Cerebrovascular accidents (hypertensive encephalopathy and hemorrhage) are rare complications during pregnancy and the postpartum period. The exact incidence of these complications during pregnancy and the first 6 weeks postpartum is unknown. Several population-based studies, however, have consistently shown that the risk of these complications is increased compared with the nonpregnant state. The issue of cerebral vascular accidents during pregnancy and the postpartum period should be of increasing relevance to obstetricians, anesthesiologists, emergency department physicians, neurologists, and critical care physicians. The incidence of stroke increases with age, and women are becoming pregnant at older ages than ever before; obstetric patients ages 45 to 50 years have become increasingly common. Obesity is also a risk factor for stroke, and pregnant women mirror American society at large, in which obesity has become epidemic. Long-standing hypertension and diabetes mellitus, both associated with obesity, further increase the risk of stroke. The risk of stroke in the postpartum period is almost certainly higher still. Postpartum strokes generally occur from 3 days to 6 weeks after delivery—a vulnerable time when significant physiologic, hematologic, and hemodynamic changes occur.
Stroke can happen at any time during pregnancy and in the postpartum period. The clinical presentation is similar to that seen in nonpregnant patients; however, the presenting signs and symptoms can mimic those seen in preeclampsia/eclampsia, and the possibility of cerebrovascular accidents may be overlooked. Table 9-1 lists the potential etiologies of cerebrovascular accidents during pregnancy and postpartum.
Vascular Causes |
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Hypertensive Causes |
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Disorders of Coagulation |
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Medications/Drugs |
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Other |
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Hypertension is one of the most common medical disorders affecting pregnancy. It complicates 12% of pregnancies and is responsible for 18% of maternal deaths in the United States. Cerebrovascular accidents have been recognized as a complication of hypertensive disorders of pregnancies for many years. Several studies have reported that hypertensive disorders of pregnancy are associated with 11% to 47% of cases of hypertensive encephalopathy and with 8% to 50% of cerebral hemorrhage during pregnancy and within the first 6 weeks postpartum.
The presenting signs and symptoms of cerebrovascular accidents in pregnancy and postpartum are summarized in Table 9-2 . In general, there is potential for the delay in making the correct diagnosis and treatment of these patients because these signs and symptoms can mimic those of preeclampsia-eclampsia. In addition, patients may hesitate to seek immediate medical care when experiencing symptoms of headache, nausea, vomiting, and epigastric pain because they are common in pregnancy and postpartum, and some women might not consider them serious enough for evaluation unless they become severe. Moreover, the presence of these symptoms may not be aggressively evaluated by obstetricians and emergency department physicians, particularly in women who are normotensive and in the late postpartum period. Therefore, it is prudent to counsel and educate patients, especially those with relevant risk factors (diagnosed gestational hypertension, preeclampsia, chronic hypertension) to seek care for these symptoms.
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The laboratory findings ( Table 9-3 ) and the neuroimaging findings ( Table 9-4 ) in patients with cerebrovascular accidents overlap with those in severe preeclampsia-eclampsia. In making the diagnosis of cerebrovascular accident, history and physical examination are critically important, although neuroimaging and other procedures such as lumbar puncture may be needed to further clarify the diagnosis and establish the etiology. A potential delay in making the correct diagnosis and initiating proper therapy may arise because of failure to perform neuroimaging and other relevant procedures secondary to the concern of theoretic risks to the pregnancy and fetus.
Laboratory Findings |
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Neuroimaging Findings |
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Maternal and perinatal complications associated with cerebrovascular accidents depend on etiology, timing of the diagnosis, maternal and fetal conditions, and gestational age at time of diagnosis, as well as the quality of management used. In general, maternal complications include death and residual neurologic deficit, whereas perinatal complications may include fetal/neonatal death, fetal hypoxia, and prematurity.
Case 1: Hypertensive Encephalopathy
A 40-year-old G1P0 presents in the first trimester with blood pressure 170/120 mm Hg. The patient gives a history of chronic hypertension for the past 5 years that was treated with angiotensin-converting enzyme (ACE) inhibitor and diuretics. With the diagnosis of pregnancy, her primary care physician discontinued the ACE inhibitor due to concern for fetal effects and switched her to oral methyldopa at a dose of 250 mg twice daily. Due to continued hypertension, the methyldopa dose was increased to 500 mg twice daily. During the subsequent prenatal visits, her blood pressure continued to worsen and the dose of methyldopa was increased to 1000 mg three times daily.
At 35 weeks’ gestation she was seen in the office with a blood pressure 170/105 mm Hg. The patient complained of a severe headache but denied shortness of breath, vision changes, and epigastric pain. Urine dipstick for protein was trace. Because of concern for preeclampsia, the patient was sent to the obstetric triage for nonstress testing and repeat blood pressure measurements. She was observed for 1 hour during which acetaminophen was given and her headache improved. A nonstress test was performed, which was reactive. Repeat blood pressure measurements during the observation period ranged between 160 to 180 and 100 to 115 mm Hg. The physician ordered oral labetalol with a first dose of 200 mg to be given prior to discharge with a prescription for 200 mg twice a day. In addition, he instructed the patient to take acetaminophen as needed if her headache returned. The triage nurse questioned the physician as to the appropriateness of these recommendations because of her concerns of the degree of hypertension and suggested admission for further monitoring and evaluation. Unfortunately, the physician did not order further evaluation in part because the urine dipstick was trace for protein, and preeclampsia laboratory tests had recently been preformed and were normal.
Previous laboratory studies as an outpatient:
AST | 30 units/L (normal <40 units/L) |
ALT | 35 units/L (normal <60 units/L) |
Uric acid | 4.5 mg/dL (normal <6 mg/dL) |
Creatinine | 0.7 mg/dL (normal <1 mg/dL) |
Platelet count | 200,000/mm 3 (normal >100,000/mm 3 ) |
Hemoglobin | 12.3 g/dL (normal >10 g/dL) |