Severe Traumatic Brain Injury: A Case Study
Hypertonic Saline versus Mannitol in the Treatment of
Severe Traumatic Brain Injury
During the recent Afghanistan and Iraq conflicts, Severe Traumatic Brain Injuries (sTBI) were a large portion of the wounded or deaths among Canadian Armed Forces (CAF) and Allies. Pannell et al. (2011) analytical study of CAF soldiers who were killed in Afghanistan from January 2006-April 2008, concluded most common causes of deaths deemed preventable during the Afghanistan conflict of CAF members were hemorrhage (38%), neurologic injury (33%) and blast injuries (16%). Neurological injuries were further defined as 10 casualties suffered penetrating head injuries and 7 casualties suffered severe closed head injuries which included midbrain avulsion, large subarachnoid …show more content…
Glasgow Coma Scale (GCS) being the most common used within the Royal Canadian Medical Service to describe the severity of brain injury; GCS 13-15 mild TBI, GCS 9-12 moderate TBI, and GCS 15mmHg, when the brain is injured the body autoregulation system will try to ensure cerebral perfusion pressure (CPP) for adequate oxygen perfusion of the brain. CPP is mean arterial pressure (MAP) minus ICP; normal CPP >50mmHg. When there is an overwhelming injury or delay in treatment CCP is decreased and symptoms of herniation symptoms can be observed. Cushing Traid: Hypertension, bradycardia (late sign) and irregular respiratory pattern (Kussmaul’s breathing) which could be the first indication of a life threatening cerebral herniation and pending brain death.
Overall, clinical management of sTBI is to prevent cerebral herniation syndrome by avoiding hypotensive events (MAP >90mmHg) and hypoxia (normocarbia pCO2 35-40mmHg), ICP monitoring to sustain ICP 65mmHg, elevating of the head of bed 30 degrees, and osmotic therapy (mannitol or HTS) to reduce cerebral edema (serum osmolality maximum 320 mOsm/L), prevent herniation syndrome and …show more content…
They use the osmotic gradient to reduce cerebral edema to decrease ICP. Mannitol mechanism of action is to reduce ICP by drawing water from the brain parenchyma, does not cross brain-blood barrier (BBB). But also causes profound osmotic diuresis by increases the osmotic pressure of glomerular filtrate, inhibits tubular reabsorption of water and electrolytes, increases urinary output if renal failure or hypovolemia is a concern could be devastating to patient’s outcome. HTS mechanism of action is the same osmotic gradient in the BBB as mannitol versus there is no profound diuresis, thus a hypovolemia or renal failure/ injury are not a risk. HTS also restores the normal cellular resting membrane potential and cell volume, stimulation of atrial natriuretic peptide release, inhibition of inflammation, and enhancement of cardiac output. This literature review will look at the efficiency and effectiveness of both in the management of increased ICP/ cerebral hypertension in sTBI with the intent to determine which is more proficient to decrease ICP, herniation and
Severe Traumatic Brain Injury
During the recent Afghanistan and Iraq conflicts, Severe Traumatic Brain Injuries (sTBI) were a large portion of the wounded or deaths among Canadian Armed Forces (CAF) and Allies. Pannell et al. (2011) analytical study of CAF soldiers who were killed in Afghanistan from January 2006-April 2008, concluded most common causes of deaths deemed preventable during the Afghanistan conflict of CAF members were hemorrhage (38%), neurologic injury (33%) and blast injuries (16%). Neurological injuries were further defined as 10 casualties suffered penetrating head injuries and 7 casualties suffered severe closed head injuries which included midbrain avulsion, large subarachnoid …show more content…
Glasgow Coma Scale (GCS) being the most common used within the Royal Canadian Medical Service to describe the severity of brain injury; GCS 13-15 mild TBI, GCS 9-12 moderate TBI, and GCS 15mmHg, when the brain is injured the body autoregulation system will try to ensure cerebral perfusion pressure (CPP) for adequate oxygen perfusion of the brain. CPP is mean arterial pressure (MAP) minus ICP; normal CPP >50mmHg. When there is an overwhelming injury or delay in treatment CCP is decreased and symptoms of herniation symptoms can be observed. Cushing Traid: Hypertension, bradycardia (late sign) and irregular respiratory pattern (Kussmaul’s breathing) which could be the first indication of a life threatening cerebral herniation and pending brain death.
Overall, clinical management of sTBI is to prevent cerebral herniation syndrome by avoiding hypotensive events (MAP >90mmHg) and hypoxia (normocarbia pCO2 35-40mmHg), ICP monitoring to sustain ICP 65mmHg, elevating of the head of bed 30 degrees, and osmotic therapy (mannitol or HTS) to reduce cerebral edema (serum osmolality maximum 320 mOsm/L), prevent herniation syndrome and …show more content…
They use the osmotic gradient to reduce cerebral edema to decrease ICP. Mannitol mechanism of action is to reduce ICP by drawing water from the brain parenchyma, does not cross brain-blood barrier (BBB). But also causes profound osmotic diuresis by increases the osmotic pressure of glomerular filtrate, inhibits tubular reabsorption of water and electrolytes, increases urinary output if renal failure or hypovolemia is a concern could be devastating to patient’s outcome. HTS mechanism of action is the same osmotic gradient in the BBB as mannitol versus there is no profound diuresis, thus a hypovolemia or renal failure/ injury are not a risk. HTS also restores the normal cellular resting membrane potential and cell volume, stimulation of atrial natriuretic peptide release, inhibition of inflammation, and enhancement of cardiac output. This literature review will look at the efficiency and effectiveness of both in the management of increased ICP/ cerebral hypertension in sTBI with the intent to determine which is more proficient to decrease ICP, herniation and