Cerebral circulation after head injury. Part 2: The effects of traumatic brain edema.
The authors have assessed the effects of subacute traumatic brain edema (BE) on cerebral circulation and metabolism, and on clinical outcome. Fifty-five severely injured, comatose, young patients who survived for more than 24 hours were studied on 78 occasions within 30 days of injury. After hematomas had been surgically evacuated, BE was diagnosed by radiological evidence of brain swelling, demonstrated by cerebral angiograms and ventriculograms. At identical levels of carbon dioxide pressure, intracranial pressure was significantly elevated in the Edema Group to twice the value in the No Edema Group (27.1 vs 14.1 torr). There were, however, no significant differences in cerebral perfusion pressure cerebral blood flow, resistance to blood flow, cerebral metabolic oxygen rate, ventricular cerebrospinal fluid acid-base, lactate, K+ or Na+ concentrations, or in clinical outcome. It is concluded that this type of subacute traumatic BE, which is significantly associated with surgical lesions, is not of major hemodynamic or clinical significance in intensively treated patients, and does not cause cerebral ischemia. Patient outcome is determined more by the severity of the initial diffuse cortical and subcortical injury than by the presence or absence of subacute BE.
D000293:Adolescent; D000328:Adult; D001921:Brain / Q000378:metabolism; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D001930:Brain Injuries / Q000150:complications*; D002560:Cerebrovascular Circulation; D002648:Child; D006801:Humans; D007773:Lactates / Q000378:metabolism; D010101:Oxygen Consumption; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D007773:Lactates; D012964:Sodium; D011188:Potassium