Children of different ages sustain various types of head traumas. The specific circumstances of head trauma must be determined, and the predisposing factors must be identified. Such information should be sought directly from an injured child whenever possible and also from observers, such as playmates, teachers, parents, ambulance attendants, or others at the scene of the accident. Under emergency circumstances, such as posttraumatic status epilepticus or acute intracranial hemorrhage,
someone other than the person treating the injured child may be needed to obtain the history. Details of the accident should be supplemented by observations of memory loss, repetitive questioning, confusion, visual disturbance, and symptoms of increased ICP, such as altered consciousness, vomiting, severe headache, and changes in vital signs. A history of previous immunizations, drug allergies, current medications, and possible drug intoxication also should be obtained.

The principal mechanisms of head injury are contact and acceleration-deceleration. Lesions caused by an object striking the head, or vice versa, include scalp laceration, skull fracture, epidural hematoma, brain contusion, and intracerebral hemorrhage. By contrast, acceleration-deceleration, which results from head movement immediately after the injury, leads to intracranial and intracerebral pressure gradients and to shear, tensile, and compressive strains. Such inertial (nonimpact) lesions are responsible for cerebral concussion, diffuse axonal injury, and acute subdural hematoma.

Vital signs demand immediate diagnostic study and sometimes mandate emergency treatment. Characteristic changes in pulse, blood pressure, and respirations may indicate shock (i.e., decreased blood pressure and increased pulse) or increased ICP (i.e., increased blood pressure, decreased or increased pulse, slowed or irregular respirations). Usually, a decrease in blood pressure in the head-injured child is caused by an injury in another location, such as thoracic, intraabdominal, or retroperitoneal hemorrhage or bleeding into soft tissues surrounding a long-bone fracture. Occasionally, however, bleeding into the scalp may be sufficient to produce shock (as with subgaleal hematoma) or bleeding inside the skull (as with epidural hematoma). Other causes for hypotension in the head-injured child are spinal cord injury, cardiac contusion or tamponade, and tension pneumothorax.

The entire body should be scrutinized for signs of trauma. Physical examination should include a search for injury to the neck, chest, abdomen, and long bones and a careful inspection of the skin. Long-bone fractures, which occur in one-third of patients with severe head injuries, may be complicated by fat embolism. The neck should be examined with care, because of possible injury. In cases of suspected neck trauma, the neck should not be moved; the neck is immobilized by sandbags and adhesive tape or a firm collar. Such injury is suggested by cervical abrasions or cervical spine tenderness. Meningismus can result from cervical trauma, subarachnoid blood, or herniation of the cerebellar tonsils.

The head must be examined carefully. The scalp should be inspected and palpated for tenderness or depression. All scalp lacerations should be probed with a sterile-gloved finger in search of a foreign body or an underlying skull fracture. Tension of the anterior fontanelle should be assessed in young infants. Transillumination of the skull in infants and young children may detect abnormal accumulations of fluid, including blood, outside or inside the skull. Cranial ultrasound examination may be helpful when the anterior fontanelle is open. Periorbital hemorrhage (raccoon-eyes sign), ecchymosis behind the ear (Battle sign), blood behind the eardrum (hemotympanum), and bleeding from the ears or nose should be noted. These signs, along with CSF otorrhea or rhinorrhea, indicate a basilar skull fracture.

The neurologic examination should include an assessment of the child’s alertness, orientation, and memory; a neuro-ophthalmologic examination; and testing of motor and sensory functions, reflexes, and coordination. When possible, testing of orientation and memory should include the child’s account of the episode that caused the head trauma. The presence and extent of any retrograde and anterograde (posttraumatic) amnesia should be determined. Additional assessment of memory should include testing of the child’s digit span and recall of several items after 5 minutes. A child’s repeated asking of the same question is reminiscent of Korsakoff psychosis, a posttraumatic, anterograde-type memory disturbance.

