Pediatric Head Injury 2013

DOI: 10.1542/pir.33-9-3982012;33;398Pediatrics in Review

Jeff E. Schunk and Sara A. SchutzmanPediatric Head Injury

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Pediatric Head InjuryJeff E. Schunk, MD,* Sara

A. Schutzman, MD

Author Disclosure

Drs Schunk and

Schutzman have

disclosed no financial

relationships relevant

to this article. This

commentary does not

contain a discussion of

an unapproved/

investigative use of

a commercial product/

device.

Educational Gap

Recent studies have provided updated guidelines for the diagnosis of head injury and the

management of patients who experience concussions. A multidisciplinary panel has re-

cently issued new guidelines for return to play after head injury.

Objectives After reading this article, readers should be able to:

1. Understand the anatomy and pathophysiology relevant to pediatric head injuries.

2. Take an appropriate history, perform an appropriate physical examination, and decide

what imaging, if any, is warranted in the case of a child with a head injury.

3. Know the characteristics of the various types of intracranial injuries.

4. Understand the proper management of both minor and severe head injuries in

children.

IntroductionPediatric head injury is extremely common. Although the vast majority of children withhead trauma have minor injuries, a small number, even among well-appearing children, willhave more serious injuries with the potential for deterioration and signicant sequelae. Theclinician is challenged to discern which few among the many injured are at high risk forintracranial complications. Clinical symptoms are neither completely sensitive nor specicfor signicant injury: vomiting may be associated with intracranial injury (ICI), but mostchildren who experience vomiting do not have a complication. Computed tomography(CT) accurately identies ICIs requiring intervention, but also identies minor lesions withunclear clinical importance (ie, not requiring intervention) and exposes developing brainsto ionizing radiation with the associated risks.

Although clinical decision rules determine which children are at highest risk and providea useful clinical framework, they may not necessarily direct care. Additionally, in this era of

reliance on imaging, it is important to remember what theclinical examination tells us regarding brain function, infor-mation that may or may not correlate with the structural in-formation provided on head CT.

The purpose of this discussion is to review important as-pects of pediatric head trauma. Sections on epidemiology,mechanisms of injury, and the pathophysiology of specicinjuries will provide a backdrop for the discussion of clinicalassessment and indications for imaging and admission. Whatfollows is a discussion of concussion, postconcussion syn-drome, and return-to-play recommendations.

EpidemiologyChildhood head injuries account formore than 600,000 emer-gency department (ED) visits per year and presumably a larger

Abbreviations

BSF: basilar skull fractureCSF: cerebrospinal uidCT: computed tomographyEDH: epidural hemorrhageGCS: Glasgow Coma ScaleICI: intracranial injuryICP: intracranial pressurePECARN: Pediatric Emergency Care Applied Research

NetworkSAH: subarachnoid hemorrhageSDH: subdural hemorrhageTBI: traumatic brain injury

*Professor, Division of Pediatric Emergency Medicine, Department of Pediatrics, University of Utah School of Medicine, Primary

Childrens Medical Center, Salt Lake City, UT.Assistant Professor, Department of Pediatrics, Harvard Medical School, Senior Associate Physician in Medicine, Division of

Emergency Medicine, Department of Medicine, Childrens Hospital Boston, Boston, MA.

Article neurologic disorders

398 Pediatrics in Review Vol.33 No.9 September 2012


number of visits and calls to primary care providers.Most pediatric head injuries are minor, including scalpand face contusions, abrasions, and lacerations that donot raise concern for signicant underlying pathology;however, trauma is the leading cause of death in chil-dren older than 1 year, and among trauma patients,head injury is the leading cause of death and disability.Pediatric head traumarelated deaths in the UnitedStates are in excess of 3,000 per year.

Although children exhibit almost limitless creativitywith regard to sustaining injury, most pediatric headtrauma results from falls, motor vehicle collisions, autoversus pedestrian incidents, bicycle-related injuries, andsports. Younger children suffer more falls and are moreoften the victims of child abuse, whereas motor vehiclecrashes and sports-related mechanisms play a greater rolein older children. This discussion focuses on blunt headtrauma rather than penetrating trauma (eg, gunshotwound) because penetrating injury is much less commonand unlikely to present to the primary care clinician.

Although the approach to head injury should considerthe potential for serious injury in all cases, some mecha-nisms can be regarded as relatively trivial and unlikely tobe associated with serious injury. These injuries includelow-velocity self-propelled contact into stationary objects(eg, the toddler runs into the door frame) and falls fromstanding or sitting height or lower. However, the pres-ence of any symptoms of head trauma despite the historyof an apparently benign mechanism would no longerqualify the head injury as trivial.

Rarely, minor mechanisms may create more serious in-jury in the presence of undiagnosed intracranial pathol-ogy (eg, hemorrhage into a brain tumor). The clinicianalso must be alert to more dangerous mechanisms thatcould be concealed, either because the child choosesnot to disclose or because the injury was inicted.

General PathophysiologyBrain injury results from the blow to the head and the in-terplay of brain parenchyma, the brains coverings, thebrains housing structure (the cranial vault), and the vas-cular supply. It is useful to consider the relevant anatomicstructures as layers from outside to inside.

