Traumatic brain injury (TBI) is defined as brain pathology or alteration of brain function caused by an external force and in children is a major cause of acquired disability as well as a leading cause of morbidity and mortality. TBI commonly results in impairments in mobility, cognition, language, swallowing, and performance of daily skills. In TBI 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 old, the leading cause of TBI that resulted in an emergency department (ED) visit from 2010 to 2014 is falls, as reported by the Centers for Disease Control and Prevention (CDC). Nonaccidental trauma is another leading cause in this age group. However, the most common cause for worldwide pediatric traumatic brain injury, as well as in the pediatric age group 14 years or older, is motor vehicle collisions. Additionally, being struck by an object caused one in four TBI ED visits in children less than 17 years old.1
Epidemiology including risk factors and primary prevention
In TBI, a bimodal age distribution is often described, with very young children (0-2 years) and adolescents (15-18) more commonly injured. Over 837,000 children ages 0-14 years sustain a TBI annually. Of these children, about 812,000 visit the ED with over 23,000 hospitalizations and about 2,000 deaths (2014).1,2 Approximately 17,000 children are permanently disabled each year. TBI most commonly occurs in the spring and summer and the rate of TBI is higher in males than females. Studies indicate children with learning disorders and hyperactivity disorder are more likely to sustain a TBI. Prevention includes primarily educating caretakers on appropriate use of helmets and transportation seats with safety belts, and improved safety engineering of automobiles.
TBI is comprised of primary and secondary mechanisms of injury. The primary injury is from direct damage and shear forces and includes contusions or penetrating lesions, 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.
Secondary injury results from several 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). A child’s head is relatively larger (head to body ratio) and has a thinner calvarium. The brain is often softer, less myelinated, increasing the susceptibility to DIA. Space-occupying hematomas are less likely in children. In general, clinical signs are less reliable in children due to limited vocabulary/communication, but do mirror adult symptoms as the child gets older. Most often the presenting symptoms include headache, nausea, vomiting, seizures, lethargy or drowsiness. Amnesia is often hard to elicit from a child. In neonates clinical signs may be hypotonia, listlessness, bulging tense fontanels and sunsetting.
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.
Second Impact syndrome is a growing but controversial topic of interest. With frequent repeat concussions, there is an increase in severity of symptoms or even fatal events following a new mild concussive episode. The syndrome is due to the repetitive frequency of brain swelling. It is believed that the multiple impacts derange auto regulatory and metabolic mechanisms enough to produce vascular engorgement. These small changes in volume lead to large changes in pressure in a child’s brain progressing to more severe changes, allowing more excitatory neurotransmitter releases. The end result is a syndrome explained by pairing of excess neurotransmitters interacting with high plasticity in a developing brain.
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 positioning with elevated head of bed, 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 due to 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. However, rehabilitation and recovery do not stop after discharge from rehabilitation centers. Cognitive and communication disorders are common and may persist – the more severe the injury, the worse the outcomes are across all cognitive domains.
Recovery is variable and may arrest at any stage of consciousness and cognition. Disorders of consciousness are defined as a transient staging system to communicate these functional cognitive outcomes. Patients in a coma lack a sleep wake cycle, eyes remain closed or cannot be aroused. In those who survive this phase, progression to a vegetative state usually happens within 2 to 4 weeks by the resumption of a sleep wake cycle and spontaneous opening of the eyes but absence of environmental awareness. In this state patients do not demonstrate language, comprehension of verbal/gestural cues, or purposeful movement. It is worth noting a controversy of the classification of permanent versus persistent categories within vegetative state. Persistent is defined as one to three months while permanent is defined as twelve months in traumatic cases. Patients who then 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. This state is reliant concurrently on intact language and motor function. Individuals who receive early rehabilitation during MCS within 6 months of brain injury have good outcomes. New studies suggest minimal sensory stimulation may be beneficial even in the ICU. The Coma Recovery Scale- Revised designed by Aspen neurobehavioral conference for adults is commonly used to help with differential diagnosis, prognostication, and further management. It is applicable to Ranchos Los Amigo levels of Cognitive Function scales 1 through 4. Cognitive recovery as measured by the revised Rancho Los Amigos Levels categorizes patients into 10 levels ranging from no response to purposeful and appropriate behavior with modified independence. Remaining in vegetative states longer than 90 days following anoxic/traumatic injury has increased mortality rate in pediatric cases.
Neuroendocrine dysfunction is common in moderate to severe head traumas. An estimated 30% of traumatic cases will have some element of dysfunction in the first year following the injury. Monitoring acutely in ICU for hyponatremia due to the frequency of syndrome of inappropriate ADH (SIADH) or hypernatremia from central diabetes insipidus (DI) is both difficult and commonplace. Unfortunately, due to the use of hyperosmolar substances, such as mannitol and 3% normal saline, as well as some sedative medications, cause of Na abnormalities can be multifactorial. When other factors have been ruled out, small vessel inflammatory responses more often than mechanical impact to the pituitary gland is proposed as the cause for change in pituitary dysfunction. Unfortunately, MRI imaging only detects 30% of pituitary injuries, as specificity of identifying radiologic details in the pituitary stalk is difficult.
