Pediatric Head Trauma

Etiology

Underlying etiologies of pediatric TBI include sporting events, falls, and motor vehicle collisions.[4] Falls resulting in head trauma are more common in young children due to 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 clinician should be cognizant of is non-accidental trauma (NAT).[5]

Epidemiology

Each year, pediatric TBI results in over 500,000 emergency department visits and about 60,000 hospitalizations in the United States.[6] 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, and trauma is the leading cause of mortality in children aged 1 or older.[1][2] In the United States, head trauma-related deaths exceed 3,000 per year in the pediatric population.[7] Across all pediatric age groups, males are more likely to present with TBI than females.[8]

Pathophysiology

The underlying pathophysiology of TBI is the excessive deformation of the brain parenchyma and the 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 be fractured along the calvarium or skull base. Leptomeningeal cysts (growing skull fractures) and "ping-pong" fractures may also be seen in the pediatric population.[9][10]

Hemorrhage may occur in multiple compartments outside and within the brain, including subarachnoid hemorrhage, subdural hematoma, epidural hematoma, contusions within the brain parenchyma itself, and cephalohematoma (birth-related injury) where a hematoma exists in the compartment between the periosteum and underlying calvarium.[11] Diffuse axonal injury (DAI) is present to some degree in the majority of patients with moderate-to-severe TBI.[12] 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 CT (computed tomography) scan but later identified on magnetic resonance imaging (MRI). DAI is a subtype of TBI that 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 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.[13] Unrestricted glutamate release subsequently triggers voltage/ligand-gated ion channels, resulting in a cortical spreading depression-like state.[13] Adenosine triphosphate (ATP) dependent ionic pumps are extensively upregulated to restore cellular hemostasis, resulting in widespread depletion of intracellular reserve and increased adenosine diphosphate (ADP).[13] As a result, neurons transition into impaired metabolism that can last 7 to 10 days following the initial injury and may be associated with alterations in cerebral blood flow.[13] 

During the impaired metabolic state, the brain is vulnerable to repeat injury and impairments in behavior and spatial learning, presenting as post-concussive symptoms. As a result of TBI, neurons may undergo cytoskeletal damage, altered neurotransmission, and axonal dysfunction.[13] Early identification and management of TBI are critical in halting the progression of the primary injury, preventing or reducing the severity of the secondary injury, and preventing subsequent primary injuries when the brain is vulnerable. 

History and Physical

The initial examination of a pediatric TBI patient should proceed stepwise to identify all injuries and optimize cerebral perfusion by maintaining hemodynamic stabilization and oxygenation. The initial survey should include a brief, focused neurological examination concerning the GCS. 

The pediatric GCS is similar to the adult GCS, with the main difference being 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 is performed with vigilance for occult injuries and attention to the following warning signs:

• Inspection for cranial nerve deficits, periorbital or postauricular ecchymoses, cerebrospinal fluid (CSF) rhinorrhea or otorrhea, or hemotympanum (signs of the base of skull fracture).[14]

• 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, before fontanelle closure, a complete and/or tense anterior fontanelle can serve as a marker for elevated ICP.

• Auscultation for carotid bruits, 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 for deep tendon reflexes. Evaluate plantar reflexes for upgoing toes (Babinski sign). Clonus, Hoffman reflex, and bulbocavernosus reflex are concerns for associated spinal cord injury

NAT should be suspected if the patient presents 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 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 facilitate the early identification of patients with elevated ICP and the implementation of primary bedside interventions. Non-contrast CT of the head is the imaging modality of choice for patients with TBI and an abnormal GCS. Several clinical decision guidelines[15] 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 score 14-15) with a low risk of clinically significant brain injuries.[16]

Children aged 2 or younger:

• GCS score ≤14 or palpable skull fracture or other signs of altered mental status: CT head recommended.

• 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 versus observation based on parental preference, age 3 or less than 3 months, worsening signs/symptoms in the emergency department, multiple versus isolated findings, and clinician experience. 

• All others: CT head is not recommended 

Children aged 2 or older:

• GCS score ≤14 or signs of basilar skull fracture or other signs of altered mental status: CT head recommended.

• History of loss of consciousness or severe headache or history of vomiting or history of a severe mechanism of injury: CT versus observation (similar to above).