The scalp consists of ve layers of soft tissue thatcover the skull. Common injuries to the skin and subcu-taneous tissue (the outer two layers) include lacerations,abrasions, and freely mobile contusions. Beneath lies thestrong galea aponeurotica that also connects musculartissue on the front and back of the skull. Underneathare the loosely applied areoloar tissue layer and thenthe pericranium.

Hemorrhages may occur in the subgaleal region fromdirect blows or as a result of bleeding from a fracture.Cephalohematomas are hematomas caused by bleedingbeneath the periosteum, a condition well known to thosewho care for newborn infants.

The skull can be divided into the calvarium or bonyskullcap and the skull base. The skullcap is composed ofthe frontal, parietal, occipital, and temporal bones. Thebase of the skull is made up of the sphenoid, palatine,and maxillary bones and portions of the temporal andoccipital bones. Injury to the calvarium results from di-rect forces, and fractures commonly are linear.

Less commonly, skull fractures may be depressed (in-truded by more than the thickness of the bone), commi-nuted (consisting of multiple fragments), diastatic (widelysplit), or open (communicating with a laceration). Fracturesinvolving the skull base, known as basilar skull fractures(BSFs), are more complicated because of adjacent anatomicstructures (eg, cranial nerves, sinuses), their association withICI, and the risk they pose for meningitis.

Within the skull are the intracranial contents, consist-ing of the brain and its covering membranes (the menin-ges), blood, and cerebrospinal uid (CSF). The meningesplay an important role in the genesis of serious ICI. Theoutermost meningeal layer, the dura mater, is attachedtightly to the inner aspect of the skull. The epidural spaceis a potential space between the dura and the skull. Menin-geal arteries course between two layers of the dura and maybecomemore grooved into the skull as the skull matures, sothat a skull fracture may injure these vessels and causebleeding into the epidural space. Meningeal arteries are par-ticularly vulnerable to injury because they run beneath thethinnest part of the skull. Channels exist within the dura forvenous drainage and these dural sinuses also may be lacer-ated. Blood collecting in the epidural space is referred to asan epidural hematoma or epidural hemorrhage (EDH).

Beneath the dura lies the arachnoid mater, a thin tissuelayer coursing close to the brain but not following thebrain sulci. This membrane separates the CSF-containingsubarachnoid space beneath it from the subdural space.Within the subdural space lie the bridging veins that re-turn blood from the brain to the dural sinuses. Thesebridging veins are susceptible to shearing forces whenthere is rapid acceleration or deceleration that movesthe brain within the skull. A hematoma in this space istermed a subdural hemorrhage (SDH).

The third, innermost meningeal layer is termed the piamater and adheres to the underlying brain, coursing overall gyri and sulci. This layer contains many small vesselsthat can be injured from direct blow or shear forces, re-sulting in a subarachnoid hemorrhage (SAH).

neurologic disorders head injury

Pediatrics in Review Vol.33 No.9 September 2012 399


Beneath themeninges lies the brain parenchyma, a semi-solid tissue that is not afxed to the skull and can movefreely within it. The CSF that bathes the brain and the spi-nal 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 im-mediately at the time of trauma from direct impact (eg,brain impacts the inner aspect of the skull or a skull frag-ment moves into the brain) or from shear forces when thegray matter and white matter move at different speedsduring deceleration or acceleration.

Secondary injury refers to ongoing derangement toneuronal cells not initially injured during the traumaticevent. Ongoing injury results from processes initiatedby the trauma, including hypoxia, hypoperfusion (localor systemic shock), metabolic derangements (eg, hypo-glycemia), expanding mass and increased pressure, andedema. Because primary injury occurs at the momentof trauma, little can be done to mitigate it other than pre-vention, so treatment during trauma resuscitation focuseson preventing secondary injury.

When considering secondary injury, two additionalconcepts warrant further discussion. The rst consider-ation relates to pressure and volume within the cranialvault. After infancy, the cranial vault is a relatively stiff,poorly compliant structure and the intracranial volumeis relatively xed. From a simplistic standpoint, the vaultcontains brain, blood, and CSF, and any increase in thevolume of one component necessitates a relative decreasein another.

If volume compensation does not occur, intracranialpressure (ICP) will increase. With progressive increasesin ICP, the patient will experience headache, vomiting,and depressed mental status, then posturing, and ulti-mately vital sign deterioration. Increasing ICP may leadto global ischemia through mechanisms discussed later inthis section. Ultimately, increased ICP will lead to brainherniation (abnormal movement of the brain across skullstructures).

Herniation can occur at several different anatomic lo-cations (Fig 1). When a mass lesion is one-sided andsupratentorial, uncal herniation may occur. This type ofherniation involves movement of the innermost part ofthe temporal lobe, the uncus, over the tentorium, withresultant pressure on the midbrain and pressure on thethird cranial nerve, impairing its parasympathetic bersand leading to ipsilateral pupillary dilation.

