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Traumatic Brain Injury
Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Diagnosis is suspected clinically and confirmed by imaging (primarily CT). Initial treatment consists of ensuring a reliable airway and maintaining adequate ventilation, oxygenation, and blood pressure. Surgery is often needed in patients with more severe injury to place monitors to track and treat intracranial pressure elevation, decompress the brain if intracranial pressure is increased, or remove intracranial hematomas. In the first few days after the injury, maintaining adequate brain perfusion and oxygenation and preventing complications of altered sensorium are important. Subsequently, many patients require rehabilitation.
In the US, as in much of the world, TBI is a common cause of death and disability. Causes include motor vehicle crashes and other transportation-related causes (eg, bicycle crashes, collisions with pedestrians), falls (especially in older adults and young children), assaults, and sports activities (see Sports-Related Concussion).
Structural changes from head injury may be gross or microscopic, depending on the mechanism and forces involved. Patients with less severe injuries may have no gross structural damage. Clinical manifestations vary markedly in severity and consequences. Injuries are commonly categorized as open or closed.
Open injuries involve penetration of the scalp and skull (and usually the meninges and underlying brain tissue). They typically involve bullets or sharp objects, but a skull fracture with overlying laceration due to severe blunt force is also considered an open injury.
Closed injuries typically occur when the head is struck, strikes an object, or is shaken violently, causing rapid brain acceleration and deceleration. Acceleration or deceleration can injure tissue at the point of impact (coup), at its opposite pole (contrecoup), or diffusely; the frontal and temporal lobes are particularly vulnerable. Axons, blood vessels, or both can be sheared or torn. Disrupted blood vessels leak, causing contusions, intracerebral or subarachnoid hemorrhage, and epidural or subdural hematomas (see Table: Common Types of Traumatic Brain Injury).
Common Types of Traumatic Brain Injury
Concussion (see Sports-Related Concussion) is defined as a transient and reversible posttraumatic alteration in mental status (eg, loss of consciousness or memory, confusion) lasting from seconds to minutes and, by arbitrary definition, < 6 h. Gross structural brain lesions and serious neurologic residua are not part of concussion, although temporary disability can occur due to symptoms, such as nausea, headache, dizziness, memory disturbance, and difficulty concentrating (postconcussion syndrome) that usually resolve within weeks.
Contusions (bruises of the brain) can occur with open or closed injuries and can impair a wide range of brain functions, depending on contusion size and location. Larger contusions may cause brain edema and increased intracranial pressure (ICP). Contusions may enlarge in the hours and days following the initial injury and cause neurologic deterioration.
Diffuse axonal injury (DAI) occurs when rotational deceleration causes shear-type forces that result in generalized, widespread disruption of axonal fibers and myelin sheaths. A few DAI lesions may also result from minor head injury. Gross structural lesions are not part of DAI, but small petechial hemorrhages in the white matter are often observed on CT and on histopathologic examination. DAI is sometimes defined clinically as a loss of consciousness lasting > 6 h in the absence of a specific focal lesion. Edema from the injury often increases ICP, leading to various manifestations (see Traumatic Brain Injury : Pathophysiology). DAI is typically the underlying injury in shaken baby syndrome.
Hematomas (collections of blood in or around the brain) can occur with open or closed injuries and may be epidural, subdural, or intracerebral. Subarachnoid hemorrhage (SAH—bleeding into the subarachnoid space—see Subarachnoid Hemorrhage (SAH)) is common in TBI, although the appearance on CT is not usually the same as aneurysmal SAH.
