STATE OF THE ART

Pediatric Minor Head Trauma From the Division of Emergency Medicine, Children’s Hospital, Harvard Medical School, Boston, MA.

Sara A. Schutzman, MD David S. Greenes, MD

Received for publication February 7, 2000. Revision received May 22, 2000. Accepted for publication June 6, 2000. Editor’s Note: This article continues a series of special contributions addressing state-of-the-art techniques, topics, or concepts. State-of-the-art articles will be featured in Annals on a regular basis in the next several volumes. Address for reprints: Sara A. Schutzman, MD, Division of Emergency Medicine, Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115; 617-355-6624, fax 617-355-6625; E-mail [email protected]. Copyright © 2001 by the American College of Emergency Physicians. 0196-0644/2001/$35.00 + 0 47/1/109440 doi:10.1067/mem.2001.109440

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Head trauma is one of the most common childhood injuries, annually accounting for more than 500,000 emergency department visits, 95,000 hospital admissions, 7,000 deaths, and 29,000 permanent disabilities; hospital care costs alone exceed $1 billion annually. The majority of patients have minor head trauma, and, although most of these injuries are insignificant, minor head trauma causes a large number of intracranial injuries. The largest reduction in head trauma mortality rates results from preventing deterioration and secondary brain injury in patients with minor or moderate head injuries who initially appear to be at low risk. The goal of the clinician, therefore, is to identify those at risk for intracranial injury and subsequent deterioration, while limiting unnecessary imaging procedures. This article reviews the current data and practice in assessing and treating minor head trauma in children. [Schutzman SA, Greenes DS. Pediatric minor head trauma. Ann Emerg Med. January 2001;37:65-74.] INTRODUCTION

Head trauma is one of the most common childhood injuries, annually accounting for more than 500,000 emergency visits, 95,000 hospital admissions, 7,000 deaths, and 29,000 permanent disabilities; hospital care costs alone exceed $1 billion annually.1-3 Most patients have minor head trauma,1,4,5 and although most of these injuries are insignificant, minor head trauma causes a large number of intracranial injuries (in some studies, >50% of all intracranial injuries occurred in patients who were awake and alert).6-8,9 The importance of minor head trauma lies not only in numbers but in preventable mortality. Klauber et al10 showed that reduced mortality rates in head trauma result not from saving patients with severe head injuries, but rather from preventing deterioration in patients with minor or moderate head injuries who initially appear to be at low risk.

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Computed tomographic (CT) scans of the head can identify intracranial injuries with high sensitivity, yet universal imaging of all children with minor head trauma would result in unnecessary tests with high costs and wasted time and resources. In addition, CT imaging of young children may require sedation, which carries risks including hypoxia, apnea, prolonged depressed level of consciousness, and aspiration.11-13 Thus, the goal of management of minor head trauma in children is to identify and treat intracranial injuries while limiting unnecessary imaging procedures. The focus of research has therefore been on identifying clinical predictors for intracranial injuries, and, conversely, identifying predictors of children at low risk, for whom imaging is unnecessary. When reviewing the literature, it should be noted that there is no standard definition for minor head trauma. In various sources, the term “minor head trauma” refers to cases in which children have Glasgow Coma Scale (GCS)14 scores of 13 to 15, 14 to 15, or 15.1,4,5,15-20 Most recently, the American Academy of Pediatrics (AAP) defined children with minor head injury as “those who have normal mental status at the initial examination, who have no abnormal or focal findings on neurologic examination, and who have no physical evidence of skull fracture.”21 In all cases, the clinician should approach these children as having apparently minor head trauma because they may harbor potentially life-threatening intracranial hematomas. INTRACRANIAL INJURIES Diagnostic evaluation

The primary focus of the diagnostic evaluation of minor head trauma is to identify those intracranial injuries that will lead to serious morbidity or mortality if left untreated. For instance, patients with an intracranial hematoma may appear well on initial evaluation but then become critically ill as intracranial pressure increases and cerebral herniation ensues.22 Cerebral contusions and diffuse brain swelling also may progress over time, so that patients who appear well initially later develop signs of increased intracranial pressure.23 The concept of the “golden hour” in trauma refers to the idea that the clinician has a short window of time to diagnose and treat certain traumatic injuries before they cause serious harm.24 Applying this concept to minor head trauma, the clinician focuses on the diagnosis of expanding intracranial hematomas, so that surgical evacuation can be performed before secondary brain injury

