Traumatic brain injury is a major cause of death and acquired neurologic impairment in childhood. Each year 600 000 children present to emergency departments for evaluation of head injuries.1 Of these children, 250000 are hospitalized.2 Brain injury is the most common cause of traumatic death, and this occurs in approximately 25 000 children annually.3 Over one third of survivors of moderate to severe brain injury will suffer varying degrees of neurologic and psychologic impairment.4'5 The economic costs of head injury are staggering. Future production losses alone total greater than $8 billion.6 Based on the morbidity, mortality, and economic drain associated with head trauma, the National Health Injury Foundation calls traumatic brain injury "the silent epidemic."7 Morbidity and mortality of acute brain injury can be significantly reduced with a systematic and well-organized approach to various factors related to pediatric head trauma.8,9 Therefore, pediatricians and other healthcare professionals involved in the care of children should have a thorough understanding of pediatric head trauma. The following discussion will include the causes of head trauma, the physiology of the immature central nervous system, as well as the pathophysiology of the injured brain, the various types of head injury, assessment, management, and prognosis of head trauma patients, and the importance of preventative measures in decreasing the number and minimizing the effects of pediatric accidental head injuries.
CAUSES OF HEAD INJURY
The cause of head injury depends in part on the age of the patient2,10 (Table 1). During the first 2 years of life, the most common cause of head injury is a fall. Severe accidental head trauma is relatively uncommon in children younger than 2 years of age, and the most frequent cause of severe injury in this age group is child abuse. Motor vehicle accidents account for a large number of both minor and severe head injuries in children younger than 2 years of age. These children are usually unrestrained passengers in an involved automobile.
Age-Related Causes of Head Injuries in Children
Between 2 and 5 years of age, falls continue to be the leading cause of head injuries. Motor vehicle accidents replace child abuse as the major cause of severe head trauma in this age group. The majority of these patients are still unrestrained passengers. However, some are the victims of being struck as pedestrians by automobiles.
Children between the ages of 6 and 12 years are involved in twice as many "pedestrian-struck" motor vehicle accidents as younger children.11 During this time period, as children become more independent and mobile, head injuries from bicycles, motor bikes, all-terrain vehicles, skateboards, and rollerskate accidents become more significant.10 Falls still play a major role in the overall number of head injuries.
In the adolescent and teenage years, sports injuries contribute to head trauma. Duiing this age period, head trauma patients are commonly drivers involved in motor vehicle accidents. Violent assaults, especially in inner-city populations, become a significant cause of traumatic brain injuries.
In all age groups of head-injured patients, boys outnumber girls. This becomes especially apparent in children older than 2 years of age.
THE DEVELOPING CENTRAL NERVOUS SYSTEM
The craniocerebral anatomy and physiology in a growing infant and child are different from those of an adult. It is important to understand these differences as they impact on the presentation, severity, and outcome of pediatric head injuries. Development of the central nervous system (CNS) is incomplete at birth. During the first 3 years of life, CNS maturation progresses at the same rate as in utero. After 3 years of age, CNS maturation continues at a slower rate into the teenage years.12
Infants are characterized by a large head in relationship to the rest of the body. The head to body ratio decreases with age. Infants also have weak neck muscles that cannot effectively support their large heads. An infant's brain, therefore, may be more prone to acceleration-deceleration injuries, because it sits in a heavy, poorly supported skull. This situation makes infants and toddlers relatively "top heavy," which may account for the seemingly great propensity of infants and toddlers to preferentially strike their heads when falling. An infant's skull is thin and easily deformable and therefore may not provide much protection to the brain from a direct blow. The thin skull is also prone to fractures and the suture lines of the cranium are not fused in infancy.
The infant's brain is not completely myelinated. Myelinization progresses rapidly in the first year of life and then continues at a slower rate into the second decade of life. The decreased myelination in die cerebral hemispheres of an infant's brain makes the brain more pliable and may protect it from deforming forces. The white matter of the infant's brain, however, is more vulnerable to shearing forces that are generated in acceleration-deceleration injuries.
Infants have relatively large subarachnoid spaces as compared with adults. The cerebral hemispheres drain blood into veins that cross the large subarachnoid space and then drain into dural venous sinuses. In acceleration-deceleration injuries, these vessels are easily disrupted which can lead to subdural hemorrhaging. Table 2 compares the infant and adult craniocerebral contents.
Anatomic Comparison Between Infants and Adults
PHYSIOLOGY AND PATHOPHYSIOLOGY OF THE CRANIAL VAULT
Severe neurologic injury following head trauma is related to the unique physiology and pathophysiology of the brain and the intracranial environment. The brain is surrounded by a layer known as the dura mater. The dura mater (which in Latin means "tough mother") is a thick, relatively poorly compliant, leathery membrane. Surrounding the brain and dura mater is the bony cranium. The cranium and the dura mater form a stiff, relatively non-yielding vault around the brain. After infancy, the skull sutures fuse, and this vault becomes even stiffer and more noncompliant.