The level of consciousness may range widely. The Glasgow Coma Scale (GCS) (Table 118.1A), with scores ranging from 3 (worst) to 15 (best), provides a useful and reproducible scoring system for quantifying the level of consciousness and for systematically following a head-injured child’s clinical course. The child’s best motor response (score, 6 to 1), best verbal response (score, 5 to 1), and eye opening (score, 4 to 1) are assessed. In the young, nonverbal child, modifications in the GCS must be made. Although a variety of coma scales have been proposed for pediatric practice, a modification of the GCS that has been particularly useful is seen in Table 118.1B. In the child younger than 1 year, with eye opening, the verbal stimulus used is a shout rather than a command and for the best motor response, spontaneous movements rather than those in response to commands are assessed. With verbal response in children 5 years or younger, a score of 5 is given for appropriate words and phrases (2 to 5 years) or babbling and cooing (0 to 2 years); a 4 is given for inappropriate words (2 to 5 years) or consolable crying (0 to 2 years); a 3 is given for persistent crying or screaming to pain (0 to 5 years); a 2 is given for grunting or moaning to pain (0 to 5 years); otherwise, the same criteria as in the older child are used in scoring the younger child’s responses. Although most studies have reported a correlation between a low GCS score and severe neurologic morbidity and substantial mortality rates, children with a low GCS score (3 to 5) sometimes do surprisingly well if the head injury has not been complicated by a hypoxic-ischemic insult. Numerous factors, including intubation, orbital swelling, sedation, and neuromuscular blockade, interfere with accurate scoring with the GCS, thus limiting its predictive value.

Neuro-ophthalmologic evaluation should include a measurement of pupillary size and reactivity. Small pupils are seen with diencephalic and pontine injuries; a unilateral dilated pupil suggests temporal lobe herniation on the same side. The fundi should be examined carefully, with evidence of retinal and preretinal (subhyaloid) hemorrhages and papilledema specifically sought. Abnormalities of ocular gaze and position may include roving eye movements, limited lateral and vertical gaze, and skew deviation. When clearly no neck injury has occurred, the oculocephalic (doll’s-eye) maneuver can be used to assess any apparent limitation of eye movements. This procedure is performed with the child supine by rotating the head to one side and then the other. When the head is moved to the left, the eyes should deviate to the right (and vice versa) if brainstem pathways controlling eye movements are functioning normally. Lateral gaze can be tested also in the comatose patient by caloric stimulation: The child’s head is elevated 30 degrees above horizontal, and one external auditory canal is irrigated with ice water. If brainstem function is normal, the eyes should turn toward the ear being irrigated. An important precaution is ascertaining that the auditory canal is clear and that the eardrum is intact before performing this test. In an alert child, testing of visual acuity, visual fields, and opticokinetic nystagmus also should be performed.

The extent of examination of the motor system will depend on the child’s alertness. When the child is comatose, abnormal posturing (e.g., decorticate, decerebrate) should be sought. Noxious stimulation, such as a sternal rub, may be required to produce such posturing. Muscle tone may be reduced (hypotonia) or increased (spasticity or rigidity) in a hemiparetic or paraparetic distribution. In a responsive child, motor impairment can be detected by testing individual muscles, examining conventional gait and stressed gait, and observing the outstretched arms for evidence of a drift. Also, performing sensory testing may be possible. The neurologic examination is completed by testing for abnormal reflexes, such as a palmar grasp, suck, or root; by eliciting deep-tendon reflexes; and by checking for plantar responses.

In moderately and severely injured children and in those in whom the cause or circumstances of the injury are unknown, additional studies may be indicated. They include complete blood cell count; serum amylase; urinalysis; platelet and clotting studies; toxic screen on blood, urine, and gastric aspirate; and skeletal survey for old and recent fractures.

The management of the child with head injury must be directed to the entire patient. The head and neck must be stabilized; with suspected neck trauma, a firm cervical collar (Philadelphia type) or sandbags or tape and Velcro straps attached to a backboard should be used. Life-threatening obstruction of the airway may result from blood, vomiting, secretions, a foreign object, or the tongue (the last especially with severe mandibular fractures). Accessible foreign objects should be removed, and patency of the airway maximized by proper positioning. Usually, a chin lift will relieve upper airway obstruction. If any concern about an accompanying cervical spine injury exists, a jaw thrust, not a chin lift, with the head kept in a neutral position, should be used to open the airway.

