Severe traumatic brain injury (TBI) in children: Initial evaluation and management

INTRODUCTION — This topic will review the initial evaluation and management of children with severe traumatic brain injury (TBI). The evaluation and management of inflicted head injury, diagnosis and management of elevated intracranial pressure, and minor head injury are discussed separately:

●(See "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children".)

●(See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis" and "Elevated intracranial pressure (ICP) in children: Management".)

●(See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation" and "Minor head trauma in infants and children: Management".)

SEVERITY CLASSIFICATION — The severity of TBI has been traditionally defined by the initial Glasgow Coma Scale (GCS) or Pediatric Glasgow Coma Scale score (table 1) [1]:

●Mild (GCS score 13 to 15)

●Moderate (GCS score 9 to 12)

●Severe (GCS score <9)

However, a significant minority of patients with TBI and a GCS score of 13 have potentially life-threatening intracranial lesions. While a revised classification has not been widely adopted, a GCS score of 9 through 13 likely best represents the TBI population at moderate risk for death or long-term disability (ie, "potentially severe").

In addition, classification of TBI in any individual patient should involve trending of the overall GCS score (as well as the individual components, eye, verbal, and motor) so that severity of the injury is not under- or over-estimated, both improvements and deterioration are recognized, and care is adjusted in a timely manner.

The GCS, including its prognostic value in children with head injury, is discussed in more detail separately. (See "Classification of trauma in children", section on 'Glasgow Coma Scale'.)

Other trauma scores that incorporate GCS or level of consciousness and that are used to identify severe injury include the Pediatric Trauma Score and the Revised Pediatric Trauma Score (table 2). (See "Classification of trauma in children", section on 'Physiologic systems'.)

EPIDEMIOLOGY — TBI is the leading cause of pediatric trauma death and disability and affects up to 280 out of 100,000 children worldwide [2,3]. In the United States alone, TBI annually impacts 475,000 children and causes over 2600 TBI-related deaths, 37,000 hospitalizations, and 435,000 emergency department (ED) visits [4,5]. Approximately 5000 children are disabled due to TBI each year. Moreover, costs of treatment for TBI approximate USD $2.6 billion annually [6].

Various mechanisms result in TBI severe enough to require hospitalization. Overall, falls and motor vehicle crashes account for the majority of injuries [7]. Inflicted head injury is a significant mechanism, particularly for infants younger than one year of age. As an example, in the United Kingdom, among infants were admitted to intensive care units with head injuries, 52 percent had been abused [8]. (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children".)

Among all children presenting to the ED in one prospective series, 98 percent had a Glasgow Coma Scale (GCS) score of 15, suggesting that most head injuries are minor [9]. However, approximately 75 percent of children with multiple trauma have TBI and almost 80 percent of all trauma deaths are associated with TBI [10,11]. Mortality rates between 17 and 33 percent have been reported in retrospective series describing children with severe brain injury [12-15]. In developed countries, TBI is the most common cause of trauma-related death and disability in childhood [16,17].

The highest pediatric morbidity and mortality is reported in children younger than four years of age, and in those with hypotension, low GCS scores at initial presentation, coagulopathy, or hyperglycemia [12,17-24]. Overall mortality among children with TBI who are treated in EDs or require hospital admission is 4.5 percent (compared with 10.4 percent among adults) [2]. Despite the higher survival in children with TBI, disability is significant with the functional long-term outcome associated with the initial injury severity [25].

TYPES OF INJURY — Brain injury can be categorized as diffuse or focal:

●Diffuse brain injury – Diffuse brain injury (DBI) is the most common type of severe TBI resulting in death in children and is usually produced by impact, acceleration, and deceleration forces. Diffuse traumatic axonal injury (DAI) is a severe form of DBI. DAI develops as the result of tissue shearing at the interface of grey and white matter [26-29]; focal injuries may also be present in patients with DAI (eg, multifocal intraparenchymal hemorrhages, subdural hematoma, or epidural hematoma).  

Although not associated with structural changes on imaging, concussion is a milder form of DBI. The definition and pathophysiology of concussion are discussed separately. (See "Concussion in children and adolescents: Clinical manifestations and diagnosis", section on 'Definitions' and "Concussion in children and adolescents: Clinical manifestations and diagnosis", section on 'Pathophysiology'.)

●Focal brain injury – Several types of focal brain injury may occur:

•Brain contusion – Brain contusions typically arise from blunt trauma between the brain and the skull after acceleration and deceleration of the head. Contusions may be in the location of impact (coup), or on the opposite side of the brain (contrecoup), or both.

