Chapter 5: Hypertensive Emergencies

Hypertensive disorders are the most common medical complications of pregnancy, affecting 5% to 10% of all pregnancies. 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 2 occasions, no less than 6 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. Abnormal proteinuria in pregnancy is defined as the excretion of greater than or equal to 300 mg/dL of protein in 24 hours, a protein:creatinine ratio of greater than or equal to 0.30 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.

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. Gestational hypertension in and of itself has little effect on maternal or perinatal morbidity or mortality when it develops at or beyond 37 weeks’ gestation. However, approximately 40% of patients diagnosed with preterm gestational hypertension will subsequently develop preeclampsia, or severe gestational hypertension. In addition, these pregnancies may result in fetal growth restriction and placental abruption. Those with severe gestational hypertension are at risk for adverse maternal and perinatal outcomes and should be managed like those with severe preeclampsia. 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 mild 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). 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:

• Nausea and vomiting

• Persistent, severe headache

• Right upper quadrant or epigastric pain

• Scotomata

• Blurred vision

• Shortness of breath

• Decreased fetal movement

• Rupture of membranes

• Vaginal bleeding

• Regular uterine contractions

A particularly severe form of preeclampsia is 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 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’ gestation, or if it persists longer than 6 months after delivery. Women with chronic hypertension are at risk of developing superimposed preeclampsia. Superimposed preeclampsia is defined as an exacerbation of hypertension and new onset of proteinuria.

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, abruptio 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) and vasoconstrictive (thromboxane A2, endothelins) substances. 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 prepregnancy levels. Because of this, serum creatinine levels in nonpreeclamptic 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 >1.1 mg/dL may occur due to renal insufficiency. In rare cases profound renal insufficiency may lead to acute tubular necrosis. This is usually seen in the presence of abruptio 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 and hepatic rupture. The latter 2 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 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). Initial work-up 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. Guidelines for expectant management are outlined in Table 5-3. Fetal well being should be assessed on a daily basis by nonstress 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. Worsening maternal or fetal status warrants delivery, regardless of gestational age (Table 5-3). Women with a nonviable fetus should be presented with the option of pregnancy termination.

Maternal blood pressure control is essential with expectant management or during delivery. Medications can be given orally or intravenously, as necessary, to maintain blood pressure between 140 to 155 mm Hg, systolic and 90 to 105 mm Hg, diastolic. The most commonly used intravenous medications for this purpose are labetalol and hydralazine. Other medications can include oral rapid-acting nifedipine. Subsequent management can include oral medications such as labetalol and long acting nifedipine. The recommended dosages of medications for acute treatment of hypertension are listed in Table 5-4. Care should be taken not to drop the blood pressure too rapidly so as to avoid reduced renal and placental perfusion.

A trial of labor is indicated in patients with severe preeclampsia if gestational age is >30 weeks and/or if cervical Bishop score is greater than or equal to 6. However, an appropriate time frame should be established regarding the achievement of active labor. Preeclamptic women receiving magnesium sulfate are also at risk for postpartum hemorrhage due to uterine atony. Patients should be closely monitored for 24 hours postpartum. Postpartum eclampsia occurs in 25% of patients; thus, MgSO₄ should be continued for 24 hours after delivery. There is usually no need for continued seizure prophylaxis beyond 24 hours postpartum. Some of these patients are at risk for pulmonary edema and exacerbation of severe hypertension at 2 to 5 days postpartum. Therefore, they should receive frequent monitoring and a short course of furosemide, if needed. It is important to avoid the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or anti-inflammatory agents for pain relief in these women due to their potential deleterious effect on maternal renal function. If needed, I recommend acetaminophen with codeine for pain relief.