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occurs. Early evacuation of subdural hematoma in adults has been shown to lead to a decrease in morbidity and mortality.25 The literature also shows that prognosis after epidural hematoma is directly related to the patient’s neurologic status before surgical evacuation.26-28 These findings suggest that patients with intracranial hematomas will have a better outcome if the lesion is diagnosed and treated early, before neurologic deterioration ensues. The available research literature indicates that few pediatric patients with minor head trauma require surgical intervention. Dacey et al29 reported in a prospective study that 3 (1.5%) of 230 children presenting to an emergency department with concussion required neurosurgical intervention. Rosenthal and Bergman30 reported on a retrospective series of 459 children with head injuries who had a history of loss of consciousness. Three (0.7%) of these 459 patients required surgical evacuation of an intracranial hematoma. Quayle et al6 reported that 1 (0.4%) of 266 subjects with head injuries and normal neurologic status required surgical evacuation of an epidural hematoma. Schunk et al31 reported that 3 (1%) of 313 children with head injuries with a normal neurologic status who had a head CT scan required surgical intervention, all for evacuation of epidural hematomas. Other studies have reported rates of surgical intervention approaching zero among pediatric patients with minor head trauma.19,32 No studies describing pediatric patients with minor head trauma have directly demonstrated an improvement in outcome associated with early diagnosis of intracranial hematoma. The low rate of surgical intervention in pediatric minor head trauma, along with the paucity of data showing a benefit to early diagnosis of these lesions, has led some authors to question the value of radiographic imaging in these patients.21 These authors argue that many of the radiographic lesions that are diagnosed in these patients have no clinical significance.33 With low but nonzero rates of surgical intervention described in the literature, many clinicians continue to fear missing the rare case that will lead to serious subsequent deterioration. Furthermore, because most studies of pediatric minor head trauma include few patients with intracranial injuries, it has been impossible to prove that patients with minor head trauma and radiographic evidence of intracranial injury will uniformly have a benign prognosis. Because of these concerns, many authors have developed imaging strategies intended to identify patients with radiographic evidence of intracranial injury, regardless of whether these injuries will require specific therapy. Radiographic evidence of intracranial injury is not uncommon

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in pediatric patients with minor head trauma. In a prospective study, Quayle et al6 reported that 16 (6%) of 266 pediatric patients with head injuries and normal neurologic status had intracranial injury noted on CT scan. Similarly, in a prospective study, Dietrich et al32 found that 11 (5%) of 195 children with head injuries and normal neurologic status had intracranial injury on CT scan. Schunk et al31 reported that 13 (4%) of 313 children with head injuries and normal results on neurologic examination who were studied retrospectively had an intracranial injury noted on head CT scan. No study of pediatric patients with minor head trauma has been able to identify a single criterion, or a small set of clinical criteria, that identify all patients with radiographic lesions. The data clearly show that patients with depressed mental status or abnormal neurologic findings on examination have a higher risk of having radiographic lesions.6,15,19,32,34,35 Among patients with a normal neurologic status, few clinical signs are useful for identifying patients with radiographic lesions. Loss of consciousness, although frequently considered a risk factor for intracranial injury,21 has poor sensitivity and specificity for identifying patients with radiographic intracranial lesions. Schunk et al31 reported that intracranial injury was noted in 2.5% of patients with loss of consciousness and in 4.7% of patients with no loss of consciousness. Davis et al19 reported that none of the 49 neurologically normal patients with isolated head trauma and a history of loss of consciousness had intracranial injury. Quayle et al 6 found that loss of consciousness was associated with intracranial injury only if the loss of consciousness lasted longer than 20 minutes. Other individual clinical symptoms and signs—such as vomiting or seizures—have similarly been found to have poor sensitivity and specificity for detecting intracranial injury (although several studies are retrospective, which raises the possibility of poor documentation rather than the true absence of signs or symptoms).6,19,31,32 Based on these findings, many authors have recommended that clinicians consider CT imaging for patients with any symptoms or signs of brain injury (ie, loss of consciousness, vomiting, seizure, headache, focal neurologic examination, depressed mental status), rather than trying to identify particular signs that indicate high risk for intracranial injury.6,15,32 The implication from these recommendations is that patients without any of these clinical symptoms or signs of brain injury do not need imaging. It is true that most children with radiographic evidence of intracranial injury described in the literature have at least some clinical signs of brain injury. However,

