Appropriate BP management following acute ischemic stroke remains controversial. Elevated BP often is a protective physiologic response to maintain cerebral perfusion. The American Heart Association (AHA) recommends initiating IV antihypertensive therapy for thrombolysis candidates when SBP >185 or DBP >110 mm Hg. For those who are not thrombolysis candidates, the recommended threshold for initiating IV antihypertensives is SBP >220 or DBP >120 mm Hg.7 The goal is to lower the BP by 15% to 25% within the first 24 hours. These goals are less aggressive than in patients with hypertensive encephalopathy without stroke.
Spontaneous intracerebral hemorrhage causes a rise in ICP with reflex systemic hypertension. Although a correlation between HTN and hematoma expansion exists, there is no evidence that shows lowering BP is protective. Two clinical trials are evaluating the effects of BP reduction to specified target levels.8 Pending those results, the AHA recommends BP reduction for patients with SBP >200 or MAP >150 mm Hg, or for patients with SBP >180 or MAP >130 mm Hg and evidence of elevated ICP.7 In both ischemic and hemorrhagic stroke, nicardipine and labetalol are appropriate first-line agents.
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Most sympathetic crises are related to the recreational use of sympathomimetic drugs, pheochromocytoma, abrupt antihypertensive withdrawal, or concurrent ingestion of monoamine-oxidase inhibitors and tyramine-containing foods. Selective beta-blockers can increase BP and worsen HTN through unopposed alpha effects.
Although labetalol traditionally has been considered the ideal agent—due to its alpha and beta antagonism—studies have failed to support its use in this clinical setting.9 Phentolamine, nicardipine, and fenoldopam are reasonable selections.
Hypertension is common in the early postoperative period following cardiothoracic, vascular, head and neck, and neurosurgical procedures. No consensus exists regarding the treatment of noncardiac surgery patients, but treatment is recommended for BP >140/90 or MAP >105 mmHg in cardiac surgery patients. Nicardipine, clevidipine, and esmolol are proven agents. All three have been shown more effective than SNP in maintaining target BP, and each is associated with less BP variability.10
In patients with pregnancy-induced hypertension, initial therapy for preeclampsia includes magnesium sulfate for seizure prophylaxis and BP control until delivery of the fetus can be safely undertaken. The FDA does not recommend any specific antihypertensive agents; however, ACE inhibitors and SNP are contraindicated. Although hydralazine is used extensively in this setting, a meta-analysis showed increased risk of maternal hypotension, Cesarean section, placental abruptions, and low Apgar scores.11 Labetalol and nicardipine appear to be safe and effective in pregnant hypertensive patients.
Back to the Case
This case represents a classic presentation of malignant hypertension with hypertensive encephalopathy, which is reversible with timely and appropriate management. The patient’s MAP is approximately 165 mmHg, well above the upper threshold of cerebral vascular autoregulation in most patients with chronic hypertension. A brain MRI should be obtained to definitively rule out stroke, as management goals would be considerably different.
If the scan is negative, treatment should be initiated immediately with a goal of reducing the MAP by no more than 25% within the first hour. Nicardipine or labetalol would be appropriate therapeutic choices, administered in an ICU with close hemodynamic monitoring.
Given the patient’s end-stage renal disease and evidence of intracranial hypertension, SNP would be a suboptimal choice. Over hours two through six, BP could be lowered gradually to 160/100, then to his baseline BP over the ensuing 24 to 48 hours, monitoring closely for signs of neurologic deterioration. Once BP is stable and there is no evidence of worsening end-organ damage, he can be safely transitioned to oral agents.