INJURY: HEAD

SARA A. SCHUTZMAN, MD AND REBEKAH MANNIX, MD, MPH

PEDIATRIC HEAD TRAUMA

Head injuries in children are common, accounting for approximately 500,000 emergency department (ED) visits per year in the United States. Although the majority of these injuries are minor, head trauma causes significant pediatric morbidity and mortality. Trauma is the leading cause of death in children older than 1 year, and traumatic brain injury is the leading cause of death and disability caused by trauma in children, resulting in more than 2,000 deaths annually.

The most common mechanism of injury for pediatric head trauma is falls, followed by motor vehicle and pedestrian accidents and bicycle injuries; the majority of fatal injuries occur secondary to motor vehicle–related accidents. The mechanism of head injury varies with age; younger children are more likely to suffer falls or abuse, whereas older children are often injured in sporting or motor vehicle accidents (in addition to falls).

Many of the serious neurologic complications of head injury are evident soon after the traumatic event; however, some life-threatening injuries can appear initially as minor head trauma. To manage head injuries best, the physician must approach the child in a systematic manner to address all injuries (global resuscitation is the first priority of cerebral resuscitation), identify and treat any neurologic complications, and prevent ongoing cerebral insult.

PATHOPHYSIOLOGY

Neurologic injury following head trauma is related to the unique physiology and pathophysiology of the brain and the intracranial environment. The brain is a semisolid structure bathed in cerebrospinal fluid (CSF) and covered by the fine inner pia-arachnoid membrane and the outer thick fibrous layer of dura, all of which are encased in the skull, which is covered by the five-layered structure of the scalp. After infancy (when the skull sutures fuse), the cranial vault becomes a stiff and poorly compliant structure housing the brain. Because the intracranial volume is relatively fixed, any change in the volume of one of the intracranial components (blood, brain, and CSF) must occur at the expense of the others; if the other components do not decrease proportionally, intracranial pressure (ICP) will increase.

Brain injury occurs in two phases: primary and secondary. The primary injury is the mechanical damage sustained at the time of trauma and can be caused by direct impact of the brain against the internal calvarial structures, by bone or foreign bodies projected into the brain, and by shear forces delivered to the white matter tracts. Secondary brain injury is further neuronal damage sustained after the traumatic event to cells not initially injured. This results from numerous causes, including hypoxia, hypoperfusion, and metabolic derangements, and may also result from sequelae of the primary injury (e.g., cerebral edema, expanding intracranial mass) or be caused by extracranial injuries (e.g., hypotension from excessive blood loss, hypoxia from pulmonary contusion). The clinician’s goal is to identify and treat any complications of primary brain injury in order to limit further neuronal damage by secondary brain injury.

One of the most common causes of secondary brain injury is cerebral ischemia resulting from impaired perfusion. Cerebral perfusion pressure is the difference between the mean arterial pressure of blood flowing to the brain and the ICP. In the healthy child, blood flow to the brain is maintained at a constant rate over a wide range of systemic blood pressures by means of autoregulatory changes in the cerebrovascular resistance so that the brain does not suffer ischemia or excessive blood flow during periods of relative hypotension or hypertension, respectively. With severe injuries, this autoregulatory control may be lost and the cerebral blood flow can become directly dependent on the cerebral perfusion pressure; with low mean arterial pressure or increased ICP, there will be inadequate blood flow and cerebral ischemia results. In addition to potential for causing decreased cerebral perfusion, increased ICP, if left unchecked, can lead to brain herniation and compression. This may be caused by a number of posttraumatic conditions, including cerebral edema and expanding intracranial mass.

Clinical symptoms of increased ICP or herniation include headache, vomiting, irritability, lethargy, visual disturbance, gait abnormalities, and weakness. Signs include depressed level of consciousness, abnormal vital signs (bradycardia, hypertension, respiratory irregularity), cranial nerve palsies, hemiparesis, and decerebrate posturing. The classic findings in transtentorial herniation are headache, decreasing level of consciousness followed by ipsilateral pupillary dilatation (cranial nerve III palsy), and contralateral hemiparesis or posturing. If the process continues unchecked, dilatation of the opposite pupil, alteration in respirations, and ultimately, bradycardia and arrest ensue (see Chapter 105 Neurologic Emergencies).

DIFFERENTIAL DIAGNOSIS

Head trauma may cause injuries of the scalp, skull, and intracranial contents. Although each is discussed here separately, the clinician must remember that these injuries may occur alone or in combination, and all potential injuries must be considered when dealing with one.