The physiologic importance of the noncompliant housing of the brain is explained by the modified Monro-Kellie doctrine, which states that the cranium is a closed box. Within this closed box are three compartments: the brain, blood, and cerebrospinal fluid (CSF). An increase in the volume of one of these three compartments, or the addition of a fourth compartment (ie, a tumor), must be accompanied by a reciprocal decrease in the other compartments; otherwise, an increase in intracranial pressure (ICP) will develop. If left unchecked, the increased ICP will impair cerebral perfusion. This will result in cell injury and brain death from ischemia.
The relationship between ICP and cerebral perfusion can be appreciated by the equation for cerebral perfusion pressure (CPP):
CPP = MAP - ICP
where MAP is the mean arterial blood pressure. Increases in ICP or decreases in MAP can decrease cerebral perfusion and cause a decrease in cerebral blood flow.
An increase in ICP will lead to displacement of CSF from the ventricular system into the spinal canal. This will decrease the volume of the CSF compartment. Autoregulation is the control of cerebral blood flow (CBF) in response to different metabolic stimuli. CBF is affected by both the oxygen and carbon dioxide content of arterial blood. Beyond the normal ranges of PaO2 and PaCO2, CBF is inversely related to PaO2 and directly proportional to PaCO2This occurs through vasoconstriction and dilatation of the cerebral vasculature.
When head trauma occurs, often the injured brain can no longer autoregulate. This increases in ICP can occur from unreciprocated increases in the volume of the brain caused by swelling and edema, hemorrhage, or hydrocephalus. The development of increased ICP is often referred to as "secondary brain injury" because of its devastating results on brain tissue.
The classification and differentiation of primary and secondary brain injuries are important concepts in head trauma. Primary injury is the injury that occurs at the time of the traumatic event and irreversibly injures and kills brain cells. Primary brain injury is usually the result of an impact blow or acceleration-deceleration force. Secondary injury refers to damage and death of healthy brain cells that initially survived the traumatic event, but succumbed as a result of sequelae of the primary injury or complications of other simultaneous injuries. The most common causes of secondary brain injury are ischemia, hypoxia or anoxia and hypercarbia. As an example, if a child is struck by a car, primary injury occurs when the child's head is struck against the car or pavement and brain cells are injured or destroyed. If increases in ICP occur or if the child goes into shock or stops breathing, secondary injury will occur and other brain cells that were not initially damaged will be injured or destroyed from ischemia and hypoxia or anoxia.
Primary brain injury is irreversible and therefore untreatable. The goal of treating any child with head trauma is to prevent or minimize secondary brain injury. This can best be accomplished by understanding the physiologic principles of the Monro-Kellie doctrine and the interrelationships of CPP, MAP, and ICP.
Figure. Clinical diagnosis of posttraumatic scalp swellings. Reprinted with permission from Rosman NP, Herskowitz J, Carter AP, O'Connor JF. Acute head trauma in infancy and childhood: clinical and radiologic aspects. Pediatr Clin North Am. 1979;26:707-736.
ACCIDENTAL HEAD INJURIES
Scalp injuries are extremely common presentations of accidental head trauma. Thousands of children each year present to private practitioners' offices and emergency departments with scalp lacerations. If no other underlying injuries have occurred, scalp injuries are usually benign. Scalp lacerations, however, may result in copious bleeding. This may be of special concern in younger children, because with their smaller total blood volumes, blood loss from a scalp laceration may become clinically significant.13 Treatment of scalp lacerations involves thorough irrigation of the wound and exploration for foreign bodies or any underlying fractures or galeal lacerations. Suturing will provide hemostasis and help protect from infection. Tetanus prophylaxis should be considered. Influences on the need for tetanus prophylaxis include the nature of the penetrating object, the extent of the wound, the length of time the wound has been unattended, and the child's immunization history, including allergic reactions to immunizations.13-14
Scalp swelling following head trauma may prove to be a diagnostic dilemma. The differential diagnosis for non-infectious posttraumatic swelling includes subgaleal hematoma, caput succedaneum, cephalhematoma, and porencephalic or leptomeningeal cysts.
In infants, transillumination of the scalp may provide clues to differentiate the etiology of scalp swelling. The Figure illustrates some of the differentiating characteristics of the various causes of scalp swelling.13 Caput succedaneum presents as diffuse scalp swelling with increased transillumination. This can be differentiated from a subgaleal hematoma, which presents as a diffuse scalp swelling with decreased transillumination. The two may also be differentiated by the age of the patient. Scalp swellings in older children are the result of subgaleal hematomas, whereas infants may present with a subgaleal hemorrhage or a caput succedaneum. A cephalhematoma usually presents as a focal scalp swelling with decreased transillumination. A porencephalic or leptomeningeal cyst presents as a diffuse scalp swelling (see next section).13
Skull fractures may be categorized as linear, growing, basilar, depressed, compound, or diastatic. The majority of skull fractures are linear. Although linear fractures in themselves are usually benign and do not necessitate treatment, they indicate that a significant impact to the skull has occurred. The child should therefore be assessed for underlying intracranial injury. A linear fracture across the petrous temporal bone should raise concern for a possible laceration of the middle meningeal artery, which may produce a resultant epidural hematoma.2,8,13
A late complication of linear skull fractures is the development of a leptomeningeal cyst or "growing fracture." Growing fractures usually develop 3 to 6 months following a linear skull fracture in children who are usually younger than 3 years of age. The initial linear fracture is associated with a dural tear. The dura mater, arachnoid membranes, and CSF evaginate into the fracture margins producing a leptomeningeal cyst. With continued evagination and CSF pulsations, the fracture site increases over time.2 Growing fractures may be the result of a porencephalic cyst, whereby a communication develops between the fracture site and the lateral ventricle. Whereas uncomplicated linear skull fractures are benign and do not necessitate treatment, growing fractures may cause seizures or other neurologic deficits and usually require surgical treatment.