HELLP Syndrome

The specific laboratory abnormalities demonstrating hemolysis, elevated liver enzymes, and low platelets are shown in Table 5-5. The clinical presentation of patients with HELLP syndrome is highly variable. However, HELLP patients generally are multiparous, white females who present at less than 35 weeks’ gestation. Sibai has noted that hypertension may be absent (20%), mild (30%), or severe (50%) in women diagnosed with HELLP syndrome. Therefore, the diagnosis of HELLP syndrome cannot necessarily be ruled out in the normotensive patient who has other signs and symptoms that are consistent with preeclampsia.

Differential Diagnosis

HELLP may be confused with other medical conditions, particularly in the face of normotension. A list of the differential diagnoses is found in Table 5-6. HELLP can be confused with other specific medical conditions, such as acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS), and lupus nephritis The differentiation among the 3 entities is based on specific laboratory findings (Table 5-7).

Management

The initial evaluation in women diagnosed with HELLP syndrome should be the same as that for preeclampsia with severe features. The patient with preterm gestation should be cared for at a tertiary care center. Management initially should include maternal and fetal assessment, control of severe hypertension (if present), initiation of magnesium sulfate infusion, correction of coagulopathy (if present), and maternal stabilization. Immediate delivery should be performed in patients at more than 34 weeks’ gestation. In patients less than 34 weeks without proven lung maturity, corticosteroids should be given and delivery planned for 48 hours thereafter, provided there is no worsening of maternal or fetal status in the meantime. The use of steroids, volume expanders, plasmapheresis, and antithrombotic agents in patients with HELLP have produced only marginal results, although some evidence suggests a benefit of steroid therapy for improvement in maternal platelet count. However, 2 multicenter placebo-controlled trials revealed that high-dose dexamethasone does not improve maternal outcome in patients with HELLP syndrome in the antepartum or postpartum period. This was later confirmed by the results of a recent meta-analysis of corticosteroid use in women with HELLP syndrome. Conservative management of HELLP syndrome poses a significant risk of abruptio placentae, pulmonary edema, adult respiratory distress syndrome (ARDS), ruptured liver hematoma, acute renal failure, DIC, eclampsia, intracerebral hemorrhage, and maternal death. Therefore, expectant management past 48 hours is not warranted for the minimal fetal benefits, when weighed against the profound maternal risk.

Patients with a favorable cervix and a diagnosis of HELLP syndrome should undergo a trial of labor, particularly if they present in labor. An operative delivery in some situations may even be harmful. However, elective cesarean section should be considered in patients, at very early gestational ages, with unfavorable cervices. The anesthetist should be updated as to the trend in platelet count for patients with HELLP. Should such a patient require cesarean delivery, platelet transfusion of approximately 6 to 10 units should be initiated en route to the operating room in patients with severe thrombocytopenia. However, platelet consumption is rapid with a platelet transfusion in this setting. Intraoperative considerations should include drain placement (subfascial, subcutaneous, or both) due to generalized oozing. Postpartum management of the HELLP patient should include close hemodynamic monitoring for at least 48 hours. Serial laboratory evaluations should also be done to monitor for worsening abnormalities. Most patients should show reversal of laboratory parameters within 48 hours. Therefore, we do not recommend postpartum administration of dexamethasone at our center.

Another potential life-threatening complication of HELLP syndrome is subcapsular liver hematoma. Clinical findings consistent with this complication include phrenic nerve pain. Pain in the pericardium, peritoneum, pleura, shoulder, and esophagus are consistent with referred pain from the phrenic nerve. Confirmation of the diagnosis can be obtained via the computed tomography, ultrasonography or magnetic resonance imaging. Conservative management in a hemodynamically stable patient with an unruptured subcapsular hematoma is appropriate, provided that close hemodynamic monitoring, serial evaluations of coagulation profiles, and serial evaluation of the hematoma with radiologic studies are performed. Should the patient decompensate hemodynamically, the diagnosis of ruptured subcapsular hematoma should be entertained. If rupture of a subcapsular liver hematoma is suspected, immediate intervention is necessary. Liver hematoma rupture with hemodynamic shock is a life threatening surgical emergency. Management should involve trauma and vascular surgeons. Correction of coagulopathy and massive blood product transfusion is essential. Typically, rupture involves the right lobe of the liver. Maternal and fetal mortality is over 25%, even with immediate intervention. The current recommendation for treating rupture of subcapsular liver hematoma in pregnancy is packing and drainage, if possible.

