Traumatic Brain injury

Author: Spyridoula Tsetsou, MD

Definition

•Traumatic brain injury (TBI) is a broad term that encompasses multiple intracranial processes (including cerebral contusion, epidural hemorrhages, subdural hemorrhages, subarachnoid hemorrhages, skull fractures, diffuse axonal injury, and cerebral edema) that occur secondary to head trauma or if the head experiences a sudden deceleration injury without external trauma resulting in an injury to the brain.¹ TBI is classified depending on the nature, mechanism, and location of injury, as summarized in Tables E1 and E2. The severity is classically assessed by Glasgow Coma Scale (GCS) and further trichotomized as mild TBI (GCS 13 to 15), moderate TBI (GCS 9 to 12), and severe TBI (GCS ≤8).^1-3
•Mild TBI is defined as loss of consciousness <30 min, a Glasgow Coma Scale (GCS) of 13 to 15, and normal imaging.
•Moderate TBI is defined as loss of consciousness for 30 min to 24 h with even longer alteration in consciousness, a GCS of 9 to 12, and may or may not have abnormal imaging.
•Severe TBI is defined as >24 h of loss of consciousness with a GCS of 3 to 8 and prolonged posttraumatic amnesia with normal or abnormal imaging.¹^,²

TABLE E1 Overview of Classification of Traumatic Brain Injury

Mechanism	Blunt		High velocity (MVC)
			Low velocity (fall, assault)
	Penetrating		GSW
			Other (stab wounds, etc.)
	Blast		Explosive devices
Severity	Mild		GCS 14-15
	Moderate		GCS 9-13
	Severe		GCS 3-8
Morphology	Skull fracture	Vault	Linear versus stellate
			Depressed/nondepressed
			Open/closed
		Basilar	With/without CSF
			With/without CN palsy
	Intracranial lesions	Focal	Epidural
			Subdural
			Intracerebral
		Diffuse	Mild concussion
			Classic concussion
			Diffuse axonal injury

CN, Cranial nerve; CSF, cerebrospinal fluid; GCS, Glasgow Coma Scale; GSW, gunshot wound; MVC, motor vehicle collision.

Adapted from Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

TABLE E2 Classification of Traumatic Brain Injury

	Mild	Moderate	Severe
Structural imaging	Normal	Normal or abnormal	Normal or abnormal
Loss of consciousness	>30 min ^a	30 min to 24 h	>24 h
Post-traumatic amnesia	0-1 day	>1 day and >7 days	>7 days
Glasgow Coma Scale score	13-15	9-12	3-8
Abbreviated Injury Scale score: Head	1-2	3	4-6

^aAny alteration in mental state at the time of the accident.

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

Synonyms

TBI
Head injury
Concussion
Intracranial contusion

ICD-10CM CODES
S06.9 X0A		Intracranial injury
S06.1X7A		Traumatic cerebral edema with loss of consciousness of any duration with death due to brain injury prior to regaining consciousness, initial encounter
S06.2X9A		Diffuse traumatic brain injury with loss of consciousness of unspecified duration, initial encounter
S06.300A		Unspecified focal traumatic brain injury without loss of consciousness, initial encounter
S06.305A		Unspecified focal traumatic brain injury with loss of consciousness greater than 24 h with return to preexisting conscious level, initial encounter
S06.309A		Unspecified focal traumatic brain injury with loss of consciousness of unspecified duration, initial encounter
S09.90		Unspecified injury of the head

Epidemiology & Demographics

Traumatic brain injury (TBI) is a leading cause of mortality in the young and elderly worldwide. In the 2022 Centers for Disease Control and Prevention (CDC) surveillance report, suicide, unintentional falls, and motor vehicle accidents (MVAs) caused the majority of TBI-related deaths.⁴

Incidence:

Globally, more than 69 million people suffer from TBI each yr, with North America and Europe showing highest incidence and Southeast Asian and Western Pacific countries experiencing the greatest burden of disease. According to one estimate, up to 4.6 million individuals suffer from TBI in the U.S. and Canada each yr.⁵ In 2014, about 2.87 million emergency department visits, including deaths and hospitalizations, were associated with TBI. The financial burden of TBI has been estimated to be greater than $80 billion/yr in the United States and is approaching $400 billion worldwide in direct and indirect costs.⁶

Prevalence:

In 2016, the global prevalence of TBI was estimated at 55.5 million. From 1990 to 2016, the age-standardized prevalence of TBI increased by 8.4%.⁷

Predominant Sex & Age:

TBI occurs more commonly in males and hospitalizations/deaths are the highest in adults >75 yr of age.⁴

Risk Factors:

•Falls
•Motor vehicle accidents
•Physical violence
•Sport injuries
•Ballistic injuries (gunshot wounds, blast injuries)

Genetics:

TBI and Apo E Ε4 synergistically are associated with a tenfold increased risk for Alzheimer disease. Apo E Ε4 is also associated with larger intracerebral hematomas and greater ischemia after TBI.⁸

Physical Findings & Clinical Presentation

TBI patients present with a spectrum of clinical symptoms (Table E3) including nausea, vomiting, headache, seizures, altered mental status, and/or coma. Stigmata of trauma, including bruises, scalp lacerations, and periorbital or mastoid ecchymosis suggesting skull base fractures, can be telltale signs of underlying traumatic brain injury. The spectrum of TBI is most commonly assessed using the GCS (Table E4), which ranges from 3 to 15 and utilizes eye, motor, and verbal exams (Table E5).