Basal skull fractures occur in the basilar portions of the frontal, ethmoid, sphenoid, temporal, or occipital bones. Basilar skull fractures are commonly associated with pediatric head trauma and suggest a significant impact to the skull has occurred. The diagnosis of a basilar skull fracture is often made clinically because radiologic evidence of a basilar skull fracture is absent in 40% of affected children.15 Clinical findings depend on the location of the fracture. Fractures in the anterior fossa may give rise to rhinorrhea, periorbital ecchymosis (raccoon eyes), anosmia, and ocular palsies. Hemotympanum, otorrhea, vertigo, mastoid ecchymosis (Battle's sign), and unilateral hearing loss may indicate middle fossa fractures. A posterior fossa fracture may cause brain stem compression and lead to respiratory irregularity, hypotension, and tachycardia.8 Meningitis is a known late complication of basilar skull fractures. Most basilar skull fractures only require observation for 24 to 48 hours. Antibiotics, as a rule, are not given prophylactically. Some investigators have suggested that hospitalization may not be necessary for children with isolated basilar skull fractures as long as they have a normal neurologic examination, a Glasgow Coma Score of 15, and no intracranial pathology on computed tomography (CT) scan.13
Depressed skull fractures may be classified as either simple or compound. Simple depressed skull fractures are the result of a local impact force to the skull. Surgery may be indicated when a focal neurologic deficit is noted, a CT scan shows either compression of the brain by the depressed bone plate or a hematoma under the fracture site. If the fractured bone plate is depressed to a greater depth than the thickness of the skull, then the likelihood of a laceration of the dura is increased and surgery may be indicated. Otherwise, these fractures do not necessarily require emergency surgery.2
Features of Concussion Frequently Observed
Infants may develop a unique simple depressed skull fracture known as a "ping pong" fracture. Ping pong fractures represent an indentation of the skull; however, the skull remains intact. Significant depressions and those that may cause noticeable cosmetic disfigurement may require elevation.8
Compound or open fractures involve laceration of skin down to the site of the fractured bone. The fracture may be linear, depressed, or comminuted. Surgical debridement and repair is usually indicated.13
Diastatic fractures represent traumatic separations of bone plates in the skull at one or more suture sites. These separations usually occur in children under 4 years of age and the most frequent suture site is the lambdoid suture. Intervention is usually not required unless a leptomeningeal or porencephalic cyst develops.13
Concussions are among the most frequently encountered problems following head trauma. Concussion is a trauma-induced alteration in mental status that may or may not involve loss of consciousness.16 A common misunderstanding is that concussion must involve loss of consciousness. In fact, loss of consciousness is not the most common neurologic abnormality seen in patients with concussions.
Confusion and amnesia are the most common and almost classic features of concussion. Confusion often presents in very subtle ways, which include disturbance of vigilance with heightened distractibility, inability to maintain a coherent stream of thought, and inability to carry out a sequence of goal-directed movements. Frank disorientation is a less common presentation of concussion-related confusion.16 Table 3 lists some frequently observed features, and Table 4 includes common neurobehavioral symptoms of concussion. Infants and young children may not develop these classic findings. These patients may present with drowsiness, pallor, and frequent vomiting.2
Symptoms of Concussion
The mechanism of concussion is unclear. It is believed to be due to shearing and stretching forces in the brain that damage both white matter and neuronal cells in the cortex and brain stem reticular formation.17 The damage to the axons and neuronal cells is termed diffuse axonal injury (DAI).17 The spectrum of symptomatology encountered in concussion is therefore related to the degree of neuronal cell and white matter damage and dysfunction.
Table 5 illustrates a grading system for concussion.18 Although most concussions are self-limiting, a known complication of concussion exists which is known as the "second impact syndrome."16 In the second impact syndrome, the patient, while still symptomatic from an earlier concussion, suffers cerebrovascular congestion or a loss of cerebrovascular autor egulation leading to malignant brain swelling and a marked increase in intracranial pressure.
Classification of Concussions
Most children with grade 1 or 2 concussions require only acetaminophen analgesia and close observation at home by a responsible adult with good instructions to observe for symptoms of increasing ICP. Children with loss of consciousness longer than 5 minutes, persistent symptoms, or inadequate home observation should have a CT scan and be hospitalized.19
Concussions are a common head injury encountered in contact sports (ie, football, hockey, rugby). Often, healthcare practitioners are asked when a child may return to play after sustaining a sportsrelated concussion. Table 6 illustrates guidelines for when a child may resume athletics following a concussion.
