• Although minor head injury is a frequent reason for emergency department (ED) visits by children, clinically significant traumatic brain injury (TBI) is uncommon.
• Clinical decision rules are available to aid the identification of mildly head-injured children not requiring a computed tomography (CT) scan.
• A concussion is a trauma-induced transient disturbance of brain function.
• The emergency physician should recommend full physical and cognitive rest and prompt medical follow-up of all children who have sustained a concussion.
Concussion, minor head injury, mild closed-head injury, and mild traumatic brain injury (mTBI) have been variably used in scientific literature.1 Minor head injury, the broadest of the terms, refers to craniocerebral trauma and extracranial injury. The term closed-head injury is applied to injuries that do not involve penetration of the skull and dural layer. Mild closed-head injury and mTBI are often used interchangeably, although technically only mTBI implies the presence of cerebral injury. It is associated with symptoms such as a brief loss of consciousness (LOC), disorientation, or vomiting. Like minor head trauma, patients with mTBI usually have Glasgow Coma Scale (GCS) scores of 13 to 15, measured approximately 30 minutes after the injury. In comparison, patients with moderate TBI generally have initial GCS scores between 9 and 12, whereas those with severe injury have GCS scores ≤8. Epidemiologically, minor head trauma is generally defined separately in children younger than 2 years of age because clinical assessment is often more difficult, infants with intracranial injuries in this age group are frequently asymptomatic, skull fractures may occur as the result of minor trauma, and inflicted injury occurs more often.2 The definition of minor head trauma for children 2 years of age and older has often been based on the GCS with some experts limiting this term to children with a GCS of 15, whereas others have included children with scores ≥13. The different definitions used by professional societies and experts for minor head injury and mTBI are provided in Table 8-1. Concussion and mTBI have been used synonymously, mTBI is a broader term defined by GCS and has structural and functional components, whereas concussion is more likely to be a subclassification of mTBI with poor relationship to GCS and is largely a functional brain injury. Further discussion on concussion occurs at the end of this chapter.
Definition(s) for Minor Head Injury and mTBI
Of the 1.7 million TBIs occurring each year in the United States, 80.7% were emergency department (ED) visits, 16.3% were hospitalizations, and 3.0% were deaths. The Centers for Disease Control and Prevention (CDC) statistics reveal an increase in TBI-related ED visits (14.4%) and hospitalizations (19.5%) from 2002 to 2006. Among children 0 to 14 years of age, there were almost half a million ED visits, 35,136 hospitalizations, and 2174 deaths. Males aged 0 to 4 years have the highest rates for TBI-related ED visits, hospitalizations, and deaths combined. Most children with head trauma are young, male, and have a mild injury. Between the years 2006 and 2009, CDC reported a 62% increase in fall-related TBI seen in EDs among children aged 14 years or less.2–4 It is estimated that there are 3.8 million concussions from sports and recreation annually in the United States. Since most of these injuries are mild, this is likely an underestimate because the number of children participating in organized sports has gone up from 40 million in 2000 to 60 million in 2008.5 Football, soccer, basketball, wrestling, lacrosse, rugby, cheerleading, and ice hockey are associated with significant rates of concussion. Girls participating in the same sports as boys have a higher rate of reported concussion. This has been attributed to possible reporting bias, smaller neck circumference, less neck strength, and a decreased head–neck segment mass compared with boys.5
INCIDENCE OF INTRACRANIAL INJURY
Although the true incidence of intracranial injury in patients with minor head trauma is unknown because of issues related to varying definitions for mTBI, selection and verification bias, the following estimates from selected populations can serve as a guide. Among children 2 years of age and older with minor head trauma and a normal neurologic examination, 3% to 7% will have an intracranial injury found on computed tomography (CT) scan and approximately 0.1% to 0.6% will have an injury requiring neurosurgical intervention. For children younger than 2 years with minor head trauma and a normal neurologic examination, approximately 3% to 10% have an intracranial injury.2,6,7
