Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Diagnosis is suspected based on history and physical examination 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 United States, as in much of the world, TBI is a common cause of death and disability.
Causes of TBI include
Falls (especially in older adults and young children)
Motor vehicle accidents and other transportation-related causes (eg, bicycle accidents, vehicles colliding with pedestrians)
Physical assault
Sports activities (eg, sports-related concussion)
Pathology of Traumatic Brain Injury
Injury from head trauma may be gross or microscopic, depending on the mechanism and forces involved. Patients with less severe injuries may have no gross structural damage. Clinical sequelae vary markedly in severity and consequences.
Injuries are commonly categorized as open or closed.
Open head 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 head 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 to this type of injury. Axons, blood vessels, or both can be sheared or torn, resulting in diffuse axonal injury. 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
Disorder | Clinical Findings | Diagnosis |
|---|---|---|
Concussion | Transient mental status alteration (eg, loss of consciousness or memory) | Based on clinical findings CT: By definition, no acute intracranial hemorrhage, lesions, or contusion present; there may be nondisplaced or minimally displaced linear skull fractures |
Brain contusion | Widely variable degrees of neurologic dysfunction or normal function | CT: Hyperdensities resulting from punctate hemorrhages of varied sizes |
Diffuse axonal injury | Loss of consciousness lasting > 6 and < 8hours but no focal deficits or motor posturing | Based on clinical findings CT: At first, may be normal or show small hyperdensities (microhemorrhages) in corpus callosum, centrum semiovale, basal ganglia, or brain stem MRI: Multiple small microhemorrhages in deep white matter or subcortical areas and brain stem |
Epidural hematoma | Headache, impaired consciousness within hours, sometimes with a lucid interval Herniation typically causing contralateral hemiparesis and ipsilateral pupillary dilation | CT: Hyperdensity in epidural space, classically lenticular-shaped and located over the middle meningeal artery (temporal fossa) due to a temporal bone fracture |
Acute subdural hematoma | Typically, acute neurologic dysfunction, which may be focal, nonfocal, or both With small hematomas, normal function possible | CT: Hyperdensity in subdural space, classically crescent-shaped Degree of midline shift important |
Chronic subdural hematoma | Gradual headache, somnolence, confusion, sometimes with focal deficits or seizures | CT: Hypodensity in subdural space (abnormality is isodense during subacute transition from hyperdense to hypodense) |
Subarachnoid hemorrhage | Typically, normal neurologic examination Occasionally, acute neurologic dysfunction | CT: Hyperdensity within subarachnoid space on the surface of the brain; often lining the sulci |
Basilar skull fracture | Leakage of cerebrospinal fluid (CSF) from the nose or ear Blood behind the tympanic membrane (hemotympanum) or in the external ear Ecchymosis behind the ear (Battle sign) or around the eye (raccoon eyes) | CT: Usually visible |
Concussion
Concussion (see also Sports-Related Concussion) is defined as a traumatically induced transient and reversible posttraumatic alteration in mental status (eg, loss of consciousness or memory, confusion) lasting from seconds to minutes and sometimes several hours. It is classified as a type of mild TBI.
Gross structural brain lesions and serious neurologic residua are not part of concussion, although temporary disability can result from symptoms (such as nausea, headache, dizziness, memory disturbance, and difficulty concentrating [postconcussion syndrome]), which usually resolve within weeks. However, it is thought that multiple concussions may lead to chronic traumatic encephalopathy, which results in severe brain dysfunction.
Brain contusions
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; surgery may be required.
Diffuse axonal injury
Diffuse axonal injury (DAI) occurs when rotational deceleration causes shear-type forces that result in generalized, widespread disruption of axonal fibers and myelin sheaths. In some cases, DAI lesions can result from minor head trauma. Gross structural lesions are not part of DAI, but small petechial hemorrhages in the white matter are often observed on CT (although MRI may be more sensitive) and on histopathologic examination.
DAI is sometimes defined clinically as a loss of consciousness lasting > 6 hours and < 8 hours in the absence of a specific focal lesion (1).
Edema from the injury often increases ICP, leading to various manifestations.
DAI is typically the underlying injury in abusive head trauma.
Hematomas
Hematomas (collections of blood in or around the brain) can occur with open or closed injuries and may be
Epidural
Intracerebral (intraparenchymal)
Subdural
Subarachnoid hemorrhage (SAH—bleeding into the subarachnoid space) is common in traumatic brain injury (TBI), although the appearance on CT is not usually the same as aneurysmal SAH. Blood from SAH secondary to TBI typically accumulates in the cerebral convexities, whereas aneurysmal SAH is predominantly centered deep in the basal cisterns or deep within the Sylvian fissure.