Ventilatory management is assisted by inserting an oral airway into the oropharynx; if needed, ventilatory support should be provided. Suctioning should be performed without touching the carina. In comatose children and in others with airway obstruction or ineffective respiratory effort with a diminished gag and cough, and in patients with a GCS of less than 8, orotracheal or nasotracheal intubation usually is needed. Nasotracheal intubation should not be used if a basal skull fracture is suspected. Intubation diminishes the risk of aspiration (of oropharyngeal secretions, blood, or vomitus) and the risk of airway obstruction, assists in tracheal suctioning, and is mandatory for controlled ventilation. The head and neck should be moved with great care, any associated neck injury is not exacerbated. Optimal conditions for intubation are provided by rapid induction of intravenous anesthesia with propofol 1 to 2 mg/kg or etomidate 1.5 to 3 mg/kg; with any hemodynamic instability, however, a combination of fentanyl, 1 to 5 μg/kg, and midazolam, 0.1 mg/kg, could be given intravenously instead. Intravenous lidocaine, 1 to 1.5 mg/kg, should be given 1 to 2 minutes before intubation, with neuromuscular blockade accomplished with intravenous high-dose vecuronium, 0.2 to 0.3 mg/kg, or vecuronium, 0.01 mg, followed by succinyl choline, 1.5 mg/kg. Oxygen (100%) should be given at 3 to 10 L/minute by bag and mask or by nasal prongs, with the P_aO₂ maintained at 90 to 100 mm Hg. Cardiac rate and rhythm should be monitored.

An intravenous line should be established; blood testing should include hematocrit, type and cross-match, and amylase (for evidence of pancreatic injury). Sites of hemorrhage must be controlled, and blood volume must be maintained. With infrequent exceptions, shock is not a sign of head injury in children. It usually is caused by associated injury, such as rupture of an abdominal organ (e.g., liver); bleeding into extracranial soft tissues (as with a pelvic fracture); peritonitis (after spillage of contents from a ruptured intestine); traumatic pancreatitis; or associated spinal cord injury (“spinal shock”). Occasionally, however, rapid intracranial bleeding into the epidural space or even into the scalp can cause shock. In all children with severe head injury, a central venous line to monitor central venous pressure should be placed, and an arterial line should be inserted to monitor arterial blood pressure, assess cerebral perfusion pressure, and facilitate blood gas measurements. Normal systolic blood pressure varies with age: 50 to 60 mm Hg in neonates; 70 to 80 in toddlers; 80 to 90 in school-aged children; and 90 to 100 in adolescents. Mean systemic arterial blood pressure should be maintained at 65 mm Hg at least to ensure adequate cerebral circulation. Hypovolemia (greater than 20% blood volume loss) is corrected by intravenous crystalloid (such as lactated Ringer solution or normal saline) or colloid (hydroxyethyl starch or 5% albumin in a bolus of 10 to 20 mL/kg, repeated as necessary to establish adequate perfusion).

A slowing in pulse rate may indicate an encouraging response to treatment for circulatory insufficiency, but it also can be a danger signal, reflecting increased ICP. Circulatory failure with a fall in blood pressure is treated with volume replacement, after which epinephrine, 0.1 to 0.5 μg/kg/minute, or norepinephrine, 0.05 to 0.2 μg/kg/minute, can be given. With cardiac arrest, in addition to ventilation and chest compressions, the child should be treated in accordance with the Pediatric Advanced Life Support (PALS) recommendations.

Accompanying injuries, such as those to the scalp, chest (especially pneumothorax), great vessels, abdominal viscera, pelvis, limbs, or spine, may require specific treatment. Chest films aimed at looking for rib fractures, hemopneumothorax, and mediastinal widening should be obtained. With suspected abdominal bleeding or intestinal perforation, abdominal ultrasonography, CT scanning, or diagnostic peritoneal lavage should be performed.

