Pediatric Traumatic Brain Injury

Author(s): Nancy Yeh, MD, Melissa Trovato, MD

Originally published:11/16/2011

Last updated:08/22/2016



Traumatic brain injury (TBI) results from trauma that involves any part of the brain and outwardly may affect ambulation, cognition, communication, swallowing, and performance of daily skills. Injuries may be primary, due to impact, and secondary, due to inciting events, such as edema, seizures, and increased intracranial pressure (ICP).


In children ages 0-14 years, the leading cause of TBI that resulted in an emergency department (ED) visit from 2006-2010 is falls, as reported by the Centers for Disease Control and Prevention (CDC). Another common cause of TBI children 0-4 years of age is non-accidental trauma. After the age of 14 years, assault and motor vehicle related trauma are included in the more prevalent causes.

Epidemiology including risk factors and primary prevention

Over 500,000 children ages 0-14 years sustain a TBI annually. Of these children, about 474,000 end up visiting the ED with over 35,000 hospitalizations and about 2,000 deaths from 2002-2006.1

Over all, the CDC reports an increase in the incidence of pediatric TBI-related ED visits almost yearly from 2001-2010. The mortality rate for pediatric TBI has been trending down from 2001-2010.

TBI most commonly occurs in the spring and summer. The rate of TBI is higher in males than females. Studies indicate children with attention deficit hyperactivity disorder are more likely to sustain a TBI. Prevention is primarily educating caretakers on appropriate use of helmets, safety engineering of automobiles, and transportation seats with safety restraints.


TBI is comprised of primary and secondary mechanisms of injury. The primary injury is from direct damage and shear forces. Primary injuries include contusions, impact depolarization from increase in extracellular potassium and glutamate, and diffuse axonal injury (DAI). DAI is a result of acceleration-deceleration and rotational forces causing shearing of the axons. It most commonly affects the white matter of the corpus callosum and other midline structures. Primary injuries can also be caused by objects penetrating the skull into the dura and possibly brain.

Secondary injury results from a number of causes such as hypoxemia, electrolyte abnormalities, seizures, excitotoxicity leading to neuronal cell death, and cerebral edema. The cerebral edema that results from increased cerebral blood volume and water content can lead to intracranial hypertension. The dangers of intracranial hypertension include ischemia and herniation.

TBIs can also be categorized into focal and diffuse injuries. Focal injuries are recognized by localized damage on imaging. Diffuse injury as a result of DAI is more readily visible on magnetic resonance imaging (MRI).

Mechanisms of recovery can occur in several ways. Neuroplasticity through neuronal regeneration and collateral sprouting can occur, along with activation of latent areas and change in synaptic communication.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Following a TBI, symptoms may include mental status changes, extremity weakness, headaches, cranial nerve deficits, and visual changes. Depending on injury severity, symptoms may progress due to cerebral edema, elevated ICP, seizures, and hydrocephalus. Management of medical issues may help determine recovery.

In the ED, the child’s airway, breathing, and circulation is assessed and managed. Glasgow Coma Scale (GCS) or the Pediatric GCS scores are obtained. Patients with a GCS of 8 or less are intubated for airway protection. The head and spine are evaluated and imaged as indicated.

Patients are assessed frequently for signs of increased ICP for which a monitor may be required. For patients with increased ICP, medical management may include the use of mannitol, hypertonic saline, and short periods of hyperventilation. If medical management fails, secondary methods are considered, including phenobarbital coma and decompressive craniectomy.

The main goal of the acute care hospitalization is prevention of secondary complications and secondary brain injury as a consequence of hypotension, hypoxia, or both. Once medically stable, a patient may be transitioned to the most appropriate rehabilitation setting.

Impairments may become more noticeable as the child recovers. All domains of functioning can be impacted, including motor, sensory, communication, cognition, and behavior. Rehabilitation is the next phase of recovery for patients with moderate to severe injury and even some with mild injury with ongoing symptoms. Rehabilitation and recovery do not stop after discharge from rehabilitation.