Subdural hematomas are collections of blood between the dura mater and the arachnoid mater. Acute subdural hematomas arise from laceration of cortical veins or avulsion of bridging veins between the cortex and dural sinuses.
Acute subdural hematomas often occur in patients with
Head trauma caused by falls or motor vehicle accidents
Underlying cerebral contusions
A contralateral epidural hematoma
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 both compression and swelling occur, mortality and morbidity can be high.
A chronic subdural hematoma may appear and cause symptoms gradually over several weeks after trauma. Chronic subdural hematomas occur more often in patients with alcohol use disorder and older patients (especially in those taking antiplatelet or anticoagulant medications or in those with brain atrophy). Older 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 1 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.
Skull fractures
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.
Most patients with simple linear fractures and no neurologic impairment are not at high risk of brain injuries, but patients with any fracture associated with neurologic impairment are at increased risk of intracranial hematomas.
Skull fractures that involve special risks include
Depressed fractures: Highest risk of tearing the dura, damaging the underlying brain, or both
Frontal bone fractures: Risk of frontal sinus violation, which may lead to higher risks of long-term mucocele and meningitis development due to an unrecognized cerebrospinal fluid (CSF) fistula
Temporal bone fractures that cross the area of the middle meningeal artery: Risk of epidural hematoma
Fractures that cross 1 of the major dural sinuses: May cause significant hemorrhage and venous epidural or venous subdural hematoma. Injured venous sinuses can later thrombose and cause cerebral infarction
Fractures of the occipital bone and base of the skull (basilar bones): Indicate a high-intensity impact, because these bones are thick and strong, and meaningfully increase risk of brain injury (eg, cerebral contusions and hematomas). 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. Basilar skull fractures may also lacerate the dura and cause CSF leakage into the ear, nose, or throat.
Fractures that involve the carotid canal: Can result in carotid artery dissection
Fractures in infants: Risk of meninges becoming trapped in a linear skull fracture of the parietal bone with subsequent development of a leptomeningeal cyst and expansion of the original fracture (growing fracture)
Pathology reference
1. Mesfin FB, G N, Shapshak AH, et al: Diffuse Axonal Injury. Treasure Island, FL. StatPearls Publishing, 2024
Pathophysiology of Traumatic Brain Injury
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.
Traumatic brain 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 intracranial pressure (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 calcium, free radicals, and cytokines), causing further cell damage, further edema, and further increases in ICP. Systemic complications from trauma (eg, hypotension from hemorrhage or hypoxia from pulmonary injuries) 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 (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. Excessive ICP can also cause short-term and long-term autonomic dysfunction that can result in significant hemodynamic disturbances that are particularly dangerous in patients with polytrauma and other internal organ injuries, fluid depletion, electrolyte imbalance, coagulopathy, hypotension, and anemia from acute blood loss.
Injury to the hypothalamus, subfornical organ, and nucleus tractus solitarius, which regulate the overall sympathetic tone, blood flow circulation, and baroreflex response, can lead to profound changes in cardiac and renal function. Hypothalamic dysfunction affects the hypothalamic-pituitary-adrenal axis, causing hemodynamic instability, hypertension, and tachycardia from a sympathetic "storm" that upregulates cardiac contractility and induces fluid retention in the kidney. These changes can subsequently cause acute kidney injury (AKI) and Takotsubo cardiomyopathy (sometimes termed neurogenic stunned myocardium, atypical Takotsubo cardiomyopathy, or stress cardiomyopathy), which manifests as acute systolic heart failure. These systemic changes can significantly increase inpatient mortality during the first few weeks after injury in fragile and susceptible polytrauma patients if unrecognized or undertreated outside an intensive care setting.
Hyperemia and increased brain blood flow may result from concussive injury in adolescents or children.
Second-impact syndrome is rare and is defined by symptoms (eg, altered level of consciousness, confusion, appearance of being stunned) that occur when there is a second traumatic insult before complete recovery from a previous concussion (1). The second traumatic insult could be mild. second-impact syndrome occurs because of a sudden increased ICP from malignant cerebral edema (rapid neurological deterioration due to the effects of space-occupying cerebral edema). The exact pathophysiology of this disease is still being debated, but the leading hypothesis holds that a loss of autoregulation of cerebral blood flow leads to vascular engorgement, increased ICP, and herniation.
