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Published on: June 21, 2019
Seizure Prophylaxis in Young Patients Following Traumatic Brain Injury
Ahmed Abdel-Aziz Bahey1, Talat Chughtai2, Ayman El-Menyar3,4
1Department of Pharmacy, Clinical Pharmacy, Trauma Surgery Section, Hamad General Hospital, Doha, Qatar.
Insights
Phenytoin did not prevent early-onset seizures (EOS) in traumatic brain injury (TBI) patients. This study suggests current use of phenytoin for seizure prophylaxis after TBI is ineffective and warrants further investigation.
Area of Science:
- Neurology
- Neurosurgery
- Pharmacology
Background:
- Phenytoin is a common anti-seizure medication.
- Its effectiveness and safety in preventing early-onset seizures (EOS) after traumatic brain injury (TBI) are debated.
- This study investigates phenytoin's utility in TBI patients.
Purpose of the Study:
- To explore the use of phenytoin as seizure prophylaxis following TBI.
- To determine if phenytoin administration is effective in preventing EOS after TBI.
Main Methods:
- Retrospective observational study of adult TBI patients.
- EOS defined as witnessed seizure within one week post-injury.
- Comparison of phenytoin versus no-phenytoin use, EOS versus no-EOS, and TBI severity groups.
Main Results:
- Phenytoin use was associated with higher rates of EOS, higher Marshall Score, lower Glasgow Coma Scale (GCS), and increased mortality.
- Toxic serum phenytoin levels and low serum albumin were independent predictors of EOS.
- Phenytoin was administered more frequently in patients with severe TBI.
Conclusions:
- Prophylactic phenytoin use was ineffective in preventing EOS post-TBI.
- Further large-scale, matched studies and defined hospital protocols are necessary for optimal phenytoin use after TBI.
Introduction:
Phenytoin is one of the commonly used anti.seizure medications in nontraumatic seizures. However, its utility and safety in young patients with traumatic brain injury (TBI) for the prevention of early-onset seizures (EOS) are debatable. We sought to explore the use of phenytoin as a seizure prophylaxis following TBI. We hypothesized that administering phenytoin is not effective in preventing EOS after TBI.
Methods:
This was a retrospective observational study conducted on adult TBI patients. EOS was defined as a witnessed seizure within a week postinjury. Data were compared as phenytoin versus no-phenytoin use, EOS versus no-EOS, and among TBI severity groups.
Results:
During 1 year, 639 TBI patients were included with a mean age of 32 years; of them, 183 received phenytoin as seizure prophylaxis, and 453 received no prophylaxis medication. EOS was documented in 13 (2.0%) patients who received phenytoin, and none had EOS among the nonphenytoin group. The phenytoin group was more likely to have a higher Marshall Score (P = 0.001), lower Glasgow Coma Scale (GCS) (P = 0.001), EOS (P = 0.001), and higher mortality (P = 0.001). Phenytoin was administrated for 15.2%, 43.2%, and 64.5% of mild, moderate, and severe TBI patients, respectively. EOS and no-EOS groups were comparable for age, gender, mechanism of injury, GCS, Marshall Score, serum phenytoin levels, liver function levels, hospital stay, and mortality. Multivariable logistic regression analysis showed that low serum albumin (odds ratio [OR] 0.81; 95% confidence interval [CI] 0.676.0.962) and toxic phenytoin level (OR 43; 95% CI 2.420.780.7) were independent predictors of EOS.
Conclusions:
In this study, the prophylactic use of phenytoin in TBI was ineffective in preventing EOS. Large-scale matched studies and well-defined hospital protocols are needed for the proper utility of phenytoin post-TBI.
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