Contusion is a bruising or tearing of brain tissue. Contusions are the most frequent brain injury seen on CT scan. Cortical contusions are usually direct coup or contrecoup injuries occurring when the brain impacts against the bony prominences of the skull. Less frequently, contusions may be caused by a penetrating foreign body. The most commonly involved regions of the brain are the temporal lobes and the subfrontal regions over the orbital cortex. Contusions are also noted underneath fracture sites. Signs and symptoms of contusion are unconsciousness, disturbance in strength or sensation, changes in visual awareness, or focal neurologic signs such as seizures. Contusions are usually not surgically treatable. Complications may include brain edema and hemorrhage into the contusion site. Delayed intracerebral hematomas may occur after 5 to 10 days following head trauma. These are believed to represent hemorrhage into an area of infarction.2, 19
Intracranial hemorrhages may be classified based on their anatomic location witliin the cranium. These include epidural, subdural, subarachnoid, and intraparenchymal hemorrhages. In each case, the hemorrhage results in a collection of blood (hematoma), which may exert a mass effect and increased intracranial pressure, according to the Monro-Kellie doctrine.
An epidural hematoma is a collection of blood in the extradural space. Epidural hematomas are most commonly associated with fractures of the temporal bone which overlies the middle meningeal artery. Fracturing of the temporal bone causes a laceration of the middle meningeal artery resulting in hemorrhage into the extradural space. Epidural hematomas are more common in older children than in toddlers and infants. This is because in children younger than 2 years of age, the middle meningeal artery is not yet embedded in the bony surface of the skull. Therefore, a fracture of the temporal bone may not cause separation and tearing of the middle meningeal artery. In adults, epidural hemorrhages are almost always arterial in origin. In children, however, 25% of epidural hemorrhages may be venous in origin involving the diplopie veins and dural sinuses.7,8
Adolescents with epidural hematomas may present with the classic lucid interval, which consists of a brief concussive state, followed by an alert and oriented period which precedes a sometimes rapid deterioration in mental status. The period of rapid mental status deterioration is due to increased ICP generated by the expanding epidural hematoma within the closed skull (again, the Monro-Kellie doctrine at work).
The classic lucid interval is rarely encountered in children. Infants often present with nonspecific and variable signs and symptoms such as altered mental status, bulging fontanelle, separation of sutures, anemia, and shock. Older children may present with signs of increasing ICP such as altered mental status or localizing signs (hemiparesis or hemiplegia, ipsilateral pupil dilation, posturing, or contralateral limb weakness). One of the most significant findings in all age groups is a progressive decrease in level of consciousness. If untreated, the increasing ICP may lead to herniation of the brain onto the brain stem with cardiorespiratory arrest. Symptomatology resulting from an arterial epidural hematoma may progress at a rapid rate (hours). Venous epidural hematomas usually produce symptoms at a slower rate (days).7,8
Epidural hematomas usually appear on CT scan as double-convex, hyperdense areas. Epidural hematomas may represent life-threatening emergencies. The treatment of symptomatic epidural hematomas is surgical evacuation. Even short delays (2 to 3 hours) in treatment can significantly increase morbidity and mortality. In cases where asymptomatic epidural hematomas are considered to be too small to warrant surgical evacuation, CT scanning should be repeated after a few hours.9 Many small, asymptomatic epidural hematomas have been shown to expand over the ensuing hours.20
A subdural hematoma is a collection of blood that lies between the dura mater and the cortex. Subdural hemorrhages are usually venous in origin from torn bilateral bridging cerebral veins. Often, there is associated cortical damage.7,8
Subdural hematomas are almost always the result of significant head trauma. Therefore, the presentation will be that of a child who has sustained significant head injury. Generally, patients will present with marked and progressive neurologic deterioration. Findings on neurologic examination will depend on the severity of injury, the size of the hematoma, and the time since injury. CT scan usually demonstrates a crescentic lesion located on the surface of the brain. There is often an underlying contusion. Brain edema and significant mass effect may also be noted.7
Definitive therapy for symptomatic large subdural hemorrhages is surgical evacuation. As in epidural hematomas, if a subdural hematoma is deemed too small for surgical evacuation, vigilant serial neurologic assessment and a repeat CT scan is indicated.
Intracerebral hematomas in children usually represent an extension or late development from a cortical contusion. These signify a tremendous injury.
These patients present with profound neurologic deterioration. Occasionally, a hematoma localized to a polar region of the brain may be evacuated surgically. Usually, the treatment for intracerebral hematomas is nonoperative.7, 9
MANAGEMENT OF CHILDREN WITH HEAD INJURY
The goal of management of patients with head trauma is to prevent and minimize, wherever possible, the occurrence of secondary injury to the brain. Secondary injuries will most likely occur as a result of hypoxia, anoxia, or ischemia. Therefore, the first and most effective step is through proper assessment and management of the patient's airway, breathing, and circulation (ABC).
When to Return to Play After Removal From Contest
The airway should be assessed and, if necessary, controlled quickly and reliably. Indications for endotracheal intubation include abnormal respiratory rate and rhythm as a result of severe underlying neurologic injury, upper airway obstruction from secretions, blood, teeth, or foreign bodies, loss of airway tone or protective airway reflexes, preexisting or subsequent pulmonary disease such as aspiration or neurogenic pulmonary edema, respiratory muscle fatigue, chest wall dysfunction, or increased intracranial hypertension.7 Intubation should be carried out by qualified personnel.