Pathophysiology reference
1. Cantu RC: Second-impact syndrome. Clin Sports Med 17(1):37-44, 1998. doi: 10.1016/s0278-5919(05)70059-4
Symptoms and Signs of Traumatic Brain Injury
Initially, most patients with moderate or severe traumatic brain injury (TBI) lose consciousness (usually for seconds or minutes), although some patients with minor injuries have only confusion or amnesia (amnesia is usually retrograde, which means 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.
Symptoms of specific types of TBI
Symptoms of various types of TBI 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
Focal neurologic deficits (eg, hemiparesis)
Pupillary dilation with loss of light reactivity in such patients usually indicates herniation. Some patients who have an epidural hematoma lose consciousness, then have a transient lucid interval, and then gradual neurologic deterioration.
Acute subdural hematomas are usually associated with alterations in orientation, level of arousal, and/or cognition. They are commonly associated with increased intracranial pressure (ICP) even when small due to underlying cerebral contusions and edema. Symptoms include
Headache
Seizures
Hemiparesis
Symptoms of increased ICP
Pupillary asymmetry, abnormal brain stem reflexes, and coma from brain stem compression due to uncal herniation
Intracerebral hematomas and contusions can cause focal neurologic deficits such as hemiparesis, progressive decrease in consciousness, or both.
Progressive decrease in consciousness may result from anything that increases intracranial pressure, or ICP (eg, hematoma, edema, hyperemia).
Autonomic dysfunction from injury to the hypothalamus and other vital subcortical structures can cause
Sympathetic hyperactivity with hypertension and tachycardia
Neurogenic (Takotsubo) cardiomyopathy with ischemic changes and decreased cardiac function
Acute kidney injury with deterioration of renal function
Increased ICP sometimes causes vomiting, but vomiting is nonspecific. Markedly increased ICP classically manifests as a combination of the following (called the Cushing triad):
Hypertension (usually with increased pulse pressure)
Bradycardia
Respiratory depression
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 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 the following:
Leakage of CSF from the nose or throat (CSF rhinorrhea) or into the middle ear (CSF otorrhea)
Blood behind the tympanic membrane (hemotympanum) or in the external ear canal if the tympanic membrane has ruptured
Ecchymosis behind the ear (Battle sign) or in the periorbital area (raccoon eyes)
Loss of smell and hearing, which is usually immediate, although these losses will 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 a step-off deformity.
© Springer Science+Business Media
© Springer Science+Business Media
© Springer Science+Business Media
Chronic subdural hematoma may manifest with increasing daily headache, fluctuating drowsiness or confusion (which may mimic early dementia), mild-to-moderate hemiparesis or other focal neurologic deficits, and/or seizures.
Diagnosis of Traumatic Brain Injury
Initial rapid trauma assessment
Neurologic examination
Glasgow Coma Scale
CT
Initial measures
An initial overall assessment of injuries should be done (see Approach to the Trauma Patient: Evaluation and Treatment). Airway adequacy and breathing are assessed. Diagnosis and treatment of TBI occur simultaneously in seriously injured patients (1).
A rapid, focused neurologic evaluation is also part of the initial assessment; it includes assessment of the components of the Glasgow Coma Scale (GCS) 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 minutes initially, then every 1 hour after stabilization). Subsequent improvement or deterioration helps estimate injury severity and prognosis.
The Glasgow Coma Scale (GCS—see table Glasgow Coma Scale) is a reproducible scoring system 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 GSC scores are associated with better recovery (2). By convention, the severity of head injury is initially defined by the GCS:
13 to 15 is mild TBI
9 to 12 is moderate TBI
3 to 8 is severe TBI
Glasgow Coma Scale*
Area Assessed | Response | Points |
|---|---|---|
Eye opening | Open spontaneously | 4 |
Open to verbal command | 3 | |
Open in response to pain applied to the limbs or sternum | 2 | |
None | 1 | |
Verbal | Oriented | 5 |
Disoriented, but able to answer questions | 4 | |
Inappropriate answers to questions; words discernible | 3 | |
Incomprehensible speech | 2 | |
None | 1 | |
Motor | Obeys commands | 6 |
Responds to pain with purposeful movement | 5 | |
Withdraws from pain stimuli | 4 | |
Responds to pain with abnormal flexion (decorticate posture) | 3 | |
Responds to pain with abnormal (rigid) extension (decerebrate posture) | 2 | |
None | 1 | |
* Combined scores ≤ 8 are typically regarded as coma. | ||
Adapted from Teasdale G, Jennett B: Assessment of coma and impaired consciousness. A practical scale. Lancet 2:81–84; 1974. | ||
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.
