Primary brain injury occurs as a result of direct mechanical damage inflicted during the traumatic event. Secondary injuries occur from metabolic events such as hypoxia, ischemia, or increased intracranial pressure. The prognosis for recovery depends on the severity of the injuries. Anatomic features, specific injuries, and intracranial pressure physiology are important components in the pathophysiology of pediatric brain injury.
The scalp is the outermost structure of the head and adjacent to the galea, which is a tendinous sheath connecting the frontalis and occipitalis muscles (Fig. 29–1). Beneath the galea is the subgaleal compartment where large hematomas may form in this space. The pericranium lies just below, tightly adhering to the skull. The outer and inner tables of the skull are separated by the diploic space. The thin, fibrous dura is next, and it contains few blood vessels compared to the underlying leptomeninges, the arachnoid, and pia. Small veins bridge the subdural space and drain into the dural sinuses. Dural attachments partially compartmentalize the brain. In the midline, the falx cerebri divides the right and left hemispheres of the brain. The tentorium divides the anterior and middle fossa from the posterior fossa, with an opening for the brain stem. Cerebrospinal fluid surrounds the brain within the subarachnoid space.
The outer structures protect the brain during everyday movements and minor trauma; however, these features can inflict damage when significant force is applied or sudden movement occurs. Movement of the brain within the vault along the uneven base of the skull may injure brain tissue. The unyielding, mature skull can contribute to brain injury when brain edema or an expanding hematoma develops. Subsequently, herniation across compartments can cause compression of vital structures, ischemia from vascular occlusion, and infarction.
In infants, the open sutures and thin calvarium produce a more flexible skull capable of absorbing greater impact. Incomplete myelinization contributes to greater plasticity of the brain as well. This flexibility permits more severe distortion between skull and dura, and cerebral vessels and brain, increasing susceptibility to hemorrhage. Finally, the disproportionately large size and weight of the head compared to the rest of the body of infants and young children contributes to an increased likelihood of head injury.
The scalp is richly vascularized and, if injured, can bleed profusely. Scalp bleeding can lead to hemodynamically significant blood loss from relatively small lacerations, especially in infants and young children. Carefully explore open scalp wounds for skull integrity, depressions, or foreign bodies. The presenting sign of a subgaleal hematoma is an extensive soft tissue swelling that occurs several hours or days after the traumatic event and is commonly associated with a skull fracture. A subgaleal hematoma can persist for several days to weeks.
Linear nondepressed skull fractures occur at the point of impact. The presence of a skull fracture indicates a significant blow to the head, and children with skull fractures are more likely to have an associated intracranial injury. However, the absence of a skull fracture does not exclude the presence of intracranial injury.4 “Growing fractures” are unique to infants and young children. They may occur after a skull fracture in children younger than 2 years of age when associated with a dural tear. Rapid brain growth postinjury may be associated with the development of a leptomeningeal cyst, which is an extrusion of cerebrospinal fluid or brain tissue through the dural defect. Thus, children younger than 2 with a skull fracture require follow-up to detect a growing fracture.2
Basilar skull fractures typically occur at the petrous portion of the temporal bone, although they may occur anywhere along the base of the skull. Clinical signs suggesting a basilar skull fracture include hemotympanum, cerebrospinal fluid otorrhea, cerebrospinal fluid rhinorrhea, periorbital ecchymosis (“raccoon eyes”), or postauricular ecchymosis (Battle's sign). Radiologic diagnosis often requires detailed computed tomography (CT) imaging of the temporal bone, since plain skull radiographs or routine head CT scans may not be diagnostic.
Epidural hematomas occur more commonly in older children than infants and toddlers.5 Most occur in combination with a temporal skull fracture and meningeal artery bleeding; the remainder are venous in origin. They may be life-threatening, but prompt diagnosis and surgical intervention make an excellent outcome possible. Signs and symptoms include headache, vomiting, and altered mental status, which may progress to signs and symptoms of uncal herniation with pupillary changes and hemiparesis. Patients classically present with an initial lucid period followed by a rapid deterioration in mental status, as the hemorrhage increases in size (Fig. 29–2).
Epidural hematoma with midline shift.
Acute subdural hematomas occur more commonly than epidural hematomas in children.2 Acute interhemispheric subdural hematomas, which occur more often in infants and young children, may be caused by shaking/impact injuries of abuse. Subdural hematomas usually result from tearing of the bridging veins and typically occur over the cerebral convexities. Subdural hematomas are often associated with more diffuse brain injury. They may progress more slowly than epidural bleeds, with symptoms commonly including irritability, vomiting, and alterations in mental status.
