Pediatric Head Injury

Abstract

Recent studies have provided updated guidelines for the diagnosis of head injury and the management of patients who experience concussions. A multidisciplinary panel has recently issued new guidelines for return to play after head injury.After reading this article, readers should be able to:Pediatric head injury is extremely common. Although the vast majority of children with head trauma have minor injuries, a small number, even among well-appearing children, will have more serious injuries with the potential for deterioration and significant sequelae. The clinician is challenged to discern which few among the many injured are at high risk for intracranial complications. Clinical symptoms are neither completely sensitive nor specific for significant injury: vomiting may be associated with intracranial injury (ICI), but most children who experience vomiting do not have a complication. Computed tomography (CT) accurately identifies ICIs requiring intervention, but also identifies minor lesions with unclear clinical importance (ie, not requiring intervention) and exposes developing brains to ionizing radiation with the associated risks.Although clinical decision rules determine which children are at highest risk and provide a useful clinical framework, they may not necessarily direct care. Additionally, in this era of reliance on imaging, it is important to remember what the clinical examination tells us regarding brain function, information that may or may not correlate with the structural information provided on head CT.The purpose of this discussion is to review important aspects of pediatric head trauma. Sections on epidemiology, mechanisms of injury, and the pathophysiology of specific injuries will provide a backdrop for the discussion of clinical assessment and indications for imaging and admission. What follows is a discussion of concussion, postconcussion syndrome, and return-to-play recommendations.Childhood head injuries account for more than 600,000 emergency department (ED) visits per year and presumably a larger number of visits and calls to primary care providers. Most pediatric head injuries are minor, including scalp and face contusions, abrasions, and lacerations that do not raise concern for significant underlying pathology; however, trauma is the leading cause of death in children older than 1 year, and among trauma patients, head injury is the leading cause of death and disability. Pediatric head trauma–related deaths in the United States are in excess of 3,000 per year.Although children exhibit almost limitless creativity with regard to sustaining injury, most pediatric head trauma results from falls, motor vehicle collisions, auto versus pedestrian incidents, bicycle-related injuries, and sports. Younger children suffer more falls and are more often the victims of child abuse, whereas motor vehicle crashes and sports-related mechanisms play a greater role in older children. This discussion focuses on blunt head trauma rather than penetrating trauma (eg, gunshot wound) because penetrating injury is much less common and unlikely to present to the primary care clinician.Although the approach to head injury should consider the potential for serious injury in all cases, some mechanisms can be regarded as relatively trivial and unlikely to be associated with serious injury. These injuries include low-velocity self-propelled contact into stationary objects (eg, the toddler runs into the door frame) and falls from standing or sitting height or lower. However, the presence of any symptoms of head trauma despite the history of an apparently benign mechanism would no longer qualify the head injury as trivial.Rarely, minor mechanisms may create more serious injury in the presence of undiagnosed intracranial pathology (eg, hemorrhage into a brain tumor). The clinician also must be alert to more dangerous mechanisms that could be concealed, either because the child chooses not to disclose or because the injury was inflicted.Brain injury results from the blow to the head and the interplay of brain parenchyma, the brain’s coverings, the brain’s housing structure (the cranial vault), and the vascular supply. It is useful to consider the relevant anatomic structures as layers from outside to inside.The scalp consists of five layers of soft tissue that cover the skull. Common injuries to the skin and subcutaneous tissue (the outer two layers) include lacerations, abrasions, and freely mobile contusions. Beneath lies the strong galea aponeurotica that also connects muscular tissue on the front and back of the skull. Underneath are the loosely applied areoloar tissue layer and then the pericranium.Hemorrhages may occur in the subgaleal region from direct blows or as a result of bleeding from a fracture. Cephalohematomas are hematomas caused by bleeding beneath the periosteum, a condition well known to those who care for newborn infants.The skull can be divided into the calvarium