Acute brain edema in fatal head injury: analysis by dynamic CT scanning

Abstract

Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p less than 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.

Decompressive craniectomy with multi-dural stabs - A combined (SKIMS) technique to evacuate acute subdural hematoma with underlying severe traumatic brain edema

“…[16] However, there is an evidence to suggest that it may be secondary to ischemia caused by the compressive hematoma or vasomotor paralysis. [17] All 225 patients at SKIMS, Kashmir, had brain edema, contusions and acute subdural clot. The 60.50% (72/119) of multi-dural stabs and 58.49% (62/106) of open-dural flaps were having a low admission GCS of 3-6 and none of all patients (225) had a GCS above 8, the results were still better for multi-dural stabs, most probable cause being the protection of brain cortex from laceration by pouting.…”

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

“…At the moment of impact, the applied pressure wave causes a sudden cessation of all electrical activity in the brain. 20,24 Because arteries under normal conditions are in a state of semicontraction, a loss of vascular tonus, that is, vasoparalysis, will cause a CPPdriven dilation of these cerebral arteries. Such dilation in turn induces an increase in cerebral blood volume that cannot be compensated for by a rapid cerebrospinal fluid transfer or by an autoregulation-mediated vasoconstriction because the autoregulation is impaired.…”

Quantitative cerebral blood flow and metabolism determination in the first 48 hours after severe head injury with a new dynamic spect device

“…Early determinations of CBF (in the first 24 hours after trauma) obtained by Yoshino [38] and Muizelaar [23] showed a trend towards higher flows and better coma scores while a significant correlation between motor score and CBF was found in the first 8 hours and was lost after 12 hours by Bouma [2].…”

“…These conditions may alter cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) much more than under normal circumstances, since the adaptive responses to these stresses may be diminished or abolished after head injury [4,12,18,22]. Many clinical studies, even in the early period [2,6,13,38], have been performed in severely head injured patients leading to an improvement in the understanding of the pathophysiological aspects of this pathology. In particular the determination of CBF's adequacy to meet the brain metabolic demands and in outcome prediction, the assessment of the responsiveness of the cerebral circulation by testing autoregulating and by evaluating the cerebrovascular reactivity to changes in paCO2, the pharmacological effects of various therapeutic regimen have been investigated [16].…”