Central herniation occurs when central brain struc-tures, including the diencephalon and temporal lobes,move caudally through the tentorium cerebelli. Cingu-late or subfalcine herniation occurs when the cingulate

gyrus is pushed across the midline under the falx cereb-rial. Although subfalcine herniation does not affect themidbrain directly, it can affect blood ow and can prog-ress to central herniation.

In tonsillar herniation, the cerebellar tonsils move downthrough the foramen magnum with compression of thelower brainstem and upper cervical spinal cord. Compressionof the brainstemmay result in severe neurologic dysfunction,cardiovascular and respiratory instability, and death.

The other important concept in considering second-ary injury involves cerebral perfusion. Cerebral perfusionpressure is the difference between the mean arterial bloodpressure and ICP. In health, cerebral blood ow is main-tained despite variable blood pressures by autoregulatorychanges in cerebral vascular resistance. When severe inju-ries occur, this ability to autoregulate may be impaired, sothat cerebral blood ow will be dependent on cerebralperfusion pressure.

In the absence of appropriate autoregulation, cerebralperfusion will diminish with elevated ICP or with sys-temic hypotension. In either instance, resultant ischemia,neuronal death, and subsequent edema all contribute tosecondary injury.

Figure 1. This figure depicts four types of brain herniation: (1)cingulated (subfalcine), (2) central, (3) uncal (transtentorial),and (4) tonsillar. (Figure is reproduced with permission fromKaye AH. Head Injuries. In: Smith JA, Tjandra JJ, Clunie GJ,Kaye AH, eds. Textbook of Surgery. 3rd ed. Oxford, UK: Wiley-Blackwell; 2006:445453.)




General Management ConsiderationsManagement focuses on prevention of secondary injury,so initial attention is directed to the ABCs of trauma re-suscitation, focusing on maintaining adequate airway,breathing (ventilation and oxygenation), and circulation(blood pressure and perfusion). Cervical spine precautionsare taken when head injury is present because head injurymay be associated with cervical spine injury. Oxygen is ap-plied, ventilation is supported as necessary to providenormocarbia (partial pressure of carbon dioxide at 3545 mm Hg), and circulatory concerns are addressed.

Hyperventilation is no longer the standard of care, al-though there is still a limited role for acutely lowering in-creased ICP in the intensive care unit or operating room.Patients with Glasgow Coma Scale (GCS)

with or without loss of consciousness. From a practicalstandpoint, concussion often is used to refer to moreminor head injury when the GCS is 14 to 15, the patienthas some symptoms (eg, headache, dizziness, vomiting,amnesia, or confusion), there is no evidence of a fracture,and there are no focal neurologic decits. A more detaileddiscussion of concussion is below.

Skull FracturesThe main importance of skull fractures is that they aremarkers for signicant impact to the head that increasesthe risk of ICI signicantly; however, it is important tonote that ICI also occurs in the absence of fractures, andmany fractures are not associated with ICI. Rarely, the frac-ture itself may lead to a complication (more common withbasilar or depressed skull fracture). Before the advent ofCT, skull radiography was an important modality to identifychildren at risk for complications; however, because plainradiographs give no direct information about ICI, currentlythey are of very limited utility. Skull fractures now are diag-nosed most commonly when a CT scan is obtained.

An exception to the lack of utility of skull radiographsoccurs when child abuse is suspected. When child mal-treatment is suspected, the presence of a skull fracture,old or new, with or without ICI, has important implica-tions; so skull radiographs, with their higher sensitivityfor fracture, are included as part of a more comprehensiveskeletal survey. Skull fractures in children younger than 2years in the absence of a history of appropriate mechanismshould prompt a more thorough evaluation for inicted

trauma (including skeletal survey) and appropriate report-ing and referrals.

Fracture of the calvarium is more common than frac-ture of the base of the skull. Most fractures are linear and,when considered in isolation (ie, not associated withICI), of little consequence. No specic therapy need bedirected to the fracture except pain management. Follow-upwith primary care is appropriate to detect the exceedinglyrare late complication of a growing fracture. Depressedskull fractures (those intruded more than the thicknessof the bone) carry increased risk of primary injury tothe brain because of intrusion of the fragment and, de-pending on the location, may have signicant cosmeticsequelae (Fig 2). Neurosurgical consultation is neces-sary for all depressed skull fractures, even in the absenceof more serious ICI.

Basilar Skull FracturesBSF requires special consideration for several reasons. Theycan have unique clinical presentations providing clinicalclues that often are readily apparent. Hemotympanumor blood draining from the ear, are the most commonsigns of a BSF. CSF draining from the ear or draining fromthe nose (attributable to a cribriform plate fracture), Battlesign, and raccoon eyes also are signs of BSF. Persistent

Table 2. Modified Coma Scale forInfants (Best Score Is 15)

Activity Best Response Score

Eye opening Spontaneous 4To speech 3To pain 2None 1

Verbal Coos, babbles 5Irritable, cries 4Cries to pain 3Moans to pain 2None 1

Motor Normal spontaneous 6Withdraws to touch 5Withdraws to pain 4Abnormal flexion 3Abnormal extension 2None 1

Figure 2. This toddler fell from a horse and CT scan showsdepressed and comminuted parietal skull fracture.




clear drainage from the nose after head trauma should alertthe clinician to the possibility of a BSF. BSF also can occurin the absence of these clinical ndings and be apparentonly on CT; conversely, CT scan may not detect all suchfractures.

