Accounts for about 1.1 million emergency department visits and one hospitalization per 1000 people each year in the U.S.
TBI is often unrecognized, misdiagnosed and undertreated.
The brain is susceptible to variations in oxygen delivery.
Reduction in oxygen delivery in other organs can be offset by increasing cardiac output, but this compensation does not necessarily apply to the brain, where cerebrovascular auto regulation enacts changes in cerebral blood flow to maintain balance between oxygen delivery and consumption.
These autoregulatory mechanisms are often impaired in acute brain injuries, resulting in significant impact of anemia in patients who are neurpcritically ill.
CDC reports 1.7 million people present to hospital emergency room with traumatic brain injury (TBI) and 1.365 million are treated and released.
It is estimated 2 million people experience TBI in the US each year.
The number of individuals who sustain severe traumatic brain injury with prolonged loss of consciousness each year is estimated to be between 56 and 170 per one million.
TBI encompasses various injuries of varying severity in causation ranging from concussions during sports, to head trauma from falls, to skull fractures, to penetrating wounds, and to many other causes of neurotrauma.
Motor vehicle accidents and falls are the main causes.
Each year, more than 1.5 million mild traumatic brain injuries with no loss of consciousness, and an equal number have injuries that impair consciousness.
Mild TBI is the most common type of TBI, resulting in approximately 2 1/2 emergency department visits per year in the US.
The highest rates of mild TBI are observed in older adults more than 75 years of age, in children younger than five years of age and adolescents age 15-24 years.
For most cases of mild traumatic brain injury, neuroimaging is not necessary, and most have unremarkable findings on neuroimaging test results.
CT brain imaging is indicated for patients with potential life-threatening complications requiring neurosurgery, such as fractures and intracranial hemorrhages.
MRI imaging is more sensitive to brain contusions and microhemorrhages than CT.
Mild TBI is seen at a higher rate in men than women at greater than 18%.
Definition of mild TBI includes a blow to or jolting of the head causing an acute disruption of brain function, manifested by a brief loss of consciousness of less than 30 minutes, confusion, or post traumatic amnesia for less than 24 hours, not accounted for by factors of psychological trauma or alcohol/drug intoxication.
Mild Trumatic brain injury typically results in physical, cognitive, and emotional symptoms that can worsen transiently with mental and physical exertion.
Previously mild traumatic brain injury was felt to be benign and self limiting but is now noted to be responsible for symptoms and disability they can persist for more than one year.
Severe traumatic brain injury is a leading cause of neurological disability, and approximately 50% of patients have long-term outcomes of death or severe disability.
Early after acute brain injury 15% of clinically unresponsive patients that do not follow commands have EEG evidence of brain activation in response to spoken motor commands.
Many individuals experiencing mild TBI such as a concussion, recover in weeks while others report symptoms to be prolonged.
Many patients with severe TBI are challenged with chronic, or even lifetime, morbidity and disability.
Traumatic brain injury, increases the risk of premature dementia and Alzheimer’s disease.
In adults leading causes of head injury are falls and motor vehicle accidents.
In the 15-24 year age group sports are second only to motor vehicle accidents as a cause of tramatic brain injury.
Estimated that 1.6 to 3.8 million sports related mild TBI’s occur in athletes annually.
It is estimated 2.5 million caregivers supporting a family member with TBI.
Patients with a history of a traumatic brain injury have higher rates of non-fatal deliberate self harm, suicide, and all cause mortality than the general population.
Traumatic brain injury patients may experience physical, cognitive, and emotional symptoms that place them at a higher risk of suicide.
An anonymous survey of college athletes revealed that 43% who had suffered a concussion deliberately concealed their symptoms.
An estimated 10 million cases of traumatic brain injury worldwide leading to hospitalization or death, annually.
A leading cause of death and disability from injury in the US.
TBI results in 142,000 emergency department visits and more than 81,000 hospitalizations and 14,300 deaths annually among older adults.
Annual burden for traumatic brain injury in the US is $60 billion (Maas AI et al).
Direct and indirect costs 76 $ billion/yr.
Traumatic brain injury (TBI) contribute about 2.4 million emergency department visits, hospitalizations, or deaths.
One third of all injury deaths include a TBI.