In addition to either SIADH or Central DI, chronic dysfunction in growth hormone, gonadotropin and hypothyroidism have been reported in children with TBI. Growth hormone deficiency is predicted to have an incidence of 20% with symptoms of fatigue, decreased exercise tolerance, depression, osteoporosis, hyperlipidemia and atherosclerosis. Gonadotropin deficiencies are predicted to occur in 10-15% of cases with symptoms of decreased libido, muscle mass, and strength. Hypothyroidism is predicted to occur in 5% of cases.
Specific secondary or associated conditions and complications
Secondary complications may include:
- Cerebral edema
- Elevated ICP
- Electrolyte disturbances
- Hearing loss
- Vision impairment
- Extremity weakness
- Joint/muscle contractures
- Speech impairment
- Cognitive impairment
- Paroxysmal autonomic instability
- Urinary and bowel incontinence
- Heterotopic ossification
- Neuroendocrine disorders
ESSENTIALS OF ASSESSMENT
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.
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 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 15.3 For children older than 16, the Galveston Orientation and Amnesia Test (GOAT) is utilized.
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, in the chronic phase, 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 skull, neck and limbs may be obtained to rule out additional injuries as indicated by physical examination There is concern around the risk of multiple radiation exposures to children, especially less than 2 years old when evaluating mild TBIs. The radiation exposure of CTs is estimated to be responsible for 1 in 1000-5000 of children to cause lethal malignancy. Some studies propose guidelines for timing of imaging based on likelihood to demonstrate clinically significant brain trauma correlating to GCS scale. Currently 1 in 3 children in North America presenting with mild TBI symptoms receive CT imaging, with only 10% revealing head trauma and fewer requiring intervention.
In terms of complications such as heterotopic ossification (HO), a triple-phase bone scan is indicated since early HO does not appear on plain films.
Supplemental assessment tools
An electroencephalogram (EEG) may be obtained to evaluate for seizures. Seizures are classified into immediate, early and late posttraumatic seizures. Incidence of posttraumatic seizures are higher in children than adults. Depending on severity and presentation, additional studies may be utilized, including assessment of hearing, vision, and swallow function.
- 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.
- As for the survival rates, 63 % of children in vegetative state, 65% of immobile and 81% of mobile MCS children survived 8 years post injury.
- In children with severe TBI and unconscious state lasting longer than 6 hours, approximately 75% regained physical independence within one year of injury.
- Delay in initiation of comprehensive rehabilitation program results in worse functional outcomes and diminished recovery and rehab efficiency in children with severe TBI.
- Time to follow commands may be the best predictor of general functional outcome.
- Volume and number of lesions on MRI correlate with severity and functional outcome.
- Pupillary abnormality is a negative predictor of motor 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, child life specialists and educators may be necessary for coping, adjustment, and reintegration into society and school. Ongoing community support groups may be available as well.
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.
REHABILITATION MANAGEMENT AND TREATMENTS
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, seizures 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 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. The need for pediatric specific rehabilitation is determined by looking at general outcomes, family behavior, cognitive, speech, language, swallow, gross and fine motor skills as well as neuropsychology evaluations and school reentry. When a rehab unit’s focus is pediatrics, the neuropsychology and cognitive outcomes are better. Also, both pediatric and CARF accredited rehabilitation units are better in achieving social reintegration and school reentry. During rehabilitation, 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.
Non-pharmacologic treatments of disorders of consciousness include sensory or nervous system stimulation. Often times, patients remain in ICUs with negative or without stimuli- lights off, noxious blood draws, excessive conversation and limited interaction. Minimal Sensory stimulation may develop into a new frontier of therapy beginning as early as the ICU for patients in vegetative and minimal conscious states. While several protocols are being developed with an assortment of sensory inputs- requiring all five sensory inputs to be used at one time within a specific therapy session, current research suggests a three week improvement in disorders of consciousness. The proposed benefits are based on the belief that deprived of stimulus brain undergoes atrophy. With stimulus, an increase in the reticular activation system increases awareness and arousal. Some imaging findings demonstrate an increase in brain activity when familiar tactile, olfactory, and visual stimuli are provided to patients. These new therapies are decreasing length of stay in ICU and duration of depressed consciousness. The limitation of studies is the absence of control groups making it difficult to differentiate results from a natural recovery.
Various other electrophysiologic stimulations are under investigation including non-invasive median nerve, dorsal column and trans cranial direct current magnetic stimulation as well as deep brain stimulation. Finally, regenerative medicine has used fetal brain cells and liver cells to provide trophic factors and direct cell-to-cell communications helping to integrate new neuronal circuits. In two case series with 17 and 18-year-old severe traumatic brain injury in coma for 5-8 weeks, there was significantly improved recovery based on Glasgow Outcome score and MRI atrophy on follow up. These cases were part of a 38 pediatric case series, where 33 cases showed significant recovery after 3-7 days following last cellular transplantation.
