Pediatric Head Trauma Clinical Presentation

Patients with head trauma may experience 1 or a combination of primary injuries, depending on the degree and mechanism of trauma. Specific types of primary injury include scalp injury, skull fracture, basilar skull fracture, concussion, contusion, intracranial hemorrhage (ICH), subarachnoid hemorrhage, epidural hematoma, subdural hematoma, intraventricular hemorrhage, penetrating injuries, and diffuse axonal injury.

Scalp injury

Often observed with traumatic brain injury (TBI), scalp injury can overlie other intracranial pathology; therefore, it necessitates careful exploration for foreign bodies or underlying skull fractures. Bleeding associated with scalp lacerations could be significant enough to cause hypotension and shock in a small infant.

Caput succedaneum and cephalohematoma are observed with birth-related head trauma. Caput succedaneum involves molding of the neonatal head and crosses the suture lines, whereas cephalohematoma involves subperiosteal bleeding and is limited by the suture lines.

Skull fracture

Skull fractures are linear, comminuted, depressed, and diastatic. In children, 90% of the fractures are linear and tend to be more diastatic; thus, the radiographic appearance is more impressive. An open fracture is a fracture overlaid by a laceration. The presence of cerebrospinal fluid (CSF) in the wound indicates a violation of the dura and warrants further exploration.

The location of the fracture is important because it may cross the path of a major vessel and be associated with an intracranial bleed.

A depressed skull fracture is defined as displacement of the inner table of the skull by more than 1 thickness of the bone. One third of depressed fractures are simple, one third are associated with dural laceration, and one fourth have cortical lacerations.

Basilar skull fracture

Basilar skull fracture is present in 6-14% of pediatric patients with head trauma and is suggested by a history of a blow to the back of the head.

Loss of consciousness, seizures, and neurologic deficits may or may not be present. Children with basilar skull fracture usually have prolonged nausea, vomiting, and general malaise, most likely because of the vicinity of the fracture to the emesis and vestibular brainstem centers. Physical findings such as Battle sign, raccoon eyes, and CSF otorrhea and rhinorrhea are pathognomonic; ocular nerve entrapment may occur in 1-10% of patients.^[11]

Concussion

Concussion is a transient loss of consciousness and occurs as the result of head trauma. Patients often have normal findings on neurologic examination; the diagnosis is usually a retrospective one.

Infants and young children have a higher incidence of posttraumatic seizures and most often increased delayed somnolence and vomiting; older children have a history of posttraumatic amnesia. Waxing and waning of mental status in the absence of any morphologic changes is also characteristic of concussion and is more often observed in older children.

Contusion

A contusion is an area of bruising or tearing of the brain tissue, caused by a direct injury to the head. The temporal and frontal lobes are the most vulnerable areas because of their anatomic relationship with the bony protuberances of the calvaria. The typical presentation is of progressive neurologic deterioration secondary to local cerebral edema, infarcts, or late-developing hematomas.

Epidural hematoma

Epidural hematomas (see the image below) develop between the skull and the dura, secondary to the laceration of an artery or vein. Those of arterial origin peak in size 6-8 hours after the injury, whereas those of venous origin may grow over 24 or more hours. Common locations are the temporal, frontal, and occipital lobes. An overlying skull fracture may be present.

Patients may present with the classic lucid interval between the initial loss of consciousness and subsequent neurologic deterioration, but this is less frequent in the pediatric population. When neurologic deterioration with hemiparesis, unconsciousness, posturing, and pupillary changes develops, it is due to the expansion of hematoma and exhaustion of compensatory mechanisms, with subsequent compression of the temporal lobe or brainstem (see the image below).

Subdural hematoma

Subdural hematoma (see the image below) develops between the dura and the cortex as a result of tearing of the bridging veins across the dura or laceration of the cortical arteries caused by acceleration-deceleration forces. It is usually associated with severe parenchymal injury, and the presentation is that of profound and progressive neurologic deterioration.

Subdural hematoma may develop secondary to birth trauma, in which case the presentation is within 12 hours of life and includes seizures, full fontanel, anisocoria, and respiratory distress. It may also be a feature of shaken baby syndrome; the usual presentation is of new-onset seizures, increased head circumference, a poorly thriving infant, and tense fontanel. Focal neurologic deficits are usually absent.

Penetrating injuries

Penetrating injuries derive from a variety of sources. They should be considered neurosurgical emergencies because rapid deterioration and fatal hemorrhages may ensue.

Intraventricular hemorrhage

Intraventricular hemorrhage (see the image below) is usually the result of minor trauma and resolves spontaneously. Large hemorrhages can lead to obstructive hydrocephalus, especially when they are located at the level of the foramen of Monroe and the aqueduct of Sylvius, in which case surgical intervention is required.

