الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Traumatic brain injury (TBI) is a serious neuro-disorder commonly caused by road traffic accidents (RTAs), sports related events or violence. It is one of the leading causes of disability and death of young adults in industrialized countries presents a major worldwide social, economic, and health problem.
TBI are classified according to severity, physical mechanism, pathophysiology and CT findings.
Secondary brain injuries are defined as the constellation of cellular and biochemical processes that are set in motion by the primary injury and then evolve over the subsequent hours and days. They include cerebral edema, hematomas, hydrocephalus, intracranial hypertension, vasospasm, metabolic derangement, infection, and seizures.
Researches aiming at reducing or preventing the neuro-logical consequences of head trauma are ongoing, but currently the clinical outcome following TBI depends on the circumstances of injury and early clinical management aiming at reducing the occurrence of secondary brain insults. No effective intervention
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has been found to reverse the pathologic events initiated by the traumatic event. Post-traumatic seizures are seizures that result from traumatic brain injury (TBI and brain damage caused by physical trauma. Post traumatic seizures classified in to immediate post traumatic seizures, early post-traumatic seizures, late post-traumatic seizures and post-traumatic epilepsy.
Anticonvulsants may be indicated in the early stages following moderate to severe TBI in order to reduce the incidence of seizures. Seizure medications can be grouped according to their main mechanism of action, although many of them have several actions and others have unknown mechanisms of action.
Phenytoin sodium, is a hydantoin-derivative anti-consultant. The mechanism of action is through limitation of seizure propagation by reduction of post-tetanic potentiation. Side effects including, hypotension if administered too rapidly through the intravenous approach, atrial or ventricular conduction depression, ventricular depression, respiratory depression, toxic hepatitis and liver damage, hematologic effects, local soft-tissue reactions and rash.
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The objective of our study is to compare the efficacy of Levetiracetam versus phenytoin in the prevention of early post traumatic seizures.
The study was conducted on 40 patients with moderate to severe traumatic brain injury admitted to the Critical Care Department of Ain Shams University Hospital.
All the forty patients will be divided into two groups A&B
Patients in group (A) will receive PTH within 1st 24 hours after TBI as 15mg/kg loading then 7mg/kg/day maintenance for 7 days.
Patients in group (B) will receive LEV syrup as 5 cc (500mg) via NGT or OGT / 12 hour.
The results of this study show that no significant effect of both treatment of blood picture, electrolytes, kidney function, liver function and vital signs.
The value of SGOT & SGPT of studied patients was described. There was no clinical significance in value of SGOT in seven days follow up between two groups. There were no clinical significance in value of SGPT between two groups in first 6 days but there were clinical significance at day seven with (P=0.0.016).
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The incidence of seizure was 2 patients (10.0%) in LEV group and 1 patient (5.0%) in phenytoin group with no statistically significant difference between the two groups (p=0.925).