BSFs are important because they are associated with ICIand have a higher incidence of complications from thefracture itself, owing to the unique anatomic location.ICI occurs in about 20% of BSF patients who have a normalneurologic 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 menin-gitis. Fractures adjacent to the paranasal or sphenoid si-nuses can lead to meningitis if bacteria from these areasenter the normally sterile subarachnoid space. The overallrisk of developing meningitis after sustaining a BSF isprobably less than a few percent, but the risk is increasedif there is CSF rhinorrhea or otorrhea.

Use of prophylactic antibiotics is controversial. If thereis ongoing CSF leakage, neurosurgical intervention maybe needed to facilitate healing of the dural tear. Anatomicadjacency of the base of the skull to cranial nerve path-ways means that BSF may cause hearing loss, facial paral-ysis, and a decreased sense of smell, as well as other cranialnerve dysfunction. Conductive hearing loss also may oc-cur from blood in the middle ear.

General Intracranial InjuriesPerhaps the most important issue for the clinician evalu-ating a head-injured child is determining if there is anICI. With improved CT images and current neurosurgicalpractice, however, detecting an ICI does not equate toa need for neurosurgery. Visible lesions on CT scan mayor may not be associated with functional issues or seriousmorbidity. The two broad classications of ICIs includefocal hemorrhage (EDH, SDH, SAH, intracerebral hem-orrhage, and cerebral contusion), which typically are visi-ble on initial imaging, and diffuse injury (cerebral edema,diffuse axonal injury), which tends to progress andmay be-come more visible on subsequent imaging.

Epidural HemorrhageWhen bleeding occurs between the skull and the duramater, the patient is said to have EDH. The bleedingsource is arterial in w30%, fewer are clearly identied asvenous, and in the remainder the source is unclear. EDHis caused most commonly by a blunt trauma mechanism,with falls most frequent. Often there is an overlying frac-ture (60% to 80%), and the EDH has a lens-shapedappearance on CT (Fig 3). Typically, the underlying brainparenchyma is not injured. Classic teaching suggested

that patients with EDH had LOC, then a lucid interval,and then deteriorated. However, that clinical presenta-tion is rare; only w20% of children with an EDH evenexperience LOC. Some children may present with markedlethargy or focal neurologic ndings and progress to morefrank signs of herniation.

However, presentation with more subtle signs, such aspersistent vomiting and headache, is more common, andmore than 30% of patients who have EDH are alert withnormal neurologic ndings at the time of diagnosis. Al-though some small epidurals may produce minimal orno symptoms, they have the potential to expand, whichcan result in cerebral herniation and death. Fear of miss-ing an expanding EDH, with its high potential for mor-tality, has, in part, fueled the marked increase in use of CTscanning occurring in recent decades.

Patients with EDH require emergent neurosurgicalconsultation and close monitoring. Patients with largerEDH, midline shift, or signicant symptoms are treatedwith emergent craniotomy and evacuation of thehematoma. Because some small EDHs do not expandsignicantly, relatively asymptomatic patients who havesmall epidurals may be managed expectantly, at the

Figure 3. This CT scan demonstrates a right epiduralhematoma with typical lens shape. The mass effect hascaused effacement of the lateral ventricle and shift of themidline to the patients left.




neurosurgeons discretion, with admission and very closemonitoring. Patients who have EDH successfully drainedemergently have a good long-term outcome in more than80% of cases.

Subdural HemorrhageWhen bleeding occurs between the dura and the arach-noid membrane, an SDH results. Usually, tearing ofthe bridging veins is the source of the bleeding and resultsfrom a direct blow, falls from signicant height, or frominicted head trauma, as seen in child abuse. SDH is notusually associated with an overlying fracture and hasa crescent shape on CT (Fig 4).

Unlike the EDH, an SDH usually is associated withunderlying brain injury and the hemorrhages may be bi-lateral. Children may present with LOC, altered mentalstatus, seizures, irritability, vomiting, lethargy, or signsor symptoms of increased ICP (eg, bulging fontanel, de-creased responsiveness). In about half the instances ofSDH, the children present in coma or signicantly de-pressed GCS.

Mortality of patients presenting with acute SDH is highand ranges from 10% to 20%. SDH in infants is associatedwith child abuse but is not diagnostic that abuse has oc-curred. Child abuse should be suspected highly when there

is no explanation for the injury, when the mechanism ofinjury does not match the degree of injury, or in instancesin which there appears to be evidence of SDH with bothnew and old blood.

A chronic SDH may occur in children with coagulo-pathies, but usually results from child abuse, and maypresent with subtle ndings, including macrocephaly, fullfontanel, fussiness, seizures, and vomiting.