In low and median income countries in which motor powered transportation is increasing, the incidence of traumatic brain injury is rising, and involves predominantly young men.
In richer countries the epidemiology of TBI is changing because of the rate of traffic incidents is decreasing with safety laws and preventive measures in place, whereas with aging population such injury in the elderly is more common..
Estimated 5.3 million individuals in US are living with TBI related disabilities.
Traumatic brain injury in sports refers to an acute alteration in mental status that may or may not involve loss of consciousness after the traumatic event.
Traumatic brain injury by blast can be related to direct damage by passage of the blast wave through the skull and/or causing acceleration and/or rotation of the head, and can cause indirect damage when kinetic energy from a blast wave is transferred through large blood vessels in the abdomen and chest to the central nervous system.
Trumatic brain injury has a spectrum of injuries ranging from concussions to devastating intracranial hemorrhage.
Intracranial bleeding is a common complication of TBI.
Ongoing intracranial bleeding can lead to an increase in intracranial pressure, as well as brain herniation and death.
Associated with an increased risk of dementia both compared with people without a history of TBI and with people with non-TBI trauma.
CT of the brain is the gold standard for rapidly identifying intracranial injuries that require prompt intervention.
Patients with Glasgow coma score 9 through 12, which is moderate or severe head trauma, or coma scale of eight or less should undergo emergency head CT.
With a Glasgow coma score of 13 or higher there is minimal or no alterations in mental status and the patients have minor head trauma.
Individuals with traumatic brain injury are six times more likely to exhibit alexithymia.
The use of brain CT scans for patients with a GCS of 13 or higher is not clear.
Minor trauma to the brain occurs in 89% of cases compared to moderate to severe trauma which occurs and 11% of cases.
No individual history or physical examination can rule out intracranial injury after minor trauma.
Following minor head trauma clinical decisions to rule out intracranial injuries with additional imaging such a CT scan include: individuals older than 60 years, intoxication, headache, vomiting, seizures, amnesia, visual trauma above the clavicles, GCS score less than 15 two hours, suspected open, depressed, or basilar skull fracture.
Patients without any of the above features above after minor head trauma can be discharged or observed, and are at low risk of severe intracranial injury
Between five and 15% with minor trauma have intracranial injuries, and only a small minority of these require neurosurgical intervention.
Almost all acute and catastrophic brain diseases increase intracranial pressure.
Traumatic brain injury, intracerebral and extracerebral hematomas, cerebral infarction, and brain swelling associated with liver failure, and brain tumors associated with increased ICP.
Acute management after TBI target physiological parameters to minimize secondary brain injury.
Rapid decrease in body temperature at your earliest possible time after injury, or prophylactic hypothermia may improve outcomes with normothermic traumatic brain injury management: but the POLAR randomized clinical trial showed that early prophylactic hypothermia compared with normothermia did not improve neurological outcomes at six months in patients with severe Traumatic brain injury.
Elevated intracranial pressure consistently associated with poor outcomes.
10 to 15% of traumatic brain injuries are severe, and most are associated with raised intracranial pressure.
The rate of death is 18.4% for patients with traumatic brain injury and increased intracranial pressure of less than 20 mmHg and 55.6% of those within intracranial pressure for more than 40 mmHg.
Direct trama can injure the cortex, while hematomas can damage subcortical structures, lead to vasospasm and ischemia injury.
Among hospitalized patients with severe traumatic brain injury 60% die or survive with severe disabilities.
Sudden movement of the skull can lead to acceleration, rotational or deceleration injury with long axons interconnecting brain lesions.
Intracranial hemorrhages may be associated with prolonged labor, hypoxia, hemorrhagic disorders, or intravascular anomalies.
Intracranial hemorrhages may originate from tears in the dura or from ruptured vessels crossing the brain.
Severe trauma can cause hemorrhage within various intracranial spaces, leading to bring contusion, diffuse axonal shearing, and brain swelling.
May cause damage to the substance of the brain with intraventricular bleeding or parenchymal bleeding.
The skull protects the brain with a bony encasement, but its irregular interior of the skull can lead to brain injuries.
Axonal disruption and contusions can lead to sensory, motor and neurocognitive syndromes.