Subdural hematomas are collections of blood between the dura mater and the pia-arachnoid mater. Acute subdural hematomas arise from laceration of cortical veins or avulsion of bridging veins between the cortex and dural sinuses. They often occur with head trauma from falls and motor vehicle crashes. Compression of the brain by the hematoma and swelling of the brain due to edema or hyperemia (increased blood flow due to engorged blood vessels) can increase ICP. When these processes both occur, mortality and morbidity can be high. A chronic subdural hematoma may appear and cause symptoms gradually over several weeks after trauma. These hematomas occur more often in alcoholics and elderly patients (especially in those taking antiplatelet or anticoagulant drugs, or in those with brain atrophy). Elderly patients may consider the head injury relatively trivial or may have even forgotten it. In contrast to acute subdural hematomas, edema and increased ICP are unusual.
Epidural hematomas are collections of blood between the skull and dura mater and are less common than subdural hematomas. Epidural hematomas that are large or rapidly expanding are usually caused by arterial bleeding, classically due to damage to the middle meningeal artery by a temporal bone fracture. Without intervention, patients with arterial epidural hematomas may rapidly deteriorate and die. Small, venous epidural hematomas are rarely lethal.
Intracerebral hematomas are collections of blood within the brain itself. In the traumatic setting, they result from coalescence of contusions. Exactly when one or more contusions become a hematoma is not well defined. Increased ICP, herniation, and brain stem failure can subsequently develop, particularly with lesions in the temporal lobes.
Penetrating injuries by definition involve fractures. Closed injuries may also cause skull fractures, which may be linear, depressed, or comminuted. The presence of a fracture suggests that significant force was involved in the injury. Although most patients with simple linear fractures and no neurologic impairment are not at high risk of brain injuries, patients with any fracture associated with neurologic impairment are at increased risk of intracranial hematomas. Fractures that involve special risks include
Depressed fractures: These fractures have the highest risk of tearing the dura, damaging the underlying brain, or both.
Temporal bone fractures that cross the area of the middle meningeal artery: In these fractures, an epidural hematoma is a risk.
Fractures that cross one of the major dural sinuses: These fractures may cause significant hemorrhage and venous epidural or venous subdural hematoma. Injured venous sinuses can later thrombose and cause cerebral infarction.
Fractures that involve the carotid canal: These fractures can result in carotid artery dissection.
Fractures of the occipital bone and base of the skull (basilar bones): These bones are thick and strong, so fractures in these areas indicate a high-intensity impact and meaningfully increase risk of brain injury. Basilar skull fractures that extend into the petrous part of the temporal bone often damage middle and inner ear structures and can impair facial, acoustic, and vestibular nerve function.
Fractures in infants: The meninges may become trapped in a linear skull fracture with subsequent development of a leptomeningeal cyst and expansion of the original fracture (growing fracture).
Brain function may be immediately impaired by direct damage (eg, crush, laceration) of brain tissue. Further damage may occur shortly thereafter from the cascade of events triggered by the initial injury.
TBI of any sort can cause cerebral edema and decrease brain blood flow. The cranial vault is fixed in size (constrained by the skull) and filled by noncompressible CSF and minimally compressible brain tissue; consequently, any swelling from edema or an intracranial hematoma has nowhere to expand and thus increases ICP. Cerebral blood flow is proportional to the cerebral perfusion pressure (CPP), which is the difference between mean arterial pressure (MAP) and mean ICP. Thus, as ICP increases (or MAP decreases), CPP decreases. When CPP falls below 50 mm Hg, the brain may become ischemic. Ischemia and edema may trigger various secondary mechanisms of injury (eg, release of excitatory neurotransmitters, intracellular Ca, free radicals, and cytokines), causing further cell damage, further edema, and further increases in ICP. Systemic complications from trauma (eg, hypotension, hypoxia) can also contribute to cerebral ischemia and are often called secondary brain insults.
Excessive ICP initially causes global cerebral dysfunction. If excessive ICP is unrelieved, it can push brain tissue across the tentorium or through the foramen magnum, causing herniation (see Brain herniation.) and increased morbidity and mortality. If ICP increases to equal MAP, CPP becomes zero, resulting in complete brain ischemia and brain death; absent cranial blood flow is objective evidence of brain death (see Brain Death).