•Intraparenchymal brain hemorrhage – Intraparenchymal brain hemorrhage develops from tears in the brain tissue and/or vasculature and may complicate blunt or penetrating trauma.

•Subdural hematoma – Subdural hematoma (SDH) forms when there is hemorrhage into the potential space between the dura and the arachnoid membranes (image 1). There are two major sources of bleeding in patients with SDH: bridging blood vessels that cross the subdural space and cerebral cortical hemorrhage caused by direct brain trauma. SDH commonly complicates severe brain injury, including abusive head trauma in children. The clinical diagnosis and management of SDH in children is discussed separately. (See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management".)

•Epidural hematoma – An epidural hematoma (EDH), also known as extradural hematoma, is a hemorrhage into the space between the dura and the overlying calvarium (image 2). After blunt trauma, an EDH may result from disruption of the middle meningeal artery, the middle meningeal vein, diploic veins, or venous sinuses. The clinical diagnosis and management of an intracranial EDH in children is discussed separately. (See "Intracranial epidural hematoma in children".)

•Subarachnoid hemorrhage – Subarachnoid hemorrhage develops from tearing of small vessels in the pia mater. It may complicate other brain injuries in children with severe head trauma or be found in isolation [30].

ASSOCIATED INJURIES — Severe TBI in children is commonly complicated by multiple trauma [13,31]. In retrospective series describing severely head injured children, up to two-thirds have sustained multiple trauma [13,32]. In these cases, death is typically a result of the head injury [15,32,33]. The management of multiple trauma in children is reviewed separately. (See "Trauma management: Approach to the unstable child".)

Cervical spine injury (CSI) must always be suspected for children with TBI or injury above the clavicle and evaluation is usually needed. CSI occurs in 1 to 2 percent of children with severe blunt trauma. Patients with severe TBI are at significant risk and can be difficult to assess. As an example, in one small observational study, almost 30 percent of children with severe TBI and continued altered mental status or need for endotracheal intubation 72 hours after injury, had comorbid findings on either computed tomography or magnetic resonance imaging of the spine [34]. (See "Evaluation and acute management of cervical spine injuries in children and adolescents".)

PATHOPHYSIOLOGY — The pathophysiology of severe TBI involves two insults:

●Primary injury is the direct trauma to the brain.

●Secondary injury is the result of a cascade of biochemical, cellular, and metabolic responses to direct injury which worsens in patients who develop hypoxia, hypotension, or both.

Initially following brain injury, cerebral blood flow appears to be decreased in children (rather than increased, as previously thought) [35-37]. Hypoperfusion in conjunction with increased metabolic demand makes the brain more susceptible to secondary insults, such as hypoxemia and hypotension. Cerebral perfusion may be particularly dependent upon maintaining adequate blood pressure (BP) because cerebral autoregulation is often impaired following severe pediatric TBI [14,38]. In addition, release of excitatory neurotransmitters, such as acetylcholine, glutamate, and aspartate causes neuronal damage [39].

Following this initial phase, cerebral swelling develops that generally peaks 24 to 72 hours after the injury. The resulting intracranial hypertension can further compromise cerebral perfusion leading to more ischemia, swelling, herniation, and death. Impaired cerebral autoregulation after initial TBI may further reduce cerebral blood flow and result in cerebral ischemia. For example, impaired cerebral autoregulation during the first week after severe TBI is associated with a poor, six-month Glasgow Outcome Score (severe disability, vegetative, or died) [40].

Diffuse cerebral swelling following severe TBI is more common among infants and children compared with adults [41]. Mechanisms that account for this age-related difference are not known. Anatomical and pathophysiological factors likely play a role. As an example, a diffuse pattern of brain injury may develop because the infant skull is more compliant and can tolerate considerable deformation before fracture occurs [42,43]. In addition, brain atrophy that probably begins in young adulthood, permits more room in the adult skull for the brain to expand. Finally, experimental data from animals suggest that pathophysiological features, such as enhanced diffusion of excitotoxic neurotransmitters, the inflammatory response of the developing brain, and changes in blood-brain-barrier permeability may also be involved [44].

The volume relationships between brain parenchyma, cerebrospinal fluid, and blood, as well as physiologic mechanisms that maintain pressure homeostasis (including the autoregulation of cerebral blood flow to maintain cerebral perfusion pressure) within the intracranial compartment are discussed separately. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Physiology'.)

PRIMARY SURVEY — As with any significantly injured child, during the initial evaluation and stabilization of the injured child (primary survey) priority is given to the maintenance of airway patency, oxygenation, ventilation, cardiovascular support, and the management of immediately life-threatening injuries according to the principles of Advanced Trauma Life Support (table 3). In children with severe TBI, rapid stabilization is particularly important to prevent secondary brain injury due to hypoxia and shock. (See "Trauma management: Approach to the unstable child", section on 'Primary survey'.)

