Traumatic Brain Injury

Updated: June 6, 2025

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Background

Traumatic brain injury (TBI) disrupts normal brain function due to trauma. It refers to brain dysfunction caused due to an external mechanical force.

Primary injury results from mechanical force through contact or acceleration-deceleration at injury occurrence.

Secondary injury is non-mechanical, may be delayed, and can exacerbate existing brain injuries from impact.

Classification as follows:

Primary injuries

Secondary injuries

A sudden trauma to the head disrupts normal brain function through blows or penetrative injuries.

TBI varies from mild concussion to severe cognitive impairment.

Biphasic injury complexity requires interventions for immediate trauma and long-term neuroprotection.

Glasgow Coma Scale (GCS) measures consciousness and neurologic function from 3 to 15 points through motor, verbal, and eye responses.

Loss of consciousness is classified as mild, moderate, or severe based on duration and symptoms.

Posttraumatic amnesia is the duration until patients can show continuous memory post-injury.

Epidemiology

Males have nearly double the hospitalization risk for TBI than females and almost three times the TBI-related death risk.

Sources indicated that individuals aged 75 or older accounted for 32% of TBI-related hospitalizations and 28% of related deaths observed.

Mortality rates post-severe TBI are notably high, with survivors more prone to death from seizures, pneumonia, digestive issues, and various external injuries compared to similarly aged individuals.

TBI is a significant global health concern to cause high mortality and disability rates. WHO predicts it will become a leading cause of death by 2030.

Anatomy

Pathophysiology

Primary injury occurs immediately due to mechanical force, while secondary injury develops later and can exacerbate existing damage to the brain from the initial injury.

They are located on the poles and inferior aspects of the frontal lobes, cortex near the operculum, and lateral temporal lobes.

Epidural hematomas involve rapid blood clots between bone and dura, as arterial bleeding increases pressure on brain tissue.

Secondary injury from TBI can arise hours or days later due to impaired cerebral blood flow.

It decreased cerebral blood flow from edema, hemorrhage, or increased ICP leads to failed ion pumps and calcium-sodium imbalance.

Etiology

The causes of TBI are as follows:

Falls

Motor Vehicle Accidents

Sports and Recreational Injuries

Assaults and Violence

Blast Injuries

Workplace and Industrial Accidents

Penetrating Injuries

Recreational and Domestic Incidents

Genetics

Prognostic Factors

Determining TBI prognosis is complex due to varied patient health statuses, injury types, severities, and treatment timings.

Retrospective cohort study showed that patients aged 45-64 years had twice the likelihood of poor outcomes and patients over 80 years had five times the likelihood compared to ages 18-44.

Patients with moderate to severe TBI experienced high long-term unemployment risk due to comorbid psychiatric symptoms and cognitive impairment.

Davis’s study found that increased GCS scores predict survival from field to emergency department.

Clinical History

Collect details including the mechanism of injury, timeline and events after injury, medical and family history to understand clinical history of patients.

Physical Examination

Head and Scalp Examination

Neurological Examination

Spine Examination

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Immediate symptoms are:

Loss of consciousness, post-traumatic seizures, vomiting, severe headache, visible trauma

Delayed symptoms are:

Subtle cognitive impairment, sleep disturbances, persistent headache, mood changes

Differential Diagnoses

Subdural hematoma

Cerebral contusion

Delirium

Syncope

Psychogenic non-epileptic seizures

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

3% saline bolus hyperosmolar therapy is recommended for ICP, with doses of 2-5 mL/kg.

Avoid midazolam and fentanyl bolus to prevent cerebral hypoperfusion risks.

Moderate hypothermia helps control ICP but not overall outcomes improvement.

Early enteral nutrition supports reduced mortality and better outcomes.

First-line imaging for suspected moderate to severe TBI or high-risk mild TBI.

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

use-of-non-pharmacological-approach-for-traumatic-brain-injury

Perform soft restraints if necessary to prevent self-harm or tube dislodgement.

Remove unnecessary equipment that causes injury during seizures.

Use shower chairs for those with impaired balance.

Home safety evaluation includes remove clutter, improve lighting, and remove throw rugs.

Proper awareness about TBI should be provided and its related causes with management strategies.

Appointments with neurologist and preventing recurrence of disorder is an ongoing life-long effort.

Use of Osmotic Agents

Mannitol:

It increases glomerular filtrate osmolarity to reduce water reabsorption.

Use of Antiepileptics

Levetiracetam:

It has antiepileptic effects that involve calcium channels and neurotransmitter release modulation.

Use of Vasopressors

Norepinephrine:

It increases cardiac output and heart rate to decrease renal perfusion.

use-of-intervention-with-a-procedure-in-treating-traumatic-brain-injury

The procedural interventions for airway and ventilation procedures include endotracheal intubation and mechanical ventilation.

Surgical interventions include craniotomy and decompressive craniectomy.

use-of-phases-in-managing-traumatic-brain-injury

In the immediate assessment and stabilization phase, the goal is to prevent secondary injury and rapid transport.

