Continuing Education Activity

Traumatic brain injury (TBI) represents one of the leading causes of death and disability in children between 1 and 18 years of age. TBI is typically classified as mild, moderate, or severe based on the Glasgow coma scale (GCS). The condition is a disruption in the normal function of the brain caused by a mechanical impact on the head. TBI ranges from mild to severe and/or fatal. TBI can be conceptualized as a primary injury occurring at the moment of impact, followed by a secondary injury which can be due to a combination of sequelae, including intracranial hematomas, ischemia (often due to elevated intracranial pressure), edema, vasospasm, and hypoxemia. This activity reviews the epidemiology, etiology, and pathophysiology of pediatric head trauma, outlines the evaluation and management of this patient population and emphasizes the importance of the interprofessional team in its management.

Objectives:

• Identify the etiology of pediatric head trauma.
• Review the pathophysiology of head trauma in children.
• Outline the treatment and management options available for pediatric head trauma.
• Describe interprofessional team strategies for improving care coordination and outcomes in children with head trauma.

Introduction

Traumatic brain injury (TBI) represents one of the leading causes of death and disability in children between 1 and 18 years of age.[1][2] TBI is typically classified as mild, moderate, or severe based on the Glasgow coma scale (GCS). Patients with a GCS of 14 to 15 are considered to have mild TBI, while patients with a GCS of 9 to 13 have moderate TBI, and those with a GCS of 3 to 8 have severe TBI.[3] Severe TBI is associated with a high risk of mortality and neurologic morbidity in children.[2] Primary prevention efforts, avoidance of secondary neurologic injury, organized trauma systems, and diagnosis and treatment of elevated intracranial pressure (ICP) can ameliorate negative outcomes of severe TBI. 

Etiology

Underlying etiologies of pediatric TBI include sporting events, falls, and motor vehicle collisions.[4] Falls resulting in head trauma are more common in very young children because of their under-developed ambulatory skills combined with disproportionately large heads, a shifted center of gravity, and immature neck muscles. A less common but potentially severe etiology that the pediatric provider should be cognizant of is non-accidental trauma (NAT).

Epidemiology

Each year, pediatric TBI results in over 500,000 emergency department visits and about 60,000 hospitalizations in the United States.[5] The majority of pediatric head injuries are minor, including scalp abrasions, with no concern for significant intracranial pathology. On the other hand, many pediatric head injuries are significant, which is evident by the fact that trauma is the leading cause of mortality in children older than one year.[1][2] In the United States, head trauma-related deaths exceed 3,000 per year in the pediatric population.[6] Across all pediatric age groups, males are more likely to present with TBI than their female counterparts.[7]

Pathophysiology

The underlying pathophysiology of TBI is the excessive deformation of the brain parenchyma and its vascular structures relative to the skull and its normal attachment sites. Specific mechanisms of TBI are diverse and may include penetrating injuries, blast injuries, contact injuries, and acceleration-deceleration inertial injuries, with many patients presenting with a combination of different mechanisms. The skull may become fractured along the calvarium or skull base. Leptomeningeal cysts (growing skull fractures) and "ping-pong" fractures may also be seen in the pediatric population. 

Hemorrhage may occur in multiple compartments within and outside of the brain, including subarachnoid hemorrhage, subdural hematoma, epidural hematoma, contusions within the brain parenchyma itself, and cephalohematoma (birth-related injury) where there is a hematoma in the compartment between the periosteum and underlying calvarium. Diffuse axonal injury (DAI) is thought to be present to some degree in the majority of patients with moderate-to-severe TBI. DAI is typically caused by a rapid rotational or deceleration force that causes stretching and tearing of neurons, leading to focal areas of hemorrhage that are not always detected on the initial (computed tomography) CT scan but later identified on magnetic resonance imaging (MRI). DAI is a subtype of TBI which can present with intractable coma without elevated ICP. 