ECLAMPSIA

The rate of eclampsia in the United States is 0.05% to 0.1%, and much higher in developing countries. Eclampsia continues to be a major cause of maternal and perinatal morbidity/mortality worldwide. The maternal mortality rate is approximately 1% to 2%. The perinatal mortality rate ranges from 13% to 30%. Eclampsia can occur antepartum (50%), intrapartum (25%), or postpartum (25%). In the postpartum period, eclampsia can develop as late as 4 weeks.

Management

During the eclamptic seizure, the main therapy is supportive care. Management of eclampsia is as follows:

1. Avoid injury: Padded bed rails, restraints

2. Maintain oxygenation: O₂, pulse oximetry, arterial blood gas assessment

3. Minimize aspiration: Lateral decubitus position, upper airway suction

4. Initiate magnesium sulfate

5. Control blood pressure

6. Move toward delivery (corticosteroids if <28 weeks and stable condition at a center with expertise in management of eclampsia)

Most seizures are self-limited, lasting 1 to 2 minutes. Magnesium sulfate is the drug of choice for the prevention of eclampsia and should also be used for prevention of recurrent seizures. Approximately 10% of eclamptic women receiving magnesium sulfate will nevertheless have more seizures. Immediately following an eclamptic seizure, it is common to see abnormalities in the fetal heart rate pattern. These include fetal bradycardia, decreased variability, late decelerations, and reflex tachycardia. They typically resolve within 5 to 10 minutes after the convulsion. It is important not to proceed directly to cesarean delivery after a seizure, if at all possible. Vaginal delivery is the preferred birth route, even after an eclamptic seizure. Cesarean delivery should be performed for obstetric indications only. Induction of labor may be performed with oxytocin or prostaglandins, with the patient maintained on magnesium sulfate throughout her labor course. Careful attention must be given to the overall fluid status of the patient. Patients with eclampsia may have profound hemoconcentration. Because of this, close hemodynamic monitoring is required in the setting of epidural anesthesia and/or of severe blood loss. Patients who are hypovolemic will not respond well to acute blood loss, yet it is also important to limit fluids, as these patients have capillary leakage and are predisposed to developing pulmonary edema. Magnesium sulfate should be continued for 24 hours postpartum. Intracranial imaging is typically not warranted unless coma or focal neurologic signs persist or the diagnosis is uncertain. Postpartum eclampsia is a diagnostic dilemma. Any woman seizing in the postpartum period should be considered to have eclampsia; however, other disorders must be ruled out. Patients who develop postpartum eclampsia usually will have symptoms prior to seizure activity including severe, persistent headache, blurred vision, photophobia, epigastric pain, nausea and vomiting, and transient mental status changes. Therefore, it is important to educate patients to report these symptoms to healthcare providers so as to initiate preeclamptic evaluation. Eclamptics should receive MgSO₄ for at least 24 hours after seizure activity. If the patient has normal laboratory values and hypertension is controlled, she can be discharged in a few days with instructions to report symptoms and to return in 1 week for outpatient evaluation.