Once the airway has been properly assessed and managed, careful attention must be paid to the patient's breathing. Pulmonary parenchymal processes, such as aspiration pneumonia or pneumonitis, pulmonary edema, lung contusions or hemorrhages (associated trauma), atelectasis, or pneumothoraces, can worsen hypoxia. In addition to furthering secondary injuries from ongoing hypoxia, cerebral blood flow will increase as a response to hypoxia. This in turn may increase ICP. If ventilation is not adequate, hypercapnia may result which can also increase ICP.7
After the airway and breathing have been secured, the patient's perfusion must be assessed and, if necessary, restored as shock will worsen secondary brain injury from ischemia. The most common cause of shock in a trauma victim is hypovolemia secondary to blood loss. In such cases, rarely is the cause of blood loss an intracranial hemorrhage. Therefore, another extracranial source of bleeding must be searched for (usually an intraabdominal hemorrhage or possibly a hemonhage secondary to a femur fracture). The initial treatment is volume resuscitation. Careful attention must be paid to the patient's fluid and electrolyte balance during fluid resuscitation as overhydration can worsen brain swelling and increase ICP. Clinical signs such as heart rate (otherwise unexplained tachycardia is the most useful indicator of hypovolemic shock), blood pressure, pulse strengrh, capillary refill, and extremity warmth are measures of the patient's perfusion.
Glasgow Coma Score (GCS)
Modified Coma Score for Infants
Once the airway, breathing, and circulation have been assessed and managed, a neurologic assessment must be completed. In the pediatric patient with head trauma, the basic components of the initial neurologic examination include an assessment of level of consciousness, brain stem function, pupil reactivity, and motor function.8
One of the most valuable components of the neurologic examination is determining the level of consciousness. The Glasgow Coma Score (GCS) is a convenient scoring system used to assess the level of consciousness and monitor the neurologic progression of a head-injured patient. The GCS rates patient performance in three major areas: eye opening, which relates to arousal and alertness; verbal ability, which relates to content and mentation; and motor ability, which reflects mentation as well as the functional integrity of the major CNS pathways.7 The GCS has gained widespread recognition as a useful neurologic assessment tool in older children and adults. Modified coma scores based on the GCS have been adapted in various ways to accept age-appropriate behavior. Tables 7 and 8 illustrate the Glasgow Coma Score and a modified coma score for infants, respectively.
Once the airway, breathing, and circulation have been assured and rhe initial neurologic assessment has been completed, a complete history, physical examination, and neurologic examination are performed. Throughout this process, constant reassessment of the patient's airway, breathing, circulation, and neurologic examination is important.
A detailed history is vital to the appropriate management of the patient. Important aspects of the history include the mechanism of injury, loss of consciousness, altered behavior, seizures, progression of symptoms, and any associated injuries. These points of information give clues as to the nature and severity of the injuries.7 The child's past medical history is also important, as prior health conditions may impact on the patient care.
A full physical and neurologic examination are then performed. It is important to look for other associated injuries as these may in themselves jeopardize the patient's safety or worsen secondary brain injury. The possibility of spinal cord injury must always be considered when evaluating a patient with head trauma.
After the initial resuscitation and evaluation have been completed, many children will require a neuroradiologic procedure. The CT scan has emerged to be the radiologic procedure of choice for evaluating patients with head trauma. Physicians, however, are confronted with the problem of selecting those children who would benefit from a CT scan. Cost effectiveness must be weighed against the consequences of failing to diagnose an intracranial injury. In an attempt to assess clinical features that might reliably predict the need for CT imaging in pediatric head trauma patients, Dietrich and colleagues demonstrated a poor correlation between the clinical symptoms of significant traumatic brain injury and findings on CT scan.1 Suggested indications for head CT scans include a GCS of 14 or less, a GCS of 15 in association with amnesia for the event, loss of consciousness, vomiting, seizures, neurologic deficits, or a concomitant condition that renders the neurologic examination unreliable or unobtainable (ie, anesthesia, intoxication, underlying neurologic conditions).1'7
Discharge Instructions ("Neuro Check") Sheet Given to Parents Upon Their Child's Discharge From the Hospital
With the advent and availability of CT scans, the indications or usefulness of skull radiographs are becoming more limited. Skull radiographs may be useful in diagnosing skull fractures. However, they do not give information regarding the brain parenchyma. Pertinent skull information can also be obtained with the CT scan and correlated with any underlying brain injury. Regardless of the radiologic procedure employed, it is crucial that before a patient is sent for a radiologic procedure, the airway, breathing, and circulation must be fully assessed and stabilized.
Intracranial Pressure Management
Several interventions can be initiated to control ICP. The child's head should be elevated 30° and placed in the midline position. This technique promotes venous drainage and helps prevent increases in cerebral blood volume. If the patient is intubated, hyperventilation to reduce the PaCO2 to 30 to 35 mmHg may decrease cerebral blood flow. Hypoxemia and hypercarbia should be prevented because of their potent vasodilatory effects on the cerebral vasculature. Seizures and hyperthermia should be controlled as they will not only cause an elevation in ICP, but also increase the brain's metabolic requirements.
Fluid administration must be performed carefully as overhydration can worsen brain swelling and elevate the ICP. It is important, however, to prevent dehydration as impaired perfusion can compromise cerebral perfusion pressure.