TABLE E3 Symptoms of Mild Traumatic Brain Injury

Physical	Cognitive	Behavior
•Nausea •Vomiting •Dizziness •Headaches •Blurred vision •Increased sensitivity to noise or light •Diminished libido •Disturbed sleep •Quickness to fatigue •Lethargy •Sensory loss	•Decreased attention •Decreased concentration •Problems with perception •Problems with memory •Problems with speech production •Problems with speech comprehension •Executive dysfunction	•Irritability •Quick to anger •Disinhibition •Emotional lability

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

TABLE E4 Glasgow Coma Scale

Response		Points
Speech
Alert, oriented, and conversant		5
Confused, disoriented, but conversant		4
Intelligible words, not conversant		3
Unintelligible sounds		2
No verbalization, even with painful stimulus		1
Eye Opening
Spontaneous		4
To verbal stimuli		3
To painful stimuli		2
None, even with painful stimuli		1
Motor
Follows commands		6
Localizes painful stimulus		5
Withdraws from painful stimulus		4
Flexor posturing with central pain		3
Extensor posturing with central pain		2
No response to painful stimulus		1

Data from Teasdale G, Jennett B: Assessment of coma and impaired consciousness: a practical scale, Lancet 2:81-84, 1974. In Vincent JL et al: Textbook of critical care, ed 8, Philadelphia, 2024, Elsevier.

TABLE E5 Useful Criteria to Assess the Severity of Head Injury ^a

Quantifying the Degree of Head Injury	Glasgow Coma Scale (GCS)	Score
Moderate TBI (GCS 9-13)	Eye Opening
Severe TBI (GCS <8)	Spontaneous	4
Significant head CT:	To speech	3
•Cerebral edema	To pain	2
•Midline shift	None	1
•Subdural/epidural bleeding	Verbal Response
•Open head injury with intracranial air	Oriented	5
	Confused conversation	4
	Inappropriate words	3
	Incomprehensible sounds	2
	None	1
	Best Motor Response
	Obeys commands	6
	Localizes pain	5
	Flexion withdrawal to pain	4
	Abnormal flexion (decorticate)	3
	Extension (decerebrate)	2
	None (flaccid)	1

TBI, Traumatic brain injury.

^aConsultation with other specialists (i.e., neurosurgeon) may be valuable for the orthopedic surgeon unfamiliar with the process of "clearing" the patient’s head injury for ischemic monomelic neuropathy (IMN) fixation.

From Browner B et al: Skeletal trauma: basic science, management, and reconstruction, ed 6, Philadelphia, 2019, Elsevier.

Etiology

•Falls, MVA, suicide, and assaults resulting in direct or indirect head trauma are the most common etiologies, with suicides being the leading cause of TBI-related deaths in the U.S.⁴ (Figs. E1 and E2). In low-income countries, MVA remains the largest cause, whereas falls are the main cause in high-income areas.
•Gunshot wounds are the most prevalent penetrating injuries (Fig. E3), accounting for 35% of deaths from TBI under the age of 45 yr in the United States. Self-inflicted injuries such as nail gun injuries can also lead to penetrating trauma (Fig. E4). Gunshot wounds are the most lethal type of brain injury, with 90% resulting in death.
•The most common mechanisms of pediatric TBI vary according to age. Falls are the leading cause of TBI in children under the age of 14 yr. Children younger than 4 yr of age are injured mainly by falls but are also affected by abusive injuries and motor vehicle accidents. Children 4 to 8 yr of age are injured in falls and motor vehicle accidents but also become more at risk for other transportation-related injuries such as bicycle-related incidents.
•Sports-related TBIs account for roughly one third of all causes of TBI, with higher incidence in males, adolescents, and young adults. Some common sports associated with TBI are football, horse riding, cycling, skateboarding, hockey, water sports, and snow sports.⁹

Figure E1 In This Drawing, a Hammer Blow to the Back of the Head Inflicts a Coup Injury to the Occipital Region and, as is Typical, a More Extensive Contrecoup Injury to the Inferior Surface of the Frontal and Anterior Tips of the Temporal Lobes

(From Kaufman DM et al: Kaufman’s clinical neurology for psychiatrists, ed 9, Philadelphia, 2023, Elsevier.)