or bony skullcap and the skull base. The skullcap is composed of the frontal, parietal, occipital, and temporal bones. The base of the skull is made up of the sphenoid, palatine, and maxillary bones and portions of the temporal and occipital bones. Injury to the calvarium results from direct forces, and fractures commonly are linear.Less commonly, skull fractures may be depressed (intruded by more than the thickness of the bone), comminuted (consisting of multiple fragments), diastatic (widely split), or open (communicating with a laceration). Fractures involving the skull base, known as basilar skull fractures (BSFs), are more complicated because of adjacent anatomic structures (eg, cranial nerves, sinuses), their association with ICI, and the risk they pose for meningitis.Within the skull are the intracranial contents, consisting of the brain and its covering membranes (the meninges), blood, and cerebrospinal fluid (CSF). The meninges play an important role in the genesis of serious ICI. The outermost meningeal layer, the dura mater, is attached tightly to the inner aspect of the skull. The epidural space is a potential space between the dura and the skull. Meningeal arteries course between two layers of the dura and may become more grooved into the skull as the skull matures, so that a skull fracture may injure these vessels and cause bleeding into the epidural space. Meningeal arteries are particularly vulnerable to injury because they run beneath the thinnest part of the skull. Channels exist within the dura for venous drainage and these dural sinuses also may be lacerated. Blood collecting in the epidural space is referred to as an epidural hematoma or epidural hemorrhage (EDH).Beneath the dura lies the arachnoid mater, a thin tissue layer coursing close to the brain but not following the brain sulci. This membrane separates the CSF-containing subarachnoid space beneath it from the subdural space. Within the subdural space lie the bridging veins that return blood from the brain to the dural sinuses. These bridging veins are susceptible to shearing forces when there is rapid acceleration or deceleration that moves the brain within the skull. A hematoma in this space is termed a subdural hemorrhage (SDH).The third, innermost meningeal layer is termed the pia mater and adheres to the underlying brain, coursing over all gyri and sulci. This layer contains many small vessels that can be injured from direct blow or shear forces, resulting in a subarachnoid hemorrhage (SAH).Beneath the meninges lies the brain parenchyma, a semisolid tissue that is not affixed to the skull and can move freely within it. The CSF that bathes the brain and the spinal cord provides some degree of cushioning for the brain.It is useful to discuss brain injury as having two phases. The primary injury is mechanical damage sustained immediately at the time of trauma from direct impact (eg, brain impacts the inner aspect of the skull or a skull fragment moves into the brain) or from shear forces when the gray matter and white matter move at different speeds during deceleration or acceleration.Secondary injury refers to ongoing derangement to neuronal cells not initially injured during the traumatic event. Ongoing injury results from processes initiated by the trauma, including hypoxia, hypoperfusion (local or systemic shock), metabolic derangements (eg, hypoglycemia), expanding mass and increased pressure, and edema. Because primary injury occurs at the moment of trauma, little can be done to mitigate it other than prevention, so treatment during trauma resuscitation focuses on preventing secondary injury.When considering secondary injury, two additional concepts warrant further discussion. The first consideration relates to pressure and volume within the cranial vault. After infancy, the cranial vault is a relatively stiff, poorly compliant structure and the intracranial volume is relatively fixed. From a simplistic standpoint, the vault contains brain, blood, and CSF, and any increase in the volume of one component necessitates a relative decrease in another.If volume compensation does not occur, intracranial pressure (ICP) will increase. With progressive increases in ICP, the patient will experience headache, vomiting, and depressed mental status, then posturing, and ultimately vital sign deterioration. Increasing ICP may lead to global ischemia through mechanisms discussed later in this section. Ultimately, increased ICP will lead to brain herniation (abnormal movement of the brain across skull structures).Herniation can occur at several different anatomic locations (Fig 1). When a mass lesion is one-sided and supratentorial, uncal herniation may occur. This type of herniation involves movement of the innermost part of the temporal lobe, the uncus, over the tentorium, with resultant pressure on the midbrain and pressure on the third cranial nerve, impairing its parasympathetic fibers and leading to ipsilateral pupillary dilation.Central