Hyperemia and increased brain blood flow may result from concussive injury in adolescents or children. Second impact syndrome is a rare and debated entity defined by sudden increased ICP and sometimes death after a second traumatic insult that is sustained before complete recovery from a previous minor head injury. It is attributed to loss of autoregulation of cerebral blood flow that leads to vascular engorgement, increased ICP, and herniation.
Initially, most patients with moderate or severe TBI lose consciousness (usually for seconds or minutes), although some patients with minor injuries have only confusion or amnesia (amnesia is usually retrograde and results in memory loss of a period of seconds to a few hours before the injury). Young children may simply become irritable. Some patients have seizures, often within the first hour or day. After these initial symptoms, patients may be fully awake and alert, or consciousness and function may be altered to some degree, from mild confusion to stupor to coma. Duration of unconsciousness and severity of obtundation are roughly proportional to injury severity but are not specific.
The Glasgow Coma Scale (GCS—see Table: Glasgow Coma Scale*) is a quick, reproducible scoring system to be used during the initial examination to estimate severity of TBI. It is based on eye opening, verbal response, and the best motor response. The lowest total score (3) indicates likely fatal damage, especially if both pupils fail to respond to light and oculovestibular responses are absent. Higher initial scores tend to predict better recovery. By convention, the severity of head injury is initially defined by the GCS:
Glasgow Coma Scale*
Prediction of the severity of TBI and prognosis can be refined by also considering CT findings and other factors. Some patients with initially moderate TBI and a few patients with initially mild TBI deteriorate. For infants and young children, the Modified Glasgow Coma Scale for Infants and Children is used (see Table: Modified Glasgow Coma Scale for Infants and Children). Because hypoxia and hypotension can decrease the GCS, GCS values after resuscitation from cardiopulmonary insults are more specific for brain dysfunction than values determined before resuscitation. Similarly, sedatives and paralytics can decrease GCS values and should be avoided before full neurologic examination is done.
Modified Glasgow Coma Scale for Infants and Children
Symptoms of various types of TBI may overlap considerably.
Epidural hematoma symptoms usually develop within minutes to several hours after the injury (the period without symptoms is the so-called lucid interval) and consist of increasing headache, decreased level of consciousness, and focal neurologic deficits (eg, hemiparesis). Pupillary dilation with loss of light reactivity usually indicates herniation. Some patients lose consciousness, then have a transient lucid interval, and then gradual neurologic deterioration. Most patients with subdural hematomas have immediate loss of consciousness. Intracerebral hematoma and subdural hematoma can cause focal neurologic deficits such as hemiparesis, progressive decrease in consciousness, or both. Progressive decrease in consciousness may result from anything that increases ICP (eg, hematoma, edema, hyperemia).
Increased ICP sometimes causes vomiting but vomiting is nonspecific. Markedly increased ICP classically manifests as a combination of hypertension (usually with increased pulse pressure), bradycardia, and respiratory depression (Cushing triad); respirations are usually slow and irregular. Severe diffuse brain injury or markedly increased ICP may cause decorticate or decerebrate posturing. Both are poor prognostic signs.
Transtentorial herniation (see Brain herniation.) may result in coma, unilaterally or bilaterally dilated and unreactive pupils, hemiplegia (usually on the side opposite a unilaterally dilated pupil), and Cushing triad.
Basilar skull fracture may result in leakage of CSF from the nose (CSF rhinorrhea) or ear (CSF otorrhea), blood behind the tympanic membrane (hemotympanum) or in the external ear canal if the tympanic membrane has ruptured, and ecchymosis behind the ear (Battle sign) or in the periorbital area (raccoon eyes). Loss of smell and hearing is usually immediate, although these losses may not be noticed until the patient regains consciousness. Facial nerve function may be impaired immediately or after a delay. Other fractures of the cranial vault are sometimes palpable, particularly through a scalp laceration, as a depression or step-off deformity. However, blood under the galea aponeurotica may mimic such a step-off deformity.