Cognitive and communication disorders are common and persist. The more severe the injury, the worse the outcomes across all cognitive domains. Recovery is variable and may arrest at any stage of consciousness and cognition. Patients in a coma lack a sleep wake cycle and their eyes remain closed. Progression to a vegetative state is characterized by the resumption of a sleep wake cycle and opening of the eyes. Patients who advance into the minimally conscious state (MCS) exhibit environmental awareness, which is inconsistent but reproducible. Emergence from the MCS is demonstrated by consistent command following and functional object use. Cognitive recovery, as measured by the as measured by the Rancho Los Amigos Levels of Cognitive Function Scale (Rancho), categorizes patients into 10 levels ranging from no response to purposeful and appropriate behavior with modified independence.

Specific secondary or associated conditions and complications

Secondary complications may include:

  • Cerebral edema
  • Elevated ICP
  • Seizures
  • Electrolyte disturbances
  • Hydrocephalus
  • Dysphagia
  • Hearing loss
  • Vision impairment
  • Extremity weakness
  • Joint/muscle contractures
  • Scoliosis
  • Speech impairment
  • Cognitive impairment
  • Paroxysmal autonomic instability
  • Urinary and bowel incontinency
  • Heterotopic ossification
  • Neuroendocrine disorders



A detailed history includes the inciting event, use of protective gear such as helmet or seatbelt, duration of loss of consciousness, initial GCS score, and associated injuries. History of the child’s baseline function, developmental history, previous history of TBI, and social history are also obtained.

Physical examination

The physical examination varies based on injury severity. A detailed neurological and musculoskeletal examination includes mental status, cranial nerves (with smell), strength, sensation, reflexes, muscle tone, cerebellar testing, fine motor testing, balance, and active and/or passive range of motion. The initial examination may be limited by the child’s tolerance and medical stability, and must be followed serially.

Functional assessment

Functional assessment will vary based on severity and age. For a child admitted to acute rehabilitation, the WeeFim and Gross Motor Function Measure may be utilized. An age appropriate assessment of alertness and orientation should also be conducted and monitored as needed. The Child Orientation and Amnesia Test (COAT) may be used in children ages 3 to 15.2 For children older than 16, the Galveston Orientation and Amnesia Test (GOAT) is utilized.

Laboratory studies

Electrolytes to evaluate for hyponatremia or hypernatremia and other laboratory abnormalities associated with dysfunction of the hypothalamic pituitary axis should be monitored. Symptoms may include polyuria, polydipsia, or decreased urine output. Other symptoms of axis dysfunction include fatigue, changes in mental status, growth failure, precocious or delayed puberty, amenorrhea and short stature.


A computed tomography (CT) scan is typically performed in the ED to assess for bleeding or swelling. MRI may be obtained later to further assess injury to deeper structures and to evaluate for DAI. X-rays of the neck and limbs may be obtained to rule out additional injuries as indicated by physical examination. If heterotopic ossification (HO) is suspected, a triple-phase bone scan is indicated. Early HO does not appear on plain films.

Supplemental assessment tools

An electroencephalogram (EEG) may be obtained to evaluate for seizures. Depending on severity, additional studies may be utilized, including assessment of hearing, vision, and swallow function.

Early predictions of outcomes

General Outcome

  • Children younger than 5 years of age with TBI have a greater mortality rate.
  • Longer length of coma is a negative predictor of outcome.
  • Best motor response score on the GCS is the best acute predictor of outcome.
  • Longer duration of posttraumatic amnesia (PTA) and total duration of impaired consciousness have worse outcomes.

Functional Outcome

  • In children with severe TBI and unconscious state lasting longer than 6 hours, approximately 75% regained physical independence within one year of injury.
  • Time to follow commands may be the best predictor of general functional outcome.
  • Volume and number of lesions on MRI correlates with severity and functional outcome.
  • Pupillary abnormality is a negative predictor of motor outcome.

Cognitive Outcome

Children with non-accidental brain injury have worse recovery based on the Glasgow Outcome Scale and have worse cognitive outcomes.