All patients with severe TBI warrant emergency involvement of a neurosurgeon with pediatric expertise.

Cervical spine motion restriction should be maintained throughout the primary survey.

Initial assessment — During the primary survey, neurologic disability should be assessed as follows:

●Assign Glasgow Coma Scale (GCS) score (table 1) – GCS score provides a global assessment of consciousness and indicates need for intervention:

•Any patient with a GCS ≤12 or higher GCS with an abnormality on head computed tomography (CT) scan warrants emergency consultation with and evaluation by a neurosurgeon.

•In addition to neurosurgery consultation, any patient with a GCS <9 or a GCS that is rapidly falling warrants emergency endotracheal intubation. Intubation should be performed by rapid sequence intubation (RSI) with cervical spine motion restriction. The clinician should perform as much of the neurologic examination as possible before sedatives and paralytic agents are administered; however, intubation should not be delayed to perform the examination. (See 'Rapid sequence intubation' below.)

●Identify signs of impending herniation – Signs of transtentorial herniation include (figure 1 and table 4):

•Hypertension with bradycardia or tachycardia using age-based standards for heart rate (table 5) and blood pressure (BP) (table 6 and table 7)  

•Unequal or fixed and dilated pupils

•Abnormal breathing pattern (eg, Cheyne-Stokes respirations)

•Hemiparesis

•Decorticate, decerebrate, or absent motor response to pain

Initial stabilization — The initial management of children with severe TBI includes meticulous attention to support airway, breathing, and circulation to prevent secondary injury caused by hypoxia or hypotension and measures to prevent and treat intracranial hypertension [45,46].

Our approach to the initial stabilization of children with severe TBI is largely consistent with the revised Brain Trauma Foundation pediatric guidelines published in 2019 [47-49].

In many children with severe TBI, life-saving supportive therapies are initiated by emergency clinicians. Whenever possible, these patients should then be managed by specialists with pediatric expertise, including neurosurgeons, radiologists, and intensivists. Some patients will go to the operating room for neurosurgery or other surgeries and anesthesiologists should also have expertise in the management of these patients.

Airway and breathing — Patients with severe TBI (ie, GCS <9) generally require intubation to protect against aspiration of gastric contents and to optimize oxygenation and ventilation. Intubation is also warranted for patients with milder TBI if they have rapidly declining mental status and/or signs of respiratory failure. Patients with milder TBI who are awake and lucid can be managed with supplemental O2 alone.

When performing intubation in a child with severe TBI, the clinician should:

●Maintain cervical motion restriction (see "Pediatric cervical spinal motion restriction", section on 'Motion restriction during airway management')

●Use a cuffed endotracheal tube (see "Technique of emergency endotracheal intubation in children", section on 'Cuffed versus uncuffed')

General principles of airway management for children (including techniques for opening and maintaining an airway, bag-mask ventilation, and tracheal intubation) are reviewed separately. (See "Basic airway management in children" and "Technique of emergency endotracheal intubation in children".)

Rapid sequence intubation — Endotracheal intubation is accomplished by using RSI (table 8) (see "Rapid sequence intubation (RSI) in children for emergency medicine: Approach"):

●Pretreatment – Although optional, atropine, is suggested for all children in shock, children ≤1 year, <5 years when receiving succinylcholine, and older children receiving a second dose of succinylcholine. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Approach", section on 'Pretreatment'.)

We do not routinely use lidocaine for RSI in patients with elevated intracranial pressure (ICP) because our experience suggests that etomidate is adequate, and RSI without lidocaine is simpler to perform. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Airway'.)

●Induction agents – We suggest etomidate as the sedative agent during RSI in children with severe TBI. Our preference is based on its neuroprotective properties and favorable hemodynamic effects (ie, it can be used safely in patients with existing or impending hemodynamic instability). Although etomidate can cause transient adrenal suppression, the benefits appear to outweigh the risks in most patients. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis", section on 'Sedation (induction) agents'.)

Thiopental and propofol also have neuroprotective properties and are reasonable alternatives to etomidate; however, they can cause hypotension, particularly in patients who are hemodynamically unstable. Furthermore, thiopental is not available in many regions.

In the past, ketamine has been thought to increase ICP and has been avoided for RSI in children with severe TBI. However, limited observational evidence in ventilated children with severe TBI indicates that it does not increase ICP and in some patients decreases ICP while maintaining cerebral perfusion pressure [50,51]. Thus, ketamine may be an alternative agent for induction during RSI [52,53].