Falls are the commonest cause of minor head injury in children. This is followed by motor vehicle crashes, pedestrian and bicycle accidents, injury due to projectiles, assaults, sports-related trauma, and abuse. Isolated head trauma occurs in the majority of patients. Falls result in the greatest number of TBI-related ED visits (523,043) and hospitalizations (62,334), whereas motor vehicle–traffic injury is the leading cause of TBI-related deaths. Infants sustain more falls and are at increased risk for inflicted injury. It is of utmost importance to identify children who have sustained an inflicted head injury, even if the injury is minor. Children who remain in the care of the alleged perpetrator are at significant risk for repeat injury.2
ANATOMY, PATHOPHYSIOLOGY, AND BIOMECHANICS
The infant’s head is disproportionately larger and heavier relative to the rest of the body. It is supported on a relatively shorter, weaker, and more flexible neck. Force applied to the head or body results in more momentum of the head and less restriction from the weaker cervical soft tissues. This increases the likelihood of injury to the brain. In infancy, the open fontanelles and sutures provide more flexibility, which can absorb greater impact as well as provide for expansion of the intracranial volume. Incomplete myelinization results in greater plasticity of the brain. This flexibility allows for more distortion between the container (the skull and dura) and its contents (the brain and the cerebral blood vessels), which results in increased susceptibility to hemorrhage. Most head trauma results from a combination of direct impact, acceleration/deceleration, or rotational shear forces. The more pliable skull of the younger child tends to bend inward on impact, applying pressure on the inner table and its underlying vessels in the epidural and subdural spaces. The surrounding areas bend outward, putting pressure on the outer table, producing a fracture which may or may not be proximate to the area of impact. Younger children and infants with isolated skull fractures tend to present with normal mental status unless there is a significant underlying brain injury with mass effect. Laboratory studies suggest that concussive brain injury is characterized by transient, functional, cellular impairments, including abrupt neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow, and impaired axonal function. Any of these conditions may lead to a state of enhanced vulnerability, during which time the patient may have symptoms of confusion or headache. A second impact before the brain is fully recovered may result in a potentially fatal loss of cerebrovascular autoregulation resulting in vasoparalysis, brain swelling, increased intracranial pressure, and death (second impact syndrome). Research indicates that, after a single brain impact, this state of increased vulnerability can persist for 3 to 5 days but usually resolves within a week. In the patient with a mild head injury, a more prolonged “postconcussion syndrome” may occur, characterized by persistent alterations in cognition, behavior, and personality changes as well as emotional swings. This can affect interpersonal relationships, school, and work. Athletes reporting posttraumatic headache up to 7 days after injury demonstrated significantly worse neurocognitive scores, possibly associated with incomplete recovery. Chronic cognitive impairments can occur in athletes who have sustained multiple, seemingly minor, head injuries and are associated with accelerated or increased neurodegeneration in specific brain regions. Clinical symptoms of concussions (confusion, amnesia, headache, attention deficits, disorientation, and loss of motor coordination) are usually transient.5
The goal of the evaluation and management of children with apparently minor head trauma is to obtain a detailed history, perform a comprehensive physical examination to identify those with TBI who may require immediate intervention (as with an epidural hematoma), or close follow-up (as with a concussion), while limiting unnecessary neuroimaging procedures, and, for the injured athlete, return to play.
Ensure that the patient is not in any danger and that the airway is patent, and that breathing and circulation are adequate. The primary injury can be exacerbated by hypotension and acidosis, leading to a secondary injury. Hypotension, which can result from a simple scalp laceration in the young child, disrupts cerebral autoregulation even more than hypertension. Fluid resuscitation may be necessary to prevent hypotension and a possible secondary brain injury. In addition, children who may have sustained an inflicted injury must be identified.
