Pediatric Head Trauma 

Trauma is a leading cause of death in children older than 1 year in the United States, with head trauma representing 80% or more of the injuries. In approximately 5% of head trauma cases, patients die at the site of the accident. Head trauma has a high emotional, psychosocial, and economic impact because these patients often have comparatively long hospital stays, and 5-10% require discharge to a long-term care facility.^[1]

Most head injuries in children occur secondary to motor vehicle accidents, falls, assaults, recreational activities, and child abuse. The percentage of each contributing factor differs between studies, and the distribution varies according to age, group, and sex.

Patients with head trauma may experience 1 or a combination of primary injuries, including scalp injury, skull fracture, basilar skull fracture, concussion, contusion, intracranial hemorrhage, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, intraventricular hemorrhage, penetrating injuries, and diffuse axonal injury.

The goal of medical care of patients with head trauma is to recognize and treat life-threatening conditions and to eliminate or minimize the role of secondary injury. Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation secondary to increased intracranial pressure (ICP).

Brain Trauma Foundation guidelines suggest that cardiopulmonary resuscitation should be the foundation upon which treatment of intracranial hypertension must be based and that in the absence of any obvious signs of increased ICP, no prophylactic treatment should be initiated, because this may directly interfere with the optimal resuscitation process.

Surgical decompression is required in the presence of a rapidly expanding epidural or subdural hematoma that causes an increase in ICP and focal compression.

The anatomic characteristics of the child’s brain render it more susceptible than the adult brain to certain types of injuries following head trauma. The head is larger in proportion to the body surface area, and stability is dependent on the ligamentous rather than bony structure. The pediatric brain has a higher water content (88%, compared with 77% in adults), which makes the brain softer and more prone to acceleration-deceleration injury. The water content is inversely related to the myelinization process.

The unmyelinated brain is more susceptible to shear injuries. Infants and young children tolerate ICP increases better because of open sutures.

Both primary and secondary injuries are described in pediatric patients with head trauma, and the presence of these injuries affects outcome.

Primary injuries

The primary injury occurs at the time of impact, either via direct injury to the brain parenchyma or via injury to the long white-matter tracts through acceleration-deceleration forces.

Direct injury to the brain parenchyma occurs as the brain makes forceful contact with the bony protuberances of the calvaria or is penetrated by bony fragments or a foreign body. In children, the compliant skull is easily deformed, and impacts on the brain at the time of the insult result in a coup injury, whereas in adults, the brain is forced against the bony protuberances opposite the point of the impact, resulting in a countercoup injury. Intracranial hemorrhage (ICH) may also result from shearing or laceration of vascular structures.

Acceleration-deceleration forces cause shearing of the long white-matter tracts, leading to axonal disruption and secondary cell death.

Secondary injuries

The secondary injury is represented by systemic and intracranial events that occur in response to the primary injury and further contribute to neuronal damage and cell death.

The systemic events are hypotension, hypoxia, and hypercapnia and may occur either as a direct result of primary injury to the central nervous system (CNS) or as a consequence of associated injuries in a person with multiple traumas.

The intracranial events are a series of inflammatory changes and pathophysiologic perturbations that occur immediately after the primary injury and continue over time. Their presence adds to the adverse outcome of the head trauma patient.

The inflammatory changes are the result of a cascade of biomolecular alterations triggered by the initial insult, leading to microcirculatory disruption and neuronal disintegration. A series of factors such as free radicals, free iron, and excitatory neurotransmitters (glutamate, aspartate) are the result of these inflammatory events, and their presence contributes to the negative outcome. The pathophysiologic events are cerebral edema, increased ICP, hyperemia, and ischemia.

Altered autoregulation of cerebral blood flow

Because the brain has minimal ability to store energy, it depends on aerobic metabolism. The delivery of oxygen and metabolic substrate to the brain is maintained by a constant supply of blood, referred to as cerebral blood flow (CBF). CBF, defined as the amount of blood in transit through the brain at any given point in time, is estimated to be 50 mL/100 g/min in a healthy adult and is known to be much higher in children. However, the minimum amount necessary to prevent ischemia remains unknown.