●Paralytic agents – Succinylcholine is preferred when there are concerns for a difficult airway. Although increased ICP with the use of succinylcholine has been reported in patients with brain tumors, there is no definitive evidence that succinylcholine causes a rise in ICP in patients with brain injury [54-56].

Otherwise, rocuronium or succinylcholine are good choices for paralytic agents. When the reversal agent for rocuronium, sugammadex, is available, then some experts prefer to use rocuronium to avoid any potential rare complications associated with succinylcholine, such as hyperkalemia in patients with undiagnosed neuromuscular disease, or malignant hyperthermia. Succinylcholine is also contraindicated in patients with acute crush injuries.  

When sugammadex is not available, succinylcholine, if not contraindicated, is preferred to other paralytics because of its shorter duration of paralysis which permits a more rapid recovery of the neurologic examination. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis", section on 'Paralytic agents'.)

Ventilation — Hyperventilation (PaCO₂ <35 mmHg) may cause cerebral ischemia as the result of decreased cerebral blood flow. Consequently, end-tidal CO₂ monitoring is essential for all intubated patients with severe TBI. End-tidal CO₂ should be maintained between 35 and 40 mmHg unless there are signs of impending herniation. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Breathing' and "Elevated intracranial pressure (ICP) in children: Management", section on 'Therapeutic hyperventilation'.)

Circulation — Cerebral perfusion must be maintained to prevent secondary ischemic injuries. Patients with severe TBI should have adequate venous access (eg, two large-bore peripheral intravenous catheters) in place so that shock can be rapidly treated. Laboratory studies should be obtained to as described below. (See 'Laboratory studies' below.)

Fluid management — Hypovolemic shock should be treated using isotonic solutions (eg, isotonic saline) with a goal of attaining a state of normal, rather than excess, circulating volume. Excess intravascular volume may exacerbate the development of cerebral edema. Hypotonic fluids, such as D5W, should be avoided because they deliver too much free water, which may exacerbate cerebral edema and cellular destruction. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Circulation'.)

General principles of the management of hypovolemic and hemorrhagic shock in children, as well as techniques for vascular access, are discussed separately. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies" and "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Fluid resuscitation'.)

Goal blood pressure — During the initial management of patients with severe TBI before the ICP monitor is placed, the clinician must make a judgement about what BP is adequate for cerebral perfusion without the ability to directly measure CPP:  

●While the optimal BP required to maintain cerebral perfusion in children with severe TBI is uncertain, we suggest targeting high-normal BP in most patients (ie, systolic BP ≥75^th to 90^th percentile for age, height, and sex (table 9)).

●Hypotension (ie, BP <5^th percentile) is clearly harmful in this setting and should be avoided [12,14,45,57-61].

●Hypertension in patients with severe TBI may indicate increased ICP. Management should first focus on measures to decrease ICP; antihypertensive medications should be avoided. (See 'Intracranial hypertension and brain herniation' below.)

Optimal BP management involves placing an ICP monitor to permit measuring the cerebral perfusion pressure (CPP; which is the difference between the mean arterial pressure and ICP). (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Cerebral perfusion pressure'.)

Many clinicians aim for a high-normal BP with the rationale that merely avoiding hypotension is insufficient to prevent cerebral ischemia. This approach is supported by a retrospective study of >10,000 children with isolated severe TBI (median GCS score of 3) in which hospital mortality was lower in patients with systolic BP ≥75^th percentile at the time of admission compared with patients with lower systolic BP [58]. However, other factors may account for the improved survival in patients with higher BPs. The optimal target remains uncertain. Our suggested target is higher than the current American College of Surgeons therapeutic target of ≥5^th percentile [12,14].

Once ICP monitoring is in place, BP and ICP should be adjusted to obtain a CPP of 40 to 50 mmHg for children five years of age and younger and 50 to 60 mmHg for children older than five years of age up to 17 years of age. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Medical treatment of sustained intracranial hypertension or impending herniation'.)

After correction of hypovolemia due to dehydration or hemorrhage, persistent hypotension may indicate cardiac dysfunction, thereby necessitating administration of vasoactive agents. Echocardiography may be warranted to definitively make the diagnosis of cardiac dysfunction. Elevated troponin has been documented, suggesting that myocardial injury occurs in severe isolated TBI [62]. Improving cardiac function may prevent multiorgan failure in TBI.