A careful history should include the time and nature of the incident, particularly the height of the fall or the force of the impact. With young infants, be alert to any feature of the history that is inconsistent with the child’s developmental milestones, since this is the age group at highest risk for nonaccidental trauma. The high-performing athlete may try to hide symptoms because of pressures to perform. Historical features that suggest an increased risk of intracranial injury include high-risk mechanism, seizure, confusion, LOC, significant headache, vomiting, and presence of preexisting conditions that place the child at risk for intracranial hemorrhage. These include arteriovenous malformation and bleeding disorder. Injury mechanisms can be categorized as2,8:
• Severe (motor vehicle crash with patient ejection, death of another passenger, or rollover; pedestrian or bicyclist without helmet struck by a motor vehicle; falls of more than 5 ft for patients aged 2 years and older, or more than 3 ft for those younger than 2 years; or head struck by a high-impact object)
• Mild (ground-level falls or running into stationary objects)
• Moderate (any other mechanism).
LOC has been reported in approximately 5% of children <2 years of age and up to 13% of children ≥2 years of age. However, the risk of TBI in the setting of brief isolated LOC without any other symptoms or signs of TBI is very low. Headache, a frequent complaint, has been reported in up to 45% of children. In preverbal children, irritability may be an indication of discomfort, such as headache. At least one episode of vomiting occurs in approximately 14% of patients, although most children who vomit following head trauma do not have intracranial injury. Nevertheless, a history of any vomiting after head trauma increases the risk of TBI to some degree. Numerous smaller studies have reported a wide range of incidence of immediate posttraumatic seizures (3%–8%) but the incidence is likely to be substantially lower, estimated at ≤0.6% in a larger study. Transient abnormalities such as cortical blindness, acute confusional states, trauma-induced migraine-equivalent phenomena, and stroke following mild head trauma have been reported in children.9–12
A meticulous neurologic examination along with documentation of a GCS must be performed. Examine the scalp for linear hematomas, especially over the temporal or occipital areas. Palpate carefully, looking for crepitus or depressions. In young infants, feel the fontanelle for fullness. Check for blood and cerebrospinal fluid leaking from the ears or the nose; look for ecchymoses around the eyes (raccoon sign) and behind the ears (Battle sign). Also look for blood behind the tympanic membrane (hemotympanum), another indicator of a basilar skull fracture. Ensure that all cranial nerves are intact and that the child is not exhibiting any stereotyped posturing. Watch the child’s movements to ensure that all extremities move equally. Observe how the child holds his head; if he moves his head about freely, it is unlikely that he has a neck injury. Palpate the neck for any step offs, swelling, or crepitus. It should be noted that skull fractures are not uncommon following minor head trauma in children, particularly in those younger than 2 years of age. Linear skull fractures are more common and 15% to 30% have associated intracranial injuries. Most children with skull fractures will have overlying scalp hematomas, but most scalp hematomas in older children are not associated with skull fractures. In infants younger than the age of 1 year, increased scalp hematoma size and location in the parietal or temporal areas suggest a higher incidence of skull fracture.
INDICATIONS FOR NEUROIMAGING
CT is the neuroimaging procedure of choice for emergently diagnosing traumatic brain injuries. Although less than 10% of CT scans in children with minor head trauma reveal traumatic brain injuries and less than 1% have injuries requiring neurosurgical intervention, in the United States, the use of CT for the evaluation of children with head trauma has increased fivefold from 1995 to 2008. This is problematic as the developing brain is particularly susceptible to radiation-induced malignancy, with lifetime risk of lethal malignancies estimated at 1 in 1000 to 1 in 5000 for a CT scan in a child.8,13 Routine skull radiography is not indicated especially if a head CT is performed. It can be considered as a part of skeletal survey, or to rule out the presence of a foreign body, or, rarely, to screen for fractures in selected asymptomatic patients 3 to 24 months of age with concerning scalp hematomas and should be performed only if a radiologist with pediatric expertise is available to provide an interpretation. If a screening skull radiograph shows a fracture, then a head CT should be performed.
