Acute regional cerebral blood flow changes caused by severe head injuries

Abstract

To evaluate the changes in cerebral blood flow (CBF) that occur immediately after head injury and the effects of different posttraumatic lesions on CBF, 61 CBF studies were obtained using the xenon-computerized tomography method in 32 severely head-injured adults (Glasgow Coma Scale score (GCS) less than or equal to 7). The measurements were made within 7 days after injury, 43% in the first 24 hours. During the 1st day, patients with an initial GCS score of 3 or 4 and no surgical mass had significantly lower flows than did those with a higher GCS score or mass lesions (p less than 0.05): in the first 1 to 4 hours, those without surgical mass lesions had a mean CBF of 27 cc/100 gm/min, which rose to 44 cc/100 gm/min by 24 hours. Patients without surgical mass lesions who died tended to have a lower global CBF than did those with better outcomes. Mass lesions were associated with a high global CBF and bihemispheric contusions with the lowest flows. By 24 hours after injury, global blood flow increased in groups that originally had low flows and decreased in those with very high initial flows, such that by 36 to 48 hours, most patients had CBF values between 32 and 55 cc/100 gm/min. Lobar, basal ganglion, and brain-stem blood flow values frequently differed by 25% or more from global averages. Brain-stem CBF varied the most but did not correlate with clinical signs of brain-stem dysfunction. Double studies were performed at two different pCO2 values in 10 patients with various posttraumatic lesions, and the CO2 vasoresponsivity was calculated. Abnormal CO2 vasoresponsivity was found with acute subdural hematomas and defuse cerebral swelling but not with epidural hematomas. In patients without surgical mass lesions, the findings suggest that CBF in the first few hours after injury is often low, followed by a hyperemic phase that peaks at 24 hours. Global CBF values vary widely depending on the type of traumatic brain injury, and brain-stem flow is often not accurately reflected by global CBF values. These findings underscore the need to define regional CBF abnormalities in victims of severe head injury if treatment is intended to prevent regional ischemia.

Cerebral Metabolic Response to Low Blood Flow: Possible Role of Cytochrome Oxidase Inhibition

“…In patients with compromised CBF, further reduction could affect the CMR O 2 . Abnormally low CBF is a common finding in patients with severe traumatic brain injury (Glasgow Coma Scale less than 8; Cold, 1989;Marion et al, 1991;Obrist et al, 1979;Overgaard et al, 1981) and hypoxia may be the single most important secondary factor affecting the outcome in these patients (Miller, 1985). Therefore, indomethacin should be used with care in the acute management of traumatic brain injury, especially in conditions of a high intracranial pressure.…”

Relationship between Flow-Metabolism Uncoupling and Evolving Axonal Injury after Experimental Traumatic Brain Injury

“…Disturbances in cerebral blood flow (CBF are also a common sequela of head injury and have been documented both experimentally (Yamakami and McIntosh, 1991;Bryan et al, 1995;Kochanek et al, 1995;Forbes et al, 1997;Hendrich et al, 1999;Lythgoe et al, 2003) and clinically (Bouma et al, 1991;Marion et al, 1991;Martin et al, 1997;Coles et al, 2002). CBF abnormalities have been shown to be an important mechanism underlying secondary brain damage experimentally (Jenkins et al, 1989;Giri et al, 2000) and clinically have been shown to be strongly associated with poor outcome (Robertson et al, 1992).…”

Delayed, Transient Neurological Deterioration After Mild Head Injury. Case Report.

“…18,26) Hyperemia in our case was interpreted as the benign hemispheric type induced by metabolic recovery from the damage done by the mild contusional and subdural hematomas. The benign type of hyperemia is considered to be secondarily induced by metabolic demands on the release of metabolic mediators during reestablishment of membrane ionic homeostasis after head injury.…”

“…5,12,[18][19][20]22,23,26,30) Complete neuroimaging examinations including CT and MR imaging, cerebral angiography, and SPECT during the period of neurological deterioration found no traces of vasospasm.…”