Chronic subdural hematoma may manifest with increasing daily headache, fluctuating drowsiness or confusion (which may mimic early dementia), and mild-to-moderate hemiparesis or other focal neurologic deficits.
Amnesia may persist and be both retrograde and anterograde (ie, for events following the injury). Postconcussion syndrome, which commonly follows a moderate or severe concussion, includes headache, dizziness, fatigue, difficulty concentrating, variable amnesia, depression, apathy, and anxiety. Commonly smell (and thus taste), sometimes hearing, or rarely vision is altered or lost. Symptoms usually resolve spontaneously over weeks to months.
A range of cognitive and neuropsychiatric deficits can persist after severe, moderate, and even mild TBI, particularly if structural damage was significant. Common problems include amnesia, behavioral changes (eg, agitation, impulsivity, disinhibition, lack of motivation), emotional lability, sleep disturbances, and decreased intellectual function.
Late seizures (> 7 days after the injury) develop in a small percentage of patients, often weeks, months, or even years later. Spastic motor impairment, gait and balance disturbances, ataxia, and sensory losses may occur.
A persistent vegetative state (see Vegetative State and Minimally Conscious State) can result from a TBI that destroys forebrain cognitive functions but spares the brain stem. The capacity for self-awareness and other mental activity is absent; however, autonomic and motor reflexes are preserved, and sleep-wake cycles are normal. Few patients recover normal neurologic function when a persistent vegetative state lasts for 3 mo after injury, and almost none recover after 6 mo.
Neurologic function may continue to improve for a few years after TBI, most rapidly during the initial 6 mo.
(For an example of how to triage, diagnose, and treat head injuries in a system in which CT and specialty trauma care are used more selectively than in the US, see also the practice guideline of the National Institute for Clinical Excellence of the United Kingdom Head injury: assessment and early management.)
An initial overall assessment of injuries should be done (see Approach to the Trauma Patient : Evaluation and Treatment). Diagnosis and treatment occur simultaneously in seriously injured patients.
A rapid, focused neurologic evaluation is part of the initial assessment, including assessment of the components of the GCS, adequacy of the airway and breathing, and pupillary light response. Patients are ideally assessed before paralytics and sedatives are given. Patients are reassessed at frequent intervals (eg, every 15 to 30 min initially, then every 1 h after stabilization). Subsequent improvement or deterioration helps estimate injury severity and prognosis.
Complete neurologic examination is done as soon as the patient is sufficiently stable. Infants and children should be examined carefully for retinal hemorrhages, which may indicate shaken baby syndrome. Funduscopic examination in adults may disclose traumatic retinal detachment and absence of retinal venous pulsations due to elevated ICP, but examination may be normal despite brain injury. Concussion is diagnosed when loss of consciousness or memory lasts < 6 h and symptoms are not explained by brain injury seen on neuroimaging. DAI is suspected when loss of consciousness exceeds 6 h and microhemorrhages are seen on CT. Diagnosis of other types of TBI is made by CT or MRI.
Imaging should always be done in patients with more than transiently impaired consciousness, GCS score < 15, focal neurologic findings, persistent vomiting, seizures, a history of loss of consciousness, or clinically suspected fractures. A case can be made for obtaining a CT scan of the head in all patients with more than a trivial head injury, because the clinical and medicolegal consequences of missing a hematoma are severe, but clinicians should balance this against the possible risk for radiation-related adverse effects from CT in younger patients.