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it is important to recognize that few data exist on CT findings in asymptomatic pediatric patients with head injuries (sometimes called cases of “trivial” head injury), because these cases have either been specifically excluded from or underrepresented in many large series.6,32 The true incidence of radiographic evidence of intracranial injury in children with asymptomatic head injuries is unknown. Most published studies and recommendations regarding pediatric head trauma have treated patients younger than 2 years differently from older children. Children younger than 2 years have traditionally been considered to present special management challenges, because they appear to have a higher risk of skull fracture and intracranial injury after minor mechanisms of injury,36,37 and because clinical detection of intracranial lesions may be more difficult in these young patients.21,38,39 In general, the younger the patient, the higher the risk of intracranial injury and the more difficult to assess. Infants in the first 3 months of life, who have a very limited behavioral repertoire and an especially high incidence of intracranial injury after minor mechanisms of injury, may be particularly challenging to assess.7 The available research data support the notion that in infants, clinical signs of brain injury are a less reliable means of identifying patients with radiographic lesions. We performed a prospective study of 608 infants younger than 2 years presenting to an urban pediatric ED.7 Fourteen (48%) of 30 patients with intracranial injury in the cohort had none of the following clinical signs of brain injury: loss of consciousness, seizures, persistent emesis, behavior change, bulging fontanel, depressed mental status, or abnormal findings on neurologic examination. In a retrospective study from the same institution, we found that 19 (19%) of 101 infants admitted to the hospital with intracranial injury had no symptoms or signs of brain injury.37 Similarly, Quayle et al6 found that 5 (4%) of 135 infants in their study had intracranial injury despite the absence of any clinical signs of brain injury. In the studies from our institution, the risk for asymptomatic intracranial injury was highest for infants younger than 6 months.7,37 As with older children, infants with intracranial injury and a normal neurologic status have a low but nonzero rate of surgical intervention. One (7%) of the 14 asymptomatic infants with intracranial injury that we described had an epidural hematoma with associated midline shift, which was treated with emergency surgical evacuation.7 Most intracranial injuries in asymptomatic infants are diagnosed because the infants have an associated skull fracture.7,37 Skull fracture is clearly a risk factor for asso-

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ciated intracranial injury. Quayle et al6 reported that skull fracture increased the risk of intracranial injury 20-fold. Shane and Fuchs40 reported that 15 (47%) of 32 infants with skull fracture who had a CT scan performed had an associated intracranial injury. Most cases of skull fracture are associated with a scalp hematoma.41,42 We found that scalp hematoma, indicative of underlying skull fracture, was a more sensitive predictor of intracranial injury than any of the clinical signs of brain injury we evaluated.7 Larger hematomas and hematomas of the parietal scalp convey an especially high risk of intracranial injury.43 Complications

As noted, children with minor head trauma who have intracranial injuries seen on head CT scan have a small risk of subsequent clinical deterioration, secondary to an increase in intracranial pressure or to seizure activity resulting from irritation of the cerebral cortex.10,22,23 Children with minor head trauma who have normal findings on head CT scan may rarely have short-term complications as well. Many patients with concussion (defined as a transient alteration in mental status after head trauma) have normal findings on head CT scan.32,44 The clinician should remember, however, that a normal head CT result does not mean that the brain has not been injured on a microscopic level. Increasing evidence suggests that patients who have a concussion have abnormal neurologic function for several days after the injury.45,46 Even more importantly, several frightening case reports of the “second impact syndrome” have appeared.47 These cases all describe football players who developed irreversible brain injury, apparently triggered by a fairly routine second head impact after a prior concussion had occurred. The cause of the second impact syndrome is poorly understood, but it is thought perhaps to be related to disordered autoregulation.47,48 The literature indicates that CT imaging is not totally sensitive for radiographically evident intracranial injuries. A number of researchers have demonstrated abnormalities on magnetic resonance imaging (MRI) of the brain in patients with head injuries whose CT scans yielded normal findings.49,50 Most such patients had small areas of contusion, or subtle evidence of diffuse axonal injury. CT imaging does seem to be very sensitive, however, for identifying lesions that will require acute medical or surgical therapy. Several studies have shown that the risk of subsequent neurologic deterioration (assuming no second impact) after normal findings on head CT scan is negligible. Davis et al51 reported that 2 (0.5%) of 400 children with initially normal findings on head CT scan had an

