OBJECTIVE: To determine the prevalence and possible etiologies of liver enzyme abnormalities in patients with acquired brain injury and to assess the impact of these abnormalities on the rehabilitative process. SETTING: University tertiary care rehabilitation center. DESIGN: Retrospective study. SUBJECTS: Fifty-six consecutive patients admitted to a brain injury unit in a 30-month period who had an intracranial hemorrhage without associated head or abdominal trauma. MAIN OUTCOME MEASURES: Liver function tests, Functional Independence Measure (FIM) scores, exposure to hepatotoxic drugs, antiepileptic medication serum levels, history of alcohol use, medical history, length of stay, and medical costs. RESULTS: There was an increase (from acute hospital admission to inpatient rehabilitation admission) in gamma-glutamyltransferase (GGT) levels from 42 to 147U/L (p=.0012). There was an increase in alkaline phosphatase from 83 to 125U/L (p=.0079). There was a significant relationship between the GGT level on rehabilitation admission and exposure to hepatotoxic drugs, particularly phenytoin (n=55, p=.0007). Similar findings were noted between alkaline phosphatase and phenytoin (n=55, p=.0022) and systemic steroids (n=50, p=.0277). History of alcohol use was not predictive of changes in liver function tests (p > .05). Correlation analysis revealed no detrimental effect of the elevated serum liver enzyme levels on the Rasch-converted FIM cognitive or motor admission or discharge scores or change in the scores while on rehabilitation (p > .05). All radiologic testing and hepatitis profiles were negative, and 10 of the 16 patients with follow-up laboratory tests showed improvement in their serum liver enzyme levels. CONCLUSIONS: After nontraumatic brain injury there is a characteristic pattern of enzyme elevation that statistically relates to phenytoin exposure. No additional etiologic abnormalities were found on further workup, suggesting that further evaluation should be guided by the patient's clinical status, not laboratory value alone.
OBJECTIVE: To determine the prevalence and possible etiologies of liver enzyme abnormalities in patients with acquired brain injury and to assess the impact of these abnormalities on the rehabilitative process. SETTING: University tertiary care rehabilitation center. DESIGN: Retrospective study. SUBJECTS: Fifty-six consecutive patients admitted to a brain injury unit in a 30-month period who had an intracranial hemorrhage without associated head or abdominal trauma. MAIN OUTCOME MEASURES: Liver function tests, Functional Independence Measure (FIM) scores, exposure to hepatotoxic drugs, antiepileptic medication serum levels, history of alcohol use, medical history, length of stay, and medical costs. RESULTS: There was an increase (from acute hospital admission to inpatient rehabilitation admission) in gamma-glutamyltransferase (GGT) levels from 42 to 147U/L (p=.0012). There was an increase in alkaline phosphatase from 83 to 125U/L (p=.0079). There was a significant relationship between the GGT level on rehabilitation admission and exposure to hepatotoxic drugs, particularly phenytoin (n=55, p=.0007). Similar findings were noted between alkaline phosphatase and phenytoin (n=55, p=.0022) and systemic steroids (n=50, p=.0277). History of alcohol use was not predictive of changes in liver function tests (p > .05). Correlation analysis revealed no detrimental effect of the elevated serum liver enzyme levels on the Rasch-converted FIM cognitive or motor admission or discharge scores or change in the scores while on rehabilitation (p > .05). All radiologic testing and hepatitis profiles were negative, and 10 of the 16 patients with follow-up laboratory tests showed improvement in their serum liver enzyme levels. CONCLUSIONS: After nontraumatic brain injury there is a characteristic pattern of enzyme elevation that statistically relates to phenytoin exposure. No additional etiologic abnormalities were found on further workup, suggesting that further evaluation should be guided by the patient's clinical status, not laboratory value alone.