herniation occurs when central brain structures, including the diencephalon and temporal lobes, move caudally through the tentorium cerebelli. Cingulate or subfalcine herniation occurs when the cingulate gyrus is pushed across the midline under the falx cerebrial. Although subfalcine herniation does not affect the midbrain directly, it can affect blood flow and can progress to central herniation.In tonsillar herniation, the cerebellar tonsils move down through the foramen magnum with compression of the lower brainstem and upper cervical spinal cord. Compression of the brainstem may result in severe neurologic dysfunction, cardiovascular and respiratory instability, and death.The other important concept in considering secondary injury involves cerebral perfusion. Cerebral perfusion pressure is the difference between the mean arterial blood pressure and ICP. In health, cerebral blood flow is maintained despite variable blood pressures by autoregulatory changes in cerebral vascular resistance. When severe injuries occur, this ability to autoregulate may be impaired, so that cerebral blood flow will be dependent on cerebral perfusion pressure.In the absence of appropriate autoregulation, cerebral perfusion will diminish with elevated ICP or with systemic hypotension. In either instance, resultant ischemia, neuronal death, and subsequent edema all contribute to secondary injury.Management focuses on prevention of secondary injury, so initial attention is directed to the ABCs of trauma resuscitation, focusing on maintaining adequate airway, breathing (ventilation and oxygenation), and circulation (blood pressure and perfusion). Cervical spine precautions are taken when head injury is present because head injury may be associated with cervical spine injury. Oxygen is applied, ventilation is supported as necessary to provide normocarbia (partial pressure of carbon dioxide at 35–45 mm Hg), and circulatory concerns are addressed.Hyperventilation is no longer the standard of care, although there is still a limited role for acutely lowering increased ICP in the intensive care unit or operating room. Patients with Glasgow Coma Scale (GCS) <8 (see below) typically are intubated during trauma management.The role of pharmacotherapy in head injury may include drugs for rapid sequence intubation, cardiovascular support, anticonvulsants when seizures occur, and medications to decrease ICP. In the most severely injured patients and those with herniation syndromes, mannitol (0.5–1.0 g/kg intravenously) and hypertonic (3%) saline can be used to promote osmotic withdrawal of water from the brain into the intravascular space in an effort to reduce ICP. Corticosteroid medications have no role in the treatment of acute brain injury; however, their use in treatment of spinal cord injury is controversial.Assuming that concerns regarding airway, breathing, and circulation have been addressed, or arrangements for transfer or emergency care are being made, a general assessment should be performed, with specific emphasis on historical features and physical findings that might be indicators of potential complications from the trauma.Historical elements should focus on details of the injury mechanism and timing of symptoms. Attention is placed on loss of consciousness, amnesia, confusion, seizure, vomiting, headache, and general behavior. Injury mechanism details should include height and surface for falls (eg, 2 feet or 2 stories; onto dirt, carpet, or concrete), use of restraining devices (eg, in car seat and car seat did not move), action of victim (eg, rolled up on car hood or thrown 20 feet), speed for crashes (eg, 10 mile per hour car crash, downhill on bike “really fast”), helmet use for sports, or velocity of object if child is struck (eg, golf club swung by teen versus 2-year-old). Other activities around the time of injury are important. Head injury can occur as the result of a medical condition (eg, seizure leads to fall with resultant head injury), and head injury in teens may occur in the presence of intoxication and drug use.Physical examination includes examination of the head for evidence of abrasions, lacerations, or scalp hematomas (location, size, and character: boggy or firm); draining or bleeding from the ears or nose; blood behind the tympanic membrane (hemotympanum); apparent bruising behind the ear over the mastoid (Battle sign); blood accumulating in periorbital tissues (raccoon eyes); depression in the skull; and continuity of the skull within lacerations.Drainage or blood from the ears and nose, hemotympanum, Battle sign, and raccoon eyes are signs of BSF, frequently associated with ICI, and they are detailed in the basilar skull fracture section. Neurologic assessment is performed and although focal findings are very uncommon, they should be sought.Assessment of mental status is of utmost importance and serves as a common triage branch point to identify patients at risk for trauma complication. This evaluation usually