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intracranial injury diagnosed subsequently, with only 1 child (0.25%) requiring surgical intervention for a subdural hematoma. This child was being treated with warfarin at the time of the injury. Schunk et al,31 in a retrospective study, reported that none of 300 patients seen in their ED with normal findings on their head CT scan subsequently received any specific therapy for their head injury at the same institution. Vogelbaum et al52 reported that none of 44 patients with isolated skull fracture (with no intracranial injury) who were admitted to the hospital had any subsequent complications. Even patients with posttraumatic seizures appear to be at low risk for subsequent seizures or other complications if they have a normal neurologic examination and normal findings on the head CT scan.53 In infants younger than 2 years, the absence of intracranial injury on CT scan is similarly reassuring. We reported that none of 167 infants with head injuries with either a normal head CT scan result or an isolated skull fracture had any subsequent complications within 2 weeks of the injury.7 Similarly, in a retrospective study of infants with isolated skull fracture admitted to the hospital, we found that none of the 101 subjects had any subsequent complications.41 There is a theoretical concern for delayed intracranial bleeding after initially normal findings on the head CT scan. Several case series of patients with delayed intracranial bleeding have been published.54-56 Virtually all of these cases, however, involved patients who either had other intracranial abnormalities on the initial head CT scan or who had an abnormal neurologic status on presentation.15,54 For patients with normal head CT findings and a normal neurologic examination, delayed intracranial bleeding appears to be a very rare event. In adults, there is mounting evidence that minor head injuries can be associated with long-term neuropsychological sequelae. Rimel et al57 prospectively studied 538 adult patients with minor head trauma and found that 84% complained of some symptoms 3 months after the injury. Furthermore, neuropsychological test scores indicated mild impairment on tests of cognitive functioning, problem-solving skills, attention, and concentration. The duration of these neuropsychological sequelae after minor head injury has been questioned. Dikmen et al58 reported that 20 adult subjects with minor head injury were found to have deficits in concentration and short-term memory when tested 1 month after the injury, but not when tested again 12 months after the injury. More recently, Collins et al59 reported that a history of prior concussion was an independent risk factor for low-

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ered neuropsychological testing performance among a sample of college football players, with a history of multiple concussions being associated with even worse performance. Matser et al60 reported that young adult soccer players had poorer performance on tests for planning and memory than control subjects who were athletes in noncontact sports, and that the number of reported concussions was inversely related to performance on the neuropsychological tests. Taken together, the strength of the data suggests that minor head trauma may be associated with subtle but measurable differences in cognitive function. There are very limited data specifically examining the consequences of minor head trauma in pediatrics. Ewing-Cobbs et al61 reported results of neuropsychological testing for 35 subjects with mild to moderate head injury. Their data suggest that subtle linguistic changes were noted 6 months after the injury, with persistence of the deficits as long as 24 months after the injury. In contrast, Anderson et al62 found that 32 subjects with mild to moderate head injury performed similarly to noninjured controls when evaluated 12 months after the injury. We were unable to find any data correlating the results of head imaging studies obtained at the time of the injury and neuropsychological outcome in pediatric patients with minor head injury. We also could find no data describing the positive effect of any educational intervention intended to improve long-term neuropsychological outcome in pediatric patients with minor head injury. SKULL FRACTURES

