fetal demise.

Further on the spectrum of hypertensive disorders of pregnancy is eclampsia (occurrence of seizures not attributable to other causes in a patient with preeclampsia). In addition, preeclampsia can be accompanied by significant end-organ damage and coagulopathy, as evidenced by the frequent presentation 183of preeclampsia with HELLP syndrome. While HELLP syndrome can present without evidence of hypertension and/or proteinuria (Roberts, 2013), it is considered in this chapter due to the shared pathophysiologic changes and frequent presentation in the context of severe preeclampsia.

Chronic hypertension is defined as hypertension predating the pregnancy or noted prior to 20 weeks gestation. Another clinical entity to be considered is preeclampsia (with or without severe features) superimposed on preexisting chronic hypertension (sometimes referred to simply as superimposed preeclampsia). Unfortunately, superimposed preeclampsia poses a significant diagnostic conundrum as women affected by chronic hypertension often have some element of baseline renal dysfunction and resultant proteinuria, in addition to elevated blood pressures. However, it is known that maternal and fetal prognosis in the setting of superimposed disease is worse than with other disease processes alone (Roberts, 2013). Therefore, clinicians must be vigilant of any increase in blood pressure or worsening of baseline proteinuria in pregnant women with previously diagnosed chronic hypertension and have a high index of suspicion for superimposed preeclampsia. Maternal risk factors for the development of preeclampsia are noted in Exhibit 17.2.

While the spectrum of hypertensive disorders in pregnancy is often referred to collectively as “pregnancy-induced hypertension,” this is not an endorsed term and only disorder-specific terms should be used.

PRESENTING SYMPTOMATOLOGY

Considering the pervasive endothelial dysfunction present in preeclampsia/eclampsia, it is not surprising that the presenting symptomatology often relates to a multitude of organ systems suffering from poor vascular perfusion. Cerebral symptoms most commonly include a persistent headache but can also include dizziness, tinnitus, fever, drowsiness, changes in respiratory rate, and tachycardia. Visual symptoms often present as diplopia, scotoma, blurred vision, and vision loss. Gastrointestinal symptoms are common and usually present with nausea, vomiting, and possible epigastric pain but can also include hematemesis. Renal symptoms may include oliguria, anuria, or hematuria. In addition, many 184pregnant women will note an increase in edema (extremities, facial). Some women with severe features of the disease who suffer from cardiopulmonary compromise and resultant pulmonary edema will report significant shortness of breath. While many of these symptoms are possible, certain symptoms are considered more ominous and indicative of preeclampsia with severe features. These include those signs of hepatic capsular distension (which can present as epigastric pain), dyspnea that is secondary to pulmonary edema, headache indicative of poor cerebral perfusion (and possible impending eclampsia), and retinal artery edema and spasm causing visual changes (Roberts, 2013).

HISTORY AND DATA COLLECTION

The gravid woman presenting to an obstetric triage setting with hypertension warrants immediate evaluation. While initial history and data collection are obtained simultaneously, steps must be taken by the care team to begin treatment of severe range blood pressures and, if present, eclamptic seizure activity. In addition, fetal status must be evaluated as soon as possible with either a modified biophysical profile (mBPP) or biophysical profile (BPP).

Maternal history includes a pertinent history of present illness focusing on classic preeclampsia symptomatology. Maternal past obstetric history (including prior preeclampsia/eclampsia), as well as history of preexisting hypertension or other medical/surgical conditions, must be obtained.

Maternal blood pressure needs to be evaluated with an appropriately sized cuff (length 1.5 times the circumference of the upper arm) to minimize inaccurate readings. Ideally, the blood pressure is obtained after a rest period of 10 minutes, without exposure to caffeine or tobacco for 30 minutes. The blood pressure is obtained with a woman sitting upright; however, it can also be evaluated with the patient lying in the left lateral position with the brachial artery at heart level (Magee et al., 2008). While some electronic devices are acceptable, in general mercury sphygmomanometry (manual blood pressure cuff) is preferred due to increased accuracy (Magee & Von Dadelszen, 2009).