SDH requires emergency neurosurgical consultation. Pa-tients who have an acute large SDH with evidence of masseffect within the cranium and altered level of consciousnessare candidates for surgical drainage. Smaller SDH and morechronic formsmay bemanagedwithout surgical decompres-sion. Children with SDH often have signicant long-termmorbidity that may include developmental delay and seiz-ures. These adverse, persistent neurologic sequelae are morelikely to occur in patients who present with coma, or whenCT scan demonstrates underlying brain injury.

Subarachnoid HemorrhageIn more severely injured patients, SAH occurs about 25%of the time. This lesion results from tearing of the smallvessels of the pia mater secondary to signicant blunttrauma and associated shearing forces. Because thebleeding is in a space that communicates with otherCSF-containing spaces (within the brain, around thebrain and spinal cord), problems related to the mass effectthat is seen with EDH and SDH rarely occur. SAH often isseen in association with other ICIs, so presentation is vari-able, but SAHs occurring in isolation may present withLOC, headache, or signs of meningeal irritation (eg, vom-iting, photophobia, nuchal rigidity).

Cerebral ContusionA cerebral contusion is essentially a brain bruise causedby a well-localized area of neuronal injury with bleeding(Fig 5). This injury results from movement of the brainagainst the skull. Blunt trauma to the head maycause a cerebral contusion near the site of impact(a coup lesion) or may cause a cerebral contusion op-posite the site of impact (a contrecoup lesion). Typicalsigns may be subtle, and can include vomiting, headache,LOC, or, less commonly, a focal neurologic nding or aseizure. In most instances, small contusions have littleacute or long-term sequelae.

Diffuse Axonal InjuryDiffuse axonal injury involves injury to the white mattertracts within the brain and is likely caused by shear forces.This type of injury is caused by severe acceleration,

Figure 4. CT scan demonstrates subdural hemorrhage leftposterior and left lateral that resulted from child abuse.




deceleration, or rotational forces, occurring most com-monly in motor vehicle crashes. The injury often is atthe gray-white matter junction but may occur deeperwithin the corpus collosum, brainstem, or cerebellum.These children usually are in coma at presentation, althoughoccasionally the child will have only concussion-typesymptoms. The CT scan shows small areas of hemorrhagelocated near the gray-white interface that do not expand.Management of diffuse axonal injury is supportive,mortality is 10% to 15%, and persistent neurologic dys-function occurs in 30% to 40%.

Diffuse Brain SwellingThis condition is seen almost exclusively in children whoexperience severe head trauma and the mechanism ap-pears to be a reaction to cellular injury. Diffuse brainswelling may not be apparent on initial imaging; subse-quent CT scans demonstrate ndings of progressiveedema. The cellular insults may be varied, and cytotoxicedema, vasogenic edema, and autoregulatory dysfunctionall may play a role. The children present with marked de-pression or deterioration of the GCS, and the main threatis the associated increase in ICP.

Who Needs Computed Tomography?The clinicians goal is to identify patients who developclinically important ICI so as to prevent deteriorationand secondary brain injury (eg, from expanding EDH),while limiting unnecessary radiographic imaging. Unfor-tunately, dening sensitive and specic clinical predictorsfor identifying high-risk patients who require a head CThas been challenging.

Several issues contribute to the challenge of evaluatinghead-injured children:

Although patients with ICI often have symptoms orfunctional derangements, many patients with thesesame symptoms have no ICI.

Patients with normal neurologic examinations who ex-hibit symptoms as common as vomiting or headachemay harbor an ICI that has the potential to becomelife-threatening. Repeated examination of the fundiis prudent because papilledema may not be present ini-tially but may develop later in the course of intracranialhypertension.

Many intracranial lesions detected by CT are onlyrarely associated with signicant morbidity (eg, smallcerebral contusion or small SAH).

AlthoughCT can effectively identify clinically importantICI, this imaging modality carries the risks of radiation,including the long-term sequelae of radiation-inducedmalignancy.

Investigators have identied several clear predic-tors of ICI:

GCS 14 or altered mental status. Focal neurologic abnormalities. Skull fracture.

Patients who have any of these ndings should un-dergo CT imaging.

However, most patients have none of these ndings(ie, they have a GCS of 15, nonfocal neurologic exami-nation, and no obvious skull fracture); yet, patientswho lack these features account for a large proportionof patients who actually have ICI. Within this group,the incidence of ICI is about 5% and the need for neuro-surgery

injuries, and more often are victims of inicted injury.In addition to the predictors of ICI found in older chil-dren, nonfrontal scalp hematomas (surrogate markers forskull fracture) were found to be predictors of ICI, withlarger hematomas in younger children of greater concern.(2)

In all age groups, because of the variability of clinicalpredictors in identifying ICI and concern for missing ICI,clinicians have adopted a very liberal approach to the use ofCT scans. ED-based studies have shown that this groupwith mild head injury undergoes CT scanning from 35%to 55% of the time. Head CT for pediatric minor head in-jury increased in Canada from 15% in 1995 to 53% in 2005for head-injured children. In the United States, use has in-creased dramatically in the face of relative stability of seri-ous injury, implying that more and more normal CT scansare being obtained.