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.
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).
Pearls & Pitfalls
|
Modified Glasgow Coma Scale for Infants and Children
Area Assessed | Infants | Children | Score* |
|---|---|---|---|
Eye opening | Open spontaneously | Open spontaneously | 4 |
Open in response to verbal stimuli | Open in response to verbal stimuli | 3 | |
Open in response to pain only | Open in response to pain only | 2 | |
No response | No response | 1 | |
Verbal response | Coos and babbles | Oriented, appropriate | 5 |
Irritable cries | Confused | 4 | |
Cries in response to pain | Inappropriate words | 3 | |
Moans in response to pain | Incomprehensible words or nonspecific sounds | 2 | |
No response | No response | 1 | |
Motor response† | Moves spontaneously and purposefully | Obeys commands | 6 |
Withdraws to touch | Localizes painful stimulus | 5 | |
Withdraws in response to pain | Withdraws in response to pain | 4 | |
Responds to pain with decorticate posturing (abnormal flexion) | Responds to pain with decorticate posturing (abnormal flexion) | 3 | |
Responds to pain with decerebrate posturing (abnormal extension) | Responds to pain with decerebrate posturing (abnormal extension) | 2 | |
No response | No response | 1 | |
* Score ≤ 12 suggests a severe head injury. Score ≤ 8 suggests the possible need for intubation and ventilation as well as the need for intracranial pressure monitoring. | |||
† If the patient is intubated, unconscious, or preverbal, the most important part of this scale is motor response. This section should be carefully evaluated. | |||
Adapted from Davis RJ et al: Head and spinal cord injury. In Textbook of Pediatric Intensive Care, edited by MC Rogers. Baltimore, Williams & Wilkins, 1987; James H, Anas N, Perkin RM: Brain Insults in Infants and Children. New York, Grune & Stratton, 1985; and Morray JP, Tyler DC, Jones TK, et al: Coma scale for use in brain-injured children. Critical Care Medicine 12:1018–1020, 1984. doi: 10.1097/00003246-198412000-00002; and Carney N, Totten AM, O'Reilly C, et al: Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery 80(1):6-15. doi: 10.1227/NEU.0000000000001432. | |||
Complete clinical evaluation
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 abusive head trauma. Funduscopic examination in adults may disclose traumatic retinal detachment and/or absence of retinal venous pulsations due to elevated intracranial pressure (ICP), but examination may be normal despite brain injury.
Concussion is diagnosed when immediate and transient alterations in brain function occur after mechanical force trauma, and symptoms are not explained by brain injury seen on neuroimaging (3).
Diffuse axonal injury (DAI) is suspected when loss of consciousness exceeds 6 hours but is less than 8 hours in duration (4) and microhemorrhages are seen on MRI, although initial CT scans show no clear signs of ICH.
Diagnosis of other types of TBI is made by CT or MRI.
Neuroimaging
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 approach against unnecessary expense and the possible risk of radiation-related adverse effects from CT in younger patients.
This CT scan shows a crescent-shaped opacity overlying brain tissue, characteristic of a subdural hematoma. There is also mass effect, with ventricular compression and midline shift.
Cavallini James/BSIP/SCIENCE PHOTO LIBRARY
Classic crescent-shaped hyperdensity extending across suture lines.
© 2017 Elliot K. Fishman, MD.
Classic lentiform (lens)-shaped hyperdensity that does not extend across suture lines.
© 2017 Elliot K. Fishman, MD.
Classic lentiform (lens)-shaped hyperdensity that does not extend across suture lines.
© 2017 Elliot K. Fishman, MD.
CT scan shows an epidural hematoma (opacity at bottom right).
Cavallini James/BSIP/SCIENCE PHOTO LIBRARY
This CT scan shows a crescent-shaped opacity overlying brain tissue, characteristic of a subdural hematoma. There is also mass effect, with ventricular compression and midline shift.
Cavallini James/BSIP/SCIENCE PHOTO LIBRARY
Classic crescent-shaped hyperdensity extending across suture lines.
© 2017 Elliot K. Fishman, MD.
Classic lentiform (lens)-shaped hyperdensity that does not extend across suture lines.
© 2017 Elliot K. Fishman, MD.
Classic lentiform (lens)-shaped hyperdensity that does not extend across suture lines.
© 2017 Elliot K. Fishman, MD.
CT scan shows an epidural hematoma (opacity at bottom right).