is done by using the GCS, which is used in most head injury research (Table 1) and provides a starting point for following the patient’s progress. For the very young child, there is a modified coma scale for infants (Table 2). It is important to judge the best response, and to follow the coma scale serially for deterioration.Although variably defined, in general a concussion is a head injury that results in alteration of mental status, with or without loss of consciousness. From a practical standpoint, concussion often is used to refer to more minor head injury when the GCS is 14 to 15, the patient has some symptoms (eg, headache, dizziness, vomiting, amnesia, or confusion), there is no evidence of a fracture, and there are no focal neurologic deficits. A more detailed discussion of concussion is below.The main importance of skull fractures is that they are markers for significant impact to the head that increases the risk of ICI significantly; however, it is important to note that ICI also occurs in the absence of fractures, and many fractures are not associated with ICI. Rarely, the fracture itself may lead to a complication (more common with basilar or depressed skull fracture). Before the advent of CT, skull radiography was an important modality to identify children at risk for complications; however, because plain radiographs give no direct information about ICI, currently they are of very limited utility. Skull fractures now are diagnosed most commonly when a CT scan is obtained.An exception to the lack of utility of skull radiographs occurs when child abuse is suspected. When child maltreatment is suspected, the presence of a skull fracture, old or new, with or without ICI, has important implications; so skull radiographs, with their higher sensitivity for fracture, are included as part of a more comprehensive skeletal survey. Skull fractures in children younger than 2 years in the absence of a history of appropriate mechanism should prompt a more thorough evaluation for inflicted trauma (including skeletal survey) and appropriate reporting and referrals.Fracture of the calvarium is more common than fracture of the base of the skull. Most fractures are linear and, when considered in isolation (ie, not associated with ICI), of little consequence. No specific therapy need be directed to the fracture except pain management. Follow-up with primary care is appropriate to detect the exceedingly rare late complication of a growing fracture. Depressed skull fractures (those intruded more than the thickness of the bone) carry increased risk of primary injury to the brain because of intrusion of the fragment and, depending on the location, may have significant cosmetic sequelae (Fig 2). Neurosurgical consultation is necessary for all depressed skull fractures, even in the absence of more serious ICI.BSF requires special consideration for several reasons. They can have unique clinical presentations providing clinical clues that often are readily apparent. Hemotympanum or blood draining from the ear, are the most common signs of a BSF. CSF draining from the ear or draining from the nose (attributable to a cribriform plate fracture), Battle sign, and raccoon eyes also are signs of BSF. Persistent clear drainage from the nose after head trauma should alert the clinician to the possibility of a BSF. BSF also can occur in the absence of these clinical findings and be apparent only on CT; conversely, CT scan may not detect all such fractures.BSFs are important because they are associated with ICI and have a higher incidence of complications from the fracture itself, owing to the unique anatomic location. ICI occurs in about 20% of BSF patients who have a normal neurologic examination and GCS of 15. (1) Therefore, when signs of a BSF are noted, CT scanning is necessary.BSF is associated also with an increased risk of meningitis. Fractures adjacent to the paranasal or sphenoid sinuses can lead to meningitis if bacteria from these areas enter the normally sterile subarachnoid space. The overall risk of developing meningitis after sustaining a BSF is probably less than a few percent, but the risk is increased if there is CSF rhinorrhea or otorrhea.Use of prophylactic antibiotics is controversial. If there is ongoing CSF leakage, neurosurgical intervention may be needed to facilitate healing of the dural tear. Anatomic adjacency of the base of the skull to cranial nerve pathways means that BSF may cause hearing loss, facial paralysis, and a decreased sense of smell, as well as other cranial nerve dysfunction. Conductive hearing loss also may occur from blood in the middle ear.Perhaps the most important issue for the clinician evaluating a head-injured child is determining if there is an ICI. With improved CT images and current neurosurgical practice, however, detecting an ICI does not equate to a need for neurosurgery. Visible lesions on CT scan may or may not be associated with functional issues or serious morbidity. The two