There is no single clinical feature that reliably predicts which children with minor head trauma should receive neuroimaging. Thus, researchers have sought to create clinical decision rules to identify those at high risk or low risk. Recent reviews have identified 14 such decision rules but concluded that the PECARN head injury rule performs best because it was derived and validated on a very large cohort and had the highest sensitivity and acceptable specificity for clinically significant intracranial injury.14,15 The three most commonly used rules are the PECARN, CATCH, and CHALICE head injury rules (Table 8-2).6–9 There is heterogeneity in these rules and their primary goals are different: the PECARN rule aims to identify children who are at low risk for clinically important TBI, whereas the CATCH and CHALICE rules aim to identify children at high risk for TBI. The findings from the PECARN head injury rule, when combined with evidence from prior observational studies, suggest that the use of low-risk criteria and judicious observation of patients in lieu of head CT can allow the clinician to avoid head CT in a significant number of children undergoing evaluation for minor head trauma without missing clinically important intracranial injury. This decision rule is clear and relatively easy to implement. A comprehensive review of recent evidence regarding the evaluation of a child with mTBI is summarized in Table 8-3. It aids the clinician with the decision of obtaining a CT scan.
Decision Rules for mTBI
Suggested Neuroimaging and Management Strategy for Children with mTBI
Indications for neurosurgical consultation include brain injury seen on the CT scan; the presence of a depressed, basilar, or widely diastatic skull fracture; or deterioration of the patient’s clinical condition. Hospital admission is indicated if any of the following conditions are present: brain injury on CT scan; depressed or basilar skull fracture; persistent, significant alteration in mental status despite normal head CT; unremitting vomiting; suspected inflicted injury; extracranial injury requiring admission, or caretakers who are unreliable or unable to return for care. The majority of children who have had isolated minor head trauma can be discharged from the ED following evaluation and a brief period of observation.
Caretakers of children who have been evaluated for minor head trauma should be provided with explicit and understandable instructions for monitoring and when to return for follow-up. It is not necessary to awaken children. Immediate medical attention is required if any of the following conditions occur: persistent or worsening headache, continued vomiting or vomiting that begins or continues 4 to 6 hours after injury, change in mental status or behavior, unsteady gait, clumsiness, incoordination or seizure. Children who have had a brief immediate posttraumatic seizure following minor head trauma and have a normal head CT may not require admission to the hospital.
Concussion is defined as a “complex pathophysiologic process affecting the brain induced by a traumatic biomechanical force.” 5,16,17 This definition was recently proposed by experts at a consensus conference in 2008. They also agreed that the prior definitions and severity grading systems for concussion be abandoned. Also, several evaluation measures to individually guide return-to-play decisions were endorsed. Concussions share five common features: (i) they are caused by a direct blow to the head, face, neck, or elsewhere on the body resulting in an “impulsive” force transmitted to the head; (ii) they typically result in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously; (iii) they may result in neuropathologic changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury; (iv) they result in a graded set of clinical symptoms that may or may not involve LOC; and (v) no abnormality on standard structural neuroimaging studies. Symptoms of concussion may be obvious such as headache and nausea or may be more subtle such as alteration in sleep patterns and memory loss (Table 8-4). LOC occurs in less than 10% of individuals with concussion. Resolution of the clinical and cognitive symptoms typically follows a sequential course; however, it is important to note that in a small percentage of cases, postconcussive symptoms may be prolonged. Concussion in athletes is particularly challenging because of their poor understanding of concussion, delayed manifestation of symptoms, and the athlete’s reluctance to be forthcoming for fear of activity restrictions.
Signs and Symptoms of Concussion
ACUTE MANAGEMENT OF THE CONCUSSED CHILD OR CHILD ATHLETE
Once the diagnosis of concussion has been made and discharge criteria are met, the emergency physician should advise complete physical and cognitive rest and prompt medical follow-up. If available, consider referral to a pediatric sports medicine practitioner or other physician with experience and expertise with the management of concussion in children. Return to full activity and return to play for the athlete is best achieved by a stepwise increase of activity (Table 8-5) under the supervision of the physician performing the follow-up.17
Return to Play Guidelines
SECOND IMPACT SYNDROME
Second impact syndrome is the usually fatal result of an additional concussive head injury before resolution of the initial concussion. The second impact may not even be direct to the head. It may be a deceleration injury. There may be a brief period of normal function followed by collapse and death within a few minutes. It is believed that the second impact to the brain causes severe loss of cerebrovascular autoregulation, resulting in massive brain swelling.