Magnesium Sulfate

The use of magnesium sulfate in the management of preeclamptic patients is for the prevention of eclamptic seizures. The exact mode of action of MgSO₄ for preventing seizures is unknown, although it has been in use since the early twentieth century to prevent recurrent seizures and other associated maternal/perinatal complications. The recommended regimen is presented in Table 5-8. The intravenous route is the preferred method, as intramuscular injection of magnesium sulfate is very painful and occasionally can cause gluteal abscess formation. Magnesium sulfate is not a benign medication. Patients receiving MgSO₄ are at increased risk for postpartum hemorrhage due to uterine atony. This should be anticipated and steps should be taken to ensure availability of crossmatched blood, if the need arises. Monitoring patients for signs of magnesium toxicity should be done throughout the course of administration; this includes eliciting deep tendon reflexes, assessing mental status, checking respiratory rate, and monitoring urine output. Table 5-8 lists the clinical findings associated with various serum magnesium levels. If a patient develops signs of magnesium toxicity, the infusion should be stopped immediately. The patient should then be evaluated for respiratory compromise by examination and pulse oximetry; oxygen should be administered and a serum magnesium level should be obtained. If magnesium toxicity is diagnosed, the patient should be treated with 10 mL of 10% calcium gluconate solution, infused over 3 minutes. Calcium competitively inhibits magnesium at the neuromuscular junction and decreases the toxic effects. The impact of calcium is transient and the patient should be closely monitored for continued magnesium toxicity. Should respiratory or cardiac arrest occur, immediate resuscitation including intubation and mechanical ventilation should be initiated.

Many agents are available for the control of hypertension. It is important to be familiar with the maternal and fetal side effects, as well as mode of action in order to choose the most effective agent for the gravida. Antihypertensive agents can exert an effect by decreasing cardiac output, peripheral vascular resistance, central blood pressure, or by inhibiting angiotensin production. Indications for therapy are listed in Table 5-9. Commonly used drugs in pregnancy are listed in Table 5-4.

Several randomized trials compared the efficacy and side effects of intravenous bolus (IV) injections of hydralazine to either IV labetalol or oral rapid-acting nifedipine as well as oral nifedipine to IV labetalol. In general, the results of these studies suggest that either IV hydralazine or labetalol or oral nifedipine can be used to treat severe hypertension in pregnancy as long as the medical provider is familiar with the doses to be used, the expected onset of action and potential side effects of each of these medications. Since both hydralazine and nifedipine are associated with tachycardia, it is recommended that they should not be used in patients with heart rate above 100 beats per minute (bpm). In these patients, labetalol is the appropriate drug to use. On the other hand, labetalol should be avoided in patients with bradycardia (heart rate <60 bpm), in those with asthma and in those with congestive heart failure. In these patients, either hydralazine or nifedipine is the drug of choice. In addition, nifedipine is associated with improved renal blood flow with resultant increase in urine output which makes it the drug of choice for treatment in those with decreased urine output, and for treatment of severe hypertension in the postpartum period. There is a theoretical concern that the combined use of nifedipine and magnesium sulfate can result in excessive hypotension and neuromuscular blockade; as a result, it was recommended that nifedipine not be used in patients receiving magnesium sulfate. However, a recent review of this subject concluded that the combined use of these drugs does not increase the risks of excessive hypotension and neuromuscular blockade in patient with severe preeclampsia.

Patients with generalized swelling and/or hemoconcentration (hematocrit ≥40%) usually have marked reduction in plasma volume. A recent review of this subject concluded that the combined use of rapid-acting vasodilators (hydralazine or nifedipine) in such patients can result in excessive hypotensive response with secondary reduction in tissue perfusion and uteroplacental blood flow. Thus, such patients should receive bolus infusion of 250 to 500 mL of isotonic saline prior to the administration of vasodilators.

On rare occasions, pregnant women may present with life-threatening clinical conditions that require immediate control of blood pressure, such as hypertensive encephalopathy, acute left ventricular failure, acute aortic dissection, or conditions characterized by increased levels of circulating catecholamines (pheochromocytoma, clonidine withdrawal, cocaine ingestion). Patients at the highest risk of these complications include those with underlying cardiac disease, chronic renal disease, hypertension requiring multiple drugs to achieve control, superimposed preeclampsia in the second trimester, and abruptio placentae in association with DIC. Although a diastolic blood pressure of 115 mm Hg or greater is usually considered a hypertensive emergency, this criterion is arbitrary; the rate of change of blood pressure may be more relevant than the absolute number. The combination of elevated blood pressure with evidence of new or progressive end-organ damage determines the seriousness of the clinical situation.