broad classifications of ICIs include focal hemorrhage (EDH, SDH, SAH, intracerebral hemorrhage, and cerebral contusion), which typically are visible on initial imaging, and diffuse injury (cerebral edema, diffuse axonal injury), which tends to progress and may become more visible on subsequent imaging.When bleeding occurs between the skull and the dura mater, the patient is said to have EDH. The bleeding source is arterial in ∼30%, fewer are clearly identified as venous, and in the remainder the source is unclear. EDH is caused most commonly by a blunt trauma mechanism, with falls most frequent. Often there is an overlying fracture (60% to 80%), and the EDH has a lens-shaped appearance on CT (Fig 3). Typically, the underlying brain parenchyma is not injured. Classic teaching suggested that patients with EDH had LOC, then a lucid interval, and then deteriorated. However, that clinical presentation is rare; only ∼20% of children with an EDH even experience LOC. Some children may present with marked lethargy or focal neurologic findings and progress to more frank signs of herniation.However, presentation with more subtle signs, such as persistent vomiting and headache, is more common, and more than 30% of patients who have EDH are alert with normal neurologic findings at the time of diagnosis. Although some small epidurals may produce minimal or no symptoms, they have the potential to expand, which can result in cerebral herniation and death. Fear of missing an expanding EDH, with its high potential for mortality, has, in part, fueled the marked increase in use of CT scanning occurring in recent decades.Patients with EDH require emergent neurosurgical consultation and close monitoring. Patients with larger EDH, midline shift, or significant symptoms are treated with emergent craniotomy and evacuation of the hematoma. Because some small EDHs do not expand significantly, relatively asymptomatic patients who have small epidurals may be managed expectantly, at the neurosurgeon’s discretion, with admission and very close monitoring. Patients who have EDH successfully drained emergently have a good long-term outcome in more than 80% of cases.When bleeding occurs between the dura and the arachnoid membrane, an SDH results. Usually, tearing of the bridging veins is the source of the bleeding and results from a direct blow, falls from significant height, or from inflicted head trauma, as seen in child abuse. SDH is not usually associated with an overlying fracture and has a crescent shape on CT (Fig 4).Unlike the EDH, an SDH usually is associated with underlying brain injury and the hemorrhages may be bilateral. Children may present with LOC, altered mental status, seizures, irritability, vomiting, lethargy, or signs or symptoms of increased ICP (eg, bulging fontanel, decreased responsiveness). In about half the instances of SDH, the children present in coma or significantly depressed GCS.Mortality of patients presenting with acute SDH is high and ranges from 10% to 20%. SDH in infants is associated with child abuse but is not diagnostic that abuse has occurred. Child abuse should be suspected highly when there is no explanation for the injury, when the mechanism of injury does not match the degree of injury, or in instances in which there appears to be evidence of SDH with both new and old blood.A chronic SDH may occur in children with coagulopathies, but usually results from child abuse, and may present with subtle findings, including macrocephaly, full fontanel, fussiness, seizures, and vomiting.SDH requires emergency neurosurgical consultation. Patients who have an acute large SDH with evidence of mass effect within the cranium and altered level of consciousness are candidates for surgical drainage. Smaller SDH and more chronic forms may be managed without surgical decompression. Children with SDH often have significant long-term morbidity that may include developmental delay and seizures. These adverse, persistent neurologic sequelae are more likely to occur in patients who present with coma, or when CT scan demonstrates underlying brain injury.In more severely injured patients, SAH occurs about 25% of the time. This lesion results from tearing of the small vessels of the pia mater secondary to significant blunt trauma and associated shearing forces. Because the bleeding is in a space that communicates with other CSF-containing spaces (within the brain, around the brain and spinal cord), problems related to the mass effect that is seen with EDH and SDH rarely occur. SAH often is seen in association with other ICIs, so presentation is variable, but SAHs occurring in isolation may present with LOC, headache, or signs of meningeal irritation (eg, vomiting, photophobia, nuchal rigidity).A cerebral contusion is essentially a brain bruise caused by a well-localized area of neuronal injury with bleeding (Fig 5). This injury results from movement of the brain against the skull. Blunt trauma to the head may cause a cerebral