Continuing Education Activity

Blunt traumatic brain injury (TBI) is a disruption in the normal function of the brain caused by a mechanical impact to the head. TBI ranges from mild to severe and/or fatal. TBI can be conceptualized as a primary event occurring at the moment of impact, followed by secondary damage due to edema and elevated intracranial pressure. This activity reviews the pathophysiology of pediatric head trauma and stresses 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

Blunt traumatic brain injury (TBI) is a disruption in the normal function of the brain caused by a mechanical impact to the head. TBI ranges from mild to severe and/or fatal. TBI can be conceptualized as a primary event occurring at the moment of impact, followed by secondary damage due to edema and elevated intracranial pressure. Early identification and management of traumatic brain injury are crucial in halting the progression of the primary insult and preventing or reducing secondary brain injury. 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.[1] Initial symptoms of moderate-severe TBI in children are similar to adults, but the ultimate functional impact in children who survive TBI becomes more apparent as the child ages and faces increased challenges in processing information, reasoning, and impaired judgment.

Etiology

The most common cause of TBI in children are falls and sports/recreation-related injuries. Falls (striking the head) 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. Less common, but more severe etiologies of TBI include non-accidental trauma and motor vehicle-related injuries including pedestrians struck by a vehicle.

Epidemiology

Each year, pediatric TBI results in over 500,000 emergency department visits and about 60,000 hospitalizations in the United States.[2] Fatal TBI in children is primarily caused by non-accidental trauma and motor vehicle-related injuries (including pedestrians struck by a vehicle). Falls and sports/recreation-related TBI rarely lead to fatal injuries but can cause post-concussive symptoms in up to 30% of patients. Falls are more common in children in the 0 to 4 year age group, while sports and recreation-related injuries are more common in the 5 to 14 year age group. Across all age groups, males are more likely to present with TBI.

Pathophysiology

Most patients with moderate-to-severe TBI have a combination of intracranial injuries. 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 and edema that are not always detected on the initial CT scan. Subarachnoid hemorrhage (SAH) due to tearing of pial vessels is considered a marker of severity, present in almost half of pediatric patients with severe TBI. Subdural and epidural hematomas are the most frequent type of mass lesion identified in TBI. Cerebral contusions occur in about one-third of patients with moderate-to-severe TBI, caused by a direct impact or acceleration-deceleration forces that cause the brain to strike the frontal or temporal regions of the skull.  Intracerebral bleeding or hematoma, caused by coalescence of contusions or a tear in a parenchymal vessel, occurs in up to one-third of patients with moderate-to-severe TBI.

History and Physical

The initial resuscitation 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 also include a brief, focused neurological examination with attention to the GCS, pupillary examination, and motor function.

The pediatric GCS is similar to the adult GCS, but the main difference is in the verbal response in which the pediatric GCS assigns a normal verbal score of 5 for babbling, cooing, or smiling appropriately, while subtracting 1 point if crying but consolable, subtracting 2 points for inconsolable crying, subtracting 3 points for moaning or grunting, and subtracting 4 points for no verbal response.

After addressing any airway 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[3], cerebrospinal fluid (CSF) rhinorrhea or otorrhea, hemotympanum (signs of the base of skull fracture)
• Fundoscopic examination for retinal hemorrhage (a potential sign of abuse in children) and papilledema (a sign of increased intracranial pressure [ICP])
• Palpation of the scalp for hematoma, crepitus, laceration, and bony deformity (markers of skull fractures). In infants fullness of the fontanelle can be a marker of intracranial hematoma or elevated ICP
• Auscultation for carotid bruits, painful Horner syndrome, or facial/neck hyperesthesia (markers of carotid or vertebral dissection)
• Evaluation for cervical spine tenderness, paresthesias, incontinence, extremity weakness, priapism (signs of spinal cord injury)
• Extremities: Motor and sensory examination (for signs of spinal cord injury)