TBI can be conceptualized as a primary injury occurring at the moment of impact, followed by a secondary injury resulting from disrupted normal cellular function. Secondary injury can result from a combination of inflammation, ischemia, apoptosis, and vasospasm. At the cellular level, the biomechanical force of TBI results in unregulated ionic flux (potassium efflux, sodium, and calcium influx), which leads to unrestricted glutamate release.[8] Unrestricted glutamate release triggers voltage/ligand-gated ion channels resulting in a cortical spreading depression-like state.[8] Adenosine triphosphate (ATP) dependent ionic pumps are then extensively upregulated to restore cellular hemostasis resulting in widespread depletion of intracellular reserve and an increase in adenosine diphosphate (ADP).[8] As a result, neurons then transition into a state of impaired metabolism that can last up to 7 to 10 days following the initial injury and may be associated with alterations in cerebral blood flow.[8] 

During this impaired metabolic state, the brain is vulnerable to repeat injury, as well as impairments in behavior and spatial learning, often presenting as post-concussive symptoms.[8] As a result of TBI, neurons may additionally experience cytoskeletal damage, altered neurotransmission, and axonal dysfunction.[8] Early identification and management of traumatic brain injury are crucial in halting the progression of the primary injury, preventing or reducing the severity of secondary brain injury, and preventing subsequent primary injuries during the period when the brain is vulnerable following traumatic brain injury. 

History and Physical

The initial resuscitation of a pediatric TBI patient should proceed in a step-wise fashion to identify all injuries, as well as optimize cerebral perfusion by maintaining hemodynamic stabilization and oxygenation. The initial survey should include a brief, focused neurological examination with attention to the GCS. 

The pediatric GCS is similar to the adult GCS, with the main difference in the verbal component of the scoring system. In the 0 to 23 month age group, a 5 is designated for babbling, cooing, or smiling appropriately, 4 points if crying but consolable, 3 points for inconsolable crying, 2 points for moaning or grunting, and 1 point for no verbal response. In the 2 to 5 age group, a 5 is designated if the child is verbalizing appropriate words and phrases, a 4 is designated if the child is verbalizing inappropriate words, a 3 if the child is crying or screaming, a 2 for moaning or grunting and a 1 for no verbal response. GCS in the >5 age group is similar to that in an adult patient. 

After stabilization of any airway, breathing, or circulatory deficits, a thorough head-to-toe physical examination must be performed with vigilance for occult injuries and careful attention to detect any of the following warning signs:

• Inspection for cranial nerve deficits, periorbital or postauricular ecchymoses, cerebrospinal fluid (CSF) rhinorrhea or otorrhea, hemotympanum (signs of the base of skull fracture)[9]
• Fundoscopic examination for retinal hemorrhage (a potential sign of abuse in children) and papilledema (a sign of elevated ICP)
• Palpation of the scalp for hematoma, crepitus, laceration, and bony deformity (markers of skull fractures). In infants, prior to fontanelle closure, a full and/or tense anterior fontanelle can serve as a marker for elevated ICP
• Auscultation for carotid bruits, painful Horner syndrome, or facial/neck hyperesthesia (markers of carotid or vertebral dissection)
• Evaluation for spine tenderness, paresthesias, incontinence, extremity weakness, priapism (signs of spinal cord injury)
• Extremities: Motor and sensory examination (for signs of spinal cord injury)
• Reflexes: Check deep tendon reflexes. Evaluate plantar reflexes for upgoing toes (Babinski sign). Check for clonus, Hoffman reflex, and bulbocavernosus reflex is a concern for associated spinal cord injury

Non-accidental trauma (NAT) should be suspected if the patients present with classical features such as:

• Multiple injuries in multiple locations with different stages of healing
• Retinal hemorrhage
• Bilateral chronic subdural hematomas in a young child
• Significant neurologic injury with minimal signs of external trauma

Symptoms/signs of pediatric patients who have sustained a TBI and are awake enough to express themselves may include headache, nausea/emesis, irritability, and diplopia, among others. Depending on the severity of the TBI, as children age, they may face challenges in information processing, reasoning, impulsivity, mood lability, and sleep disturbance. 

Evaluation

Serial neurological examinations allow for early identification of patients with elevated intracranial pressure (ICP) and subsequent implementation of primary bedside interventions to improve venous outflow and reduce metabolic demands. 