Figure E2 Meningeal Arterial Bleeding, Which Usually Results from a Blow Forceful Enough to Fracture the Skull, Causes an Epidural Hematoma

In Contrast, Venous Bleeding, Usually Slower and Under Less Pressure, Causes Subdural Hematoma. Ruptured Aneurysms and Head Trauma Often Cause Subarachnoid Hemorrhage (SAH). In SAH, Blood Spreads Within the Subarachnoid Space over the Convexities, Between the Gyri, into the Interhemispheric Fissure, and Down into the Spinal Canal.

(From Kaufman DM et al: Kaufman’s clinical neurology for psychiatrists, ed 9, Philadelphia, 2023, Elsevier.)

Figure E3 Image of a gunshot wound to the head-a penetrating injury.

The bullet leaves a path of destructions marked by blood, bone, and bullet fragments. Brain tissue around the bullet path is also damaged by the propagating pressure wave. However, this is not visible on computed tomography (axial computed tomography).

(From Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.)

Figure E4 Another Form of Penetrating Injury is Shown on This Anteroposterior x-Ray of the Skull, with Two Nails from a Nail Gun Stuck in the Skull and Penetrating the Right Frontal Lobe

This Patient was Neurologically Intact on Presentation. The Difficulty in Such a Case is that Bleeding Can Occur Deep in the Brain When the Nails are Removed. This Patient was Also at High Risk for Developing Pseudoaneurysm Later on.

(From Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.)

Diagnosis ⬆ ⬇

Differential Diagnosis

Differential diagnosis of TBI is quite limited; however, there are several considerations and diagnoses that should be considered, especially regarding mechanism of fall or circumstances that led to an MVA. Prodromes, signs, and symptoms should be looked for, followed by detailed workup as needed.

Workup

TBI workup is always a part of the advanced trauma life support (ATLS) protocol. Primary and secondary survey followed by imaging studies constitutes the standardized approach to TBI. Focused TBI workup includes:

•History: Including timing of injury, duration of loss of consciousness if applicable, events leading up to the injury, mechanism of injury, seizures (if any), comorbidities (Fig. E5), use of anticoagulants and antiplatelet agents (requires reversal in the event of intracranial blood on imaging).
•Neurologic examination: Glasgow Coma Scale, cranial nerves, motor/sensory exam. Assess for scalp lacerations, specifically overlying a skull fracture as well as cerebrospinal fluid (CSF) otorrhea or rhinorrhea.
•Computed tomography (CT) imaging of the head if there is a significant history of impact to the head, polytrauma, positive loss of consciousness, or stigmata of trauma to the head. Factors to consider regarding the need for CT imaging in head-injured patients are described in Table E6.

Figure E5 Assessment of the Behavioral and Emotional Changes after Traumatic Brain Injury (TBI)

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

TABLE E6 Factors to Consider Regarding the Need for Computed Tomography in Head-Injured Patients

Indications for urgent CT include the following:
•Evidence of skull fracture-basal, depressed, or open
•Abnormal results of neurologic examination
•Seizure
•Vomiting more than once
•High-risk mechanism (e.g., ejection from vehicle; injury to pedestrian or cyclist vs. car occupant)
•Decreasing GCS score or persistently decreased GCS score below 15
•Indications for lower threshold for CT scan include the following:
1. 1.Age >60 yr
2. 2.Persistent anterograde amnesia
3. 3.Retrograde amnesia >30 min
4. 4.Coagulopathy
5. 5.Fall >5 stairs or >3 ft
6. 6.Intoxication (examination unreliable)
7. 7.LOC >30 min
8. 8.Mechanism and location of injury
9. 9.Social factors (e.g., abusive situation at home, language barriers precluding an accurate history)

CT, Computed tomography; GCS, Glasgow Coma Scale; LOC, loss of consciousness.

From Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

Laboratory Tests

•Basic labs including CBC, basic metabolic panel, prothrombin time, activated partial thromboplastin time, urine drug screen, and ethanol blood level.
•Thromboelastography (TEG) or rotational thromboelastometry (ROTEM).
•Consider tests for platelet function analysis for unknown antiplatelet use.
•Consider cardiac evaluation (troponin, ECG, and echocardiography) in patients with history pointing to a cardiac event leading to TBI.
•Various biomarkers have been investigated so far, with glial fibrillary acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase L1 (UCH L1) having the higher diagnostic accuracy for intracranial injury prediction.¹⁰

Imaging Studies (Table E7

CT scan is the cornerstone of imaging modalities for head trauma; however, it is not always necessary. Patients over the age of 16 with minimal head injury (i.e., no history of loss of consciousness, amnesia, and confusion), not on blood thinners, and without associated seizure generally do not need a CT scan. Canadian CT head rules (Box E1) for patients with GCS 13 to 15 who do have history of loss of consciousness, amnesia, and/or confusion are a useful guide in determining utility of obtaining a CT scan. If any of these risk factors are present, a CT scan of the head should be performed.

CSF, Cerebrospinal fluid; CT, computed tomography; GCS, Glasgow Coma Scale.