Scalp

The scalp consists of five layers of soft tissue that cover the skull; contusions and lacerations of this structure are common results of head trauma. The outermost layers of the scalp are skin and the subcutaneous tissue; edema and hemorrhage here may produce a mobile swelling. The third layer, the galea aponeurotica, is a strong membranous sheet that connects the frontal and occipital bellies of the occipitofrontalis muscle. The remaining two layers deep to the galea are the loose areolar tissue and pericranium. Subgaleal hematomas may result from more forceful blows as vessels in the fourth layer bleed and dissect the galea from the periosteum, or they may be signs of an underlying skull fracture. In subperiosteal hematomas, or cephalohematomas, the swelling is localized to the underlying cranial bone and most frequently occurs with birth trauma. Scalp lacerations may occur with or without underlying contusions or fractures and they often require suturing. Given the high vascularity of the scalp, these injuries can result in significant blood loss if not recognized and treated appropriately.

Skull

Skull fractures occurring in the calvarium, or bony skullcap, include frontal, parietal, temporal, and occipital fractures and may be linear, diastatic, depressed, comminuted, or compound. Fractures in the base of the skull are termed basilar. Most simple fractures require no intervention but are important in that they are a marker of significant impact to the head and are associated with at least a fivefold increased risk of intracranial injury (ICI).

Linear fractures account for 75% to 90% of skull fractures in children and often manifest with localized swelling and tenderness. Diastatic fractures are traumatic separations of cranial bones at a suture site or fractures that are widely split. A depressed skull fracture is present when the inner table of the skull is displaced by more than the thickness of the entire bone. These may be palpable and are diagnosed with tangential skull radiographs (SRs) or computed tomography (CT) scans. Compound fractures are those that communicate with lacerations.

Basilar skull fractures typically produce signs specific to their fracture location that lead to the diagnosis. Fractures of the petrous portion of the temporal bone may cause hemotympanum, hemorrhagic or CSF otorrhea, or Battle sign (bleeding into mastoid air cells with postauricular swelling and ecchymosis). Fracture of the anterior skull base may cause a dural laceration with subsequent drainage of CSF into paranasal sinuses and rhinorrhea. Anterior venous sinus drainage may cause blood leakage into the periorbital tissues (raccoon eyes). Given the location of basilar skull fractures, associated cranial nerve palsies may occur. There is a high incidence of associated ICI in children with basilar skull fracture, even in those with a Glasgow Coma Scale (GCS) score of 15 and normal neurologic examination results. Of note, not all basilar skull fractures are evident on CT; however, a patient with classic clinical signs should be considered to have this fracture even without demonstrable fracture on CT.

Intracranial Injury

Insults to intracranial contents include functional derangements without demonstrable lesions on CT scan (concussion, posttraumatic seizures), hemorrhage (cerebral contusion, epidural hematoma [EDH], subdural hematoma [SDH], subarachnoid hemorrhage, and intracerebral hemorrhage), and cerebral edema. Rarely, penetrating brain injuries occur in children. ICIs may also be classified as focal (e.g., contusions, hematomas, lacerations) or diffuse (e.g., diffuse axonal injury, with cerebral edema). Focal injuries are usually apparent on the initial CT scan, even if clinically asymptomatic. Diffuse injuries, in contrast, may not demonstrate striking abnormalities on early CT imaging, even if the patient manifests significant alteration in neurologic function.

Concussion

Concussion is typically a minor brain injury characterized by posttraumatic alteration in mental status that may or may not involve loss of consciousness (LOC). No consistent associated pathologic lesion has been identified on neuroimaging. The child may have a depressed level of consciousness, pallor, vomiting, amnesia, and confusion. The clinical picture often normalizes within several hours, however, in a small number of patients symptoms may persist for days or weeks. For more details please see Chapter 121 Neurotrauma.

Posttraumatic Seizure

Posttraumatic seizures can be divided temporally into immediate, early, and late, and they occur in 5% to 10% of children hospitalized for head trauma.

Immediate seizures occur within seconds of the trauma and may represent traumatic depolarization of the cortex. They usually are generalized and rarely recur.

Early seizures occur within 1 week of the trauma (the majority within 24 hours). Skull fractures, intracranial hemorrhage, and focal signs are associated with increased risk of early posttraumatic seizures; therefore, an early seizure should prompt investigation of these possibilities.

Late seizures occur more than 1 week after the traumatic event and may be attributed to scarring associated with local vascular compromise, distortion, and mechanical irritation of the brain. These seizures are more likely to occur in children with severe head injuries, dural lacerations, and intracranial hemorrhages. A substantial number of patients will have subsequent seizures.