Diagnosing intracranial injury to minimize secondary brain injury is the main goal of evaluating minor head trauma in children. Identifying skull fractures is a secondary focus, both because fractures are predictors for intracranial injuries and because fractures in themselves occasionally lead to complications. The incidence of skull fractures in outpatients presenting for evaluation of head trauma ranges from 2% to 20% and occurs at a higher incidence in younger children (particularly those younger than 1 to 2 years).63,6,32,64-69 In infants, who have thinner cranial bones, skull fractures may result even from short falls (≤3 to 4 ft); however, the mechanism is typically more significant for older children and adolescents. The parietal bone is the most commonly fractured (approximately 60% to 70%), followed by the occipital, frontal, and temporal bones.40,41,64-69 Linear fractures are the most common type (approximately

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60% to 90%), followed by depressed and basilar fractures.31,32,41,65,66,69 Most linear fractures have an overlying hematoma or soft tissue swelling (in most studies, >90%), although the swelling may not be detectable if the child is evaluated within a short period of the trauma or if the swelling is underlying the patient’s hair.36,41,42 Larger hematomas or hematomas in the temporal or parietal regions are more likely to indicate fracture.43 Palpable bony abnormalities may be evident in children with a significantly depressed fracture but are rarely noted with linear fractures.41 Clinical findings such as hemotympanum, Battle’s sign, cerebrospinal fluid (CSF) rhinorrhea, or cranial nerve palsies are evident in approximately 80% of cases of basilar skull fracture.71 Fifteen percent to 30% of linear skull fractures are associated with intracranial injury.7,15,31,36,40,70 Conversely, 40% to 100% of cases of intracranial injury have an associated skull fracture,6,7,15,26,31,32,72,73 and the presence of a fracture increases the likelihood of an intracranial injury 4- to 20-fold.6,29,73 There are limited data describing the rate of intracranial injury among children with minor head trauma who have depressed skull fractures. Approximately 30% of closed, depressed skull fractures have an associated intracranial injury, and the deeper the depression, the higher the risk of dural tear and brain laceration.6,31,74 Kadish and Schunk71 reported that of 144 basilar skull fractures in children who had a normal neurologic status, 21% had intracranial injuries. Linear fractures almost always heal without complications; however, growing skull fractures may very rarely occur. Growing skull fractures are those that enlarge over time, producing a cranial defect. Growing skull fractures result from a tear in the underlying dura, which allows pulsation of either CSF or the herniated meninges to remodel the bone, and typically occur in infants or young children with diastatic fractures (those with separation of the edges by >3 mm).75,76 Growing skull fractures can present months to years after the initial injury (median 18 months) with a skull defect or swelling, enlargement of the fracture on plain skull radiographs, seizure, or neurologic defect. Most require surgical correction. In addition to intracranial hemorrhage, complications of depressed skull fractures include underlying dural laceration, compression of underlying brain parenchyma or intraparenchymal bone fragments (which may cause posttraumatic seizures or focal neurologic deficits), and cosmetic deformity.74,77 Insufficient data are available regarding the incidence of complications and surgical repair for alert patients with depressed skull fracture.

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Basilar skull fractures frequently occur through the temporal bone with resultant bleeding into the middle ear, and they can also disrupt the mastoid air cells or paranasal sinuses. The fracture may cause a dural tear, which can lead to CSF leak and exposure to microorganisms of the upper airway (with potential for meningitis). The rate of CSF otorrhea or rhinorrhea in children with basilar skull fracture is approximately 15% to 30%.71,78-80 Although most CSF leaks spontaneously resolve without complication within 1 week, operative intervention may be needed for persistent leaks. The incidence of meningitis in basilar skull fracture ranges from 0.7% to 5%; for patients with no intracranial hemorrhage and GCS scores of 13 or higher, the rate is 1% or less.71,81 Current data do not indicate that prophylactic antibiotic therapy significantly reduces the incidence of meningitis.82,83 Basilar skull fractures may also dislocate the bones of the auricular chain, disrupt the otic canal, or compress cranial nerves that pass through the basal foramina, leading to hearing loss or cranial nerve impairment. Hearing loss occurs in up to half of patients, can be conductive or sensorineural, and may be permanent in a small number of patients.78,80 Cranial nerve impairment (most commonly nerves VI, VII, or VIII) has been reported in 1% to 23% of patients with basilar skull fracture and may be transient or permanent.71,78,79 Limited data exist regarding the incidence of hearing and cranial nerve impairment specifically for children with minor head trauma. Skull fractures can be diagnosed by skull radiography or CT scanning. Most studies report that skull radiographs are 94% to 99% sensitive for detecting linear or depressed skull fractures,6,7,40,41 although Dietrich et al32 reported a sensitivity of only 64%. CT imaging has a lower sensitivity, ranging from 47% to 94%.6,7,32,41,84 Despite their higher sensitivity for fracture, skull radiographs have limited utility because they give little to no information about intracranial injuries. However, skull radiographs have the advantage of being more universally available than CT scanning and do not require sedation. N O N A C C I D E N TA L T R A U M A