BOX E1 Clinical Decision Rules for Neuroimaging in Adults With Mild Traumatic Brain Injury Canadian Computed Tomography Head Rule (CCHR)

High-Risk Injury (May Require Neurologic Intervention)

•GCS score <15 at 2 h after injury
•Suspected open or depressed skull fracture
•Any sign of basal skull fracture (hemotympanum, raccoon eyes, CSF otorrhea or rhinorrhea, Battle sign)
•Vomiting >2 episodes
•Age >65 yr

Medium-Risk Injury (May Have Important Brain Injury on CT)

•Amnesia before impact ≤30 min
•Dangerous mechanism (pedestrian struck by vehicle, occupant ejected from vehicle, fall from elevation >3 feet [five stairs])

New Orleans Criteria (NOC)

•Headache
•Vomiting
•Age >60 yr
•Drug or alcohol intoxication
•Persistent anterograde amnesia
•Trauma above the clavicle
•Seizure

Nexus II Criteria

•Evidence of significant skull fracture
•Scalp hematoma
•Neurologic deficit
•Altered level of alertness
•Abnormal behavior
•Coagulopathy
•Persistent vomiting
•Age >65 yr

From Walls RM et al: Rosen’s emergency medicine, concepts and clinical practice, ed 10, Philadelphia, 2023, Elsevier.

TABLE E7 Comparison of Head Imaging Modalities

	Computed Tomography Scans	Magnetic Resonance Imaging	Angiography	Skull Radiography
Advantages	Fast Patient accessible for monitoring Defines acute hemorrhages, mass effects, bone injuries, hydrocephalus, intraventricular blood, edema	Defines contusions and pericontusion edema, posttraumatic ischemic infarction, brainstem injuries	Helps localize acute traumatic lesions Defines vascular injuries, injuries to venous sinuses Detects mass effects	Readily available May help screen some patients for further imaging studies
Disadvantages	Artifacts arise from patient’s movement, foreign bodies Streak artifacts may obscure brainstem or posterior fossa	Slow Patients not easily accessible for monitoring Does not define most acute hemorrhagic lesions Not useful for bone injuries	Does not define nature of acute lesion Does not detect infratentorial masses	Does not indicate presence or absence of intracranial injury
Indications	Acute severe head trauma Acute moderate head trauma Suspected depressed skull fracture High-risk minor head trauma Suspected child abuse in minor head trauma Deteriorating neurologic status	Persistent symptoms with postconcussive syndrome Suspected posttraumatic ischemic infarction Suspected contusions not seen on CT scan	Suspected vascular injury CT scan not available	CT scan may not be done Penetrating head trauma

CT, Computed tomography.

From Marx JA et al: Rosen’s emergency medicine, concepts and clinical practice, ed 7, Philadelphia, 2010, Elsevier.

High Risk:

•Failure to reach GCS of 15 within 2 h
•Suspected open or depressed skull fracture
•Any signs of basal skull fracture (hemotympanum, "raccoon" eyes, CSF otorrhea/rhinorrhea, Battle’s sign)
•Two or more episodes of vomiting
•Age older than 65
•Dangerous mechanism of injury or polytrauma
•Retrograde amnesia to the event >30 min

Usually, in addition to a plain CT of the head (Fig. E6), computed tomography angiography (CTA) head/neck or CT of the spine is necessary if arterial or C-spine injury is suspected, respectively. Other imaging modalities such as MRI can be helpful in certain situations but are typically adjuncts in the acute setting to CT-guided management.

Figure E6 Non-Contrast-Enhanced Computed Tomography Scan of Acute Epidural Hematoma at the Level of Right Midconvexity

There is an associated mass effect and moderate midline shift.

(From Walls RM et al: Rosen’s emergency medicine, concepts and clinical practice, ed 10, Philadelphia, 2023, Elsevier.)

Pathologies that can be identified with imaging are noted in the following:

•Primary extraaxial: Epidural, subdural, subarachnoid hemorrhage
•Primary intraaxial: Axonal injury, cortical contusion, intracerebral or intraventricular hemorrhage, encephalomalacia (from prior TBI or vascular insult)
•Skull fracture: Linear, depressed, open, involving frontal sinus or skull base
•Penetrating brain injury: Gunshot wounds, sharp objects resulting in parenchymal and vascular injury
•Vascular injury: Dissection, traumatic carotid-cavernous fistula (CCF), dural arteriovenous fistula (dAVF), pseudoaneurysm formation
•Secondary acute injury: Diffuse cerebral swelling/dysautoregulation (seen more commonly in children from posttraumatic hyperemia), infarction, infection from penetrating trauma, brain herniation from mass lesion or cerebral edema
•Secondary chronic injury: Hydrocephalus (posttraumatic due to disruption of normal CSF absorption pathways), encephalomalacia, CSF leak (from skull base fractures, manifests as otorrhea or rhinorrhea), leptomeningeal cyst (seen most commonly in infants, skull fracture resulting in underlying dural injury)