Parenchymal contusions are bruises or tears of brain tissue. Bony irregularities of the skull cause these cerebral contusions as the brain moves within the skull. A coup injury occurs at the site of impact, while a contrecoup injury occurs at a site remote from the impact. Intraparenchymal hemorrhages may also occur from shearing injury or penetrating wounds. They often occur in association with intracranial hematomas or skull fractures. Signs and symptoms may include decreased level of consciousness, focal neurologic findings, and seizures.
Penetrating injuries result from sharp-object penetration or gunshot wounds. Extensive brain injury is common and severity depends on the path of the object and location and degree of associated hemorrhage.
A concussion is defined as a “trauma-induced alteration in mental status that may or may not involve a loss of consciousness.”6 Additional symptoms may include vomiting, headache, dizziness, visual changes, as well as cognitive impairments and abnormal behavior. Most symptoms resolve after 48 hours; however, some symptoms may linger for weeks to months in a “postconcussive” syndrome.7,8
Diffuse brain swelling occurs more often in children than in adults.9 The swelling usually results from a shearing or acceleration–deceleration injury. Prolonged coma or death may occur.
Nonaccidental trauma in infants and young children may result in the constellation of subdural hematoma, subarachnoid hemorrhage, and localized or diffuse brain edema (Fig. 29–3). Retinal hemorrhages, rib fractures, long bone fractures, and external signs of injury may also be present. Common symptoms of nonaccidental traumatic brain injury in infants may include lethargy, vomiting, irritability, seizures, and apnea. Many of these children may have severe alteration in consciousness.10,11
Right-sided subdural hematoma with associated midline shift and right hemispheric edema in an infant with nonaccidental head trauma.
Intracranial Pressure and Herniation Syndromes
The total volume of the intracranial vault is constant. Approximately 70% of this volume is brain, 20% is cerebrospinal and interstitial fluid, and 10% is blood. If any one of these three components increases in volume, then the other two compartments must decrease or intracranial pressure rises. The main component of compensation is a displacement of cerebrospinal fluid into the spinal canal. Once this compensatory mechanism is maximized, any additional increases in volume cause elevation of intracranial pressure to abnormal levels (>15–20 mm Hg). Cerebral perfusion becomes impaired and irreversible ischemic damage to the brain ensues.
An intracranial mass or hematoma will occupy the fixed intracranial space, compress the normal brain tissue, and reduce blood flow. Cytotoxic cerebral edema occurs with fluid accumulation within damaged brain and glial cells. Interstitial cerebral edema results from decreased absorption of fluid following brain trauma. Vasogenic cerebral edema occurs as the endothelial cell barrier is compromised and leakage of fluid into the perivascular brain tissue occurs.
The volume of cerebrospinal fluid may also increase despite the compensatory redistribution of the fluid into the spinal canal. As brain and blood volumes increase, the ventricular spaces become compressed until redistribution is not possible. Additionally, if the cerebrospinal fluid pathways are compressed by edematous tissue, cerebrospinal fluid outflow ceases and ventricular dilation and hydrocephalus can occur.
Cerebral blood volume in head-injured children may be increased as a result of brain injury. The mechanisms of autoregulation of cerebral blood flow are complex; however, flow is often increased in head-injured children, possibly due to a loss of normal autoregulatory mechanisms leading to increased risk for brain swelling. Hypoxia and hypotension of the injured patient may also contribute to diffuse brain edema. Causes of diffuse brain swelling are likely multifactorial, including hyperemia, excitotoxic neurotransmitters, enhanced inflammatory response, and increased blood–brain permeability.
Diffusely or focally increased intracranial pressure may produce herniation. Cingulate herniation occurs as one cerebral hemisphere is displaced underneath the falx cerebri to the opposite side. A transtentorial or uncal herniation is of major clinical significance (Fig. 29–4). A mass lesion or hematoma forces the ipsilateral uncus of the temporal lobe through the space between the cerebral peduncle and the tentorium. This causes ipsilateral compression of the oculomotor nerve and an ipsilateral dilated nonreactive pupil. The cerebral peduncle is compressed causing a contralateral hemiparesis. As the intracranial pressure increases and the brain stem is compressed, consciousness wanes. If herniation continues, ongoing brain stem deterioration occurs, progressing to apnea and death. Uncal herniation may be bilateral if there are bilateral lesions or diffuse edema. Herniation of the cerebellar tonsils downward through the foramen magnum occurs infrequently in children. Medullary compression from this herniation causes bradycardia, respiratory arrest, and death.
Anterior view of transtentorial uncal herniation caused by a large epidural hematoma. (With permission from American College of Emergency Physicians. Emergency Medicine: A Comprehensive Study Guide. 3rd ed. New York: McGraw-Hill; 1992.)