Hypertensive disorders are the most common medical complications of pregnancy, which affect 5% to 10% of all pregnancies.¹ Approximately 30% of hypertensive disorders in pregnancy are due to chronic hypertension and 70% are due to gestational hypertension—preeclampsia. The spectrum of the disease ranges from mildly elevated blood pressures with minimal clinical significance to severe hypertension and multiorgan dysfunction. Understanding the disease process and its impact on pregnancy is of utmost importance, as hypertensive disorders remain a major cause of maternal and perinatal morbidity and mortality worldwide (Table 5-1).

Hypertension is defined as a systolic blood pressure greater than or equal to 140 mm Hg or a diastolic blood pressure greater than or equal to 90 mm Hg. These measurements must be made on at least two occasions, no less than 4 hours and no more than a week apart. It is important to note that choosing the appropriate blood pressure cuff size will help to eliminate inaccurate blood pressure measurements.¹ Abnormal proteinuria in pregnancy is defined as the excretion of greater than or equal to 300 mg of protein in 24 hours, a protein:creatinine ratio of greater than or equal to 0.30, or a urine dipstick of at least 1+ on occasions. The most accurate measurement of total urinary excretion of protein is with the use of a 24-hour urine collection. However, in certain instances the use of semiquantitative dipstick analysis may be the only measurement available to assess urinary protein. Table 5-2 lists the classification of hypertension.¹

Gestational Hypertension

Gestational hypertension is the elevation of blood pressure during the second half of pregnancy or in the first 24 hours postpartum, without proteinuria, without abnormal blood tests (elevated liver enzymes, low platelets, or elevated serum creatinine), and without symptoms. Normalization of blood pressure occurs in the postpartum period, usually within 10 days. Treatment is generally not warranted since most patients will have mild hypertension. Mild gestational hypertension in and of itself has little effect on maternal or perinatal morbidity or mortality when it develops at or beyond 37 weeks of gestation. However, approximately 40% of patients diagnosed with preterm gestational hypertension will subsequently develop preeclampsia. In addition, these pregnancies may result in fetal growth restriction and placental abruption.² If a woman with gestational hypertension receives antihypertensive therapy, she should be considered to have severe disease. Therefore, antihypertensive drugs should not be used during ambulatory management of these women.

Preeclampsia and Eclampsia

The classic triad of hypertension, proteinuria, and/or symptoms defines the syndrome of preeclampsia. Symptoms of preeclampsia include headache, visual changes, epigastric or right upper quadrant pain, and shortness of breath. Preeclampsia may be subdivided into preeclampsia and preeclampsia with severe features. The distinction between the two is based on the severity of hypertension as well as the involvement of other organ systems (Table 5-2).¹ Close surveillance of patients with preeclampsia is warranted, as either type may progress to fulminant disease. Therefore, all women with suspected or diagnosed preeclampsia should be instructed to immediately report any of the symptoms listed below:

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  Nausea and vomiting

  
  
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  Persistent, severe headache

  
  
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  Right upper quadrant or epigastric pain

  
  
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  Scotomata

  
  
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  Blurred vision

  
  
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  Shortness of breath

  
  
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  Decreased fetal movement

  
  
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  Rupture of membranes

  
  
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  Vaginal bleeding

  
  
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  Regular uterine contractions

A particularly severe form of preeclampsia is hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome, which is an acronym for hemolysis (H), elevated liver enzymes (EL), and low platelet count (LP). The diagnosis may be deceptive because blood pressure measurements may be only marginally elevated. A patient diagnosed with HELLP syndrome is automatically classified as having severe preeclampsia. Another severe form of preeclampsia is eclampsia, which is the occurrence of seizures in a patient with preeclampsia not attributable to other causes.

Chronic Hypertension

Hypertension complicating pregnancy is considered chronic if a patient is diagnosed with hypertension before pregnancy, if hypertension is present prior to 20 weeks of gestation, or if it persists longer than 6 months after delivery. Women with chronic hypertension are at risk of developing superimposed preeclampsia with or without severe features (Table 5-2).

The risk to the fetus in patients with preeclampsia relates largely to the gestational age at delivery. Risk to the mother can be significant and includes the possible development of disseminated intravascular coagulation (DIC), intracranial hemorrhage, renal failure, retinal detachment, pulmonary edema, liver rupture, abruption placentae, and death. Therefore, astute and experienced clinicians should be in charge of the care of women with preeclampsia.