Treatment ⬆ ⬇

Prevention of secondary injury is the primary goal of prehospital and early in-hospital management. Most common mechanisms of secondary injury are either intracranial (increased intracranial pressure [ICP], hematoma) or systemic (hypoxia, hypovolemia, hypotension). Early categorization of head trauma patients according to the severity (based on GCS) and transport to facilities equipped with personnel and technology to deal with issues pertaining to head trauma has improved the overall management of head injury patients and prevention of secondary injury. Assessment and treatment recommendations for mild TBI are summarized in Table E8. Airway, breathing, and circulation along with bleeding control remain the most important parameters to be stabilized and both directly and indirectly affect GCS and overall outcome. Trauma guidelines suggest intubation should be performed in any patient with a GCS of 8 or less to prevent respiratory failure. Recent evidence suggests normo-ventilation for patients with severe TBI, with hyperventilation only being used as a temporary measure in patients with TBI and ICP crisis, until other methods of reducing ICP are employed.¹¹ Hypotension should also be avoided in patients with TBI, as it has been shown to increase mortality.¹¹ Transfer to and care in a Level 1 trauma center is associated with better outcomes. Monitoring and treatment recommendations for severe TBI are summarized in Table E9.

TABLE E8 Assessment and Treatment Recommendations for Mild Traumatic Brain Injury

Function	Assessment	Treatment
Overall recovery	Standardized symptom checklist	Physical rest 1-2 days ¹ followed by subsymptomatic aerobic exercise ²
Headache	Determine the type	HA persisting more than 3-4 days may require abortive treatment tailored to phenotype (migraine, tension-type, occipital neuralgia, etc.)
Vertigo	Romberg test, dynamic standing, tandem gait	If Hallpike Dix is normal, or if Epley maneuver does not relieve symptoms, consider physical therapy for vestibular rehabilitation
Eye movements	Examine cranial nerves 3, 4, 6 for tracking, saccades, diplopia, nystagmus	Physical therapy evaluation for vestibular rehabilitation
Near vision	Near-point accommodation and binocular convergence	Ophthalmologic evaluation for vision therapy
Cognitive function	Symptoms, cognitive testing, neuropsychologist evaluation	Sleep hygiene, neuropsychology evaluation for cognitive rehabilitation ³

HA, Headache.

¹Thomas DG et al: Benefits of strict rest after acute concussion: a randomized controlled trial, Pediatrics 135:213-223, 2015.

²Kurowski BG et al: Aerobic exercise for adolescents with prolonged symptoms after mild traumatic brain injury: an exploratory randomized clinical trial, J Head Trauma Rehabil 32:79-89, 2017.

³Cooper DB et al: Cognitive rehabilitation for military service members with mild traumatic brain injury: a randomized clinical trial, J Head Trauma Rehabil 32:E1-E15, 2017.

From Goldman L, Schafer AI: Goldman-Cecil medicine, ed 27, Philadelphia, 2024, Elsevier.

TABLE E9 Guidelines for the Management of Severe Traumatic Brain Injury

Topic	Level 1	Level 2	Level 3
Blood pressure and oxygenation	Insufficient data	Avoid systolic blood pressure <90 mm Hg.	Avoid hypoxia (PaO₂<60 mm Hg or O₂ saturation <90%).
Hyperosmolar therapy	Insufficient data	Mannitol is effective for control of raised ICP at doses of 0.25 g/kg to 1 g/kg body weight.	Restrict mannitol use prior to ICP monitoring in patients with signs of transtentorial herniation.
Prophylactic hypothermia	Insufficient data	Insufficient data	Pooled data indicate that prophylactic hypothermia is not significantly associated with decreased mortality as compared with normothermic controls.
Infection prophylaxis	Insufficient data	Periprocedural antibiotics for intubation should be administered to reduce the incidence of pneumonia. Early tracheostomy should be performed to reduce days on mechanical ventilation with pneumonia.	To reduce infection, routine ventricular catheter exchange or prophylactic antibiotic use for ventricular catheter placement is not recommended.
Deep venous thrombosis prophylaxis	Insufficient data	Insufficient data	Intermittent pneumatic compression stockings are recommended. Low-molecular-weight heparin or low-dose unfractionated heparin should be used in combination with mechanical prophylaxis.
Indications for ICP monitoring	Insufficient data	ICP should be monitored in all salvageable patients with a GCS score of 3-8 after resuscitation and an abnormal CT scan.	ICP monitoring is indicated in patients with severe TBI with a normal CT scan if >40 yr of age with blood pressure <90 mm Hg.
ICP pressure-monitoring technology	N/A	N/A	N/A
ICP thresholds	Insufficient data	Treatment should be initiated with ICP >22 mm Hg	A combination of ICP values and clinical and brain CT findings should be used to determine the need for treatment
Cerebral perfusion thresholds	Insufficient data	Aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors should be avoided because of the risk of acute respiratory distress syndrome.	CPP of <50 mm Hg should be avoided. The CPP value to target lies within the range of 60-70 mm Hg. Patients with intact pressure autoregulation tolerate higher CPP values. Ancillary monitoring of cerebral parameters that include blood flow, oxygenation, or metabolism facilitates CPP management.
Brain oxygen monitoring and thresholds	Insufficient data	Insufficient data	Jugular venous saturation (<50%) or brain tissue oxygen tension (<20 mm Hg) are treatment thresholds
Anesthetics, analgesics, sedatives	Insufficient data	Prophylactic administration of barbiturates to induce burst suppression electroencephalogram is not recommended. High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Hemodynamic stability is essential before and during barbiturate therapy. Propofol is recommended for the control of ICP but not for improvement in mortality or 6-mo outcome.	N/A
Nutrition	Insufficient data	Patients should be fed to attain full caloric replacement by day 7 postinjury.	N/A
Antiseizure prophylaxis	Insufficient data	Anticonvulsants are indicated to decrease the incidence of early PTS (within 7 days of injury).	N/A
Hyperventilation	Insufficient data	Prophylactic hyperventilation (PaCO₂ of 25 mm Hg or less) is not recommended.	Hyperventilation is recommended as a temporizing measure for the reduction of ICP. Hyperventilation should be avoided during the first 24 h after injury, when cerebral blood flow is often critically reduced. If hyperventilation is used, jugular venous oxygen saturation (SjO₂) or brain-tissue oxygen tension (PbtO₂) measurements are recommended to monitor oxygen delivery.
Steroids	The use of high-dose methylprednisolone is associated with increased mortality and is contraindicated.	N/A	N/A