Diuretics such as furosemide or mannitol have been employed in an attempt to control brain swelling. It is again important not to cause dehydration and shock from aggressive diuresis as brain perfusion may suffer.
Steroids have been used in the past to combat brain swelling. Currently, there is no clear-cut evidence of the clinical benefit or improved outcome with their use in head trauma.21,22
Some children will require intracranial pressure monitoring. Suggested indications for ICP monitoring include children who will require general anesthesia for neurosurgical or other operative procedures where the neurologic examination will be obscured, have a GCS of less than 8, or require prolonged paralysis for ventilatory management.7
After a full assessment and resuscitation are completed, a disposition for the patient should be made. Decisions regarding the triaging of patients must be individualized to meet the specific needs of each patient.
Children who may be considered for discharge to their home include those who are alert (GCS 14-15) and have sustained negligible trauma (by history) with no serious injuries, normal brain CT scans, normal neurologic examination, no severe or progressive symptoms of headache, no evidence of a basilar skull fracture, and a stable home environment with a responsible adult caretaker.3,7, 19 Parents must be advised about signs and symptoms of head injury. Table 9 is a "neuro check" list of signs and symptoms which parents should be given prior to their child's discharge.
Criteria for hospitalization may include loss of consciousness (by history), coma, seizures, or any altered mental status, focal neurologic deficits, persistent vomiting, or severe and persistent headaches, alcohol or drug intoxication interfering with a reliable examination, suspicion of child abuse, lack of a reliable adult caretaker, and underlying medical or surgical conditions that place die child at risk.3,7,19 These criteria not only suggest die need for admission, but also the duration of hospitalization and the potential need for admission to a pediatric intensive-care unit.
The outcome spectrum for head injury is broad. Although some injuries prove fatal, others may result in survival with a variety of neurologic outcomes, including intact neurologic function, mild motor or cognitive impairments, and severe vegetative states. Many investigators have attempted to identify various factors related to prognosis following head injuries.5,23-28
Rimel and colleagues found that clinical outcome (survival and neurologic function) of head trauma patients was directly related to the Glasgow Coma Score (GCS). Patients with the highest scores had the best outcome, those with the lowest scores had the worst outcome, and those patients with intermediate scores fell in between.23 Knights and colleagues found that when the severity of head injury was defined by the GCS, cognitive deficits were related to the severity of injury. Very few children with mild and moderate head injuries were noted to have behavioral changes, whereas 90% of children with severe head injuries had learning or behavioral problems.24 Casey and colleagues, however, found that among children who sustained minor head trauma, behavioral problems were reported significantly more often than for the standard normal population.25 Ruijs and colleagues reported that among children with severe closed head injuries, die duration of coma and of posttraumatic amnesia correlated strongly with the occurrence of neurologic, behavioral, and intellectual residual sequelae.26 In a 23-year follow-up study, Klonoff and colleagues found that among patients who suffered head trauma as children, there was an increased incidence of psychosocial adaptation problems which included educational lag, unemployment, current psychologic/psychiatric complaints, and problematic family relationships. The severity of the head injury was identified as the primary contributory factor in the reconstitution process and in the prediction of long-term outcomes.5 Bowen and colleagues studied brain CT scans of children with head trauma, and found that those children whose scans showed diffuse severe injury performed more poorly on cognitive, memory, and motor testing than those who did not.27 These investigators also found that the mechanism of injury was related to neurologic outcome. The children who performed poorest on cognitive, memory, and motor tests were those who sustained their injuries riding in a vehicle, as opposed to being hit by a vehicle while walking or riding a bicycle.27 Lishman noted that patients who have sustained varying grades of concussion may suffer from long-term intellectual impairment, seizures, and emotional and psychosocial difficulties.28 It is apparent then that even children who sustain minor head injuries (ie, minor concussions) are at risk for a variety of long-term neurologic and emotional complications.
Children who have sustained head injury have continuing difficulties and special needs long after discharge from the hospital. The importance and benefits of early, structured rehabilitation in a multidisciplinary framework are becoming increasingly appreciated.29,30
Rehabilitation of traumatic brain injury involves an interdisciplinary team approach of professionals who coordinate the treatment and recovery of the patient with the child's family. The multidisciplinary team of physicians, nurses, therapists, teachers, social workers, psychologists, and child life specialists work with the patient and the family in the rehabilitation process. Rehabilitation, through the interdisciplinary process, improves the impairment and thereby decreases the disabilities and handicaps suffered by the head-injured patient and his or her family.
The patient's primary care physician often plays a pivotal role by working with the various team members, the child, and the family to optimize the outcome of rehabilitation.
One of the most effective ways of dealing with this "silent epidemic" or any epidemic is tlurough education and prevention. Educational and preventative measures should be directed at the various causes of pediatric head trauma listed in Table 1.
Because child abuse represents a leading cause of severe head injury in infants and young children, pediatricians should try to identify (or refer) patients, families, or communities who would benefit from educational and interventional programs regarding child abuse. These healthcare professionals may then make an impact on injuries resulting from child abuse.