Studies have estimated that 6% to 10% of young children brought to the ED with traumatic injury are victims of child abuse,85,86 and abusive head trauma is the most common cause of traumatic death in infancy.3,87 In a study of admitted children younger than 2 years with head trauma, Duhaime et al70 reported that 24% of the injuries resulted from inflicted trauma.

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The mechanisms of injury in abusive head trauma typically involve blunt impact (such as striking the child with an object or dropping or throwing the child) and/or acceleration/deceleration injuries (as with shaking).88 The clinician’s ability to recognize inflicted injury is critical both for guiding appropriate medical therapy and for preventing further trauma from an abusive caretaker. In a study of 173 children younger than 3 years with a diagnosis of abusive head trauma, Jenny et al89 found that 54 (31%) cases were missed at the initial medical visit. Fifteen (28%) of 54 were reinjured before child abuse was diagnosed, and the authors believe that earlier diagnosis might have prevented 4 deaths. Risk factors for abuse include young age (<1 to 2 years), low socioeconomic status, unstable family situations, and disability or low birth weight of the child.88,90-96 An accurate history is rarely present for children with inflicted head injuries. The history provided is typically one of a minor blunt impact to the head (eg, falling off a bed or couch), no explanation for the injuries, or merely medical complaints such as irregular breathing, apnea, irritability, lethargy, seizure, vomiting, or decreased appetite.70,86,90,91 Inflicted head injury is significantly more common in cases of traumatic head injury with no history of trauma reported.86,95 Physical findings often include signs of blunt impact to the head (eg, swelling, contusion, bony abnormalities, bulging fontanel), although these findings may be absent in cases of shaking injuries.97 Overall, retinal hemorrhages are present in up to 65% to 90% of children admitted with inflicted head injury; however, there are no incidence data for children with apparently minor head trauma.87,91,94,97 Retinal hemorrhages are strongly associated with inflicted head injury but may very rarely be related to accidental trauma, in this setting usually resulting from mechanisms of enormous force.98,96 Extracranial abnormalities (including fractures, burns, and visceral injury) occur in 35% to 70% of children with inflicted head injuries, and are more likely to be present than with accidental head injury.89,95,97,99 Compared with unintentional injuries, diagnosed abusive injuries tend to be more severe86,96; however, children with abusive head trauma may be awake and alert at presentation.89 To date, no study has directly addressed the incidence, signs, and symptoms of children with apparently minor head trauma resulting from inflicted injury. Radiographic documentation of injuries is critical to define the extent of the injuries and to document abuse. Although CT imaging is the preferred study for acute

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evaluation of suspected intracranial injury, MRI gives superior detail for many of the lesions associated with abusive head injury.93,100 The most common intracranial lesions diagnosed in cases of abuse are subarachnoid hemorrhage, subdural hemorrhage, interhemispheric blood, and cerebral edema.70,94,95,101 These same lesions are uncommon in cases of accidental head trauma unless high-force mechanisms of injury are involved.70,102,103 Any skull fracture resulting from abuse can also occur with accidental trauma; therefore, no fracture is diagnostic of inflicted trauma. However, compared with unintentional injuries, fractures inflicted by abuse are more commonly multiple, bilateral, crossing suture lines (involving more than a single cranial bone), diastatic, nonparietal, and associated with intracranial subdural hematomas.104,105 Skull fractures that occur in young children from short falls (≤3 ft) are typically simple, linear fractures.41,70,106 R E C O M M E N D AT I O N S