Risk of Head Computed Tomography ScanningWidespread imaging has increased concerns regardingsafety, specically related to sedation and radiation risk.Concern for adverse events from sedation is justied,but with increasing speed of scanners, the need for sedationshould decrease. Clinical experience and research in pedi-atric sedation has blossomed, and overall hospital practicesin this regard have become safer, so that sedation-relatedadverse events are less of a concern.

The potential for ill effects from ionizing radiation can-not be overlooked. Evidence for this risk assessment comesprimarily from information on radiation exposure follow-ing nuclear bomb detonation and data derived from ther-apeutic use of radiation. It is estimated that CT scanningwill induce a new malignancy at a rate ofw1 in 5,000 CTscans. It appears that the greatest lifetime risk occurs in theyoungest patients (both because of life-years remainingand susceptibility of tissues), and overall risk decreases asage increases. From the standpoint of an individual or in-dividual clinician, this rate does not seem high, but whenone considers the tens of thousands of normal head CTscans being performed each year, the public health impactmay not be trivial.

Recent InvestigationsRecent investigations (3)(4) have better identied moremeaningful predictors by using multicenter design, includ-ing large numbers of head-injured children, focusing ongroups at relatively low risk, and determining decisionrules to aid clinicians determining the need for CT. Someof these large studies also altered the primary outcomemeasure from presence of an ICI, as previous studies

had done, to clinically important traumatic brain injury(TBI). In a study through the Pediatric Emergency CareApplied Research Network (PECARN) involving morethan 42,000 pediatric patients at 23 centers, a clinicallyimportant TBI was dened as death, need for neurosur-gery, intubation >24 hours, or hospitalization for 2nights. (3)

Decision rules are developed to guide the clinicians ina more thoughtful approach to CT scanning so as to avoidoveruse while still identifying clinically important ICI. Norules eliminate all risk unless all patients are scanned, butthey provide a needed framework for risk assignment.The clinician who appropriately elects not to scan shouldunderstand the risk of serious ICI.

In the PECARN study, (3) when only children withGCS of 14 to 15 are considered, high-risk criteria (w4%incidence of clinically important ICI) were GCS 14,other signs of altered mental status, and palpable skull frac-ture (if age 2 years) forwhich CT was recommended.

Other risk factors (w1% incidence of clinically impor-tant ICI) for age >2 years: loss of consciousness, severeinjury mechanism, vomiting, and severe headache; andfor age

at least 4 to 6 hours from the time of injury is a reasonablealternative.

It is clear from a subanalysis of the PECARN study thatclinicians sometimes use observation before deciding toobtain a CT. When observation is chosen, the appearanceof additional new symptoms, evidence of worsening symp-toms, or clinical deterioration should prompt imaging. Ininstances in which multiple risk factors are present orsymptoms are more severe, imaging probably is favored.Other factors that may inuence the decision to image in-clude quality of observation (eg, caretaker reliability, timeof day), the ability to return for worsening symptoms, phy-sician experience, and parental preference. Table 6 lists cri-teria typical of patients for whom imaging is not necessary.

DispositionIn general, patients with depressed skull fracture or anyICI should be hospitalized with emergent neurosurgicalconsultation for their lesions; however, some small cere-bral contusions or SAHs may have little short- or long-term clinical signicance, and deterioration is rare. Patientswith normal CT scans and resolution of symptoms typically

do not require hospitalization. Patients with persistentsymptoms (despite normal CT scans) who would not be

Table 3. Emergent HeadComputed Tomography Scan IsRecommended

Penetrating injuryGlasgow Coma Scale (GCS) 14 or other evidence of

altered mental statusFocal neurologic abnormalitiesSigns of depressed or basilar skull fractureWorsening headacheProlonged loss of consciousness (LOC) (more than a

few minutes)Clinical deterioration during observation or significant

worsening of symptomsSeizure (other than impact seizure) or any prolonged

seizurePre-existing condition that places child at increased risk

for intracranial hemorrhage (eg, bleeding disorder)In addition for children

managed easily at home (persistent vomiting, severe head-ache, abnormal mental status) also should be admitted.For any child deemed stable for discharge (both those withand without imaging), symptoms concerning for ICIshould be reviewed with reliable caretakers who are ableto return to the ED should concerns arise.

Home Management of Minor Head InjuryCalls to practitioners from caregivers regarding pediatrichead injury are frequent. In many instances, ongoing ob-servation at home without an ED or ofce visit is reason-able, if there is a reliable caretaker with the means to seekadditional care if needed, if there is no concern for inictedinjury, and if there are no underlying conditions that wouldpredispose the child to an ICI. In cases in which there isa low-risk mechanism (typically a ground level fall fromchilds own height) and there are no other injuries, noLOC or mental status changes, no vomiting (one episodeshortly after injury is of less concern), no signicant head-ache, and no nonfrontal scalp hematomas (for children

studies. Both sets of guidelines share some commonrecommendations.

Athletes suspected of having a concussion should beremoved from participation immediately and they shouldnot return while signs or symptoms are present. Athletessymptomatic for >15 minutes should not return to playuntil they are asymptomatic for 1 week.