Motor vehicle accidents remain the leading cause of severe head injuries in children of all ages. The proper use of seatbelts and air bags have been estimated to reduce the risk of fatal injury and severe brain injury by 45% to 55%.31,32 Parents, adolescents, teenagers, and communities need to be made aware of the importance of seatbelts, car seats, and safe driving habits.
Competitive and recreational sports are a cause of hundreds of thousands of mild, moderate, severe, and fatal head injures each year. Proper use of helmets in sports such as bicycling, rollerskating, skateboarding, football, hockey, soccer, lacrosse, skiing, and horseback riding would greatly reduce the incidence of head injuries and fatalities in these sports.33-39 Pediatricians should become active advocates for the use of helmets in these sports as well as for the need for proper adult supervision during these activities. We should also consider advising patients to avoid sports such as boxing where severe head injuries are not only common, but the goal of the sport ("knocking an opponent out" is a euphemism for intentionally inducing a Grade 3 concussion). The American Academy of Pediatrics has formally "vigorously opposed boxing as a sport for any child, adolescent, or young adult," and the American Academy of Neurology has formally called for a ban on boxing.40,41
Altering our physical and social environments could also have a great impact on preventing head injuries. Each year, thousands of brain injuries might be prevented if playgrounds had a safe, soft surface.42 Educational programs regarding the use of safety items such as window bars and stair gates, as well as the avoidance of products such as child walkers, would also greatly reduce childhood head injuries. Drug and alcohol awareness and prevention programs would also help in reducing head injuries associated with substance abuse. Finally, as more children each year are being injured as a result of firearms, hundreds of brain injuries each year could be avoided if parents put a limit on children's access to firearms.42
Clearly, there remains an extremely important role for healthcare providers in supporting and promoting various preventative and educational measures and programs that may reduce head injuries in children. Healthcare professionals are encouraged to contact the non-profit Brain Injury Association (202-2966443) for more information on the etiology, shortand long-term management, and prevention of childhood head injuries.
Head trauma remains an epidemic with a significant morbidity and mortality in the pediatric patient population. Healthcare professionals should be aware of the causes as well as the various presentations of head injuries in children. A proper understanding of the physiology of the central nervous system as well as the pathophysiology involved in brain injury is essential in order to properly assess and manage children with head trauma. An organized, systematic, multidisciplinary team approach is necessary for managing the acute medical problems and long-term rehabilitation needs of those children who have sustained head injuries. Educational and preventative programs and measures would greatly reduce the morbidity and mortality associated with pediatric brain injuries. In this regard, healthcare practitioners must take an active role in supporting and promoting programs that may lessen the severity of this "silent epidemic."
1. Dietrich AM, Bowman MJ, Ginn-Pease ML Kosnik E, King DR. Pediatric head injuries: can clinical factors reliably predict an abnormality on computed tomography? Ann Emerg Med. 1993;22:1535-1540.
2. Bruce DA. Head injuries in the pediatric population. Curr Probl Pediatr. 1990;20:61-107.
3. Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39:1093-1123.
4. Levin HS, Aldrich EF, Saydjari C, et al. Severe head injury in children: experience of the traumatic coma data bank. Neurosurgery. 1992;31:435-444.
5. Klonoff H, Clark C, Klonoff PS. Long-term outcome of head injuries: a 23 year follow up study of children with head injuries. Journal of Neurology, Neurosurgery and Psychiatry. 1993;56:410-415.
6. Division of Injury Control, Center for Environmental Health and Injury Control, Centers for Disease Control. Childhood injuries in the United States. Am J Dis Child. 1990;144:627-646.
7. Davis RJ, Tait VF, Dean JM, Goldberg AL, Rogers MC. Head and spinal cord injury. In: Rogers MC, ed. Textbook of Pediatric Intensive Care. Baltimore, Md: Williams & Wilkins; 1992:805-857.
8. Vemon-Levett P. Head injuries in children. Critical Care Nursing Clinics of North America. 1991;3:411-421.
9. Miller JD. Head injury, journal of Neurology, Neurosurgery and Psychiatry. 1993;56:440-447.
10. Zimmerman RA, Bilaniuk LT. Pediatric head trauma. Neuroimapng Cloues of North America. 1994;4:349-366.
11. Dandrinos-Smith S. The epidemiology of pediatric trauma. Critical Care Nursing Clinics of North America. 1991;3:387-389.
12. Fletcher JM, Miner ME, Ewing-Cobbs L- Age and recovery from head injury in children: developmental issues. In: Levin H, Grafman J, Eisenberg H, eds. Neurobehavior Recovery From Head Injury. New York, NY: Oxford University Press; 1987:279-291.
13. Rosman NP, Herskowitz J, Carter AP, O'Connor JF. Acute head trauma in infancy and childhood; clinical and radiologic aspects. Pediatr Clin North Am. 1979;26:707736.
14. Committee on Infectious Diseases American Academy of Pediatrics. Tetanus. In: Peter G, Halsey NA, Marcuse EK, Pickering LK, eds. 1994 Red Book: Repon of the Committee on Infectious Diseases. 23rd ed. Elk Grove Village, 111: American Academy of Pediatrics; 1994:458-463.
15. Kadish HA, Schunk JE. Pediatric basilar skull fracture: do children with normal neurologic findings and no intracranial injury require hospitalization? Ann Emerg Med. 1995;26:37-41.