Pharmacologic therapy is effective in the treatment phase as it includes the use of osmotic agents, antiepileptics, and vasopressors.

In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.

The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.

Medication

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Traumatic Brain Injury

Updated : June 6, 2025

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Traumatic brain injury (TBI) disrupts normal brain function due to trauma. It refers to brain dysfunction caused due to an external mechanical force.

Primary injury results from mechanical force through contact or acceleration-deceleration at injury occurrence.

Secondary injury is non-mechanical, may be delayed, and can exacerbate existing brain injuries from impact.

Classification as follows:

Primary injuries

Secondary injuries

A sudden trauma to the head disrupts normal brain function through blows or penetrative injuries.

TBI varies from mild concussion to severe cognitive impairment.

Biphasic injury complexity requires interventions for immediate trauma and long-term neuroprotection.

Glasgow Coma Scale (GCS) measures consciousness and neurologic function from 3 to 15 points through motor, verbal, and eye responses.

Loss of consciousness is classified as mild, moderate, or severe based on duration and symptoms.

Posttraumatic amnesia is the duration until patients can show continuous memory post-injury.

Males have nearly double the hospitalization risk for TBI than females and almost three times the TBI-related death risk.

Sources indicated that individuals aged 75 or older accounted for 32% of TBI-related hospitalizations and 28% of related deaths observed.

Mortality rates post-severe TBI are notably high, with survivors more prone to death from seizures, pneumonia, digestive issues, and various external injuries compared to similarly aged individuals.

TBI is a significant global health concern to cause high mortality and disability rates. WHO predicts it will become a leading cause of death by 2030.

Primary injury occurs immediately due to mechanical force, while secondary injury develops later and can exacerbate existing damage to the brain from the initial injury.

They are located on the poles and inferior aspects of the frontal lobes, cortex near the operculum, and lateral temporal lobes.

Epidural hematomas involve rapid blood clots between bone and dura, as arterial bleeding increases pressure on brain tissue.

Secondary injury from TBI can arise hours or days later due to impaired cerebral blood flow.

It decreased cerebral blood flow from edema, hemorrhage, or increased ICP leads to failed ion pumps and calcium-sodium imbalance.

The causes of TBI are as follows:

Falls

Motor Vehicle Accidents

Sports and Recreational Injuries

Assaults and Violence

Blast Injuries

Workplace and Industrial Accidents

Penetrating Injuries

Recreational and Domestic Incidents

Determining TBI prognosis is complex due to varied patient health statuses, injury types, severities, and treatment timings.

Retrospective cohort study showed that patients aged 45-64 years had twice the likelihood of poor outcomes and patients over 80 years had five times the likelihood compared to ages 18-44.

Patients with moderate to severe TBI experienced high long-term unemployment risk due to comorbid psychiatric symptoms and cognitive impairment.

Davis’s study found that increased GCS scores predict survival from field to emergency department.

Collect details including the mechanism of injury, timeline and events after injury, medical and family history to understand clinical history of patients.

Head and Scalp Examination

Neurological Examination

Spine Examination

Immediate symptoms are:

Loss of consciousness, post-traumatic seizures, vomiting, severe headache, visible trauma

Delayed symptoms are:

Subtle cognitive impairment, sleep disturbances, persistent headache, mood changes

Subdural hematoma

Cerebral contusion

Delirium

Syncope

Psychogenic non-epileptic seizures

3% saline bolus hyperosmolar therapy is recommended for ICP, with doses of 2-5 mL/kg.

Avoid midazolam and fentanyl bolus to prevent cerebral hypoperfusion risks.

Moderate hypothermia helps control ICP but not overall outcomes improvement.

Early enteral nutrition supports reduced mortality and better outcomes.

First-line imaging for suspected moderate to severe TBI or high-risk mild TBI.

Physical Medicine and Rehabilitation

Perform soft restraints if necessary to prevent self-harm or tube dislodgement.

Remove unnecessary equipment that causes injury during seizures.

Use shower chairs for those with impaired balance.

Home safety evaluation includes remove clutter, improve lighting, and remove throw rugs.

Proper awareness about TBI should be provided and its related causes with management strategies.

Appointments with neurologist and preventing recurrence of disorder is an ongoing life-long effort.

Physical Medicine and Rehabilitation

Mannitol:

It increases glomerular filtrate osmolarity to reduce water reabsorption.

Physical Medicine and Rehabilitation

Levetiracetam:

It has antiepileptic effects that involve calcium channels and neurotransmitter release modulation.

Physical Medicine and Rehabilitation

Norepinephrine:

It increases cardiac output and heart rate to decrease renal perfusion.

Physical Medicine and Rehabilitation

The procedural interventions for airway and ventilation procedures include endotracheal intubation and mechanical ventilation.

Surgical interventions include craniotomy and decompressive craniectomy.

Physical Medicine and Rehabilitation

In the immediate assessment and stabilization phase, the goal is to prevent secondary injury and rapid transport.

Pharmacologic therapy is effective in the treatment phase as it includes the use of osmotic agents, antiepileptics, and vasopressors.

In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.

The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.

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