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Head trauma is classified as blunt or penetrating based on the mechanism of injury. In children, the vast majority of head trauma is caused by blunt force with the underlying mechanism varying according to the age of the patient. In younger children, the most common causes of head trauma are falls and assaults/child abuse.6 In fact, in children under 2 years of age, nonaccidental trauma is the leading cause of death due to head trauma. In older children, falls, sports and recreation, assault, and, increasingly, motor vehicle collisions are more common. Penetrating injuries are most frequently related to dog bites in infants or gunshot wounds in older children. In the largest study of pediatric minor head injury to date, including over 42,000 patients, radiographically documented intracranial injuries were found in approximately 1.8% of children with minor head injury who presented to the ED for evaluation, and only 0.9% required intervention.4 This is a lower number than cited in prior studies, likely due to the inclusion and clinical follow-up of lower-risk children not undergoing CT. The true incidence of intracranial injuries is probably even lower, because many children with mild injuries do not present to the ED.
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The pattern of injury is different in children compared to adults. In children, diffuse injuries are proportionally more common, and in adults, focal injuries such as epidural and subdural hematomas and cerebral contusions are more common.6
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The differences in brain development and pediatric anatomy explain the specific pattern of childhood injuries compared to adults. In blunt head injury, rotation of the brain around its center of gravity leads to more diffuse injuries (diffuse axonal injury and subdural hematoma), whereas linear forces are generally less damaging to the brain and cause local (coup and contrecoup injury) rather than diffuse injury. The type and severity of the injury are determined both by the type of deceleration and its magnitude.7 Younger age is a significant risk factor for intracranial injury. Even among infants, the greatest risk for intracranial injury is in children under 3 months of age.2
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More details of physiology are discussed in chapter 257, "Head Trauma."
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Skull fractures can involve the calvarium or the base of the skull. The presence of skull fractures is a risk factor for underlying brain injury in infants under 2 years of age (Figures 138-1 and 138-2).4
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However, significant brain injury can occur in the absence of skull fractures in 50% of cases.8 Plain films of the skull should therefore not be obtained as a replacement for CT to evaluate for underlying brain injury.9 Depressed skull fractures occur in response to the application of significant force and require neurosurgical consultation, as surgical elevation is often required. Compared to adults, skull fractures in children are more common but less frequently associated with underlying brain injury.6
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A growing fracture can occur when the leptomeninges are torn beneath the fracture, allowing for the formation of a cerebrospinal fluid leptomeningeal cyst that forces apart the fracture edges and leads to nonunion. Growing skull fractures typically present weeks to months following an injury resulting in skull fracture. This rare complication is unique to infants and requires neurosurgical repair.
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INTRACRANIAL INJURIES
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An epidural hematoma (Figure 138-3) is a collection of blood between the inner skull and the dura and can occur from rapid arterial bleeding from the middle meningeal artery or the dural or diploic vasculature.
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The classic presentation is a lucid interval after head trauma followed by rapid deterioration. The presence of a bi-convex hyperdense extra-axial lesion that does not cross the suture lines is indicative of an epidural hematoma on CT.10 The long-term prognosis depends on the preoperative GCS and the extent of other underlying brain injury,11 but is generally good if surgical evacuation can be undertaken in a timely manner.
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Subdural hematomas (Figure 138-4), located between the arachnoid and the internal dural layer, are more common than epidural hematomas, particularly in infants and younger children. Subdural hematomas are caused by tearing of the subdural veins, are often extensive and bilateral (80% of cases), are frequently associated with underlying brain injury, and have a worse prognosis than epidural hematomas.
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Radiographically, a subdural hematoma appears as a crescent-shaped fluid collection with the concavity facing the brain surface. Immediately after the injury, the subdural hematoma appears more dense (brighter white) than adjacent brain tissue. Due to the metabolism of blood products within the hematoma, its radiographic appearance changes over time. In the subacute phase (1 to 3 weeks after injury), the hematoma progressively assumes the same density of the brain tissue and can thus be difficult to recognize. Flattening of the sulci and the presence of a mass effect are indirect evidence of the presence of a subdural hematoma. Subsequently, in the chronic phase, the hematoma appears as a hypodense fluid collection, with a density similar to cerebrospinal fluid.10 In infants, loss of gray-white matter differentiation and diffuse hypodensity has been described with subdural hematoma.7
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Cerebral contusions (Figure 138-5) are located in the cortex underlying the area of direct impact of a significant force (coup lesions) or on the opposite side (contrecoup lesions) where the brain has struck the cranial surface.
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The severity ranges from minor CT findings in an asymptomatic patient to severe brain edema. On CT, the presence of ill-defined hyperdense areas within the cortex of the frontal and temporal lobe represent parenchymal contusions.
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Traumatic subarachnoid hemorrhage is often associated with significant trauma and diffuse axonal injury (Figures 138-6 and 138-7). Infants more commonly present with diffuse injury and cerebral edema compared to adults because developmental differences render them susceptible to rotational and deceleration forces. Clinically, the child with diffuse axonal injury presents with a profoundly depressed level of consciousness. Radiographic findings on CT may be minimal in the acute setting. MRI is more sensitive in the detection of diffuse axonal injury, which can be both hemorrhagic and nonhemorrhagic.10
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Figure 138-8 provides noncontrast head CT images of a variety of cerebral injuries.
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The pathophysiology of concussion is complex. Although cerebral blood flow is increased in some children immediately following a concussion, the predominant pattern is transiently decreased blood flow. This is followed by a period of hyperemia from days 1 to 3, followed by return of the low-flow state.12 In more than one third of concussed children, this phenomenon continues for a month or more.13 Concussions do not cause gross structural changes, making them difficult to diagnose by conventional radiography. However, animal models indicate that the acceleration-deceleration forces of a concussion initiate a neurochemical cascade that results in neuronal membrane disruption and axonal stretching. This in turn leads to significant ion flux, initially coupled with a transient increase in the cerebral glucose metabolism, followed by hypometabolism lasting days to weeks. Cytokine-mediated inflammation, stretch-mediated axonal disconnection, and neurotransmitter-mediated oxidative dysfunction also contribute to concussion-related impairments.12