Etiology

The etiologic agent responsible for the development of preeclampsia remains unknown. The syndrome is characterized by vasoconstriction, hemoconcentration, and possible ischemic changes in the placenta, as well as maternal kidney, liver, and brain. These abnormalities are usually seen in women with preeclampsia with severe features.

Pathophysiology

Cardiovascular

The hypertensive changes seen in preeclampsia are attributable to intense vasoconstriction thought to be due to increased vascular reactivity. The underlying mechanism responsible for increased vascular reactivity is presumed to be dysfunction in the normal interactions of vasodilatory (prostacyclin, nitric oxide, angiogenic) and vasoconstrictive (thromboxane A2, endothelin, anti-angiogenic) substances.¹ Another hallmark of severe disease is hemoconcentration. Accordingly, some patients with preeclampsia have lower intravascular volumes and less tolerance for the blood loss associated with delivery.

Hematologic

The most common hematologic abnormality in preeclampsia is thrombocytopenia (platelet count <100,000/mm³). The exact mechanism for thrombocytopenia is unknown. Another occasional hematologic abnormality is microangiopathic hemolysis, as seen in association with HELLP syndrome. It can be diagnosed by the presence of schistocytes on peripheral smear and by increased lactate dehydrogenase or bilirubin levels or reduced haptoglobin levels. Interpretation of the baseline hematocrit level in a preeclamptic patient may be difficult. A low hematocrit may signify hemolysis and a high hematocrit may be due to hemoconcentration.

Renal

Vasoconstriction in preeclampsia leads to decreased renal perfusion and subsequent reductions in the glomerular filtration rate (GFR). In normal pregnancy, the GFR increases by as much as 50% above pre-pregnancy levels. Because of this, serum creatinine levels in non-preeclamptic patients rarely rise above normal pregnancy levels (0.9 mg/dL). Close monitoring of serum creatinine is necessary in patients with preeclampsia, as elevated levels of creatinine more than 1.1 mg/dL may occur due to renal insufficiency. In rare case, profound renal insufficiency may lead to acute tubular necrosis. This is usually seen in the presence of abruption placentae, HELLP syndrome and unrecognized, severe blood loss that is not corrected.

Hepatic

Hepatic damage in association with preeclampsia can range from mildly elevated liver enzyme levels to subcapsular liver hematomas with or without rupture. The latter two are usually associated with severe thrombocytopenia. Liver lesions seen on biopsy and at autopsy include periportal hemorrhages, ischemic lesions, and fibrin deposition.

Central Nervous System

Eclamptic convulsions are perhaps the most disturbing central nervous system (CNS) manifestation of preeclampsia and remain a major cause of maternal mortality in developing countries. The exact etiology of eclampsia is unknown, but may be attributable to hypertensive encephalopathy or ischemia from vasoconstriction. Radiologic studies may show evidence of cerebral edema, particularly in the posterior hemispheres, which may explain the visual disturbances seen in preeclampsia. Other CNS abnormalities include headaches, altered mentation, scotomata, blurred vision, and rarely, temporary blindness.

Management of Preeclampsia with Severe Features

Any patient with severe features should be admitted and initially observed in a labor and delivery unit (Fig. 5-1).³ Initial workup should include assessment for fetal well-being, monitoring of maternal blood pressure, symptomatology and laboratory evaluation. Laboratory assessment should include hematocrit, platelet count, serum creatinine, and aspartate aminotransferase (AST). An ultrasound for fetal growth and amniotic fluid index should also be obtained. Candidates for expectant management should be carefully selected. They should also be counseled regarding the risks and benefits of expectant management.³ Guidelines for expectant management are outlined in Table 5-3. Fetal well-being should be assessed on a daily basis by non-stress testing and weekly amniotic fluid index determination. The patient should also be instructed on fetal movement assessment. An ultrasound for fetal growth should be performed every 2 to 3 weeks. Maternal laboratory evaluation should be done daily or every other day. If the patient maintains a stable maternal and fetal course, she may be expectantly managed until 34 weeks.³ Worsening maternal or fetal status warrants delivery, regardless of gestational age (Table 5-3).³ Women with a nonviable fetus (<23 weeks) should be presented with the option of pregnancy termination.¹