The target BP required to maintain the minimum cerebral perfusion pressure (mean arterial pressure minus ICP) necessary to meet cerebral metabolic demands in infants and children with severe TBI has not been established and is likely an age-dependent continuum. Systolic BP should be maintained at least above the fifth percentile for age (table 9) because outcomes such as mortality and neurologic disability for children with severe TBI who are hypotensive at the initial evaluation are typically poor [12,14,45,57-61] .

In the absence of ICP monitoring, with no possibility of assessing CPP, the optimal BP target is unknown. Until ICP monitoring is established, some clinicians base their management on a particular systolic BP percentile for age, height, and sex (eg, >75^th to 90^th percentile) because they feel that merely avoiding hypotension is insufficient to prevent cerebral ischemia. Evidence also suggests that a higher target systolic BP may be associated with improved clinical outcomes. For example, in a retrospective study of over 10,000 children with isolated severe TBI (median GCS 3), hospital mortality was lower in patients with systolic BP ≥75^th percentile at the time of admission compared with patients with lower systolic BP [58]. However, other factors may account for the improved survival in patients with higher BPs. This study used <75^th percentile as its definition of hypotension during resuscitation, which is higher than the current American College of Surgeons therapeutic target of ≥5^th percentile [12,14].

Once ICP monitoring is in place, BP and ICP should be adjusted to obtain a CPP of 40 to 50 mmHg for children 5 years of age and younger and 50 to 60 mmHg for children older than 5 years of age up to 17 years of age. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Medical treatment of sustained intracranial hypertension or impending herniation'.)

Intracranial hypertension and brain herniation — Basic measures for stabilization of children with elevated ICP and interventions for impending herniation or sustained elevations are described in the algorithm (algorithm 1) and discussed in detail separately. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Treatment of elevated ICP'.)  

Whenever possible, a neurosurgeon with pediatric expertise should guide decisions regarding the use of hyperosmolar agents and hyperventilation to treat intracranial hypertension.

Temperature management — Children with severe TBI should be prevented from becoming febrile through the use of antipyretics, and if necessary, cooling blankets. Most pediatric centers do not use hypothermia early in treatment. However, some centers still reserve the use of hypothermia therapy for control of refractory intracranial hypertension. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Temperature control'.)

SECONDARY SURVEY — Once the injured patient has undergone a primary survey and had all immediately life-threatening injuries stabilized, the next step in management involves a head-to-toe assessment (secondary survey) including ancillary studies to identify all injuries and proceed with definitive treatment. (See "Trauma management: Approach to the unstable child", section on 'Secondary survey'.)

Cervical spine motion restriction should be maintained during evaluation until serious spine and spinal cord injury has been excluded by patient examination and imaging. (See 'Cervical spine imaging' below.)

The remainder of this discussion will focus on the evaluation specific to head injured patients, including the recognition of signs and symptoms that may adversely affect outcomes.

The evaluation of children with minor head injury is discussed separately. (See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation".)

History — For most children with severe TBI, the history of the injury will be straightforward and consistent with a significant mechanism (eg, high speed motor vehicle crash or fall from a significant height).

Historical features may also identify children who do not appear to have had a significant head injury, but have in fact, sustained a severe TBI and whose condition may deteriorate. In addition to mechanism of injury, several key symptoms are important to identify (see "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation", section on 'Common findings' and "Minor blunt head trauma in children (≥2 years): Clinical features and evaluation", section on 'Common findings'):

●Prolonged loss of consciousness and/or abnormal mental status

●Persistent vomiting

●Severe headache

●Progression of symptoms

Physical examination

General assessment — Vital signs must include pulse oximetry and an assessment of ventilation (chest wall movement, breath sounds, or end-tidal CO2 measurement). Hypoxia, hypoventilation, and hypotension should be immediately identified and treated. (See 'Airway and breathing' above and 'Goal blood pressure' above.)

Respiratory depression, bradycardia, and/or hypertension may indicate impending herniation, which require emergency intervention (algorithm 1). (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Acutely elevated ICP'.)

Open wounds to the head and neck, including penetrating wounds, should be identified during the secondary survey. Management of these injuries may require surgery. In addition, children may lose significant amounts of blood from scalp lacerations. (See "Assessment and management of scalp lacerations".)

Neurological assessment — The initial assessment of the child with severe TBI should include a focused neurological examination, including the Glasgow Coma Scale (GCS) score (table 1).

A focused neurologic examination should include the following:

●Level of consciousness

●Pupillary examination for size, reactivity, and symmetry

●Extra-ocular movements

●Funduscopic examination

●Brainstem reflexes (corneal and gag reflexes)

●Deep tendon reflexes

●Response to pain

Any abnormalities in this examination may suggest increased intracranial pressure (ICP) with impending transtentorial herniation that requires immediate intervention. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Acutely elevated ICP' and 'Ongoing management' below.)