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

• Multiple bruises over the body of different stages of healing
• Retinal hemorrhage
• Acute subdural hemorrhage

Evaluation

Non-contrast cranial computed tomography (CT) is the imaging modality of choice for patients with TBI and an abnormal GCS. CT findings associated with a poor outcome in TBI include midline shift, subarachnoid hemorrhage into the verticals, and compression of the basal cisterns. MRI may be indicated when the clinical picture remains unclear after a CT to identify more subtle lesions. Several clinical decision guidelines[4] have been validated and can be applied to determine which children with a normal or near-normal GCS can safely avoid CT.

Fundoscopy is needed to look for the presence of retinal hemorrhages in cases suspected with NAT. Abusive head trauma (shaken baby syndrome) is the most common cause of death in patients sustaining NAT.[5]

Treatment / Management

Airway adjuncts are indicated in patients not able to maintain an open airway, or not able to maintain greater than 90% oxygen saturation with supplementary oxygen. Oxygenation parameters should be monitored using continuous pulse oximetry with a target of greater than 90% oxygen saturation. Ventilation should be monitored with continuous capnography with an end-tidal pCO2 target of 35 to 40 mm Hg. Placement of a definitive airway is recommended in a patient with a GCS of less than 9.  

Systemic hypotension negatively impacts the outcome in the setting of TBI, and current studies have demonstrated improved outcomes in patients with a systolic BP = 120 mm Hg. Isotonic crystalloids should be used to prevent and correct hypotension; colloidal solutions have not been shown to improve outcomes.

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. Mortality in TBI is due to elevated ICP.

Initial bedside approaches to increased ICP include:

1. Elevate the head of the bed to 30 degrees.
2. Determine that the cervical collar is not impeding venous outflow.
3. Appropriate analgesics and sedation: Pain and anxiousness can elevate the ICP.  Opiates and benzodiazepines are frequently used, and neuromuscular blockade may be required to prevent maneuvers that increase ICP such as coughing, straining, and fighting against the ventilator.[6]
4. Hyperventilation: Routine hyperventilation in TBI is not recommended, but in the setting of impending herniation, it remains one of the fastest, short-term methods to lower ICP.[7] 
5. ICP monitoring may be considered in infants and children with severe TBI.[8]
6. Osmotic agents: Hypertonic saline (3%) or mannitol are the common hyperosmolar agents used to reduce ICP.[7]
7. Barbiturates: Patients with elevated ICP, refractory to other therapies, may benefit from barbiturates which are thought to decrease ICP by decreasing cerebral metabolic rate.[7]
8. Decompressive hemicraniectomy: As part of a surgical procedure to evacuate hematoma, or as a primary treatment of refractory ICP, decompressive hemicraniectomy reduces ICP due to the removal of part of the skull.[9]
9. Hypothermia has not been shown to improve outcomes in children.[10]

Differential Diagnosis

A thorough head-to-toe physical examination must be performed with vigilance for occult injuries.

Glutaric aciduria type I patients may present with macrocephaly and bilateral subdural hemorrhages which can be mistaken for NAT.

Prognosis

Nearly 90% of patients are discharged home from the emergency department after their head injury,[6] but about 1% of patients with a GCS of 14 to 15 have a clinically significant intracranial injury on CT,[11] and patients with severe TBI have mortality as high as 20%.

Complications

Complications depend on the severity of the head injury. It can vary from mild cognitive impairment to seizures, neurological deficits, and even death.

Deterrence and Patient Education

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

Enhancing Healthcare Team Outcomes

The management of pediatric head trauma is done by an interprofessional team that consists of a pediatric neurosurgeon, emergency department physician, nurse practitioner, pediatrician, and a radiologist. Most children with mild head trauma are discharged. 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 for no more than 2 to 3 days followed by scheduled increases in activities with close monitoring for 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 CDC website is a helpful source for up-to-date guidelines.[12]