Anesthetic management of patients with traumatic brain injury

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Anesthetic management of patients with traumatic brain injury

By: Vlad Nevazhno

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Predisposing factors such as hypoxia, hypercarbia and hypotension only exacerbate the severity of these changes. Intensive therapy for traumatic brain injury is aimed at preventing secondary brain injury. All anesthetic drugs and techniques of anesthesia violate intracranial hemo-and liquorodynamics. Therapeutic activities undertaken in the light of pathophysiological changes, significantly improve the outcome in traumatic brain injury.

Epidemiology

Head injury is the leading cause of disability and death in young people. It is estimated that in the United States, traumatic brain injury occurs with a frequency of 200 cases per 100,000 population in god.1 Each year about 500,000 people received serious head injury, of which 450.000 get to the hospital and 50,000 die before treated in hospital. Among the 450.000 people who are sent to the hospital, cases of significant disability occur in approximately 100,000 people per year. Brain injury is most common in young people aged 15 to 24 years. According to statistics, men get this type of injury is two to three times more likely than women in all age groups. More than 50% of all cases of brain injury and 70% of deaths in traumatic brain injury accounted for by road traffic in the densely populated cities proisshestviy.1 use of firearms defines a large percentage of cases of brain injury. The second main reason is the drop. More than 50% of patients with severe traumatic brain injury observed multiple injuries that result in significant blood loss, systemic hypotension and gipoksii.2

Classification of severe traumatic brain injury conducted by coma Glasgow, which allows to estimate the severity of neurological damage, taking into account the results of tests on the opening of the eyes, verbal and performance tests on motor funktsii.3 total maximum possible score is 15, a serious brain injury talk when 6 hours or more total calculated score of 8 or less. Glasgow Coma Scale and the scale of its outcome in Glasgow can compare the severity of neurological damage in different patients and to predict the outcome sostoyaniya.1 In general, mortality is highly dependent on the amount originally received scores of coma Glasgow. However, for the same injury and same number of points the elderly have a worse prognosis than younger lyudi.1

Pathophysiology

Brain injury leads to brain damage that develops in two stages. The primary damage caused by the influence of biomechanical forces on the skull and brain at the time of injury, and is developing it for a millisecond. At this point, there is contusion of the brain substance with diffuse neuronal damage and cerebral white matter, and there is a rupture of arteries and veins, which leads to multiple petechial hemorrhages. Primary injury includes concussion and contusion of the brain, blood vessels rupture and formation of hematoma (epidural, subdural, subarachnoid or intracerebral). It is still not offered any way to therapy of primary damage.

Secondary damage develops within a few minutes or hours after the injury and is a complex pathological changes that occur as a result of primary damage and lead to ischemia, swelling and brain edema, intracranial hemorrhage, intracranial hypertension and the formation of hernial protrusion. The secondary factors that contribute to the primary injury are such as hypoxia, hypercarbia, hypotension, anemia, and hyperglycemia. Warning or proper treatment of these secondary pathological conditions improves outcome in traumatic brain injury. Seizures, infectious complications and sepsis, which may arise at a later date after traumatic brain injury (a few hours or days) to further enhance the brain damage, so they should also be careful to fight and prevent their occurrence.

After traumatic brain injury on the background of severe generalized or focal disturbances, irreversible neuropathological changes in areas due to one of two reasons: 1) cerebral blood flow becomes inadequate, or 2) the metabolic needs of the brain increase dramatically. Cerebral blood flow may become inadequate systemic blood pressure reduction and increased intracranial pressure, since these factors lead to a significant reduction in cerebral perfusion pressure and cause ischemic brain damage. Increased metabolic demands of the brain, such as hyperthermia or status epilepticus, since under these conditions the brain needs oxygen and glucose to exceed the capacity of the cardio-pulmonary system in their delivery. Not yet fully established, the reasons for traumatic brain injury breaks blood circulation in the vessels of the brain, but this factor is involved in secondary injury mozga.4 Thus, an imbalance in the ratio of oxygen delivery to the brain / brain oxygen demand and failure mechanisms of adaptation in cerebrovascular system leads to the fact that the brain becomes more vulnerable to the damaging effect of additional factors, such as fluctuation of blood pressure, impaired blood rheology or hypoxia.

Traumatic brain injury triggers a cascade of potentially harmful biochemical changes. There is a shift in the intracellular calcium content, oxygen free radicals are released and vasoactive metabolites of arachidonic acid, which damages the vascular endothelium and membrane neyronov.5, 6 In addition, there is a steady accumulation of "excitatory" amino acids such as glutamate and aspartate, and this process is to faster than the heavier brain injury and fewer stocks vysokoergicheskih fosfatov.7 Ongoing clinical studies have as their objective to assess whether calcium channel blockers, scavengers of free radicals and other groups of drugs can affect the course of biochemical reactions that occur during ischemia and damage the brain. If these drugs are administered early after traumatic brain injury, their use can theoretically prevent the pathophysiological changes and improve the outcome of the state.

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Head injury is the leading cause of death among young people. Arising after the initial brain damage pathophysiological changes lead to secondary damage. Pulse oximeter.

