Large hemispheric infarction, deterioration, and intracranial pressure

Abstract

Neurologic deterioration from large hemispheric infarction with edema (LHIE) often leads to the use of therapies directed at decreasing intracranial pressure (ICP). Many of these ICP therapies can potentially accentuate tissue shifts from unilateral mass lesions and lead to rebound ICP elevations. We sought to determine whether ICP elevation is a common cause of deterioration from LHIE by measuring the initial ICP and cerebral perfusion pressure (CPP) in 19 patients deteriorating to stupor from LHIE within 3 hours of deterioration, after ruling out metabolic aberrations, medication side effects, infection, and seizures and prior to commencement of any ICP-lowering therapies. We evaluated 19 patients aged 23 to 77 years—14 with complete middle cerebral artery and five with complete internal carotid artery territory infarctions. Stupor began 59 ± 37 hours after the stroke onset. ICP monitoring (12 ipsilat-eral Camino, five contralateral ventriculostomy, and two ipsilateral epidural) demonstrated elevation of ICP (>15 mm Hg) in only five patients (26.3%), with group mean initial ICP = 13.4 ± 10 mm Hg. Similarly, the initial CPP was diminished (>55 mm Hg) in only two patients (10.5%), with group mean initial CPP = 74.9 ± 14 mm Hg. Globally elevated ICP is not a common cause of initial neurologic deterioration from LHIE mass effect.