CBF is influenced by mean arterial blood pressure (MAP), ICP, blood viscosity, metabolic products, and brain vessel diameter. CBF should not be confused with cerebral blood volume (CBV), which represents the amount of blood present in the brain vasculature. CBV is the major contributor to the ICP and depends on the diameter of intracranial vessels. When CBV is increased, the pressure gradient across the compartment is decreased, and CBF is decreased.

The brain maintains constant blood flow through a mechanism known as autoregulation. This process occurs over a wide range of blood pressures through changes in cerebral resistance in response to fluctuations in MAP pressure. At a MAP of 60-150 mm Hg, CBF is maintained. At 60 mm Hg, the cerebral vasculature is maximally dilated, and at 150 mm Hg, it is maximally constricted. Fluctuations of MAP beyond either end of this range lead to alterations in CBF and contribute to ischemia or disruption of the blood-brain barrier.

Several mechanisms are known to affect autoregulation of CBF; they may be divided into the following categories:

• Metabolic products
• Arterial blood gas content
• Myogenic factor
• Neurogenic factors
• Endothelium-dependent factors

The effects of these mechanisms are not fully known, and their mechanism of action is still under experimental investigation.

CBF is closely linked to cerebral metabolism. Although the mechanism of coupling is not clearly defined, it is suspected to involve vasodilators released from neurons. Several factors have been implicated, such as adenosine and free radicals. Pathophysiologic states that are known to increase the metabolic activity (eg, fever and seizure activity) lead to an increase in CBF.

CBF can be altered by changes in the partial pressure of oxygen or carbon dioxide. Alteration in the partial pressure of oxygen acts on the vascular smooth muscle through mechanisms that remain unclear. Hypoxia causes vasodilatation with significant increase in CBF. Increases in oxygen pressure cause vasoconstriction but to a lesser degree than hypoxia does.

Hypercarbia increases CBF up to 350% of normal; hypocapnia produces a decrease in blood flow. The mechanism appears to involve alteration in tissue pH that leads to changes in arteriolar diameter. This mechanism is preserved even when autoregulation is lost.

The myogenic mechanism was long considered to be the most important in the autoregulation process. Changes in the actin-myosin complex were thought to lead to rapid changes in the vasculature diameter, thus affecting the CBF. It has now been shown that changes in the actin-myosin complex mostly cause dampening of arterial pulsation and have little direct effect on cerebral autoregulation.

The neurogenic mechanism is represented by the effect of the sympathetic system on the cerebral vasculature. The sympathetic nervous system shifts autoregulation toward higher pressures, whereas sympathetic blockade shifts it downward.

Studies have identified nitric oxide (NO) as one of the factors affecting cerebral autoregulation; it does so by producing relaxation of cerebral vessels. NO is present in several conditions, such as ischemia, hypoxia, and stroke. It is generated by different cells at rest but also under direct stimulation by factors such as cytokines.

Traumatic brain injury (TBI) may lead to loss of autoregulation through alteration of any of these mechanisms. One study found that mild TBIs are more likely than orthopedic injuries to cause transient or persistent increases in postconcussive symptoms during the first year after injury.^[2] These mechanisms represent the foundation on which the medical management of increased ICP and cerebral perfusion pressure (CPP) is based in patients with traumatic brain injury.

Most head injuries occur secondary to motor vehicle accidents, falls, assaults, recreational activities, and child abuse. The percentage of each contributing factor differs between studies, and the distribution varies according to age, group, and sex. A few factors (eg, seizure disorder, attention deficit disorder, and alcohol and drug use) are known to enhance the vulnerability of the child or adolescent to this type of trauma. Infants and young children are more vulnerable to abuse because of their dependency on adults.

Motor vehicle accidents account for 27-37% of all pediatric head injuries. In most cases involving children younger than 15 years, the victim is a pedestrian or a bicyclist; pedestrian accidents in children aged 5-9 years are the second most frequent cause of death. Young adults aged 15-19 years tend to be passengers in the accidents, and alcohol is often a contributing factor.