Signs of herniation that must be recognized include the following (see "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Acutely elevated ICP'):

●Signs of uncal herniation, including a third cranial nerve palsy, followed immediately by hemiplegia.

●Progressive changes in respiratory pattern, pupil size, vestibuloocular reflexes, and posture that correlate with the anatomic level of brain involvement (figure 1).

●Cushing's triad, which includes hypertension, bradycardia, and slow irregular respirations.

Abusive head trauma — For children with abusive head trauma, the history is inconsistent with the degree of injury or is absent. Abused children also often have associated findings of retinal hemorrhages, fractures, unexplained bruises, apnea, and/or seizures (table 10). A thorough evaluation by a multidisciplinary child abuse team should be performed whenever there is suspicion that an injury is inflicted. The evaluation and diagnosis of inflicted head injury is discussed in greater detail separately. (See "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children", section on 'Children with intracranial injury'.)

Laboratory studies — Laboratory evaluation depends upon the type and extent of injuries identified during the primary and secondary surveys. Most children with multiple injuries, including severe TBI due to blunt trauma warrant (see "Trauma management: Approach to the unstable child", section on 'Laboratory studies' and "Approach to the initially stable child with blunt or penetrating injury"):

●Rapid blood glucose (hyperglycemia is a poor prognostic indicator for children with severe TBI)

●Type and cross

●Arterial or venous blood gas

●Rapid hemoglobin or hematocrit

●Complete blood count

●Serum electrolytes

●Serum osmolarity (if hyperosmolar therapy with mannitol will be administered)

●Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) to assist with identifying intraabdominal injury

●Urinalysis to identify gross hematuria

●Prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR)  

Biomarkers are not routinely obtained for prognostication or clinical care.

Imaging — At minimum, children with severe TBI require further imaging of the cervical spine and head in addition to plain radiographs (eg, lateral cervical spine, AP chest, and AP pelvis) and focused assessment with sonography for trauma (FAST) typically obtained during the primary survey of critically injured children.

Cervical spine imaging — All patients with severe TBI require imaging of the cervical spine, typically consisting of plain radiographs of the cervical spine and/or computed tomography. The approach to imaging in the trauma patient with severe TBI and altered consciousness is provided in the algorithm (algorithm 2) and discussed separately. (See "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Cervical spine clearance'.)

Children with severe TBI and no abnormality identify on initial cervical spine imaging still warrant continued cervical spine motion restriction until recovery of mental status permits an accurate physical examination or more definitive imaging (eg, magnetic resonance imaging) and consultation with a spine service has occurred.

Neuroimaging — All pediatric patients with severe TBI should undergo unenhanced CT of the head [45]. CT readily identifies lesions that require emergency surgery (eg, epidural hematoma) and other focal injuries, such as contusions and hemorrhage.

The head CT may be normal initially in some patients despite the suggestion of significant brain injury based upon the clinical history and physical examination. In such cases, magnetic resonance imaging (MRI) can be useful because it is more sensitive for identifying diffuse axonal injury and associated cerebral edema. However, MRI can generally be deferred until after initial stabilization and treatment. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Magnetic resonance imaging'.)

Abdominal imaging — Because the abdominal examination is not reliable in children with severe TBI, imaging for intraabdominal injury (eg, contrast-enhanced computed tomography [CT] of the abdomen and pelvis) is also required in most children with high-force blunt multiple trauma (eg, motor vehicle crash). (See "Pediatric blunt abdominal trauma: Initial evaluation and stabilization", section on 'Radiologic evaluation'.)

ONGOING MANAGEMENT — Our approach to managing children with severe TBI is largely consistent with the 2019 guidelines for management of severe TBI in infants, children, and adolescents [63,64] and the principles of Emergency Neurologic Life Support [65].

Ongoing care of the child with severe TBI should occur in a pediatric intensive care unit at a trauma center under the guidance of a neurosurgeon with pediatric expertise whenever possible and requires repeated neurological examinations to detect deterioration and/or improvement of neurological status because GCS is a continuum, and children admitted with GCS suggesting moderate TBI (9 to 13) may deteriorate.

Key aspects of management include [47-49,63]:

●Address focal injuries that require neurosurgical intervention – These injuries should be quickly identified and surgically managed:

•Epidural hematomas (image 2) (see "Intracranial epidural hematoma in children", section on 'Subsequent management')

•Acute subdural hematomas, particularly if associated with midline shift (image 3) (see "Intracranial subdural hematoma in children: Clinical features, evaluation, and management", section on 'Operative decision')  

•Penetrating brain injuries (see "Approach to the initially stable child with blunt or penetrating injury", section on 'Head trauma')

●Maintain stable cardiopulmonary status and avoid secondary brain injury – This includes:

•Avoidance of hypoxemia – Oxygen saturation (SpO₂) is maintained 95 to 99 percent in the initial post-injury period.