CT, Computed tomography; CPP, cerebral perfusion pressure; ICP, intracranial pressure; GCS, Glasgow Coma Scale; PTS, posttraumatic seizures; TBI, traumatic brain injury.

From Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

Figure E7 Algorithm for the Management of Traumatic Brain Injury (TBI)

Cpp, Cerebral Perfusion Pressure; CSF, Cerebrospinal Fluid; CT, Computed Tomography; DVT, Deep Venous Thrombosis; Hob, Head of Bed; ICP, Intracranial Pressure; ICU, Intensive Care Unit; Pud, Peptic Ulcer Disease.

(From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.)

Details of in-hospital management including critical care and surgical intervention is beyond the scope of this text. Some important points are summarized below:

•Advanced trauma life support (ATLS) protocol (airway, breathing, circulation, disability, exposure) and control bleeding.
•Ventilatory support.
•Optimization of oxygenation, ventilation, and fluid status. Goal-directed parameters for head injury are summarized in Table E10.
•CT head (Fig. E8) to evaluate for mass lesion (hematoma) or cerebral edema. These findings may necessitate either surgical intervention or ICP/PbO₂ monitor placement.
•In case of either a severe TBI (GCS 8 or less) or a moderate TBI (GCS 8 to 13) with an unreliable neurologic exam, patients should be admitted to the intensive care unit for frequent neurologic checks. TBI guidelines suggest ICP monitor placement for GCS 8 or less to monitor intracranial pressure closely.¹¹ Commonly used ICP monitors include intraparenchymal ICP monitors and external ventricular drains (EVDs). Subarachnoid or epidural bolt devices are rarely used. EVDs are considered gold standard, as they can provide diagnostic values and therapeutic management. Research has also supported the use of multimodality monitoring with brain tissue oxygen monitoring for severe TBI patients.¹¹
•Surgical decompression may involve evacuation of hematoma (epidural, subdural, intraparenchymal, contusion) through craniotomy (replacement of bone after completion of operation) or decompressive craniectomy (complete removal of bone without replacement). Skull fractures are treated depending on the morphology and location of the fracture. Open, depressed fractures require surgical debridement and elevation in most cases, in addition to broad-spectrum antibiotics.
•Elevation of head of bed at midline position to allow better venous drainage to reduce intracranial pressure.
•ICP management (Table E11), which may include the following: Drainage of cerebrospinal fluid via external ventricular drain, surgical hematoma evacuation, administration of hyperosmotic fluids to reduce edema, pharmacologic sedation and paralysis, pentobarbital-induced coma, and surgical decompression of the brain.¹¹
•Decompressive craniectomy in patients with TBI and refractory intracranial hypertension may reduce intensive care unit (ICU) stay but does not clearly improve outcomes. DECRA ¹² and RESCUEicp ¹³ are two randomized controlled trials that assessed decompressive craniectomy (DC) for reduction in ICP vs. medical management. Both trials were unable to provide definite evidence for or against DC, indicating that the decision to proceed with DC should be made on case-by-case basis, after assessment of individual risks and benefits.
•Normothermia: In patients with TBI, hypothermia can reduce intracranial hypertension, but recent trials in patients with an intracranial pressure of more than 20 mm Hg after TBI, therapeutic hypothermia, plus standard care to reduce intracranial pressure did not result in outcomes better than those with standard care alone. Prophylactic hypothermia is not recommended.¹¹
•Prevention of seizures in the acute setting. Seizure prophylaxis can be considered for the first 7 days in moderate and severe TBI. Phenytoin or levetiracetam is usually used.¹⁴ Seizure prophylaxis, however, has not been shown to prevent long-term development of traumatic epilepsy.
•Deep vein thrombosis (DVT) prophylaxis is recommended in almost all patients on hospital day 1 or 2 in addition to sequential compression devices (SCDs) for immobile or bedbound patients to prevent DVTs.¹⁵
•Early initiation of parenteral nutrition.
•Early initiation of rehabilitation.
•Early tracheostomy for ventilator-dependent patients can be considered to reduce mechanical ventilation days and ventilator-dependent complications.