Cavallini James/BSIP/SCIENCE PHOTO LIBRARY
Although radiographs can detect some skull fractures, they cannot help assess the brain and they delay more definitive brain imaging; thus, plain radiographs are usually not taken.
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 diffuse axonal injury.
CT can show the following:
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 intracranial pressure (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, diffuse axonal injury, and brain stem injury. MRI is usually more sensitive than CT for the diagnosis of very small acute or isodense subacute and isodense chronic subdural hematomas. Magnetic resonance imaging has been viewed as a promising tool for improving outcome prediction after TBI. In a study from the TRACK-TBI Investigators, MRI was found to improve prediction of unfavorable outcome at 3 months after mild TBI (5).
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).
Diagnosis references
1. National Institute for Health and Care Excellence: Head Injury: Assessment and Early Management. NICE guideline [NG232]. Published May 18, 2023. Accessed September 13, 2024.
2. Agarwal N, Iyer SS, Patil V et al: Comparison of admission GCS score to admission GCS-P and FOUR scores for prediction of outcomes among patients with traumatic brain injury in the intensive care unit in India. Acute Crit Care 38(2); 226-233 2023. doi: https://doi.org/10.4266/acc.2023.00570
3. Agarwal N, Thakkar R, Than K: Concussion. American Association of Neurological Surgeons (AANS). Published April 29, 2024. Accessed September 13, 2024.
4. Mesfin FB, G N, Shapshak AH, et al: Diffuse Axonal Injury. Treasure Island, FL. StatPearls Publishing, 2024
5. Ferrazzano PA, Rebsamen S, Field AS, et al: MRI and Clinical Variables for Prediction of Outcomes After Pediatric Severe Traumatic Brain Injury. JAMA Netw Open. 2024;7(8):e2425765. Published 2024 Aug 1. doi:10.1001/jamanetworkopen.2024.25765
Treatment of Traumatic Brain Injury
For mild injuries, observation at home
For moderate and severe injuries, optimization of ventilation, oxygenation, and brain perfusion; treatment of complications (eg, increased intracranial pressure [ICP], seizures, hematomas); and rehabilitation
Multiple noncranial injuries, which are likely with motor vehicle accidents 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 (Glasgow Coma Scale [GCS] and pupillary reaction), blood pressure (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
Severity | GCS Score | Management |
|---|---|---|
Mild | 13–15 | Observation at home |
Moderate | 9–12 | Observation in hospital |
Severe | 3–8 | Rapid sequence intubation Intensive supportive care Monitoring and treatment of increased intracranial pressure as indicated |
GCS = Glasgow Coma Scale. | ||
The cornerstone of management for all patients with traumatic brain injury (TBI) 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 preferably 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.
Mild traumatic brain injury
Patients with mild injury who did not lose consciousness or lost it only briefly and have stable vital signs, a normal head CT scan, and normal mental status and neurologic function (including resolution of any intoxication), may be discharged home, provided family members or friends can observe them closely for an additional 24 hours. These observers are instructed to return patients to the hospital if any of the following develop:
Decreased level of consciousness
Focal neurologic deficits
Worsening headache
Vomiting
Deterioration of mental status (eg, seems confused, cannot recognize people, behaves abnormally)
Seizures
Patients who lost consciousness for longer than a brief moment or have any abnormalities in mental status or neurologic function and/or cannot be observed closely after discharge are usually observed in the emergency department or admitted to the hospital.
Follow-up CT may be done in 8 to 12 hours if symptoms persist. Patients who have no neurologic changes but have minor abnormalities on head CT (eg, small contusions, small subdural hematomas with no mass effect, punctate or small traumatic subarachnoid hemorrhage) may need only a follow-up CT within 24 hours. If CT is stable and neurologic examination results are normal, these patients may be discharged home.
Moderate and severe traumatic brain injury
Patients with moderate injury should be admitted and observed even if head CT is normal. They often do not initially require intubation and mechanical ventilation (unless other injuries are present) or ICP monitoring. Patients may deteriorate and develop additional neurologic changes (eg, worsening mental status or seizures).
Patients with severe injury 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.
Management of patients with severe TBI should be based on information from ICP monitoring, which allows for interventions that reduce in-hospital and 2-week postinjury mortality (1, 2). However, some evidence suggests that use of a combination of clinical and radiographic evaluations alone results in equivalent outcomes (3). Cerebral perfusion pressure (CPP) monitoring has also been recommended as part of management because evidence suggests that it may help decrease 2-week postinjury mortality (4). For all approaches to monitoring, close monitoring using the GCS and pupillary response should continue, and CT is repeated, particularly if there is an unexplained rise in ICP.