Although plain x-rays can detect some skull fractures, they cannot help assess the brain and they delay more definitive brain imaging; thus, plain x-rays are usually not done. CT is the best choice for initial imaging, because it can detect hematomas, contusions, skull fractures (thin cuts are obtained to reveal clinically suspected basilar skull fractures, which may otherwise not be visible), and sometimes DAI. On CT, contusions and acute bleeding appear opaque (dense) compared with brain tissue. Arterial epidural hematomas classically appear as lenticular-shaped opacities over brain tissue, often in the territory of the middle meningeal artery. Subdural hematomas classically appear as crescent-shaped opacities overlying brain tissue. A chronic subdural hematoma appears hypodense compared with brain tissue, whereas a subacute subdural hematoma may have a similar radiopacity as brain tissue (isodense). Isodense subdural hematoma, particularly if bilateral and symmetric, may appear only subtly abnormal. In patients with severe anemia, an acute subdural hematoma may appear isodense with brain tissue. Among individual patients, findings may differ from these classic appearances. Signs of mass effect include sulcal effacement, ventricular and cisternal compression, and midline shift. Absence of these findings does not exclude increased ICP, and mass effect may be present with normal ICP. A shift of > 5 mm from the midline is generally considered to be an indication for surgical evacuation of the hematoma.
Pearls & Pitfalls
MRI may be useful later in the clinical course to detect more subtle contusions, DAI, and brain stem injury. It is usually more sensitive than CT for the diagnosis of very small acute or isodense subacute and isodense chronic subdural hematomas. Preliminary, unconfirmed evidence suggests that certain MRI findings predict prognosis. Angiography, CT angiography, and magnetic resonance angiography are all useful for the evaluation of vascular injury. For example, vascular injury is suspected when CT findings are inconsistent with the physical examination findings (eg, hemiparesis with a normal or nondiagnostic CT due to suspected evolving ischemia secondary to vascular thrombosis or embolism due to a carotid artery dissection).
In the US, adults with severe TBI who are treated have a mortality rate of about 25 to 33%. Mortality is lower with higher GCS scores. Mortality rates are lower in children ≥ 5 yr (≤ 10% with a GCS score of 5 to 7). Children overall do better than adults with a comparable injury.
The vast majority of patients with mild TBI retain good neurologic function. With moderate or severe TBI, the prognosis is not as good but is much better than is generally believed. The most commonly used scale to assess outcome in TBI patients is the Glasgow Outcome Scale. On this scale the possible outcomes are
Over 50% of adults with severe TBI have a good recovery or only moderate disability. Occurrence and duration of coma after a TBI are strong predictors of disability. Of patients whose coma exceeds 24 h, 50% have severe persistent neurologic sequelae, and 2 to 6% remain in a persistent vegetative state at 6 mo. In adults with severe TBI, recovery occurs most rapidly within the initial 6 mo. Smaller improvements continue for perhaps as long as several years. Children have a better immediate recovery from TBI regardless of severity and continue to improve for a longer period of time.
Cognitive deficits, with impaired concentration, attention, and memory, and various personality changes are a more common cause of disability in social relations and employment than are focal motor or sensory impairments. Posttraumatic anosmia and acute traumatic blindness seldom resolve after 3 to 4 mo. Hemiparesis and aphasia usually resolve at least partially, except in the elderly.
Multiple noncranial injuries, which are likely with motor vehicle crashes and falls, often require simultaneous treatment. Initial resuscitation of trauma patients is discussed elsewhere (see Approach to the Trauma Patient).
At the injury scene, a clear airway is secured and external bleeding is controlled before the patient is moved. Particular care is taken to avoid displacement of the spine or other bones to protect the spinal cord and blood vessels. Proper immobilization should be maintained with a cervical collar and long spine board until stability of the entire spine has been established by appropriate examination and imaging (see Spinal Trauma : Diagnosis). After the initial rapid neurologic assessment, pain should be relieved with a short-acting opioid (eg, fentanyl).
In the hospital, after quick initial evaluation, neurologic findings (GCS and pupillary reaction), BP, pulse, and temperature should be recorded frequently for several hours because any deterioration demands prompt attention. Serial GCS and CT results stratify injury severity, which helps guide treatment (see Table: Management of Traumatic Brain Injury Based on Severity of Injury).