Approximately 35-45% of patients with moderate to severe TBI have a coagulopathy, with an elevation of prothrombin time of activated PTT, with or without thrombocytopenia, which is detected early in the hospitalization.
Rates of coagulopathy following TBI are higher with more severe injuries and with the presence of cerebral edema.
The presence of coagulopathy with TBI suggests a poor prognosis.
TBI is associated with microthrombi in the cerebral circulation and is more prevalent in contused areas than in contralateral areas.
The presence of microthrombi may predispose patients to stroke.
After TBI apoptosis, necrosis, paraptosis, and regeneration of brain vessel cells occur and may lead to susceptibility
to focal ischemic injury and stroke.
Following TBI the risk of thrombotic events such as thromboembolism and stroke increases substantially.
Anticoagulation after TBI reduces the risk of thrombotic events but their benefit must be balanced against the potential for higher risk of intracranial bleeding.
Estimated 10% of college football players and 20% of high school players sustain brain injuries.
Can cause chronic traumatic encephalopathy, with amnesia, executive dysfunction, aggression, depression, and parkinsonism (SterN RA et al).
Chronic traumatic brain injury is associated with tau-immunoreactive neurofibrillary tangles preferentially involving the superficial cortical layers, astrocytic tangles and neurities (McKee AC et al ).
Stroke may be a long- term consequence of TBI.
The greater the severity of TBI the more the association with the risk of stroke and post stroke mortality.
TBI is a risk factor for stroke independent convention vascular risk.
About 2% of patients with head trauma develop post-traumatic seizures.
About 12% of patients with severe traumatic brain injury develop seizures.
About 50% of those with penetrating missile injuries develop seizures.
Prophylactic anti-seizure medicines decrease the risk of developing early (those occurring within 7 days of injury) post-traumatic seizures.
Prophylactic anti-seizure medicines do not decrease the risk of developing late (those occurring after 7 days of injury) post-traumatic seizures.
Following traumatic brain injury increased intracranial pressure caused by cerebral edema is an important secondary insult.
Monitoring of ICP is standard of care in patients with severe traumatic brain injury, however it lacks efficacy.
Tranexamic acid (TXA) is an antifibrinolytic agent used to treat or prevent excessive blood loss, significantly reduces mortality from traumatic brain injury (TBI).
Administration of tranexamic acid within 3 hours of head trauma is associated with a 20% reduction in deaths among those with mild to moderate TBI, with no evidence of adverse effects or complications.
In a controlled trial of patients with traumatic brain injury, with care focused on maintaining monitored ICP at 20 mm Hg or less, there was no superiority to care based on imaging and clinical examination (Chesnut RM et al).
First tier therapies are utilized after traumatic brain injury to control increased intracranial pressure.
With severe traumatic brain injury raised intracranial pressure may be refractory to first tier measures and require surgical decompressive craniectomy.
In a randomized, controlled trial, the Decompressive Craniectomy (DECRA) trial testing the efficacy of bifrontotemporoparietal decompressive craniectomy in adults under the age of 60 years with traumatic brain injuiry failing first tier measures for intracranial pressure:: early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure, duration of mechanical ventilation, and length of stay in the ICU but was associated with more unfavorable outcomes at 6 months, as measured by the Extended Glasgow Outcome Scale (Cooper DJ et al).
Previously patients with mild Traumatic brain injury were recommended to rest until symptoms were completely resolved: Patients were advised to avoid physical activity that elevates the heart rate, avoid participating in cognitively demanding tasks and exposure to sensory stimuli.
Recent evidence for TBI sugges 24-72 hour resumption of usual activities may lead to a faster recovery if the patient does not exacerbate symptoms, while prolong rest is associated with more symptoms and longer recovery times.
Aerobic exercise shortens recovery time by four days compared with stretching exercise after TBI.
Among patients with moderate to severe traumatic brain injury, treatment with continuous 20% hypertonic sailing compared with standard care did not result in the other neurological status at six months (Roquilly, A).
In critically, ill patients with TBI and anemia, a liberal transfusion strategy did not reduce the risk of an unfavorable neurologic outcome at six months.
In the TRAIN study group patients with acute brain injury and anemia randomized to a liberal transfusion strategy were less likely to have unfavorable neurological outcome than those randomized to restrictive strategy.