الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Traumatic Brain Injury [TBI] is a major cause of death and disability, leading to great personal suffering to victim and relatives, as well as huge direct and indirect costs to society. A clear, concise definition of Traumatic Brain Injury is fundamental for reporting, comparison and interpretation of studies on TBI.
According to the World Health Organization [WHO], traumatic brain injury will be the major cause of death and disability by the year 2020. With an estimated 10 million people affected annually by traumatic brain injury, the burden of mortality and morbidity that this condition imposes on society, makes TBI a pressing public health and medical problem.
Traumatic brain injury [TBI] is defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force.
There are different systems for classifying traumatic brain injury [TBI]. Systems include classifying by severity, morphology and further classification systems include classification of TBI by outcome and prognosis.
In terms of the classification of severity, historically TBI was classified as mild, moderate or severe by using the Glasgow Coma Scale [GCS], a system used to assess coma and impaired consciousness. The Glasgow Coma Scale is divided into three components: eye opening, verbal response and motor responses. These are usually summed to produce a total score.
• Mild traumatic brain injury: GCS score [14-15].
• Moderate traumatic brain injury: GCS score [9-13].
• Severe traumatic brain injury: GCS score [3-8].
Brain edema is recognized as one of the major causes of mortality, as well as poor neurologic outcome, because severe brain edema that is not successfully treated can lead to progressive intracranial hypertension, cerebral ischemia, brain herniation, and eventual progression to death.
Cerebral edema is defined as an increase in brain water leading to an increase in total brain mass.
Hyperosmolar therapy is the primary medical management strategy for brain edema and raised intracranial pressure.
Osmolarity refers to the osmotic concentration of a solution expressed as osmoles of solute per liter of solution. Osmolality refers to the osmotic concentration of a solution expressed as osmoles of solute per kilogram of solution.
Mannitol is a sugar alcohol that is not significantly metabolized and is excreted unchanged in the urine after IV infusion. Mannitol’s primary effect is to increase the osmotic gradient across the BBB, if it remains intact, and it promotes osmosis of water from the brain parenchyma, thereby decreasing brain water content and increasing intravascular volume acutely.
In spite of many years of effective use of mannitol for the treatment of brain edema and raised intra cranial pressure, the use of hypertonic saline has become more and more popular in the past decade.
Hypertonic saline refers to any saline solution with a concentration of sodium chloride (NaCl) higher than physiologic (0.9%). Hypertonic saline has similar osmotic effects as mannitol but is a less potent diuretic, so the initial advantage in certain clinical situations is that hypertonic saline expands the intravascular volume, increases blood pressure, increases cardiac output, and, theoretically, increases cerebral blood flow.
Management depends on the patient’s fluid and electrolyte status and overall clinical condition. After HTS therapy has been discontinued, serum sodium levels do not need to be monitored frequently.
Hypertonic saline is an important part of the treatment of patients with severe TBI. HTS can prevent and treat cerebral edema and its disastrous sequelae. Its complex physiologic actions mandate that HTS administration include careful monitoring of laboratory values and vigilant assessment for potential side effects.
This study was conducted on 40 patients of both sex admitted to the units of Critical Care Medicine Department of Alexandria Main University Hospital, Egypt divided into two groups group A: twenty patients were treated with hypertonic saline 3% intravenous through central venous catheter by loading dose 5ml/kg followed by 2ml/kg every 6 hours for 48 hours as maintenance dose. group B: twenty patients were treated with mannitol 20% intravenous through central venous catheter by loading dose 1gm/kg followed by 0.25gm/kg every 6 hours for 48 hours as maintenance dose.
All patients included in the study were subjected to the following parameters:
9. Demographic data.
10. Habits.
11. Past history of heart failure or renal failure.
12. Routine laboratory investigations including:
- Daily complete blood count [CBC].
- Serum sodium Na and serum chloride Cl every 12 hours.
- Blood urea nitrogen [BUN], serum creatinine every 12 hours and creatinine clearance [ml/min] by cockroft-Gault equation.
- Serum blood glucose level every 12 hours.
- Calculated serum osmolarity every 12 hours.
13. Hemodynamic parameters including: blood pressure [BP], heart rate [HR], respiratory rate [RR] and temperature every 2 hours.
14. Central venous pressure monitoring every 2 hours by cmH2O.
15. CT scan of brain at the start of hyperosmolar therapy and after 48 hours.
16. Glasgow coma score [GCS] every 6 hours for 48 hours.
As regard demographic data of the two studied groups.
group A: included 13 males and 7 females, their ages ranged between 21 and 54 years with a mean of 33.20 + 9.73 and median 33.5 years, while group B included 15 males and 5 females, their ages ranged between 21 and 56 years with a mean of 34.35 + 9.25 and a median 32.5 years.
There was no statistical significance between the two studied groups as regard age or sex.
As regard CT brain findings before treatment there was no statistical significance between the two studied groups.
As regard CT brain criteria after treatment and responding to treatment patients responding significantly better to with hypertonic saline 3% more than Mannitol 20%.
There was no statistical significance between the two studied groups as regard hematocrit level at all stages of the study, but we found that mannitol 20% decreases hematocrit significantly after 36 hours and 48 hours.
There was no statistical significance between the two studied groups as regard creatinine level at all stages of the study but mannitol 20% significantly increased creatinine level after 24 hours.
As regard creatinine clearance by Cockroft-Gault equation, creatinine clearance was significantly lower in Mannitol 20% group than hypertonic saline 3% group after 36 hours and 48 hours.
Both Mannitol 20% and hypertonic saline 3% elevated the calculated serum osmolarity after 12 hours to the end of the study and was statistically significant elevation for both.
Glasgow Coma Scale (GCS) improved significantly in Mannitol 20% group and also improved significantly in hypertonic saline 3% group but hypertonic saline 3% improved GCS significantly more than mannitol after 24 hours.