Pseudosubluxations of the cervical spine, especially at C2 to C3 and C3 to C4, found normally in approximately 20% of children in the first decade of life, may be sources of unnecessary concern. Fractured limbs should be splinted. The stomach should be emptied by nasogastric intubation (to prevent vomiting, aspiration, and pressure on the diaphragm, causing secondary respiratory compromise), and the bladder should be catheterized. Fever should be controlled by sponging and antipyretics. When circulatory status is adequate, the intake of iso-osmolar fluids should be given at or slightly above normal maintenance. Electrolyte abnormalities and coagulation defects should be corrected. Vital signs should be followed with care. An elevation of systolic blood pressure, a slowing or speeding of the pulse, and slowed or irregular respirations are indicative of intracranial hypertension (see section, Raised Intracranial Pressure). When seizures occur, anticonvulsants should be given (see section, Posttraumatic Seizures).

Children, adolescents, and young adults frequently are evaluated in emergency departments after sustaining minor head trauma. Useful data concerning the management of such children are few in number and not uncommonly conflicting. Thus, the American Academy of Pediatrics (AAP) and the American Academy of Family Practice (AAFP) have developed a Clinical Practice Guideline to assist in managing patients between 2 and 20 years of age who have sustained an isolated, minor, closed head injury. By definition, such patients show a normal mental status on initial examination, have no focal or otherwise abnormal findings on neurologic examination, and have no physical evidence of skull fracture. Additionally, they may or may not have sustained a brief (less than a minute) loss of consciousness, they may have had a seizure immediately after their head injury, they may have vomited, and they may have developed headache and lethargy.

When no loss of consciousness has occurred in such children, following a thorough history and physical and neurologic examinations, the child should be observed for at least 24 hours in the clinic, office, emergency department, and/or at home under the care of a competent adult; careful observation should continue for the next several days, watching for any change in the patient’s clinical status. CT scanning, skull radiographs, or MRI rarely are needed. When a brief loss of consciousness has occurred following such head injury, a slightly increased risk of an intracranial injury (1% to 5% versus less than 1% with no loss of consciousness) exists. Again, following a thorough history and physical and neurologic examinations, the child should be observed in any of the above settings and/or at home under the care of a competent adult. Because of its sensitivity and specificity, cranial CT scanning may be useful in identifying the small number of such patients in whom some intracranial abnormality is present, although only rarely are medical, neurosurgical, or other interventions needed. Factors that may indicate a clearer need for CT scanning include a delay from the time of injury until the time when the patient is first seen, a scalp hematoma overlying the course of the middle meningeal artery, and those few patients with minor head trauma in whom clinical worsening occurs. Skull radiographs or MRI are almost never needed. If imaging seems desirable, cranial CT scanning is the best modality to use; if the CT scan is normal, an adverse outcome is very unlikely.

In children younger than 2 years of age who have had a minor head injury, the risk for skull fracture and intracranial injury is higher than in older patients. Additionally, clinical assessment is more difficult in very young children, and their risk for nonaccidental injury is higher. Thus, based on the assessed risk for intracranial injury, four guidelines have been suggested for the evaluation and management of children younger than 2 years old following a minor head injury:

It is important to stress that, whereas all the above guidelines are reasonable suggestions, proposed by health professionals knowledgeable about pediatric head injuries, these guidelines are not supported by large numbers of controlled clinical studies. In some cases, clinical judgment should take precedence, and if the clinician is concerned, even if the child looks well, CT scanning should be performed.

Many factors influence the decision concerning whether to hospitalize head-injured children. Hospitalization is indicated or should be considered seriously with changing vital signs; posttraumatic seizures; altered mental status, particularly prolonged unconsciousness; persisting memory deficit; focal neurologic signs; depressed skull fracture; basilar skull fracture; enlarging scalp swelling; persisting severe headache, especially with neck stiffness; recurrent vomiting; unexplained fever; neuroradiologic abnormalities of concern; and an unexplained injury raising the question of possible child abuse.

Early posttraumatic seizures or early posttraumatic epilepsy, which occurs within the first week after head injury, develops in approximately 5% of children hospitalized after encurring a head trauma. Of these children, 20% to 30% will have additional seizures beyond the first week. Infants and young children are at greater risk for the development of early posttraumatic seizures than are older children and adults. The incidence of early posttraumatic seizures that occur after severe traumatic brain injury in children varies from 20% to 40%. The risk is greater with lower GCS scores. After adjustment for the GCS and the duration of coma, the risk of early posttraumatic seizures occurring after severe head injury is three times greater in infants than in older children to age 12 years.