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In hypertensive encephalopathy (HTE), prompt reduction of blood pressure (BP) is essential to prevent permanent neurologic and other damages. Radiologically, HTE is characterized by white-matter edema affecting preferentially the occipital lobes and other posterior structures.1 The clinical and radiologic manifestations of HTE usually resolve completely after correction of hypertension.1,2⇓ We report two patients in whom neurologic deterioration occurred paradoxically with treatment of HTE.
Case reports.
Patient 1.
A previously healthy 36-year-old Filipino man presented with acute headache, confusion, bilateral visual loss, and BP of 260/130. There was no other focal neurologic deficit on admission. Retinal examination was unremarkable. Brain CT revealed white-matter edema at the occipital lobes. After 50 mg bolus of IV labetalol, BP was reduced with the lowest reading at 140/110. Two hours later, he developed acute pulmonary edema and generalized seizures. He was transferred to the Intensive Care Unit (ICU) and was ventilated under sedation. EKG showed no evidence of myocardial ischemia. His condition was stabilized, and he was extubated 40 hours later. Physical …
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