Rajat Dhar1, Ralph Dacey, Theresa Human, Gregory Zipfel. 1. Department of Neurology, Division of Neurocritical Care, Washington University School of Medicine, St. Louis, Missouri 63110, USA. dharr@neuro.wustl.edu
Abstract
BACKGROUND AND IMPORTANCE: Hemodynamic treatment of subarachnoid hemorrhage-induced vasospasm is associated with a number of systemic and cerebral risks. However, hypertensive encephalopathy has rarely been reported in the setting of induced hypertension. Recognition of this complication is nonetheless critical because failure to lower blood pressure may lead to worsening of deficits and even permanent injury. CLINICAL PRESENTATION: This report details a case of unilateral hypertensive encephalopathy (also referred to as posterior reversible encephalopathy syndrome [PRES]) in a subarachnoid hemorrhage patient who was being treated with induced hypertension for symptomatic vasospasm affecting the contralateral hemisphere. This patient developed right hemispheric deficits associated with angiographic vasospasm of the right middle cerebral artery, which responded to induced hypertension. However, within 24 hours of raising blood pressure, the patient deteriorated with new left hemispheric deficits that paradoxically worsened when blood pressure was raised further in response. Computed tomography imaging was suspicious for evolving infarction in the left hemisphere, but on reevaluation, concern for PRES was raised. Magnetic resonance imaging confirmed left hemispheric PRES, and a dramatic neurological improvement occurred almost immediately after lowering blood pressure. Repeat CT showed resolution of the left hemispheric edema. CONCLUSION: This is the first reported case of unilateral PRES in the setting of subarachnoid hemorrhage. It likely occurred because right-sided vasospasm attenuated ipsilateral distal perfusion pressures, leaving the left hemisphere vulnerable to the consequences of induced hypertension. Hypertensive encephalopathy should be considered in patients with unilateral or asymmetric vasospasm when neurological worsening occurs in the contralateral hemisphere during induced hypertension and/or the patient paradoxically worsens despite raising blood pressure.
BACKGROUND AND IMPORTANCE: Hemodynamic treatment of subarachnoid hemorrhage-induced vasospasm is associated with a number of systemic and cerebral risks. However, hypertensiveencephalopathy has rarely been reported in the setting of induced hypertension. Recognition of this complication is nonetheless critical because failure to lower blood pressure may lead to worsening of deficits and even permanent injury. CLINICAL PRESENTATION: This report details a case of unilateral hypertensive encephalopathy (also referred to as posterior reversible encephalopathy syndrome [PRES]) in a subarachnoid hemorrhagepatient who was being treated with induced hypertension for symptomatic vasospasm affecting the contralateral hemisphere. This patient developed right hemispheric deficits associated with angiographic vasospasm of the right middle cerebral artery, which responded to induced hypertension. However, within 24 hours of raising blood pressure, the patient deteriorated with new left hemispheric deficits that paradoxically worsened when blood pressure was raised further in response. Computed tomography imaging was suspicious for evolving infarction in the left hemisphere, but on reevaluation, concern for PRES was raised. Magnetic resonance imaging confirmed left hemispheric PRES, and a dramatic neurological improvement occurred almost immediately after lowering blood pressure. Repeat CT showed resolution of the left hemispheric edema. CONCLUSION: This is the first reported case of unilateral PRES in the setting of subarachnoid hemorrhage. It likely occurred because right-sided vasospasm attenuated ipsilateral distal perfusion pressures, leaving the left hemisphere vulnerable to the consequences of induced hypertension. Hypertensiveencephalopathy should be considered in patients with unilateral or asymmetric vasospasm when neurological worsening occurs in the contralateral hemisphere during induced hypertension and/or the patient paradoxically worsens despite raising blood pressure.