These recommendations are intended for children with acute closed head trauma who are alert or easily aroused to voice or light touch. These recommendations are not intended for children with birth trauma, penetrating injury, existing neurologic disorder, bleeding diathesis, prior intracranial surgery, or multiple trauma, given their additional issues and risks. Based on the literature reviewed and presented, physicians should obtain CT imaging for any child with even mildly altered mental status (ie, GCS score of 13 to 14), focal neurologic deficits, or evidence of a depressed or basilar skull fracture. CT imaging should also be considered for children with symptoms including a history of loss of consciousness, amnesia, seizure, headache, persistent vomiting, irritability, or behavioral change. The longer the duration and the more intense the symptoms, the more strongly the clinician should consider head imaging. For children with mild symptoms, careful observation at home may be an alternative approach, with reevaluation and CT imaging for persistent or worsening symptoms. Children who are awake, alert, and asymptomatic (including no history of loss of consciousness) do not require imaging. Clinicians should have a lower threshold for imaging in infants and children younger than 1 to 2 years, given their higher incidence of skull fracture and intracranial injury from minor trauma, their risk for asymptomatic intracranial injury, and their increased risk for abuse. Any symptom in these children should prompt strong consid-

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eration for CT imaging, and the younger the infant, the more strongly the clinician should consider imaging. The clinician may also consider CT imaging even for asymptomatic infants younger than 2 to 3 months, particularly if the mechanism was more than trivial or if a scalp hematoma is present. Imaging should also be considered for children younger than age 2 with significant scalp findings, especially for those who are younger or have hematomas that are larger and nonfrontal in location. Skull radiographs may also be a useful screen for skull fracture for alert, asymptomatic infants with scalp hematomas, who would not otherwise undergo CT imaging. In these well-appearing young infants, skull radiographs offer the advantage of requiring no sedation. If a fracture is detected, CT imaging is indicated to assess for associated intracranial injury. Inflicted injury should be considered in the infant or young child with head trauma who presents with no history of injury; inconsistencies or changes in the history; a delay in seeking medical care; a history of repeated injury or hospitalization; a mismatch of the history with the physical findings; or when the child exhibits multiple injuries, injuries in various stages of healing, or overall poor care. Radiographic imaging is important both for identifying injuries as well as documenting and diagnosing abuse. CT imaging is indicated for any infant or child at risk of intracranial injury, and skeletal survey is indicated if concern for abusive trauma exists. Ophthalmologic examination should be strongly considered for any child with suspected inflicted head injury. If the suspicion of abuse has been established (based on the history, physical findings, results of radiographic imaging, and interactions with the caretakers), the physician is mandated to report the case to designated authorities. Although state laws vary, generally mandated reporters are afforded legal immunity if the allegations of abuse are deemed to be unfounded after investigation. Mandated reporters can be penalized for failure to report suspected abuse.107,108 If a diagnosis of skull fracture or intracranial injury is made, management and disposition depend on a thorough consideration of the abnormalities, and, when warranted, consultation with an appropriate subspecialist. In general, a neurosurgeon should be consulted for children with intracranial injury or skull fracture that is depressed, basilar, or widely diastatic. Most of these children require hospital admission, and the need for acute intervention is determined in conjunction with the neurosurgeon. Hospital admission should also be considered for patients with persistent neurologic deficits (despite normal CT

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findings), significant extracranial injuries, unremitting vomiting, or caretakers who are unreliable or unable to return if necessary. Admission should also be considered for any child with suspected nonaccidental trauma. The risk of delayed deterioration is low but not zero in any child who is discharged. It is therefore mandatory that discharge instructions are provided to competent caretakers regarding signs and symptoms of complications of head trauma and that caretakers are able to bring the child to medical care. The patient may be given acetaminophen for headache, but more potent analgesics are best avoided so that any progression of symptoms can be detected. If the child has no significant symptoms, quiet play or activities can be allowed. Because of concerns regarding the second impact syndrome, the American Academy of Neurology has published recommendations for activity restrictions for athletes who have sustained a concussion. A summary of the recommendations has been published by the Centers for Disease Control and Prevention (Table).47 Children with symptoms or isolated skull fractures should follow up with their physician within 24 hours. Infants and young children with skull fracture should be

Table.