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<h1>Anesthetic management of patients with traumatic brain injury</h1><p> Predisposing factors such as hypoxia, hypercarbia and hypotension only exacerbate the severity of these changes. Intensive therapy for traumatic brain injury is aimed at preventing secondary brain injury. All anesthetic drugs and techniques of anesthesia violate intracranial hemo-and liquorodynamics. Therapeutic activities undertaken in the light of pathophysiological changes, significantly improve the outcome in traumatic brain injury.<br /> <br /> Epidemiology<br /> <br /> Head injury is the leading cause of disability and death in young people. It is estimated that in the United States, traumatic brain injury occurs with a frequency of 200 cases per 100,000 population in god.1 Each year about 500,000 people received serious head injury, of which 450.000 get to the hospital and 50,000 die before treated in hospital. Among the 450.000 people who are sent to the hospital, cases of significant disability occur in approximately 100,000 people per year. Brain injury is most common in young people aged 15 to 24 years. According to statistics, men get this type of injury is two to three times more likely than women in all age groups. More than 50% of all cases of brain injury and 70% of deaths in traumatic brain injury accounted for by road traffic in the densely populated cities proisshestviy.1 use of firearms defines a large percentage of cases of brain injury. The second main reason is the drop. More than 50% of patients with severe traumatic brain injury observed multiple injuries that result in significant blood loss, systemic hypotension and gipoksii.2<br /> <br /> Classification of severe traumatic brain injury conducted by coma Glasgow, which allows to estimate the severity of neurological damage, taking into account the results of tests on the opening of the eyes, verbal and performance tests on motor funktsii.3 total maximum possible score is 15, a serious brain injury talk when 6 hours or more total calculated score of 8 or less. Glasgow Coma Scale and the scale of its outcome in Glasgow can compare the severity of neurological damage in different patients and to predict the outcome sostoyaniya.1 In general, mortality is highly dependent on the amount originally received scores of coma Glasgow. However, for the same injury and same number of points the elderly have a worse prognosis than younger lyudi.1<br /> <br /> Pathophysiology<br /> <br /> Brain injury leads to brain damage that develops in two stages. The primary damage caused by the influence of biomechanical forces on the skull and brain at the time of injury, and is developing it for a millisecond. At this point, there is contusion of the brain substance with diffuse neuronal damage and cerebral white matter, and there is a rupture of arteries and veins, which leads to multiple petechial hemorrhages. Primary injury includes concussion and contusion of the brain, blood vessels rupture and formation of hematoma (epidural, subdural, subarachnoid or intracerebral). It is still not offered any way to therapy of primary damage.<br /> <br /> Secondary damage develops within a few minutes or hours after the injury and is a complex pathological changes that occur as a result of primary damage and lead to ischemia, swelling and brain edema, intracranial hemorrhage, intracranial hypertension and the formation of hernial protrusion. The secondary factors that contribute to the primary injury are such as hypoxia, hypercarbia, hypotension, anemia, and hyperglycemia. Warning or proper treatment of these secondary pathological conditions improves outcome in traumatic brain injury. Seizures, infectious complications and sepsis, which may arise at a later date after traumatic brain injury (a few hours or days) to further enhance the brain damage, so they should also be careful to fight and prevent their occurrence.<br /> <br /> After traumatic brain injury on the background of severe generalized or focal disturbances, irreversible neuropathological changes in areas due to one of two reasons: 1) cerebral blood flow becomes inadequate, or 2) the metabolic needs of the brain increase dramatically. Cerebral blood flow may become inadequate systemic blood pressure reduction and increased intracranial pressure, since these factors lead to a significant reduction in cerebral perfusion pressure and cause ischemic brain damage. Increased metabolic demands of the brain, such as hyperthermia or status epilepticus, since under these conditions the brain needs oxygen and glucose to exceed the capacity of the cardio-pulmonary system in their delivery. Not yet fully established, the reasons for traumatic brain injury breaks blood circulation in the vessels of the brain, but this factor is involved in secondary injury mozga.4 Thus, an imbalance in the ratio of oxygen delivery to the brain / brain oxygen demand and failure mechanisms of adaptation in cerebrovascular system leads to the fact that the brain becomes more vulnerable to the damaging effect of additional factors, such as fluctuation of blood pressure, impaired blood rheology or hypoxia.<br /> <br /> Traumatic brain injury triggers a cascade of potentially harmful biochemical changes. There is a shift in the intracellular calcium content, oxygen free radicals are released and vasoactive metabolites of arachidonic acid, which damages the vascular endothelium and membrane neyronov.5, 6 In addition, there is a steady accumulation of "excitatory" amino acids such as glutamate and aspartate, and this process is to faster than the heavier brain injury and fewer stocks vysokoergicheskih fosfatov.7 Ongoing clinical studies have as their objective to assess whether calcium channel blockers, scavengers of free radicals and other groups of drugs can affect the course of biochemical reactions that occur during ischemia and damage the brain. If these drugs are administered early after traumatic brain injury, their use can theoretically prevent the pathophysiological changes and improve the outcome of the state.<br /> <p><h2>Author Info</h2>Head injury is the leading cause of death among young people. Arising after the initial brain damage pathophysiological changes lead to secondary damage. <a href="http://www.pulseoximeterok.com/">Pulse oximeter</a>. More <a href="http://www.articlesroom.com">free articles</a> from <a href="http://www.articlesroom.com">http://www.articlesroom.com</a>

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