The terms 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 these 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 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 when 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 for many reasons: clinical assessment is often more difficult as infants in this age group with intracranial injuries 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—some experts limit this term to children with a GCS of 15, whereas others have included children with scores ≥13. The definitions used by professional societies and experts for minor head injury and mTBI are provided in Table 9-1. 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 can be found at the end of this chapter.

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, the CDC reported a 62% increase in fall-related TBI seen in EDs among children aged 14 years or less.^2–4 An estimated 3.8 million concussions from sports and recreation occur annually in the United States. Since most of these injuries are mild, this is likely an underestimation because the number of children participating in organized sports has increased 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

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

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 “post-concussion 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 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 as:^2,8

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  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 feet for patients aged 2 years and older, or more than 3 feet for those younger than 2 years; or head struck by a high-impact object)

  
  
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  Mild (ground-level falls or running into stationary objects)

  
  
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  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 post-traumatic 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