Non-contrast cranial computed tomography (CT) of the head is the imaging modality of choice for patients with TBI and an abnormal GCS. Several clinical decision guidelines[10] have been validated and can be applied to determine which children with a normal or near-normal GCS can safely avoid CT. The PECARN algorithm, as outlined below, resulted in these recommendations for obtaining head CT in the pediatric patient after identifying children with a mild TBI (GCS 14-15) with a very low risk of clinically significant brain injuries.[11]

Children <2

1. GCS ≤ 14 or palpable skull fracture or other signs of altered mental status: CT head recommended
2. History of loss of consciousness for ≥5 seconds or severe mechanism of injury or occipital, parietal, or temporal scalp hematoma, or "not acting normally" per the parent or guardian: CT head vs. observation based on parental preference, age ≤ 3 months, worsening signs/symptoms in the emergency department, multiple vs. isolated findings, and physician experience. 
3. All others: CT head is not recommended 

Children ≥ 2

1. GCS ≤ 14 or signs of basilar skull fracture or other signs of altered mental status: CT head recommended 
2. History of loss of consciousness or severe headache or history or vomiting or history of a severe mechanism of injury: CT vs. observation (similar to above)
3. All others: CT head not recommended 

Despite CT's utility in initial TBI evaluation, there is little supporting evidence for routine repeat imaging in children.[12] Magnetic resonance imaging (MRI) may be indicated when the clinical picture remains unclear after CT imaging to identify more subtle lesions or if the patient's neurologic status has not improved following multiple days into admission. Vessel imaging, such as CT angiography (CTA) or magnetic resonance angiography (MRA), may be helpful if there is a concern for vascular injury or contributing underlying vascular malformation, aneurysm, etc., which may have preceded the trauma. 

Fundoscopy is necessary to look for the presence of retinal hemorrhages in cases suspected of NAT. 

Treatment / Management

Airway adjuncts are indicated in patients who cannot maintain an open airway or are unable to maintain adequate oxygen saturation with supplementary oxygen. Oxygenation parameters should be monitored using continuous pulse oximetry. Ventilation should be monitored with continuous capnography with an end-tidal pCO2 target of 35 to 40 mm Hg. Within the first 48 hours, prophylactic hyperventilation to an arterial carbon dioxide tension (PaCO2) <30 mm Hg should be avoided if possible.[13] Placement of a definitive airway, such as an endotracheal tube, is recommended in a patient with a GCS of less than 9 due to the patient's inability to secure their airway.  

Systemic hypotension negatively impacts the outcome in the setting of TBI. Isotonic crystalloids should be used to prevent and correct hypotension; colloidal solutions have not been shown to improve outcomes. 

Post-traumatic seizures are associated with severe TBI.[14] The prophylactic use of phenytoin for seven days post-injury in severe TBI patients have been found to reduce the incidence of early post-traumatic seizures (within seven days of injury) but not late post-traumatic seizures (>7 days following injury).[14] Levetiracetam may also serve as a beneficial alternative anti-epileptic medication but is less well-studied than phenytoin.[15]

Prolonged elevations of ICP greater than a threshold of 20 mm Hg are associated with poor neurologic outcomes in the pediatric population.[16] It has been suggested that in addition to controlling elevated ICPs, maintaining a minimum cerebral perfusion pressure (CPP) of 40 mm Hg in the pediatric TBI patient reduces mortality and improves neurologic outcomes.[17] It bears mentioning that similar to blood pressure, ICP and CPP are age-dependent, resulting in variable threshold ranges that differ from those recommended for the adult population. 