Untreated essential hypertension progresses to a hypertensive crisis in up to 1% to 2% of cases. In patients with long-standing chronic hypertension, hypertensive encephalopathy is usually seen in patients with systolic blood pressures above 220 mm Hg or diastolic pressures above 120 mm Hg. Patients with acute onset of hypertension may develop encephalopathy at lower pressure levels than those with chronic hypertension. Normally, cerebral blood flow is approximately 50 mL/100 g tissue per minute. To maintain this level of perfusion, cerebral arterioles dilate when blood pressure falls; the converse occurs when blood pressure rises. This mechanism usually remains operative between diastolic pressures of 60 and 120 mm Hg. Hypertensive encephalopathy is considered to be a derangement of cerebral arteriolar autoregulation, which occurs when the upper limit of autoregulation is exceeded. Typically, hypertensive encephalopathy has subacute onset over 24 to 72 hours.

During a hypertensive crisis, other evidence of end-organ damage may also be present: cardiac, renal or retinal dysfunction may arise secondary to impaired organ perfusion from loss of vascular autoregulation. Ischemia of the retina (with flame-shaped retinal hemorrhages, retinal infarcts, or papilledema) may occur, causing decreased visual acuity. Impaired regulation of coronary blood flow and marked increase in ventricular wall stress may result in angina, myocardial infarction, congestive heart failure, malignant ventricular arrhythmia, pulmonary edema, or dissecting aortic aneurysm. Necrosis of the afferent arterioles of the glomerulus results in hemorrhage of the cortex and medulla, fibrinoid necrosis, and proliferative endarteritis, resulting in serum creatinine greater than 3 mg/dL, proteinuria, oliguria, hematuria, hyaline or red blood cell casts, and progressive azotemia. Severe hypertension for several hours may result in abruptio placentae with DIC. In addition, high levels of renin, angiotensin II, aldosterone, norepinephrine and vasopressin accompany ongoing vascular damage. These circulating hormones increase relative efferent arteriolar tone, resulting in natriuresis and hypovolemia. The impact of these endocrine changes may be important in maintaining the hypertensive crisis. Therefore, attention to fluid balance and electrolytes is important.

Treatment of Hypertensive Encephalopathy

The goal of hypertensive therapy is to prevent the occurrence of a hypertensive emergency. Patients at risk for hypertensive crisis should receive intensive management during labor and for 48 hours after delivery. Although pregnancy may complicate the diagnosis, once life-threatening conditions are recognized, pregnancy should not slow or alter the mode of therapy. The only reliable clinical criterion for confirming the diagnosis of hypertensive encephalopathy is prompt response to antihypertensive therapy. Headache and sensorium often clear dramatically; sometimes within 1 to 2 hours after treatment. The overall recovery may be somewhat slower in patients with uremia and in whom the symptoms have been present for a prolonged period before therapy was initiated. Sustained cerebrovascular deficits should suggest other diagnoses such as stroke

Patients with hypertensive encephalopathy or other hypertensive crises should be hospitalized. Intravenous lines should be inserted for the administration of fluids and medications. Although there is a tendency to restrict sodium intake in patients with a hypertensive emergency, volume contraction from natriuresis may be present. A marked drop in diastolic blood pressure with a concommittent rise in heart rate upon rising from the supine position is evidence of volume contraction. Infusion of normal saline solution during the first 24 to 48 hours to achieve volume expansion should be considered. Saline infusion may help decrease the activity of the renin-angiotensin-aldosterone axis and result in better blood pressure control. Simultaneous repletion of potassium losses with continuous monitoring of blood pressure, volume status, urinary output, electrocardiographic readings, and mental status is mandatory. An intra-arterial line may provide the most accurate blood pressure readings. Laboratory studies include complete blood count with differential diagnosis and blood chemistries. A urinalysis can be obtained to survey for protein, glucose, blood, casts, and bacteria. Assessment for end-organ damage in the central nervous system, retinas, kidneys and cardiovascular system should be done periodically. Antepartum patients with viable fetuses should undergo continuous electronic fetal heart rate monitoring.