contusion near the site of impact (a “coup” lesion) or may cause a cerebral contusion opposite the site of impact (a “contrecoup” lesion). Typical signs may be subtle, and can include vomiting, headache, LOC, or, less commonly, a focal neurologic finding or a seizure. In most instances, small contusions have little acute or long-term sequelae.Diffuse axonal injury involves injury to the white matter tracts within the brain and is likely caused by shear forces. This type of injury is caused by severe acceleration, deceleration, or rotational forces, occurring most commonly in motor vehicle crashes. The injury often is at the gray-white matter junction but may occur deeper within the corpus collosum, brainstem, or cerebellum. These children usually are in coma at presentation, although occasionally the child will have only concussion-type symptoms. The CT scan shows small areas of hemorrhage located near the gray-white interface that do not expand. Management of diffuse axonal injury is supportive, mortality is 10% to 15%, and persistent neurologic dysfunction occurs in 30% to 40%.This condition is seen almost exclusively in children who experience severe head trauma and the mechanism appears to be a reaction to cellular injury. Diffuse brain swelling may not be apparent on initial imaging; subsequent CT scans demonstrate findings of progressive edema. The cellular insults may be varied, and cytotoxic edema, vasogenic edema, and autoregulatory dysfunction all may play a role. The children present with marked depression or deterioration of the GCS, and the main threat is the associated increase in ICP.The clinician’s goal is to identify patients who develop clinically important ICI so as to prevent deterioration and secondary brain injury (eg, from expanding EDH), while limiting unnecessary radiographic imaging. Unfortunately, defining sensitive and specific clinical predictors for identifying high-risk patients who require a head CT has been challenging.Several issues contribute to the challenge of evaluating head-injured children:Investigators have identified several clear predictors of ICI:Patients who have any of these findings should undergo CT imaging.However, most patients have none of these findings (ie, they have a GCS of 15, nonfocal neurologic examination, and no obvious skull fracture); yet, patients who lack these features account for a large proportion of patients who actually have ICI. Within this group, the incidence of ICI is about 5% and the need for neurosurgery <1%. Identifying reliably sensitive and specific clinical indicators has been difficult, however, because studies have found conflicting evidence regarding the significance of LOC, vomiting, seizures, and headache.Children younger than 2 years should be considered separately. Younger children are more difficult to assess clinically, are more easily injured even from short falls, have a higher incidence of asymptomatic or occult injuries, and more often are victims of inflicted injury. In addition to the predictors of ICI found in older children, nonfrontal scalp hematomas (surrogate markers for skull fracture) were found to be predictors of ICI, with larger hematomas in younger children of greater concern. (2)In all age groups, because of the variability of clinical predictors in identifying ICI and concern for missing ICI, clinicians have adopted a very liberal approach to the use of CT scans. ED-based studies have shown that this group with mild head injury undergoes CT scanning from 35% to 55% of the time. Head CT for pediatric minor head injury increased in Canada from 15% in 1995 to 53% in 2005 for head-injured children. In the United States, use has increased dramatically in the face of relative stability of serious injury, implying that more and more normal CT scans are being obtained.Widespread imaging has increased concerns regarding safety, specifically related to sedation and radiation risk. Concern for adverse events from sedation is justified, but with increasing speed of scanners, the need for sedation should decrease. Clinical experience and research in pediatric sedation has blossomed, and overall hospital practices in this regard have become safer, so that sedation-related adverse events are less of a concern.The potential for ill effects from ionizing radiation cannot be overlooked. Evidence for this risk assessment comes primarily from information on radiation exposure following nuclear bomb detonation and data derived from therapeutic use of radiation. It is estimated that CT scanning will induce a new malignancy at a rate of ∼1 in 5,000 CT scans. It appears that the greatest lifetime risk occurs in the youngest patients (both because of life-years remaining and susceptibility of tissues), and overall risk decreases as age increases. From the standpoint of an individual or individual clinician, this rate does not seem high, but when one considers the tens of thousands of normal head CT scans being performed each year, the