TABLE E10 Goal-Directed Parameters for Head Injury

Pulse oximetry ≥95%	ICP 20-25 mm Hg	Serum sodium 135-145 mEq/L
PaO₂≥100 mm Hg	PbtO₂≥15 mm Hg	INR ≤1.4
PaCO₂ 35-45 mm Hg	CPP ≥60 mm Hg *	Platelets ≥75 × 10³/mm³
SBP ≥100 mm Hg	Temperature 36°-37.5°C	Hemoglobin ≥7 g/dl
pH 7.35-7.45	Glucose 80-180 mg/dl

CPP, Cerebral perfusion pressure; ICP, intracranial pressure; INR, international normalized ratio; PaCO2, partial pressure of carbon dioxide; PaO2, partial pressure of oxygen; PbtO2, brain tissue oxygen tension; SBP, systolic blood pressure.

^*Depending on status of cerebral autoregulation.

From Vincent JL et al: Textbook of critical care, ed 8, Philadelphia, 2024, Elsevier.

Figure E8 Indications for acute seizure prophylaxis in severe head trauma.

(From Walls RM et al: Rosen’s emergency medicine, concepts and clinical practice, ed 7, Philadelphia, 2010, Elsevier.)

TABLE E11 Elevated ICP Management

•Verify ICP
1. 1.Check if EVD is still patent
2. 2.Check to see if EVD waveform is present and adequate
3. 3.Check to see if EVD ICP correlates with intraparenchymal monitor if present
•Check for 30-degree head elevation and head position at midline
•Loosen cervical collar if in place
•Open EVD for ICP >22 mm Hg for 10 min and then close and transduce ICP
1. 1.Repeat once
2. 2.If ICP >22 mm Hg, keep open at 15 mm Hg above midbrain and proceed with ICP module
•Treat temperature >37.5° C initial with acetaminophen
•Sedation
1. 1.Titrate propofol to a Ramsay score of 4
  1. a.Do not exceed 5 mg/kg/h for more than 24 h
  1. b.Check potassium, triglycerides, creatine kinase, and urinalysis for myoglobinuria q8h for 24 h
  1. c.If maximal dose of propofol is reached and ICP >22 mm Hg, add fentanyl drip
•Hyperosmolar therapy
1. 1.3% hypertonic saline bolus of 250 ml or 23.4% 30 ml
2. 2.Mannitol 20% 1-1.5 mg/kg bolus once
3. 3.Check sodium and serum osmolality q4h × 2 after every bolus
4. 4.If sodium >160 mEq/L or serum osmolality >320 sOsm/L, no further benefit can be achieved
•If core body temperature ≥37.5° C despite acetaminophen, start normothermia protocol
•Hyperventilation: goal of PaCO2 of 30-35 mmHg until ICP is controlled
•Radiology
1. 1.Refractory ICP >22 mm Hg despite intervention, obtain head CT without contrast
  - •Consider surgical decompression if patient is a candidate
  - •Consider pentobarbital coma induction
2. 1.Order continuous EEG monitoring if not already in place
3. 2.Have norepinephrine drip ready at the bedside for CPP <60 mm Hg
4. 3.Pentobarbital bolus/loading: 10 mg/kg once over 60 min, then 5 mg/kg qh × 4 or until burst suppression
5. 4.Pentobarbital maintenance dose: 1 mg/kg/h titrated to burst suppression

CBF, Cerebral blood flow; CPP, cerebral perfusion pressure; EEG, electroencephalography; EVD, external ventricular drain; ICP, intracranial pressure; MAP, mean arterial pressure; PbtO2, Brain tissue oxygen.