Approaches to reduce elevated ICP include: 

1. Elevate the head of the bed to 30 degrees.
2. Determine that the neck is in a neutral position and that the cervical collar is not impeding venous outflow.
3. Appropriate analgesics and sedation: Pain and agitation can elevate ICP. Opiates and benzodiazepines are frequently used. In refractory cases, neuromuscular blockade may be used to prevent maneuvers that increase ICP, such as coughing, straining, and fighting against the ventilator.[18]
4. Hyperventilation: Routine hyperventilation in TBI is not recommended, though, in the setting of impending herniation, it remains one of the fastest, short-term methods to lower ICP en route to the operating room.[14] 
5. ICP monitoring may be considered in infants and children with severe TBI who do not have a reliable neurologic exam where elevated ICPs resulting in a decline in neurologic status would be readily detected.[19] It should be noted, however, that recent evidence in the adult TBI literature suggests that ICP monitoring is not associated with improved outcomes.[20] 
6. Osmotic agents: Hypertonic saline (3%) or mannitol are the common hyperosmolar agents used to reduce ICP.[14] Bolus or continuous dosing of hypertonic saline may be used with the minimum dose needed to achieve and maintain ICP <20 mm Hg.[14] Mannitol is less well-studied in the pediatric population but has not been shown to be ineffective in reducing elevated ICPs or detrimental to the pediatric TBI patient. 
7. Barbiturates: Patients with elevated ICP, refractory to other therapies, may benefit from barbiturates which are thought to decrease ICP by decreasing cerebral metabolic demand.[14] 
8. Decompressive hemicraniectomy: As part of a surgical procedure to evacuate hematoma or as a primary treatment of refractory ICP, decompressive hemicraniectomy can be used to reduce medically refractory ICP via the removal of part of the skull.[21] It is recommended that when used, the bone flap should be large, the bone flap should be completely removed, and there should be extensive duraplasty.[14] 
9. Hypothermia has not been shown to improve outcomes in children and remains investigational at this period.[22] In contrast, hyperthermia should be avoided as it is potentially harmful to the injured brain. 
10. Cerebrospinal fluid (CSF) diversion may be employed to reduce medically refractory ICP, typically via external ventricular drain (EVD) or lumbar drain if not contraindicated.[23]
11. Corticosteroids: There is no evidence to support corticosteroids improving neurologic outcomes.[23] Corticosteroids are associated with increased systemic complications.[23]

Differential Diagnosis

A thorough head-to-toe physical examination must be performed with vigilance for occult injuries or alternative etiologies. Glutaric aciduria type 1 patients may present with macrocephaly and bilateral subdural hemorrhages, which can be mistaken for NAT.[24]

Prognosis

Nearly 90% of patients are discharged home from the emergency department after their head injury.[18] Approximately 1% of patients with a GCS of 14 to 15 have a clinically significant intracranial injury on CT.[11] In the severe TBI population, modern mortality rates have been reported to range between 20-39%.[25] Abusive head trauma (shaken baby syndrome) is the most common cause of death in patients sustaining NAT.[26]

Prognosticating outcomes following TBI has long been a goal of investigators. The ability to accurately prognosticate serves a great value in assisting treating physicians, researchers, and patient's families. The International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) study provides an advance in TBI prognostication and is available online for use.[27] 

Complications

Complications depend on the severity of the head injury and can vary from mild cognitive impairment to seizures, long-term neurological deficits, and even death. Systemic complications may also occur, particularly in the severe TBI cohort secondary to immobility, and may include pneumonia, deep venous thrombosis, and pulmonary embolus, among others. If patients cannot be successfully weaned from a ventilator, they may require temporary or long-term airway and nutritional support via a tracheostomy and gastrostomy tube, respectively. 

Deterrence and Patient Education

Parents of a child who sustains a head injury should be aware of the warning symptoms of elevated ICP. Informed consent, including all the likely complications (including the long-term ones), should be obtained if the child is being planned for any surgical intervention.

Enhancing Healthcare Team Outcomes

The management of pediatric head trauma is performed by an interprofessional healthcare team that includes a combination of a pediatric neurosurgeon, emergency department physician, nurse practitioner, pediatrician, trauma physician, radiologist, and others. Most children with mild head trauma are discharged from the emergency department. However, patients discharged after a head injury, or concussion should be instructed to return to physical activities in a step-wise approach. The initial step is a period of physical and cognitive rest, followed by scheduled increases in activities with close monitoring for the recurrence of symptoms. Any recurrence of symptoms indicates the need for further limitation of activities. Recommendations for return-to-activities continue to change as new studies are published, and the center for disease control (CDC) website is a helpful source for up-to-date guidelines.[28]