•Maintaining normal ventilation – End-tidal CO₂ should be maintained between 35 and 40 mmHg unless there are signs of impending herniation. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Breathing' and "Elevated intracranial pressure (ICP) in children: Management", section on 'Therapeutic hyperventilation'.)

•Maintaining euvolemia, adequate blood pressure (BP), and cerebral perfusion pressure (CPP) – The target CPP varies by age (40 to 50 mmHg for children ≤5 years old, 50 to 60 mmHg for children >5 years old). (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Medical treatment of sustained intracranial hypertension or impending herniation'.)

●Manage intracranial hypertension – Optimal management of children with severe TBI includes placement of an ICP monitor for continuous ICP and CPP monitoring. The approach to managing intracranial hypertension (ie, ICP >20 mmHg) is summarized in the algorithm (algorithm 1) and discussed in detail separately. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Treatment of elevated ICP'.)

●Provide adequate sedation and analgesia – Sedation and analgesia are necessary to facilitate ventilation and ensure safety and comfort in patients receiving invasive mechanical ventilation. In addition, adequate sedation and control of pain also help to prevent abrupt increases in ICP related to painful procedures (eg, suctioning the endotracheal tube, placement of invasive lines and tubes). Sedatives may also be used to control ICP in patients with refractory intracranial hypertension (barbiturates are typically used in for this purpose). (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Refractory intracranial hypertension'.)  

●Other supportive care – Close attention should be paid to other physiologic parameters that can impact cerebral metabolism and ICP. General supportive care includes:

•Maintaining a normal body temperature – Fever should be avoided by using antipyretics, and if necessary, cooling blankets. Most centers do not use therapeutic hypothermia for management of severe TBI. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Temperature control'.)

•Providing adequate nutrition – Nutrition is generally started within the first 72 hours [63]. Enteral nutrition is preferred, when possible. (See "Overview of enteral nutrition in infants and children", section on 'Critical illness and postoperative states' and "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription".)

•Avoidance of hypo- and hyperglycemia. (See "Approach to hypoglycemia in infants and children", section on 'Treatment' and "Glycemic control in critically ill adult and pediatric patients".)

Use of evidence-based guidelines that incorporates these interventions decreases variation in the care of children with TBI and is associated with improved survival [46,66].

DISPOSITION — Outcomes appear to be improved for children with severe pediatric TBI who are treated at trauma centers with expertise in caring for children [67,68]. Experts recommend that patients in the field with a Glasgow Coma Scale (GCS) score ≤12 (table 1) or Pediatric Trauma Score ≤8 be transported directly to a pediatric trauma center whenever possible (table 2) [69-72].

Children with the following GCS scores, who are initially treated at a community hospital, should be transferred to a pediatric trauma center once their life-threatening conditions are stabilized:

●GCS <9

●GCS ≤12 with associated major injuries

●Deterioration in clinical condition, including decrease in GCS

OUTCOMES — Adherence to key components of the TBI guidelines is associated with decreased mortality and improved functional survival [46,63]. For example, in a study of the Pediatric Guideline Adherence and Outcomes (PEGASUS) program, adherence to key components of the best-practice guidelines was examined in 199 children, most of whom had severe TBI (median GCS score of 3 on emergency department [ED] admission and 6 on pediatric intensive care unit [PICU] admission) [63]. Of these patients, 80 percent survived to discharge, and 68 percent had a favorable discharge disposition (discharge to home or rehabilitation service). Adherence by each indicator was:

●When intracranial pressure (ICP) monitoring is in place, maintain cerebral perfusion pressure >40 mmHg: 64 percent

●Avoid hypocarbia (partial pressure of carbon dioxide [PaCO₂] <30 mmHg) in the absence of herniation: 72 percent (n = 105)

●Initiate nutrition within 72 hours: 81 percent  

After adjustment for injury severity, adherence to each additional indicator was associated with higher survival (relative risk [RR] 1.27, 95% CI 1.12-1.44) and favorable discharge disposition (RR 1.46, 95% CI 1.23 to 1.72) in a dose-response fashion.