• All others: CT head not recommended 

Although CT is valid in the initial evaluation of TBI, little evidence exists supporting routine repeat imaging in children.[17] MRI may be indicated when the clinical picture remains unclear after CT imaging to identify subtle lesions or if the patient's neurologic status has not improved multiple days into admission. Cerebral vascular imaging, such as CT angiography (CTA) or magnetic resonance angiography (MRA) of the head, may be helpful if there is a concern for vascular injury or underlying vascular malformation, aneurysm, etc, which may have preceded the trauma. Ophthalmologic evaluation with 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 cannot 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 partial pressure of carbon dioxide (PaCO₂) target of 35 to 40 mm of mercury (mm Hg). Within the first 48 hours, prophylactic hyperventilation to a PaCO₂ <30 mm Hg is avoided.[18] 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 the airway. Systemic hypotension negatively impacts the outcome in the setting of TBI. Isotonic crystalloids should be used to prevent and correct hypotension; colloidal solutions do not tend to improve outcomes. (B2)

Post-traumatic seizures are associated with severe TBI.[19] The prophylactic use of phenytoin for 7 days post-injury in severe TBI patients reduces the incidence of early post-traumatic seizures (within 7 days of injury) but not late post-traumatic seizures (>7 days following injury).[19] Levetiracetam may also serve as a beneficial alternative anti-epileptic medication but is less well-studied than phenytoin.[20]

Prolonged elevations of ICP greater than a threshold of 20 mm Hg are associated with poor neurologic outcomes in the pediatric population.[21] In addition to controlling elevated ICP, maintaining a minimum cerebral perfusion pressure (CPP) of 40 mm Hg in the pediatric TBI patient reduces mortality and improves neurologic outcomes.[22] Like blood pressure, ICP and CPP are age-dependent, resulting in variable threshold ranges that differ from those recommended for adults. (B2)

Approaches to reduce elevated ICP include: 

1. Elevate the head of the bed to 30°.
2. Determine that the neck is neutral 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 prevent maneuvers that increase ICP, such as coughing, straining, and fighting against the ventilator.[23]
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.[19] 
5. ICP monitoring may be considered in infants and children with severe TBI who do not have a reliable neurologic exam where elevated ICP resulting in a decline in neurologic status is detected.[24] Recent evidence in the adult TBI literature suggests that ICP monitoring is not associated with improved outcomes.[25] 
6. Osmotic agents: Hypertonic saline (3%) or mannitol are the common hyperosmolar agents to reduce ICP.[19] Bolus or continuous dosing of hypertonic saline may be used with the minimum dose needed to achieve and maintain ICP <20 mm Hg.[19] Mannitol is less well-studied in the pediatric population but is ineffective in reducing elevated ICP and is potentially detrimental to pediatric TBI patients. 
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.[19] 
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.[26] The bone flap should be large and completely removed, with extensive duraplasty.[19] 
9. Hypothermia does not improve outcomes in children and remains investigational at this period.[27] In contrast, hyperthermia should be avoided as it is potentially harmful to the injured brain. 
10. If not contraindicated, CSF diversion may reduce medically refractory ICP, typically via external ventricular drain (EVD) or lumbar drain.[28]
11. Corticosteroids: No evidence supports corticosteroids improving neurologic outcomes. Corticosteroids are associated with increased systemic complications.[28]
(A1)

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 extra-axial fluid collections, which may be mistaken for NAT.[29]

Prognosis

Nearly 90% of patients are discharged home from the emergency department after a head injury.[23] On admission CT, approximately 1% of patients with a GCS of 14 to 15 have a clinically significant intracranial injury.[16] In the severe TBI population, modern mortality rates have been reported to range between 20% and 39%.[30] Abusive head trauma (shaken baby syndrome) is the most common cause of death in patients sustaining NAT.[31]

Prognosticating outcomes following TBI has long been a goal of current research. The ability to accurately prognosticate assists treating clinicians, researchers, and patients' families. The International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) study advances TBI prognostication and is available online.[32] 

Complications

Complications depend on the severity of the head injury and can vary from mild cognitive impairment to seizures, long-term neurological deficits, and death. Systemic complications may also occur, particularly in severe TBI cohorts 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.