Most recently, amultidisciplinary panel published a con-sensus guideline advocating abandoning acute gradingscales in favor of clinical measures of recovery. (5) Returnto play should be based on resolution of symptoms andnormalization of neurocognitive function for the individ-ual, rather than based on a predetermined amount of time.Recommendations are for physical and cognitive rest untilasymptomatic, followed by a graduated, monitored returnto play. This graduated return to play guideline from thisconsensus paper is presented in Table 7.

Postconcussion SyndromePostconcussive symptoms develop within a few days of theinitial concussion and can last anywhere from a few days toa few months. Typical symptoms include headache, fatigue,dizziness, cognitive impairment (particularly concentra-tion), and neuropsychiatric symptoms. Some children andteens may experience long-term behavioral and cognitiveproblems temporally related to experiencing a concussion.

About 80% of high school athletes who experiencesports-related concussions have resolution of symptoms

within 1 week, and fewer than 2% are symptomatic longerthan 1month. For patients whose symptoms persist beyonda few weeks, referral to a pediatric neurologist, neuropsy-chologist, sports medicine physician, or other specialist withexpertise in head injury probably is indicated. Investigationsinto understanding postconcussion syndrome risk and ef-fectiveness of interventions is limited.

References1. Kadish HA, Schunk JE. Pediatric basilar skull fracture: do childrenwith normal neurologic ndings and no intracranial injury requirehospitalization? Ann Emerg Med. 1995;26(1):37412. Greenes DS, Schutzman SA. Clinical signicance of scalp abnor-malities in asymptomatic head-injured infants. Pediatr Emerg Care.2001;17(2):8892

Table 7. Graduated Return to Play

Stage Activity Stage Objective

No activity Complete physical and cognitive rest RecoveryLight aerobic exercise Walking, swimming, stationary cycling, low

moderate intensityIncrease heart rate

Sport-specific exercise Skating drills ice hockey, running drills, no impact Add movementNoncontact training More complex training drills (eg, passing drills), may start

progressive resistance trainingExercise, coordination, cognitive

effortFull-contact practice Normal training activities after medical clearance Assess skills by coaches; restore

confidenceReturn to play Normal game play

In general, the athlete who has sustained a concussion should proceed to the next level if without symptoms at the current level. Each step generally takes 24hours. If symptoms recur, then the patient drops back to previous asymptomatic level. (Adapted from Table in Consensus statement on concussion in sport. JClin Neuroscience. 2008;16:755763, with permission.)

Summary

Pediatric head injury is very common and usuallyminor but can result in serious morbidity and is themost common cause of lethal trauma.

Based on strong research evidence, a thorough historyand physical examination with emphasis on neurologicstatus and signs of skull fracture (including size,character, and location of scalp hematomas in infants)provide the clues necessary to assess the relative risk ofserious intracranial injury (ICI). (1)(3)(4)(6)

Based on strong research evidence, computedtomography (CT) scan remains a highly useful adjunctin evaluation of the head-injured child but should beused selectively for children at higher risk for ICI. (2)(3)(4)

Based on research evidence or consensus opinion,observation can be used selectively in lieu of CTscanning for patients who are not at higher risk for ICI,minimizing the risks of CT-associated ionizingradiation. Any concerns during the observation periodshould prompt CT imaging. (3)(7)(8)

Concussion from head injury in athletics has recentlyreceived increased public attention. Based onconsensus opinion, premature return to play mayconfer increased risk to the athlete. (9)(10)




3. Kuppermann N, Holmes JF, Dayan PS, et al; Pediatric EmergencyCare Applied Research Network (PECARN). Identication of childrenat very low risk of clinically-important brain injuries after head trauma:a prospective cohort study. Lancet. 2009;374(9696):116011704. Osmond MH, Klassen TP, Wells GA, et al; Pediatric EmergencyResearch Canada (PERC) Head Injury Study Group. CATCH:a clinical decision rule for the use of computed tomography inchildren with minor head injury. CMAJ. 2010;182(4):3413485. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statementon concussion in sportthe 3rd International Conference on con-cussion in sport, held in Zurich, November 2008. J Clin Neurosci.2009;16(6):7557636. Schutzman SA. Minor head trauma in infants and children. In:Wiley JF, ed. UpToDate. 2011. Accessed at http://www.uptodate.com/contents/minor-head-trauma-in-infants-and-children7. Brenner DJ, Hall EJ. Computed tomographyan increasing sourceof radiation exposure. N Engl J Med. 2007;357(22):227722848. Nigrovic LE, Schunk JE, Foerster A, et al; Traumatic BrainInjury Group for the Pediatric Emergency Care Applied ResearchNetwork. The effect of observation on cranial computed tomog-raphy utilization for children after blunt head trauma. Pediatrics.2011;127(6):106710739. Evans RW. Concussion and mild traumatic brain injury. In:Wilterdink JL, ed. UpToDate. 2011. Accessed at http://www.uptodate.com/contents/concussion-and-mild-traumatic-brain-injury10. Halstead ME, Walter KD, Council on Sports Medicine andFitness. American Academy of Pediatrics. Clinical reportsport-relatedconcussion in children and adolescents. 2010;126(3):597615