Increased intracranial pressure
Treatment principles for patients with increased ICP include
Rapid-sequence orotracheal intubation
Monitoring of ICP and CPP
Sedation as needed
Maintaining euvolemia and serum osmolality of 295 to 320 mOsm/kg (295 to 320 mmol/kg)
For intractable increased ICP, possibly cerebrospinal fluid (CSF) drainage, temporary hyperventilation, decompressive craniotomy, or pentobarbital coma
Rapid-sequence oral intubation (using paralysis) is used rather than awake nasotracheal intubation if patients with TBI require airway support or mechanical ventilation. Nasotracheal intubation can cause coughing and gagging and thereby raise the ICP. Medications for sedation and analgesia are given prior to paralytics to minimize the ICP increase when the airway is manipulated.
Adequacy of oxygenation and ventilation should be assessed using pulse oximetry and arterial blood gases (if possible, end-tidal CO2). 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 for ICP that is unresponsive to other measures.
ICP monitoring and CPP monitoring and control, when used, are recommended for patients with severe TBI who cannot follow simple commands, especially those with an abnormal head CT, as well as for patients with TBI who have a GCS of 3 to 8 after resuscitation (1). However, ICP monitoring has not been shown to consistently decrease mortality (5, 6), but there are data that show a direct correlation between mortality and lower ICP in severe TBI (7).
The goal is to maintain ICP at < 25 (sometimes a cutoff of 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 to drain CSF and thus lower the ICP (3). However, interpretation of these findings is controversial, in part because care was provided in settings that differ from those in the United States, limiting extrapolation of results.
Sedation can be used to prevent agitation, excessive muscular activity (eg, due to delirium), and help mitigate response to pain and thus 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. The most common adverse effect is hypotension. Prolonged use at high doses can cause pancreatitis. Benzodiazepines (eg, midazolam, lorazepam) and dexmedetomidine, which are both preferred over propofol for children, 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. If paralytics are needed to prevent patients from moving or accidentally dislodging medical devices, adequate sedation must be ensured.
Adequate pain control often requires opioids.
Maintaining euvolemia and normal serum osmolality (iso-osmolar or slightly hyperosmolar; target serum osmolality 295 to 320 mOsm/kg [295 to 320 mmol/kg]) is important. To control ICP, hypertonic saline solution (3% or 23.4%) is a more effective osmotic agent than mannitol (8). It is given as a bolus of 2 to 3 mL/kg IV as needed to maintain an ICP of 20 to 25 mmHg or as a continuous infusion of 1 mL/kg/h. Serum sodium level is monitored and kept ≤ 155 mEq/L (155 mmol/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 minutes 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 every 6 to 8 hours); 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 sodium, 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.
Decompressive craniectomy may be considered when increased ICP is refractory to other interventions and sometimes as a primary measure (eg, at the time of surgery to drain a significant hematoma). For craniectomy, a significant portion of the skull is removed en bloc (to be replaced later), and duraplasty is done to allow outward brain swelling. The amount and location of bone removal depends on the injury, but the opening must be sufficient to keep the swelling from compressing brain tissue against the margins of the defect. One study suggested decreased brain herniation and improved mortality rates in patients who undergo a standard trauma craniectomy (12 cm × 15 cm bone flap) compared with a smaller limited craniectomy (6 m × 8 cm bone flap) (9). In a randomized trial comparing craniectomy and medical management, overall mortality at 6 months was reduced after craniectomy, but rates of severe disability and vegetative state were higher, and rate of good functional recovery was similar (10). In a different randomized trial, patients undergoing craniectomy had less time with elevated ICPs and shorter ICU stays when compared to those who stayed in a medical management group; however, 6-month mortality was similar between the 2 groups (11).
Pentobarbital coma is a more involved and currently less popular option for intractable increased ICP. Coma is induced by giving a loading dose of pentobarbital and then a maintenance infusion adjusted to suppress bursts of electroencephalogram (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 in a large multicenter trial (12).
High-dose corticosteroids had previously been advocated to decrease cerebral edema and ICP. However, corticosteroids are not useful to control ICP and are not recommended. In a large randomized, placebo-controlled study, corticosteroids given within 8 hours of TBI increased mortality and severe disability in survivors (13).
A variety of neuroprotective agents have been and are being studied, but thus far, none has demonstrated efficacy in clinical trials.
Seizures
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 antiseizure medication should be considered.
If phenytoin is used, a typical 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). 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 week, antiseizure medications should be stopped because their value in preventing future seizures is not established.