Measurement of Patient Outcomes
Tools for measurement of outcomes include:
- Child Behavior Checklist: caregiver report form defining child behavior
- Child Health Questionnaire: internationally recognized scale to evaluate quality of life in children
- Coma Recovery Scale- Revised (JFK Coma recovery scale): assess disorder of consciousness
- Coma/Near Coma scale: developed to measure neurobehavioral changes in sustained TBI
- Disorders of Consciousness Scale: tool used to detect subtle changes in neurobehavioral functioning during severe traumatic brain injury.
- Functional Independence Measure for Children (WeeFIM): pediatric version of Functional Independent Measures: method for evaluating functional and cognitive outcomes.
- Glasgow Coma Outcome Score: objective scale of patients with brain injury, in groups of cases for research purposes
- Gross Motor Function Measure: tool to measure gross motor function over time, specifically designed for cerebral palsy population but has been adapted for TBI.
- Pediatric Evaluation of Disability Inventory (PEDI): samples key functional capability and performance in children from 6 months to 7.5 years
- Sensory Modality Assessment Rehabilitation Technique: valid and reliable assessment for vegetative state and minimally conscious state
- Vineland Adaptive Behavior Scale: instrument for evaluating intellectual and developing disabilities
- Western NeuroSensory Stimulation Profile:a tool for assessing slow-to-recover head-injured patients
- Post-Acute Level of Consciousness scale: for assessment of young patients in vegetative and minimally conscious state
CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE
Recovery from coma prognosis is predictably worse with the longer time spent in a coma, vegetative or minimally conscious state. This data could possibly be due to the limited participation in therapy. In children more so than adults, pharmacological agents are promising to help shorten the time in a disordered consciousness state. Trials with amantadine, dopamine agonists and GABA agonists are currently small in sample population but encouraging. A study of amantadine in 184 individuals 16-65 years of age showed an increase in functional recovery at 4-16 weeks based on changes in Ranchos Los Amigos and length of Post Traumatic Amnesia. A pediatric study of 54 children using amantadine duplicated these results but did not increase Wee FIM scores. Dopamine agonists’ studies have been extremely small but are thought to increase attention and behavioral alertness. These studies need to be broadened before any recommendations can be made. GABA agonists while thought to depress CNS function normally, in traumatic brain injuries, may be useful in reversing neurotransmitter signals and restoring balance of excitation and inhibition. These limited studies have shown improvement in Coma Near Coma scale and Ranchos Los Amigos.
Non-invasive brain stimulation or (NIBS) is on a frontier showing some promise in multiple points along acquired TBI pediatric cases. More classically investigated in neonatal cerebral palsy, it is beginning to be applied due to the similar pathophysiology between the two disorders. The principle relies upon an immature brain of a neonate/child less than two years old without fully mature myelination that can undergo neuronal migration, myelin formation, and dendritic/axonal remodeling. While several types of NIBS have been tested, repetitive transcranial magnetic stimulation (rTMS) using a parallel field coil has shown limited significance in predicting functional motor deficits, decrease posttraumatic seizures, and is being investigated in altering behavioral/cognitive functions. Further investigation will require larger cohorts in both adults and children with more standardized methodology.
Recent studies are investigating biomarkers for predictability in outcomes. s100B, neuron specific enolase, myelin basic protein all show promise in predicting severity of TBI when comparing the concentration over time from initial presentation to rehabilitation setting. Currently, these markers could be screening tools as their sensitivity for intracranial injury reaches 100% but specificity is roughly 33%. The different biomarkers vary mostly with length of time to peak and length of time to detection. These specific biomarkers are limited in usefulness due to other extra cranial processes that may produce elevated concentrations- such as hemolysis. Glial fibrillary acid protein shows promise in correlation of severity over a 6-month period and does not have an extra cranial production source. More studies will need to be performed to investigate the biomarker use in predicting functional outcomes of TBI.
GAPS IN THE EVIDENCE-BASED KNOWLEDGE
Research behind the neuropharmacology and ability to predict specific long-term outcomes remain limited, especially in the pediatric population.
Definitive assessment tools and/or inter assessment reliability of disorders of consciousness continue to be discussed across the field. Research behind therapeutic interventions is progressing but limited due to natural progression of recovery in comparison to new interventions. Virtual reality therapies are intriguing, however, remain novel in terms of intervention in many disorders including traumatic brain injury.
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Original Version of the Topic:
Melissa Trovato, MD. Pediatric Traumatic Brain Injury. 11/16/2011
Previous Revision(s) of the Topic
Nancy Yeh, MD, Melissa Trovato, MD. Pediatric Traumatic Brain Injury. 08/22/2016
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