Delayed Brain Injury after Head Trauma

Stein, Sherman C.; Young, Gary; Talucci, Raymond C.; Greenbaum, Barbara H.; Ross, Steven E.

doi:10.1227/00006123-199202000-00002

Cited by 218 publications

(57 citation statements)

References 34 publications

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“…Acute ethanolism blunts hemodynamic and respiratory drive after head injury, which may promote cerebral ischemia; 57-59 it increases the permeability of the bloodbrain barrier (BBB), thereby exacerbating cerebral edema formation; 2,16,42 and it impairs the hemostatic and fibrinolytic cascades, which may contribute to posttraumatic coagulopathy and progressive hemorrhagic intracranial injury. 3,6,9,12,18,39,49,52 More recently, in vitro studies have shown that acute ethanol exposure strongly inhibits N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity and may therefore be neuroprotective. 7,32,51 Overall, these investigations indicate that preinjury alcohol consumption promotes an array of secondary injury processes, yet simultaneously affords neuroprotection.…”

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confidence: 99%

Paradoxical effects of acute ethanolism in experimental brain injury

Kelly

Lee²,

Pinanong³

et al. 1997

Journal of Neurosurgery

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Acute ethanol intoxication is a frequent complicating factor in human head injury, yet its impact on neurological outcome remains poorly defined. This study was undertaken to assess the effect of varying levels of preinjury ethanol on early postinjury mortality, recovery of motor function, and degree of neural degeneration after cortical contusion injury in the rat. Adult rats were pretrained on a beam-walking task, then randomized to one of five groups: low-dose ethanol and injury (1 g/kg, 16 animals); moderate-dose ethanol and injury (2.5 g/kg, 11 animals); high-dose ethanol and injury (3 g/kg, 17 animals); no ethanol and injury (nine animals); or ethanol and sham injury (seven animals). Forty minutes after intraperitoneal injection of ethanol or saline, the rats received a pneumatic piston-induced contusion injury of the left primary motor cortex. Their beam-walking ability was assessed daily for the next 7 days. At 4 weeks postinjury, the brains were sectioned and the dimensions of the cortical lesions were determined. Preinjury ethanol administration was associated with an acute postinjury mortality rate of 29.5% (p < 0.05); the highest mortality rate (47.1%) occurred in the high-dose ethanol group, whereas no deaths occurred in the animals in the no ethanol or sham-injured groups (p < 0.01). However, injured animals receiving low- and moderate-dose ethanol had significantly less severe beam-walking impairment initially, and a more rapid return to normal beam-walking ability, compared to the no and high-dose ethanol groups (p < 0.05). Additionally, the mean lesion volumes were significantly smaller in the low- and moderate-dose ethanol treatment groups compared to the no and high-dose ethanol groups (23.2 +/- 8 mm3 and 29 +/- 6.7 mm3 vs. 52 +/- 8.8 mm3 and 53.7 +/- 10.9 mm3, respectively, p < 0.01). In this cortical contusion model, the presence of ethanol before injury appears to exert a potent neuroprotective effect when administered in low or moderate doses. This action is postulated to result from ethanol-induced inhibition of N-methyl-D-aspartate receptor-mediated excitotoxicity. The loss of neuroprotection and increased mortality rates observed with high-dose ethanol may be related to ethanol-induced hemodynamic and respiratory depression.

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confidence: 99%

Paradoxical effects of acute ethanolism in experimental brain injury

Kelly

Lee²,

Pinanong³

et al. 1997

Journal of Neurosurgery

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“…Some studies have shown a correlation between the outcome of head injury and changes in PT, aPTT, fibrinogen level, FDP and platelet count among adults [5, 16, 17, 18], yet few studies have addressed hemocoagulative abnormalities and head injury among children, where, in a retrospective study, PT was reported to be delayed [1]. The cause of posttraumatic coagulopathy is difficult to determine [19, 20].…”

Section: Discussionmentioning

confidence: 99%

The Influence of Hemocoagulative Disorders on the Outcome of Children with Head Injury

et al. 2001

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Background: Although disseminated intravascular coagulation (DIC) and other hemocoagulative abnormalities are severe complications of head injury, their effect on clinical outcome remains unclear, particularly among children. Objectives: To evaluate the frequency of hemocoagulative abnormalities and their influence on outcome among children with head injury. Study Design: We conducted a prospective observational study among 60 children with head injury, immediately evaluating severity of head injury (Glasgow Coma Scale, GCS); cerebral axial tomography; prothrombin time; activated partial thromboplastin time (aPTT); fibrinogen level; concentration of fibrin-fibrinogen degradation products (FDP), and platelet count. Two months after injury, we applied the Glasgow Outcome Score (GOS). Associations with GOS were evaluated using univariate and multivariate logistic models. Results: Among children with severe head injury, 22.2% (6/27) developed DIC, all of whom died and had shown severe brain edema. Among those with severe head injury yet without DIC, the mortality was only 14.2%. A low GOS was significantly and independently associated with a low GCS, multiple trauma, delayed aPTT, low fibrinogen level, elevated FDP and low platelet count. Brain edema was also associated with a low GOS, though not significantly. Conclusions: In addition to GCS, type of trauma, type of brain lesion and certain coagulation abnormalities are predictors of GOS.

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“…3,9 Previous studies indicate that this condition may occur in between 15 and 76% of patients with TBI and may be responsible for a significant proportion of in-hospital mortality and unfavourable outcome. 2,4,6,7,[10][11][12][13][14][15] It is also suggested that early diagnosis and reversal of coagulation abnormalities could benefit patients with head injury. 3,16 Despite the fact that DIC is often accompanied with manifest laboratory abnormalities, no individual test is sensitive and specific enough to diagnose DIC, which historically has not had precise criteria for its diagnosis.…”

Section: Introductionmentioning

confidence: 99%