Fosphenytoin, a form of phenytoin that has no cardiac toxicity and 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 commonly used, particularly in patients with liver disorders.
Other critical care issues in TBI
Anemia and thrombocytopenia are common problems in patients who have had a TBI. However, blood transfusions may result in significantly more complications and higher mortality; thus, the threshold for transfusion in patients with TBI should be high—the same as that for other intensive-care patients.
Hyperglycemia predicts increased risk of increased ICP, impaired cerebral metabolism, urinary tract infection, and bacteremia; thus, careful glycemic control has been attempted in patients with a TBI. However, in a randomized controlled trial comparing intensive regimens (to maintain glucose < 80 to 120 mg/dL [4.4 to 6.7 mmol/L]) with traditional regimens (to maintain glucose < 220 mg/dL [12.2 mmol/L]), GCS scores were the same at 6 months, but incidence of hypoglycemic episodes was higher with the intensive regimen (14).
Various degrees of hypothermia have been advocated to improve neurologic recovery by improving neuroprotection and decreasing ICP in the acute period after TBI. However, multiple randomized controlled trials have shown that early (within 2.5 hours), short-term (48 hours postinjury) prophylactic hypothermia does not improve outcomes in patients with severe TBI compared with standard medical treatment, and it increases the risk of coagulopathy and cardiovascular instability (12, 15).
Calcium channel blockers have been used in an attempt to prevent cerebral vasospasm after TBI, to maintain blood flow to the brain, and thereby to prevent further damage. However, a review of randomized controlled trials of calcium channel blockers in patients with acute TBI and traumatic subarachnoid hemorrhage concluded that their effectiveness remains uncertain (16).
Skull fractures
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 (17).
Frontal bone fractures are repaired, especially if there is significant anterior and posterior table displacement (for cosmetic reasons) or CSF leakage into the nose from an underlying dural laceration (18).
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Use of antibiotic prophylaxis is controversial because of limited data on its efficacy and the concern that it promotes drug-resistant strains.
Surgery for intracranial hematomas
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 emergent surgery include
Midline brain shift of > 5 mm
Compression of the basal cisterns
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.
Rehabilitation
When neurologic deficits persist, rehabilitation is needed. Rehabilitation after brain injury 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. Brain injury support groups may provide assistance to the families of brain-injured patients.
For patients whose coma exceeds 24 hours, 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.
Treatment references
1. Carney N, Totten AM, O'Reilly C, et al: Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery 80(1):6–15, 2017. doi: 10.1227/NEU.0000000000001432
2. Alali AS, Fowler RA, Mainprize TG, et al: Intracranial pressure monitoring in severe traumatic brain injury: Results from the American College of Surgeons Trauma Quality Improvement Program. J Neurotrauma 30(20):1737–1746, 2013. doi: 10.1089/neu.2012.2802
3. Chesnut RM, Temkin N, Carney N, et al: A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med 367(26):2471–2481, 2012. doi: 10.1056/NEJMoa1207363
4. Gerber LM, Chiu YL, Carney N, et al: Marked reduction in mortality in patients with severe traumatic brain injury. J Neurosurg 119(6):1583–1590, 2013. doi: 10.3171/2013.8.JNS13276
5. Shafi S, Diaz-Arrastia R, Madden C, et al: Intracranial pressure monitoring in brain-injured patients is associated with worsening of survival. J Trauma 64(2):335-340, 2008. doi: 10.1097/TA.0b013e31815dd017
6. Lane PL, Skoretz TG, Doig G, et al: Intracranial pressure monitoring and outcomes after traumatic brain injury. Can J Surg 43(6):442-448, 2000
7. Kostić A, Stefanović I, Novak V, et al: Prognostic significance of intracranial pressure monitoring and intracranial hypertension in severe brain trauma patients. Med Pregl64(9-10):461-465, 2011
8. Gharizadeh N, Ghojazadeh M, Naseri A, et al: Hypertonic saline for traumatic brain injury: A systematic review and meta-analysis. Eur J Med Res 2022 Nov 20;27(1):254. doi: 10.1186/s40001-022-00897-4
9. Jiang JY, Xu W, Li WP, et al: Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: A multicenter, prospective, randomized controlled study. J Neurotrauma 22(6):623-628, 2005. doi: 10.1089/neu.2005.22.623
10. Hutchinson PJ, Kolias AG, Timofeev IS, et al: Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med 375(12):1119–1130, 2016. doi: 10.1056/NEJMoa1605215