As a patient evolves following moderate to severe TBI, he or she may go through a stage of confusion and agitation. During the agitation phase, environmental modifications may be necessary. This includes decreasing external stimuli and reducing demands on the patient by:

  • Reducing noise from TV and monitors if possible
  • Grouping vitals, medication administration, and cares to reduce interruptions
  • Limiting the number of visitors
  • Allowing for down-time
  • Providing frequent orientation
  • Identifying and treating pain

Social role and social support system

Following TBI, changes may be noted in a child’s emotional, behavioral, and social interactions. Patient and family support is important through all phases after TBI. Social workers, psychologists, and educators may be necessary for coping, adjustment, and reintegration into society and school. Ongoing community support groups may be available as well.

Professional Issues

If abuse is suspected, the child should be further evaluated by the medical team for signs of non-accidental trauma. Please see the Knowledge NOW submission on Child Abuse for further details regarding evaluation and reporting requirements.



At different disease stages

New onset/acute: In the acute care setting, treatment will focus on the management of ICP and other injuries. Prevention of secondary complications of immobility such as contractures and skin breakdown should also occur. Acute care physical and occupational therapists can fabricate temporary splints for the extremities as needed to maintain range of motion. Medication management may be necessary for treatment of paroxysmal autonomic instability, electrolyte disturbances, and spasticity or dystonia.

Subacute: The subacute management of TBI includes ongoing monitoring of range of motion and splinting as needed, management of spasticity or dystonia as it evolves, constipation and incontinence management, monitoring of nutritional status with appropriate assessment and supplementation, and assessment and treatment of swallow function as alertness improves.

Therapy services are to include physical therapy, occupational therapy, speech therapy, and neuropsychological testing/tracking of alertness, command following, and post-traumatic amnesia. The goals of therapy include preventing secondary complications, teaching strategies to compensate for impaired or lost function, optimizing the use of abilities as they return, and educating and supporting the family.

Behavioral psychology services may be necessary if the patient is agitated, and may also be needed for coping and adjustment. A special educator should work with the team to facilitate school re-entry and creation of an Individualized Education Plan (IEP) as needed.

Chronic/stable: Impairments in all domains may continue long-term. The goal will be to decrease the effect of a chronic disability on growth and development. Following TBI, significant recovery may be seen over the first year and may continue at a slower pace over time. Ongoing monitoring of impairments and impact on the child’s functioning will be important. Splinting, therapy, and educational needs may vary over time.

Children who are younger at the time of injury may not show the true nature of their cognitive deficits until they reach school age and cognitive demands are increased. For adolescents and young adults, recommendations for a driving evaluation and vocational rehabilitation services may be appropriate.

Coordination of care

An interdisciplinary approach is required for individuals requiring inpatient and outpatient rehabilitation services.

Patient & family education

Patient education at an appropriate developmental and cognitive level is important to assist with coping and adjustment. Depending on injury severity, this may occur in the acute phase, subacute and/or chronic phase. Family education starts in the acute phase and carried throughout all phases. Education is to be adjusted as the deficiencies become more apparent and the interventions require changing. Important topics will include prevention of repeat injury, contact sports guidelines, transition to home and school, legal resources, educational resources, advocacy, and transition to adulthood.

Emerging/unique interventions


Tools for measurement of outcomes include:

  • Functional Independence Measure for Children (WeeFIM)
  • Gross Motor Function Measure
  • Pediatric Evaluation of Disability Inventory
  • Glasgow Coma Outcome Score
  • The Coma/Near Coma scale
  • Child Health Questionnaire
  • Functioning After Brain Injury
  • Child Behavior Checklist
  • Vineland Adaptive Behavior Scale


Cutting edge concepts and practice

Current research looks at neurotransmitter levels and the severity of TBI, as well as the role of neuroprotective agents in rat models.


Gaps in the evidence-based knowledge

Research behind the neuropharmacology and ability to predict specific long-term outcomes remains limited, especially in the pediatric population.


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Original Version of the Topic:

Melissa Trovato, MD. Pediatric Traumatic Brain Injury. Publication Date: 2011/11/16.

Author Disclosure

Nancy Yeh, MD
Nothing to Disclose

Melissa Trovato, MD
Nothing to Disclose

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