PHYSICAL EXAMINATION

While initial steps toward the treatment of the hypertensive emergency begin and laboratory evaluations are obtained, a thorough physical examination is performed. Classic physical examination findings of preeclampsia, while not diagnostic, include edema, hyperreflexia, and clonus. Retinal artery changes (due to localized retinal vascular narrowing and segmental spasm) occur in 50% of patients with preeclampsia (Roberts, 2013). Other less common and significantly more ominous findings on physical examination include ascites and hydrothorax (associated with marked edema, increased neck vein distension, and rales on pulmonary examination) consistent with pulmonary edema/congestive heart failure, hepatic enlargement and tenderness indicative of hepatic capsular distension, and petechiae, bruising, or bleeding associated with disseminated intravascular coagulation (DIC).

A complete physical examination is performed, including cardiovascular, pulmonary, abdominal, ophthalmologic, neurologic, skin, and extremity evaluation. A cervical examination is also performed to evaluate the Bishop’s score for cervical readiness and possible delivery planning. The fetal status is evaluated as soon as possible using external fetal monitoring and by ultrasound evaluation.

185LABORATORY AND IMAGING STUDIES

Laboratory studies include complete blood count (CBC), creatinine, liver function tests, uric acid, lactate dehydrogenase (LDH), coagulation profile, urinalysis, and urine protein:creatinine ratio. Consideration can be given to sending a urine toxicology screen as sympathomimetic drugs such as amphetamines can elevate blood pressure.

The diagnosis of preeclampsia does not require the presence of proteinuria, though proteinuria is common. Proteinuria is defined as 1+ or greater protein on a urine dip or greater than 300 mg protein/24-hour period noted on a 24-hour urine collection specimen. Proper collection of a 24-hour urine specimen involves discarding the first void of the day followed by complete collection for 24 subsequent hours with an adequate volume of urine obtained. Adequacy is determined by 24-hour urine creatinine excretion equal to 15 to 20 mg/kg prepregnancy body weight. Recently, obstetric providers have adopted the use of the urine spot protein:creatinine ratio, which is a favored method of proteinuria evaluation in the nonpregnant population (Eknoyan et al., 2003) and has gained support in the medical literature as a valid way to evaluate proteinuria in the pregnant population (ACOG, 2013; Côté et al., 2008; Neithardt, Dooley, & Borensztajn, 2002; Papanna, Mann, Kouides, & Glantz, 2008).

Common abnormalities noted on laboratory analysis include evidence of hemoconcentration (elevated hematocrit), hemolysis (thrombocytopenia, elevated LDH), renal compromise (elevated creatinine), hepatic damage (elevated liver function tests), coagulopathy (elevated prothrombin time [PT], elevated international normalized ratio [INR], elevated partial thromboplastin time [PTT], low fibrinogen), and elevated uric acid. Approximately 20% of patients with preeclampsia with severe features will have HELLP syndrome with laboratory findings as noted in Table 17.2 (Sibai et al., 1993). Frequent laboratory reevaluation in the situation of markedly abnormal maternal labs, changing clinical status, or expectant management of severe preeclampsia needs to be considered.

There are no specific imaging studies required in the context of maternal hypertensive emergencies. While the exact incidence of cerebral hemorrhage in nonfatal eclampsia is unknown, it has been reported that 50% of reversible, pregnancy-related ischemic strokes do occur in the context of preeclampsia (Zeeman, 2009). If persistent neurologic changes suspicious for maternal intracranial pathology after resolution of seizure activity are noted, CT imaging of the head is indicated. If pulmonary edema is suspected, an urgent chest radiograph is warranted. If congestive heart failure is suspected, maternal echocardiogram can be obtained once the maternal and fetal status is stabilized.

TABLE 17.2 Criteria for the Diagnosis of HELLP Syndrome and Corresponding Laboratory Findings

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