Summary of recommendations for return to sports activity after concussion. Grade 1 Concussion • Definition: Transient confusion, no loss of consciousness, and duration of mental status abnormalities <15 minutes. • Management: Return to sports activity same day only if all symptoms resolve within 15 minutes; if a second grade 1 concussion occurs, no sports activity until asymptomatic for 1 week. Grade 2 Concussion • Definition: Transient confusion, no loss of consciousness, and a duration of mental status abnormalities of ≥15 minutes. • Management: No sports activity until asymptomatic for 1 full week; if a grade 2 concussion occurs on the same day as a grade 1 concussion, no sports activity until asymptomatic for 2 weeks. Grade 3 Concussion • Definition: Concussion involving loss of consciousness (LOC). • Management: No sports activity until asymptomatic for 1 week if loss of consciousness is brief (seconds); no sports activity until asymptomatic for 2 weeks if loss of consciousness is prolonged (minutes or longer). For a second grade 3 concussion, no sports activity until asymptomatic for 1 month. If an intracranial pathology is detected on CT or MRI, no sports activity for remainder of season and the athlete should be discouraged from future return to contact sports. Modified from Centers for Disease Control and Prevention. Sports-related recurrent brain injuries—United States. MMWR Morb Mortal Wkly Rep. 1997;46:224-227.

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evaluated for signs of growing skull fracture 2 months after the injury. F U T U R E D I R E C T I O N S : E VA L U AT I O N O F MANAGEMENT GUIDELINES

The AAP published consensus guidelines for the management of children older than 2 years with minor head injury in December 1999.21 Our guidelines differ in scope, in that we include children younger than age 2, those with intentional injuries, and those with basilar or depressed skull fractures. The AAP guidelines recommend no head imaging for most children with minor head injury unless there is a history of loss of consciousness, in which case head CT imaging should be considered. Our proposed guidelines differ in 2 principal ways: (1) we do not use a history of loss of consciousness as the main determinant for which children should undergo CT imaging as we do not consider a history of loss of consciousness to be an especially strong indication of intracranial injury in subjects who now appear well; and (2) we allow the clinician to consider head CT imaging in patients with no loss of consciousness but with worsening or persistent symptoms such as headache, dizziness, or vomiting. In a recent review of minor head trauma, Quayle109 made recommendations that are similar to those we propose. Future studies prospectively comparing the clinical and cost-effectiveness of the various proposed guidelines will be important in resolving the ongoing debate about how best to treat children with minor head injuries. REFERENCES 1. Kraus JF, Rock A, Hemyari P. Brain injuries among infants, children. adolescents, and young adults. Am J Dis Child. 1990;144:684-691. 2. Rivara FP. Childhood injuries. III: epidemiology of non-motor vehicle head trauma. Dev Med Child Neurol. 1984;26:81-87. 3. Centers for Disease Control and Prevention. Childhood injuries in the United States. Division of Injury Control. Center for Environmental Health and Injury Control, Centers for Disease Control. Am J Dis Child. 1990;144:627-646. 4. Kraus JF, Fife D, Conroy C. Pediatric brain injuries: the nature, clinical course, and early outcomes in a defined United States’ population. Pediatrics. 1987;79:501-507. 5. Tepas J, DiScala C, Ramenofsky ML, et al. Mortality and head injury: the pediatric perspective. J Pediatr Surg. 1990;25:92-95. 6. Quayle KS, Jaffe DM, Kuppermann N, et al. Diagnostic testing for acute head injury in children: when are head computed tomography and skull radiographs indicated? Pediatrics. 1997;99:E11. 7. Greenes DS, Schutzman SA. Clinical indicators of intracranial injury in head-injured infants. Pediatrics. 1999;104:861-867. 8. Dos Santos AL, Plese JP, Ciquini Junior O, et al. Extradural hematomas in children. Pediatr Neurosurg. 1994;21:50-54. 9. Chan KH, Mann KS, Yue CP, et al. The significance of skull fracture in acute traumatic intracranial hematomas in adolescents: a prospective study. J Neurosurg. 1990;72:189-194.

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