Falls are the most common cause of injury in children younger than 4 years, contributing to 24% of all cases of head trauma.

Recreational activities have a seasonal distribution, with peaks during spring and summer months. They represent 21% of all pediatric brain injuries, with the largest vulnerable group aged 10-14 years.

Assault accounts for 10% of all pediatric brain injuries, and firearm-related injuries account for 2%. Child abuse has been identified as the cause of brain injury in 24% of pediatric patients younger than 2 years; it was suspected in another 32%.

In children younger than 3 years, the depth of head injury can be successfully used to determine injury causes and mechanisms.^[3]

In the United States, the estimated annual incidence of pediatric head injury is approximately 200 per 100,000 population. This number includes all head injuries that result in hospitalization, death, or both in persons aged 0-19 years.

Age-, sex-, and race-related demographics

The distribution of head trauma is relatively stable throughout childhood. An increase in the incidence of head trauma was identified in 2 age groups. At approximately age 15 years, a dramatic increase occurs, mainly in males, related to their involvement in sports and driving activities. Infants younger than 1 year also have an elevated incidence of head trauma, which is attributed to falls and child abuse.^[4]

Males are twice as likely to sustain head injuries as females and have 4 times the risk of fatal trauma. Black adolescent boys account for most of the firearms-related CNS injuries in the pediatric population.

The overall outcome for children with head injuries is better than that for adults with the same injury scores.^{[5, 6, 7]} Time to maximum recovery after injury is longer in children (months to years) than in adults (typically about 6 months). Patients with multiple organ injuries, including head trauma, generally have a far worse outcome than those with head injury alone.

Outcome assessment based on the Pediatric Glasgow Coma Scale (PGCS) can be used as an early predictor, but this scale has limitations regarding long-term outcome. Mechanism of injury appears to be a significant predictor of clinical and functional outcomes at discharge for equivalently injured patients.^[8]

According to the National Center for Health Statistics, mortality from head trauma is 29% in the pediatric population. These data are based on death certificate information, and 29% could be an underestimation of the actual rate. Data reported by studies in trauma centers show that head injury represents 75-97% of pediatric trauma deaths.

Patients with severe head trauma and a PGCS score of 3-5 have a mortality of 6-35%; this figure increases to 50-60% for those with a PGCS score of 3. Of those with a PGCS score of 3-5 who survive, 90% require rehabilitation after hospital discharge, and most of them eventually return to school.

Short-term memory problems and delayed response times are reported in 10-20% of children with moderate-to-severe head injury (PGCS score, 6-8), especially if the coma lasts longer than 3 weeks. Patients with a PGCS score of 6-8 are most likely to regain consciousness within 3 weeks, but one third are left with focal neurologic deficits and learning difficulties, especially when coma persists beyond 3 weeks.^[9]

More than half of children with a PGCS score of 3-5 have permanent neurologic deficits. Patients with a PGCS score of 3 have particularly poor neurologic outcomes.

A study that primarily investigated adult TBI patients revealed that diabetic TBI victims had an unfavorable mortality odds ratio (1.5), with the trend being worse for insulin-dependent diabetes patients than for noninsulin-dependent ones.^[10] The study raises the question of how insulin deficiency may contribute to TBI mortality, either along with or independent of glucose changes after TBI.

At the very least, this study points out that meticulous insulin and glucose management of diabetic TBI patients, matching insulin to carbohydrate administration as needed, may help reduce TBI mortality in this population. Care must still be taken not to induce hypoglycemic events in these critically ill patients while trying to avoid potentially harmful insulin deficiency.^[10]

Children should be referred for early intervention and rehabilitation services. Both children and their families should be referred for psychosocial counseling. Children should be referred for neuropsychiatric testing, especially when learning difficulties are present.

For patient education resources, see the Back, Ribs, Neck, and Head Center, the Back, Neck, and Head Injury Center, and the Eye and Vision Center, as well as Concussion, Bicycle and Motorcycle Helmets, Black Eye, and Child Passenger Safety. Also see Repetitive Head Injury Syndrome and the Web site ImPACT.