Management of Traumatic Brain Injury Based on Severity of Injury
The cornerstone of management for all patients is maintenance of adequate ventilation, oxygenation, and brain perfusion to avoid secondary brain insult. Aggressive early management of hypoxia, hypercapnia, hypotension, and increased ICP helps avoid secondary complications. Bleeding from injuries (external and internal) is rapidly controlled, and intravascular volume is promptly replaced with crystalloid (eg, 0.9% saline) or sometimes blood transfusion to maintain cerebral perfusion. Hypotonic fluids (especially 5% D/W) are contraindicated because they contain excess free water, which can increase brain edema and ICP.
Other complications to check for and to prevent include hyperthermia, hyponatremia, hyperglycemia, and fluid imbalance.
Injury is mild (by GCS score) in 80% of patients who have TBI and present to an emergency department. If there is brief or no loss of consciousness and if patients have stable vital signs, a normal head CT scan, and normal mental and neurologic function (including resolution of any intoxication), they may be discharged home provided family members or friends can observe them closely for an additional 24 h. These observers are instructed to return patients to the hospital if any of the following develop:
Patients who have had loss of consciousness or have any abnormalities in mental or neurologic function and cannot be observed closely after discharge are generally observed in the emergency department or overnight in the hospital, and follow-up CT may be done in 8 to 12 h if symptoms persist. Patients who have no neurologic changes but minor abnormalities on head CT (eg, small contusions, small subdural hematomas with no mass effect, or punctuate or small traumatic subarachnoid hemorrhage) may need only a follow-up CT within 24 h. With a stable CT and normal neurologic examination results, these patients may be discharged home.
(See also the practice guideline of the Brain Trauma Foundation of the American Association of Neurological Surgeons Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents.) Injury is moderate in 10% of patients who have TBI and present to an emergency department. They often do not require intubation and mechanical ventilation (unless other injuries are present) or ICP monitoring. However, because deterioration is possible, these patients should be admitted and observed even if head CT is normal.
Injury is severe in 10% of patients who have TBI and present to an emergency department. They are admitted to a critical care unit. Because airway protective reflexes are usually impaired and ICP may be increased, patients are intubated endotracheally while measures are taken to avoid increasing ICP. Close monitoring using the GCS and pupillary response should continue, and CT is repeated, particularly if there is an unexplained ICP rise.
Treatment principles for patients with increased ICP include
Rapid sequence orotracheal intubation
Monitoring of ICP and CPP
Ongoing sedation as needed
Maintaining euvolemia and serum osmolality of 295 to 320 mOsm/kg
For intractable increased ICP, possibly CSF drainage, temporary hyperventilation, decompressive craniotomy, or pentobarbital coma
Patients with TBI who require airway support or mechanical ventilation undergo rapid sequence oral intubation (using paralysis) rather than awake nasotracheal intubation (see Overview of Respiratory Failure), which can cause coughing and gagging and thereby raise the ICP. Drugs are used to minimize the ICP increase when the airway is manipulated—eg, lidocaine 1.5 mg/kg IV 1 to 2 min before giving the paralytic. Etomidate is an excellent induction agent because it has minimal effects on BP; IV dose in adults is 0.3 mg/kg (or 20 mg for an average-sized adult) and in children is 0.2 to 0.3 mg/kg. An alternative, if hypotension is absent and unlikely, is propofol 0.2 to 1.5 mg/kg IV. Succinylcholine 1.5 mg/kg IV is typically used as a paralytic.
Pulse oximetry and ABGs (if possible, end-tidal CO2) should be used to assess adequacy of oxygenation and ventilation. The goal is a normal Paco2 level (38 to 42 mm Hg). Prophylactic hyperventilation (Paco2 25 to 35 mm Hg) is no longer recommended. The lower Paco2 reduces ICP by causing cerebral vasoconstriction, but this vasoconstriction also decreases cerebral perfusion, thus potentiating ischemia. Therefore, hyperventilation (target Paco2 of 30 to 35 mm Hg) is used only during the first several hours and if ICP is unresponsive to other measures.