Suggested ReadingCommittee on Quality Improvement. The management of minor

closed head injury in children. Committee onQuality Improvement,American Academy of Pediatrics. Commission on Clinical Policiesand Research, American Academy of Family Physicians. Pediatrics.1999;104:14071415

Halstead ME, Walter KD; Council on Sports Medicine andFitness. American Academy of Pediatrics. Clinical reportsport-related concussion in children and adolescents. Pedi-atrics. 2010;126(3):597615

Blackwell CD, Gorelick M, Holmes JF, Bandyopadhyay S,Kuppermann N. Pediatric head trauma: changes in use ofcomputed tomography in emergency departments in the UnitedStates over time. Ann Emerg Med. 2007;49(3):320324

Evans RW. Postconcussion syndrome. In: Wilterdink JL, ed.UpToDate. 2011. Accessed at http://www.uptodate.com/contents/postconcussion-syndrome

Frush DP, Donnelly LF, Rosen NS. Computed tomography andradiation risks: what pediatric health care providers shouldknow. Pediatrics. 2003;112(4):951957

Greenes DS. Neurotrauma. In: Fleisher GR, Ludwig S, eds.Textbook of Pediatric Emergency Medicine. 6th ed. Philadelphia,PA: Lippincott Williams & Wilkins; 2010:14221440

Greenes DS, Schutzman SA. Occult intracranial injury in infants.Ann Emerg Med. 1998;32(6):680686

Schutzman SA, Barnes P, Duhaime AC, et al. Evaluation andmanagement of children younger than two years old withapparently minor head trauma: proposed guidelines. Pediatrics.2001;107(5):983993

PIR QuizThis quiz is available online at http://www.pedsinreview.aappublications.org. NOTE: Since January 2012, learners cantake Pediatrics in Review quizzes and claim credit online only. No paper answer form will be printed in the journal.

New Minimum Performance Level RequirementsPer the 2010 revision of the American Medical Association (AMA) Physicians Recognition Award (PRA) and creditsystem, a minimum performance level must be established on enduring material and journal-based CME activities thatare certified for AMA PRA Category 1 CreditTM. In order to successfully complete 2012 Pediatrics in Review articles forAMA PRA Category 1 CreditTM, learners must demonstrate a minimum performance level of 60% or higher on thisassessment, which measures achievement of the educational purpose and/or objectives of this activity.

Starting with the 2012 issues of Pediatrics in Review, AMA PRA Category 1 CreditTM may be claimed only if 60% ormore of the questions are answered correctly. If you score less than 60% on the assessment, you will be givenadditional opportunities to answer questions until an overall 60% or greater score is achieved.

1. A 5-year-old boy was in a motor vehicle collision as a restrained back seat passenger. He has a large lacerationon his right forehead. On arrival to the emergency department, he opens his eyes with painful stimuli, but doesnot open his eyes when his name is called. He is mumbling, but is not using words. He withdraws to pain. Hisbrain injury is best described as a

A. mild traumatic brain injuryB. moderate concussionC. moderate traumatic brain injuryD. severe concussionE. severe traumatic brain injury




2. A 15-month-old girl is seen for fussiness, crying, and poor oral intake. On physical examination, she is fussy,but consolable. Her vital signs are stable. She is well hydrated. She has unilateral hemotympanum. The mostappropriate initial intervention at this time is

A. computed tomography (CT) scan of the brainB. magnetic resonance imaging of the brainC. prescription for antibioticsD. skull radiographic filmsE. skeletal survey

3. You see a 6-month-old girl with history of vomiting who presents with lethargy and irregular respirations.After intubating and stabilizing her, you obtain CT imaging of the brain that shows a parietal skullfracture and a crescent-shaped intracranial hemorrhage underlying the fracture. This radiographic finding ismost consistent with a

A. cerebral contusionB. diffuse axonal injuryC. epidural hematomaD. subarachnoid hemorrhageE. subdural hemorrhage

4. A 15-year-old boy was the unrestrained passenger in a motor vehicle collision. He was ejected from the vehicleand was found unconscious 20 feet from the vehicle. A CT scan shows areas of hemorrhage at the gray-whitejunction. His clinical presentation and radiographic findings are most consistent with

A. cerebral contusionB. diffuse axonal injuryC. epidural hematomaD. subarachnoid hemorrhageE. subdural hemorrhage

5. You are evaluating a 6-year-old boy who sustained a head injury when he fell out of a tree. Clear fluid is notedto be draining from his nose. His parents deny any recent respiratory infection or history of nasal allergy. Youorder a CT scan. The most likely abnormality to show up on the scan will be

A. basilar skull fractureB. cerebral contusionC. depressed skull fractureD. epidural hemorrhageE. subdural hemorrhage




DOI: 10.1542/pir.33-9-3982012;33;398Pediatrics in Review

Jeff E. Schunk and Sara A. SchutzmanPediatric Head Injury

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