Lowering Blood Pressure

The drug of choice in hypertensive crisis is sodium nitroprusside. Other drugs such as nitroglycerin, nifedipine, trimetaphan, labetalol, and hydralazine can also be used. There are risks associated with too rapid or excessive lowering of blood pressure. The aim of the therapy is to reduce the mean arterial pressure by no more than 15% to 25%. Small reduction in blood pressure in the first 60 minutes of therapy, working toward a systolic level of 155 to 160 mm Hg and a diastolic level of 100 to 110 mmHg, is recommended. In chronic hypertensives who have a rightward shift of the cerebral autoregulation secondary to medial hypertrophy of the cerebral vasculature, lowering blood pressure too rapidly may result in cerebral ischemia, stroke, or coma. Coronary blood flow, renal perfusion, and uteroplacental blood flow also may deteriorate, resulting in myocardial infarction, acute renal failure, fetal distress, or death. Hypertension that proves increasingly difficult to control is an indication for delivery. If the patient’s outcome appears grave, consideration of and preparation for possible perimortem cesarean delivery should be made.

Sodium Nitroprusside

Sodium nitroprusside causes arterial and venous relaxation by interfering with both the influx and intracellular activation of calcium. It is given as an intravenous infusion at 0.25 to 5.0 μg/kg/min. The onset of action is immediate and its effect may last 3 to 5 minutes after discontinuation. Thus, hypotension caused by nitroprusside should subside within a few minutes of stopping the drip because of the short half-life. If it does not, other causes of low blood pressure should be considered. The effect of nitroprusside on uterine blood flow is unclear. Nitroprusside is metabolized into thiocyanate, which is excreted in the urine. Cyanide can accumulate as a result of large doses (>10 μg/kg/min) or prolonged administration (>48 hours), if there is renal insufficiency or if there is decreased hepatic metabolism. Signs of toxicity include anorexia, disorientation, headache, fatigue, restlessness, tinnitus, delirium, hallucinations, nausea, vomiting, and metabolic acidosis. When infused at less than 2 μg/kg/min, however, cyanide toxicity is unlikely. A maximum rate of 10 μg/kg/min should never be continued for more than 10 minutes. The few published reports regarding nitroprusside use in pregnancy have stated that thiocyanate toxicity rarely occurs if used in standard doses. Indeed, tachyphylaxis generally occurs before toxicity. Whenever toxicity is suspected, however, therapy should be initiated with 3% sodium nitrite at a rate not to exceed 5 mL/min, up to a maximum of 15 mL. Next, administration of 12.5 g of sodium thiosulfate in 50 mL of 5% dextrose in water infused over a 10-minute period should be started.

Nitroglycerin

Nitroglycerin is an arterial, but mostly venous dilator. It is given as an intravenous infusion at an initial rate of 5 μg/min that is gradually increased every 3 to 5 minutes, titrated to blood pressure, to a maximum dose of 100 μg/min. It is the drug of choice in preeclampsia associated with pulmonary edema and for control of hypertension associated with tracheal manipulation. Side effects include a headache, tachycardia, and methemoglobinemia. It is contraindicated in hypertensive encephalopathy because it increases cerebral blood flow and intracranial pressure.

Patients with severe preeclampsia, HELLP syndrome, and hypertensive emergencies are at risk of maternal and perinatal morbidity and mortality. Every effort should be made to optimize outcomes for both. The risk to the fetus relates largely to the gestational age at delivery. Risks to the mother can be significant and include development of DIC, intracranial hemorrhage, renal failure, retinal detachment, pulmonary edema, liver rupture, abruptio placentae, and death. Therefore, astute and experienced clinicians should provide care for these women.