In patients with severe TBI who cannot follow simple commands, especially those with an abnormal head CT, ICP and CPP monitoring (see Monitoring and Testing the Critical Care Patient : Intracranial Pressure Monitoring) and control are recommended. The goal is to maintain ICP at < 20 mm Hg and CPP as close as possible to 60 mm Hg. Cerebral venous drainage can be enhanced (thus lowering ICP) by elevating the head of the bed to 30° and by keeping the patient’s head in a midline position. If needed, a ventricular catheter can be inserted for CSF drainage to lower the ICP. A recent multicenter study found no difference in TBI recovery with ICP treatment directed by an ICP monitor versus care directed by clinical and CT findings. However, interpretation of these findings is controversial, in part because care was provided in settings that differ from those in the US, limiting extrapolation of results.
Preventing agitation, excessive muscular activity (eg, due to delirium), and pain can also help prevent increases in ICP. For sedation, propofol is often used in adults (contraindicated in children) because it has quick onset and very brief duration of action; dose is 0.3 mg/kg/h continuous IV infusion, titrated gradually upward as needed (up to 3 mg/kg/h). An initial bolus is not used. The most common adverse effect is hypotension. Prolonged use at high doses can cause pancreatitis. Benzodiazepines (eg, midazolam, lorazepam) can also be used for sedation, but they are not as rapidly acting as propofol and individual dose-response can be hard to predict. Antipsychotics can delay recovery and should be avoided if possible. Rarely, paralytics may be needed; if so, adequate sedation must be ensured. Opioids are often needed for adequate pain control.
Patients should be kept euvolemic and iso-osmolar or slightly hyperosmolar (target serum osmolality 295 to 320 mOsm/kg). To control ICP, recent studies have found that hypertonic saline solution (usually 2% to 3%) is a more effective osmotic agent than mannitol. It is given as a bolus of 2 to 3 mL/kg IV as needed or as a continuous infusion of 1 mL/kg/h. Serum Na level is monitored and kept ≤ 155 mEq/L. Osmotic diuretics (eg, mannitol) given IV are an alternative to lower ICP and maintain serum osmolality. However, they should be reserved for patients whose condition is deteriorating or used preoperatively for patients with hematomas. Mannitol 20% solution is given 0.5 to 1 g/kg IV (2.5 to 5 mL/kg) over 15 to 30 min and repeated in a dose ranging from 0.25 to 0.5 g/kg (1.25 to 2.5 mL/kg) given as often as needed (usually q 6 to 8 h); it lowers ICP for a few hours. Mannitol must be used cautiously in patients with severe coronary artery disease, heart failure, renal insufficiency, or pulmonary vascular congestion because mannitol rapidly expands intravascular volume. Because osmotic diuretics increase renal excretion of water relative to Na, prolonged use of mannitol may also result in water depletion and hypernatremia. Furosemide 1 mg/kg IV is also helpful to decrease total body water, particularly when the transient hypervolemia associated with mannitol is to be avoided. Fluid and electrolyte balance should be monitored closely while osmotic diuretics are used.
When increased ICP is refractory to other interventions, decompressive craniotomy can be considered. For this procedure, a bone flap is removed (to be replaced later), and duraplasty is done to allow outward brain swelling.
A more involved and currently less popular option for intractable increased ICP is pentobarbital coma. Coma is induced by giving pentobarbital 10 mg/kg IV over 30 min, 5 mg/kg/h for 3 h, then 1 mg/kg/h maintenance infusion. The dose may be adjusted to suppress bursts of EEG activity, which is continuously monitored. Hypotension is common and managed by giving fluids and, if necessary, vasopressors.
Therapeutic systemic hypothermia has not proved helpful. Corticosteroids are not useful to control ICP and are not recommended; they were associated with a worse outcome in a previous multinational study. A variety of neuroprotective agents are being studied, but thus far, none has demonstrated efficacy in clinical trials.