11. Cooper DJ, Rosenfeld JV, Murray L, et al; DECRA Trial Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group: Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 364(16):1493-1502, 2011. doi: 10.1056/NEJMoa1102077. Erratum in: N Engl J Med 365(21):2040, 2011
12. Clifton GL, Valadka A, Zygun D, et al: Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): A randomised trial. Lancet Neurol 10(2):131-139. doi: 10.1016/S1474-4422(10)70300-8
13. Edwards P, Arango M, Balica L, et al: Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet 365(9475):1957–1959, 2005. doi: 10.1016/S0140-6736(05)66552-X
14. Bilotta F, Caramia R, Cernak I, et al: Intensive insulin therapy after severe traumatic brain injury: A randomized clinical trial. Neurocrit Care 9(2):159–166, 2008. doi: 10.1007/s12028-008-9084-9
15. Andrews PJD, Sinclair HL, Rodriguez A, et al: Hypothermia for intracranial hypertension after traumatic brain injury. N Engl J Med 373(25):2403–2412, 2015. doi: 10.1056/NEJMoa1507581
16. Vergouwen MDI, Vermeulen M, Roos YBWEM: Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: A systematic review. Lancet Neurol 5(12):1029–1032, 2006. doi: 10.1016/S1474-4422(06)70582-8
17. Bullock MR, Chesnut R, Ghajar J, et al; Surgical Management of Traumatic Brain Injury Author Group: Surgical management of depressed cranial fractures. Neurosurgery 58(3 Suppl):S56-60, 2006; discussion Si-iv. doi: 10.1227/01.NEU.0000210367.14043.0E
18. Heary RF, Hunt CD, Krieger AJ, et al: Nonsurgical treatment of compound depressed skull fractures. J Trauma 1993 Sep;35(3):441-7. doi: 10.1097/00005373-199309000-00018
Prognosis for Traumatic Brain Injury
In the United States, adults with severe traumatic brain injury (TBI) who are treated have a mortality rate of about 25 to 33% (1). Mortality is lower when Glasgow Coma Scale (GCS) scores are higher. Mortality rates are lower in children. Children overall do better than adults with a comparable injury.
Amnesia may persist and be both retrograde (ie, for events that occurred before the injury) and anterograde (ie, for events following the injury).
Postconcussion syndrome, which commonly follows a moderate or severe concussion, includes persistent 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
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 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 generally 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 months after injury, and almost none recover after 6 months.
Neurologic function may continue to improve for a few years after TBI, most rapidly during the initial 6 months.
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
Good recovery (return to previous level of function)
Moderate disability (capable of self-care)
Severe disability (incapable of self-care)
Vegetative (no cognitive function)
Death
Other prognostic grading systems based on CT findings, such as the Marshall classification system and the more recently developed Rotterdam CT score, can also be used to estimate long-term survival (2, 3).
Over 40% of adults with severe TBI have a good recovery or only moderate disability (4). Occurrence and duration of coma after a TBI are strong predictors of disability. Of patients whose coma exceeds 24 hours, 50% have severe persistent neurologic sequelae, and up to 6% remain in a persistent vegetative state at 6 months. In adults with severe TBI, recovery occurs most rapidly within the initial 6 months. Few patients recover normal neurologic function when a persistent vegetative state lasts for 3 months after injury, and almost none recover after 6 months. 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 months. Hemiparesis and aphasia usually resolve at least partially, except in older patients.
Prognosis references
1. USA Facts: How Common Are Traumatic brain Injuries in the US? Accessed September 11, 2024.
2. Maas AI, Hukkelhoven CW, Marshall LF, et al: Prediction of outcome in traumatic brain injury with computed tomographic characteristics: A comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery 57(6):1173–1182, 2005. doi: 10.1227/01.neu.0000186013.63046.6b
3. Charry JD, Falla JD, Ochoa JD, et al: External validation of the Rotterdam computed tomography score in the prediction of mortality in severe traumatic brain injury. J Neurosci Rural Pract 8(Suppl 1):S23–S26, 2017. doi: 10.4103/jnrp.jnrp_434_16
4. Centers or Disease Control and Prevention: About Potential Effects of a Moderate or Severe TBI. Accessed September 11, 2024.
Key Points
TBI can cause a wide variety of neurologic symptoms, sometimes even in the absence of detectable structural brain damage on imaging studies.
Follow initial assessment (trauma assessment and stabilization, GCS scoring, rapid and focused 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, or possibly other findings.
Discharge most patients home if TBI is mild; they can be observed at home if neuroimaging is normal or not indicated 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).