16. Kelly JP, Rosenberg JH. Diagnosis and management of concussion in sports. Neurology. 1997;48:575-580.
17. Magnuson DK, Maier RV. Pathophysiology of injury. In: Eichelberger MR, ed. Pediatric Trauma Prevention, Acute Care, Rehabilitation. St Louis, Mo: Mosby Year Book; 1993:59-83.
18. Quality Standards Subcommittee of the American Academy of Neurology. Pract ice parameter: the management of concussion in sports summary statement). Report of the Quality Standards Subcommittee. Neurology. 1997;48:581-585.
19. Dolan M. Head trauma. In: Barkin RM, ed- Pediatric Emergency Medicine: Concepts and Clinical Practice. 2nd ed. St Louis, Mo: Mosby Year Book; 1997:236-251.
20. Knuckey NW, Gelbard S, Epstein MH. The management of 'asymptomatic' epidural hematomas. A prospective study. J Neurosurg. 1989;70:392-396.
21. Saul TG, Ducket TV, Saloman M, Carro E. Steroids in severe head injury: a prospective randomized clinical trial. J Neurosurg. 1981;54:596-600.
22. Gudeman SK, Miller JD, Becker DP. Failure of high-dose steroid therapy to influence intracranial pressure in patients with severe head injury. ) Neurosurg. 1979;51:301-306.
23. Rimel RW, Giordani B, Barth JT, Jane JA. Moderate head injury: completing the clinical spectrum of brain trauma. Neurosurgery. 1982;11:344-351.
24. Knights RM, Ivan LP, Ventureyra ECG, et al. The effects of head injury in children on neuropsychological and behavioral functioning. Brain Inj. 1991;5:339-351.
25. Casey R, Ludwig S, McCormick MC. Morbidity following minor head trauma in children. Pediatrics, 1986;78:497-502.
26. Ruijs MBM, Gabreels FJM, Keyset A. The relation between neurological trauma parameters and long-term outcome in children with closed head injury. Eur J Pediatr. 1993;152:844-847.
27. Bowen JM, Clark E, Bigler ED, Gardner M, Nilsson D, Gooch J. Childhood traumatic brain injury: neuropsychological status at the time of hospital discharge. Dev Med Child Neurol. 1997;39:17-25.
28. Lishman WA, Physiogenesis and psychogenesis in the 'post-concussional syndrome.· Br J Psychiatry. 1988;153:460-469.
29. Scott-jupp R, Marlow N, Seddon N, Rosenbloom L. Rehabilitation and outcome after severe head injury. Arch Dis ChM. 1992;67:222-226.
30. Sriahani B, Scheinberg L. Neurologic rehabilitation. Neurol Clin. 1987;5:519-522.
31. National Highway Traffic Safety Administration. Final regulatory impact analysis: Amendments of FMVSS No 208-passenget car front seat occupant protection. Washington DC: Department of Transportation; 1984.
32. Hartlage LC, Rattan G. Brain injury from motor vehicle accidents. In: Templer DL, Hardage LC, Cannon WG, eds. Preventable Brain Damage: Brain Vulnerability and Brain Health. New York, NY: Springer Publishing Co; 1992:3-14.
33. Wilberger JE. Minor head injuries in American football: prevention of long term sequelae. Sports Med. 1993;15:338-343.
34. Zemper ED. Analysis of cerebral concussion frequency with the most commonly used models of football helmets. Journal of Athletic Training. 1994;29:44-50.
35. Deady B, Brison RJ, Chevrier L. Head, face and neck injuries in hockey: a descriptive analysis. J Emerg Med. 1996;14:645-649.
36. Finvers KA, Strother RT, Mohtadi N. The effect of bicycling helmets in preventing significant bicycle-related injuries in children. Clin J Sports Med. 1996;6:102-107.
37. Condie C, Rivara F, Bergman AB. Strategies of a successful campaign to promote the use of equestrian helmets. Public Health Rep. 1993;108:121-126.
38. Powell EC, Taru RR. In-line skate and rollerskate injuries in childhood. Pediatra Emerg Care. 1996;4:259-262.
39. Research and Training Center in Rehabilitation and Childhood Trauma. Sports injuries on snow and ice. Facts from the National Pediatric Trauma Registry. Fact Sheet #3; Oct 1993.
40. American Academy of Pediatrics Committee on Sports Medicine and Fitness. Participation in boxing by children, adolescents, and young adults. Pediatrics. 1997;99:134-135.
41. American Academy of Neurology. Policy statement, 'The American Academy of Neurology opposes the practice of boxing.' Executive Board Meeting, American Academy of Neurology; May 1983.
42. Perlmutter C, Sangiorgio M. 10 quick lifesavers for kids. Prevention. 1993:45:5363,127-128.
Age-Related Causes of Head Injuries in Children
Anatomic Comparison Between Infants and Adults
Features of Concussion Frequently Observed
Symptoms of Concussion
Classification of Concussions
When to Return to Play After Removal From Contest
Glasgow Coma Score (GCS)
Modified Coma Score for Infants
Discharge Instructions ("Neuro Check") Sheet Given to Parents Upon Their Child's Discharge From the Hospital