Seizures can worsen brain damage and increase ICP and therefore should be treated promptly. In patients with significant structural injury (eg, larger contusions or hematomas, brain laceration, depressed skull fracture) or a GCS score < 10, a prophylactic anticonvulsant should be considered. If phenytoin is used, a loading dose of 20 mg/kg IV is given (at a maximum rate of 50 mg/min to prevent cardiovascular adverse effects such as hypotension and bradycardia). The starting maintenance IV dose for adults is 2 to 2.7 mg/kg tid; children require higher doses (up to 5 mg/kg bid for children < 4 yr). Serum levels should be measured to adjust the dose. Duration of treatment depends on the type of injury and EEG results. If no seizures develop within 1 wk, anticonvulsants should be stopped because their value in preventing future seizures is not established. Newer anticonvulsants are under study. Fosphenytoin, a form of phenytoin that has better water solubility, is being used in some patients without central venous access because it decreases the risk of thrombophlebitis when given through a peripheral IV. Dosing is the same as for phenytoin. Levetiracetam is used increasingly, particularly in patients with liver disorders.
Aligned closed fractures require no specific treatment. Depressed fractures sometimes require surgery to elevate fragments, manage lacerated cortical vessels, repair dura mater, and debride injured brain. Open fractures may require surgical debridement unless there is no CSF leak and the fracture is not depressed by greater than the thickness of the skull. Use of antibiotic prophylaxis is controversial because of limited data on its efficacy and the concern that it promotes drug-resistant strains.
Intracranial hematomas may require urgent surgical evacuation to prevent or treat brain shift, compression, and herniation; hence, early neurosurgical consultation is mandatory. However, not all hematomas require surgical removal. Small intracerebral hematomas rarely require surgery. Patients with small subdural hematomas can often be treated without surgery. Factors that suggest a need for surgery include a midline brain shift of > 5 mm, compression of the basal cisterns, and worsening neurologic examination findings. Chronic subdural hematomas may require surgical drainage but much less urgently than acute subdural hematomas. Large or arterial epidural hematomas are treated surgically, but small epidural hematomas that are thought to be venous in origin can be followed with serial CT.
When neurologic deficits persist, rehabilitation is needed. Rehabilitation is best provided through a team approach that combines physical, occupational, and speech therapy, skill-building activities, and counseling to meet the patient’s social and emotional needs (see also Rehabilitation for Other Disorders : Brain injury). Brain injury support groups may provide assistance to the families of brain-injured patients.
For patients whose coma exceeds 24 h, 50% of whom have severe persistent neurologic sequelae, a prolonged period of rehabilitation, particularly in cognitive and emotional areas, is often required. Rehabilitation services should be planned early.
TBI can cause a wide variety of neurologic symptoms, sometimes even in the absence of detectable structural brain damage on imaging studies.
Follow assessment (trauma assessment and stabilization, GCS scoring, rapid and focussed neurologic examination) with a more detailed neurologic examination when the patient is stable.
Obtain neuroimaging (usually CT) acutely if patients have more than transiently impaired consciousness, GCS score < 15, focal neurologic findings, persistent vomiting, seizures, a history of loss of consciousness, clinically suspected fractures, and possibly other findings.
Most patients can be discharged home if TBI is mild; they can be observed at home if neuroimaging (if indicated) is normal and neurologic examination is normal.
Admit patients with severe TBI to a critical care unit and, to avoid secondary brain insult, treat them aggressively to maintain adequate ventilation, oxygenation, and brain perfusion.
Treat increased ICP usually with rapid sequence intubation, ICP monitoring, sedation, maintenance of euvolemia and normal serum osmolality, and sometimes surgical interventions (eg, CSF drainage, decompressive craniotomy).
Treat some lesions surgically (eg, large or arterial epidural hematomas, intracranial hematomas with midline brain shift of > 5 mm, compression of the basal cisterns, worsening neurologic examination findings).