The postconcussive syndrome is characterized by a sustained set of symptoms related to the initial concussion. The World Health Organization definition requires the presence of three or more of the following symptoms after a head injury: headache; dizziness; fatigue; irritability; difficulty with concentrating and performing mental tasks; impairment of memory; insomnia; and reduced tolerance to stress, emotional excitement, or alcohol. A recently proposed definition of postconcussive syndrome is the presence of cognitive, physical, or emotional symptoms of a concussion lasting longer than expected. A threshold of 1 to 6 weeks of persistent symptoms after a concussion is required to make the diagnosis. Long-term sequelae of concussion, particularly repeated concussion, may potentially include persistent postconcussive syndrome, dementia, or parkinsonism.
Although minor head trauma is exceedingly common, clinically significant TBI is rare in children. Meticulous history and physical examination along with judicious use of CT scanning are the pillars of assessment and management. Large studies on children with minor head injury suggest that it is possible to obviate CT scans by using clinically available criteria to aid decision making and improving quality of care. For children that have sustained a concussion, the emergency physician should recommend full physical and cognitive rest and prompt medical follow-up to supervise return to full activity and for the child athlete, return to play.
1. Kirkwood MW, Yeates KO, Taylor GH, Randolph C, McCrea M, Anderson VA. Management of pediatric mild traumatic brain injury; a neuropsychological review from injury through recovery. Clin Neuropsychol. 2008;22:769–800.
2. Schutzman S. Minor head trauma in infants and children. www.uptodate.com. Accessed February 10, 2013.
3. Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2004.
4. Cassidy JD, Carroll LJ, Peloso PM, et al. Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on mild traumatic brain injury. J Rehab Med. 2004;43(suppl):28–60.
5. Upshaw JE, Gosserand JK, Williams N, Edwards JC. Sports related concussions. Pediatr Emerg Care. 2012;28:926–932.
6. Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374:1160.
7. Osmond MH, Klassen TP, Wells GA, et al. CATCH: a clinical decision rule for the use of computed tomography in children with minor head injury. CMAJ. 2010;182:341.
8. Brenner DJ, Hall EJ. Computed tomography–an increasing source of radiation exposure. N Engl J Med. 2007;357:2277.
9. Dunning J, Daly JP, Lomas JP, et al. Derivation of the children’s head injury algorithm for the prediction of important clinical events decision rule for head injury in children. Arch Dis Child. 2006;91:885.
10. Da Dalt L, Marchi AG, Laudizi L, et al. Predictors of intracranial injuries in children after blunt head trauma. Eur J Pediatr. 2006;165:142.
11. Da Dalt L, Andreola B, Facchin P, et al. Characteristics of children with vomiting after minor head trauma: a case–control study. J Pediatr. 2007;150:274.
12. Holmes JF, Palchak MJ, Conklin MJ, Kuppermann N. Do children require hospitalization after immediate posttraumatic seizures? Ann Emerg Med. 2004;43:706.
13. Brody AS, Frush DP, Huda W, et al. Radiation risk to children from computed tomography. Pediatrics. 2007;120:677.
14. Maguire JL, Boutis K, Uleryk EM, Laupacis A. Should a head-injured child receive a head CT scan? A systematic review of clinical prediction rules. Pediatrics. 2009;124:e145.
15. Pickering A, Harnan S, Fitzgerald P, Pandor A, Goodacre S. Clinical decision rules for children with minor head injury: a systematic review. Arch Dis Child. 2011;96:414–421.
16. Jotwani V, Harmon KG. Postconcussion syndrome in athletes. Curr Sports Med Rep. 2010;9:21–26.
17. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med. 2009;43:i76–i84.