In a separate study, adherence to the prior version of these guidelines [45,46] was also cost effective [73].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Increased intracranial pressure and moderate-to-severe traumatic brain injury" and "Society guideline links: Pediatric trauma".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Head injury in adults (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Definition – The severity of traumatic brain injury (TBI) is traditionally defined by the initial Glasgow Coma Scale (GCS) or Pediatric Glasgow Coma Scale score (table 1) (see 'Severity classification' above):

•Mild (GCS score 13 to 15)

•Moderate (GCS score 9 to 12)

•Severe (GCS score <9)

However, a significant minority of patients with TBI and a GCS score of 13 have intracranial lesions with a moderate risk for death or long-term disability (ie, "potentially severe").  

●Primary survey – Initial priority is given to the maintenance of oxygenation, ventilation, cardiovascular support, and the management of immediately life-threatening injuries according to the principles of Advanced Trauma Life Support (table 3). In children with severe TBI, rapid stabilization is also important to prevent secondary brain injury due to hypoxia and shock. (See 'Primary survey' above.)

•Cervical spine motion restriction – Cervical spine motion restriction should be maintained during evaluation until serious spine and spinal cord imaging has been excluded by patient examination and, for patients with severe TBI, further imaging and specialty consultation. The approach to imaging in the trauma patient with altered consciousness is provided in the algorithm (algorithm 2) and discussed separately. (See "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Cervical spine clearance'.)

•Airway and breathing – Children with severe TBI generally require intubation using rapid sequence intubation (RSI) to protect against aspiration of gastric contents and to optimize oxygenation and ventilation. (See 'Airway and breathing' above.)

For most patients with severe TBI, we suggest etomidate as the induction (sedative) agent during RSI (Grade 2C). If the patient is hemodynamically stable, propofol or thiopental (where available) are reasonable alternatives. Either rocuronium or succinylcholine are acceptable choices for muscle relaxation. (See 'Rapid sequence intubation' above and "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis".)

After intubation, end-tidal CO₂ should be continuously monitored and maintained between 35 and 40 mmHg, unless there are signs of impending herniation. (See 'Ventilation' above and "Elevated intracranial pressure (ICP) in children: Management", section on 'Breathing'.)

•Circulation – Patients with severe TBI require adequate venous access (eg, two large-bore peripheral intravenous catheters) in place so that shock can be rapidly treated using isotonic solutions (eg, isotonic saline) with a goal of attaining a state of normal, rather than excess, volume status. Hypotension should be avoided. (See 'Circulation' above and 'Fluid management' above.)

During the initial management of patients with severe TBI before the intracranial pressure (ICP) monitor is placed, we suggest targeting high-normal blood pressure (BP) in most patients (ie, systolic BP ≥75^th to 90^th percentile for age, height, and sex (table 9)) (Grade 2C). (See 'Goal blood pressure' above.)

•Intracranial hypertension – During the primary survey, neurologic disability should be assessed by assigning a GCS score and identifying signs of herniation (figure 1 and table 4). The presence of hypertension with bradycardia or tachycardia should be determined using age-based standards (table 5 and table 6 and table 7). (See 'Initial assessment' above.)

Emergency consultation with a neurosurgeon with pediatric expertise should occur for all children with moderate to severe TBI. Basic measures for stabilization of children with elevated ICP and interventions for impending herniation or sustained elevations are described in the algorithm (algorithm 1). Antihypertensive medications should be avoided. (See 'Intracranial hypertension and brain herniation' above.)

•Temperature management – Children with severe TBI require treatment to prevent fever with antipyretics, and if necessary, cooling blankets. Most pediatric centers do not use hypothermia early in treatment.

●Secondary survey – Once all immediately life-threatening injuries stabilized, the secondary survey consists of a focused history, head-to-toe assessment (secondary survey), and ancillary studies to identify all injuries. (See 'Secondary survey' above.)

Laboratory evaluation depends upon the type and extent of injuries identified during the primary and secondary surveys. Most children with multiple injuries, including severe TBI due to blunt trauma, warrant extensive testing as described above. (See 'Laboratory studies' above.)

All pediatric patients with severe TBI should undergo unenhanced computed tomography (CT) of the head to identify focal brain injuries that may require neurosurgical intervention. (See 'Neuroimaging' above.)

●Ongoing management – In patients whose brain injury is not amenable to surgical correction, further care is focused on preventing hypoxia or hypotension and monitoring for and treating intracranial hypertension as discussed separately (see "Elevated intracranial pressure (ICP) in children: Management", section on 'Treatment of elevated ICP'). Ongoing care of the child with severe TBI should occur in a pediatric intensive care unit at a trauma center under the guidance of a neurosurgeon with pediatric expertise, whenever possible. (See 'Disposition' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Neil Dooney, MBBS, and Pichaya Waitayawinyu, MD, who contributed to an earlier version of this topic review.