Modified from Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

Chronic Rx

•TBI can lead to short- and long-term emotional (Table E12), physiologic, and cognitive sequelae (Table E13). Patients suffering from TBI are shown to benefit from neurocognitive (Fig. E9), occupational, and physical therapy. The Glasgow Outcome Scale is a comprehensive measure of severity and eventual outcome of brain injury. Posttraumatic amnesia, age, length of coma, GCS score within the first 24 h, and imaging study scales are some of the factors that impact long-term outcomes.
•Chronic treatment addresses several sequelae of TBI, including, but not limited to, the following: Dysautonomia, agitation, sleep disturbance, posttraumatic epilepsy, spasticity, dysphagia, syndrome of the trephined, posttraumatic hydrocephalus, apathy, fecal/urinary incontinence, headache, and neuropathic pain syndromes.
•Medication guidelines for patients with TBI and side effects of concern are described in Boxes E2 and E3. Neurostimulants such as amantadine, modafinil, and methylphenidate are used to accelerate recovery, but good randomized controlled trials (RCTs) are lacking in this area.

TABLE E12 Personality and Behavioral Changes Associated With Traumatic Brain Injury

Aggression		Need for immediate gratification
Apathy		Mood lability
		Erratic and difficult to predict temper outbursts and mood swings
Lack of goal-directed activity
Lack of empathy		Abnormal jocularity
Distractible		Irritability and reduced tolerance for frustration
Difficulty learning from mistakes		Disinhibition
Impulsivity

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

TABLE E13 Cognitive Changes

Impaired Attention	Impaired Memory	Language Deficits	Executive Dysfunction
•Basic arousal •Selective attention •Sustained attention •Divided attention •Span of attention •Speed of processing	•Post-traumatic amnesia •Retrograde amnesia •Acquisition, storage, and retrieval of new information •Prospective memory •Working memory •Procedural memory •Kinesthetic memory •Episodic memory •Declarative memory •Prospective memory •Semantic memory •Confabulation	•Word-finding •Decreased fluidity •Dysarthria •Receptive aphasia •Expressive aphasia •Anomic aphasia •Paraphasic errors •Circumlocution •Paucity of speech	•Setting and attaining goals •Initiating and monitoring behavior •Inhibiting competing impulses •Correcting behavior in response to feedback •Error recognition •Insight and empathy •Decision-making •Perseveration •Rigidity

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

Figure E9 Treatment of emotional and behavioral disturbances after traumatic brain injury.

(From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.)

BOX E3 Medication Side Effects of Concern for Patients With Traumatic Brain Injury

•Sedation
•Impaired memory
•Impaired learning
•Dry mouth
•Constipation
•Tachycardia
•Urinary retention
•Diplopia
•Confusion
•Hypotension
•Seizures

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

BOX E2 Medication Guidelines for Patients With Traumatic Brain Injury

•Eliminate biologic sources first.
•Alter the environment.
•Treat symptoms over diagnosis.
•Start low and go slow.
•Target the lowest effective dose.
•Make one change at a time.
•Remove unnecessary medications.
•Routinely review continued need for medications.
•Supplement with psychotherapy.

From Stern TA et al: Massachusetts General Hospital comprehensive clinical psychiatry, ed 3, Philadelphia, 2025. Elsevier.

Disposition

•Patients may require admission to a rehabilitation facility or discharge to home with outpatient neurocognitive therapy depending on the severity of head injury.
•Despite individual clinical variability, several common neurobehavioral sequelae of moderate to severe TBI can be identified (Table E14). Cognitive recovery is protracted for moderate to severe TBIs, with most improvements occurring in the first yr but measurable recovery of cognitive functioning still occurring several yr after the injury. However, even after a prolonged length of time, individuals may not return to preinjury levels.

TABLE E14 Common Neurocognitive Sequelae of Moderate to Severe Traumatic Brain Injury

Cognitive Domain		Clinical Manifestation of Impairment
Attention		Difficulty with sustained attention
		Poor concentration
		Psychomotor impersistence
Memory		Problems with acquiring and retaining new verbal or nonverbal information
		Problems in retrieving verbal and nonverbal memories
Speed of information processing		Slowed sensorimotor skills and information processing
Executive functioning		Problems in convergent and divergent reasoning
		Poor judgment
		Difficulty planning
		Problems in self-monitoring and self-correcting behavior
Awareness of symptoms		Difficulty recognizing deficits
		Unrealistic expectations concerning the recovery of functions
		Problems related to poor treatment compliance
Language and communication		Problems in word comprehension
		Impaired reading, spelling, and writing ability
		Tendency to become fragmented in free speech
Integrative functions		Problems in adequate or time-efficient execution of various perceptual-motor-spatial-sequential tasks

From Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

Referral

Early transfer to a Level 1 Trauma Center with neurosurgical personnel if high-risk findings are noted on clinical exam or CT head, and is associated with better outcomes.

Depression		Cognitive and motor disturbances
Profound feelings of hopelessness, despair, worthlessness		Emotional lability
Loss of sense of integrity		Impulsivity
Prior history of suicide attempt		Inflexibility
Male		Hyperactivity
Mid-adolescence to mid-twenties		Poor problem-solving
Lower socioeconomic level		Inability to identify alternatives
Drug or alcohol use
Cluster B personality disorder
		Social isolation

section name header

Basic Information ⬇

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Pearls & Considerations ⬆ ⬇

Reference(s) ⬆