Subarachnoid hemorrhage

Subarachnoid hemorrhage, the most common form of hemorrhage associated with head trauma, results from disruption of the small vessels on the cerebral cortex. The usual location is along the falx cerebri or tentorium and the outer cortical surface. Common symptoms include nausea, vomiting, headache, restlessness, fever, and nuchal rigidity caused by blood in the subarachnoid space.

Diffuse axonal injury

Diffuse axonal injury is the result of rapid acceleration-deceleration forces that cause disruption of the small axonal pathways. The most commonly affected areas are the basal ganglia, thalamus, deep hemispheric nuclei, and corpus callosum. The increased vulnerability of these structures to shear injuries is attributed to their having a different momentum from the rest of the brain at the time of the injury.

Patients usually present with various states of altered mentation and often remain in a vegetative state for long periods. A marked discrepancy between the highly abnormal neurologic examination findings and the lack of findings on computed tomography is observed. Occasionally, small petechial hemorrhages may be present. The prognosis for full recovery is often poor.

Head trauma patients often have multiple organ injuries. Assessment of patients with severe head injuries includes a primary survey and a secondary survey. The primary survey is a focused physical examination directed at identifying and treating life-threatening conditions present in a trauma patient and thereby preventing secondary brain injury. The secondary survey of patients with head trauma is a detailed examination and assessment of individual systems with the goal of identifying all traumatic injuries and directing further treatment.

Primary survey

Airway

Airway inspection should be directed at identifying the presence of foreign bodies, loose teeth, facial lacerations and bone instability, deviation of trachea, and circumoral cyanosis indicative of hypoxia. Auscultation of the airway may suggest the presence of upper airway obstruction, especially when a turbulent flow pattern is noted.

Breathing

Apnea and hypoventilation secondary to pulmonary or neurologic causes are common findings in patients with head trauma. When present, they warrant immediate intervention and endotracheal intubation.

Circulation

The Cushing triad (ie, bradycardia, hypertension, and alteration of respiration), if present, is a late manifestation indicative of herniation.

When hypotension is present, it should not be attributed solely to ICH. Several other causes may lead to this finding, such as internal hemorrhages, spinal cord injury, cardiac contusion, and dysrhythmias with secondary impaired cardiac output. Hypotension associated with bradycardia in a trauma patient should be considered highly suggestive of spinal cord injury.

Neurologic examination

Responsiveness is assessed with the alert, verbal, pain, unresponsive (AVPU) system and with the Glasgow Coma Scale (GCS) and its pediatric modification, the Pediatric Glasgow Coma Scale (PGCS). The PGCS was developed for children younger than 5 years as a more accurate tool that would avoid the errors that occur when the GCS is applied to children and infants with limited verbal skills. A total PGCS score of 13-15 represents minor injury, a score of 8-12 represents moderate injury, and a score lower than 8 represents severe injury (see the tables below).

Table 1. Pediatric Glasgow Coma Scale: Eye Opening (Open Table in a new window)

Table 2. Pediatric Glasgow Coma Scale: Best Motor Response (Open Table in a new window)

Table 3. Pediatric Glasgow Coma Scale: Best Verbal Response (Open Table in a new window)

The GCS and the PGCS do not include a pupillary examination. For this reason, pupillary assessment should be performed each time a neurologic assessment is conducted. Assessment of pupillary size and response to light may yield the following significant findings:

• Ipsilateral pupillary dilatation with no response to direct or consensual stimulation to light - This is caused by transtentorial herniation and compression of the parasympathetic fibers of cranial nerve III
• Bilateral, dilated, and unresponsive pupils - This finding constitutes an ominous sign indicative of either bilaterally compressed cranial nerve III or global cerebral anoxia and ischemia

Motor ability is assessed through direct observation of spontaneous and symmetric movement, through application of pressure to the nail bed, or through central application of painful stimuli (eg, a sternal rub). Findings may include the following:

• Decreased spontaneous movement or flaccidity, indicating potential local or spinal cord injury
• Decerebrate posturing, suggesting damage to the midbrain
• Decorticate posturing, indicating damage to the cerebral cortex, white matter, or basal ganglia

Secondary survey

Head

Cervical deformity, swelling, pain with palpation, stepoff, or malalignment could suggest an unstable injury of the cervical spine and should prompt immobilization of the cervical spine until further diagnostic tests are obtained.

Lacerations and depressions, when present, warrant further exploration for foreign bodies and underlying bone and dural disruption.

Battle sign or ecchymosis in the retroauricular and mastoid area is pathognomonic for basilar skull fracture. It is the result of blood dissecting in the occipital and mastoid area from the disrupted skull cortex. Raccoon eyes or periorbital ecchymosis is indicative of basilar skull fracture. It is also the result of blood dissecting from the disrupted skull cortex into the soft tissue of periorbital region.

Hemotympanum (blood behind the tympanic membrane) indicates fracture of the petrous temporal bone and may be associated with disruption of cranial nerves VII and VIII.

CSF otorrhea and rhinorrhea are also present with basilar skull fracture and are the result of disruption of the leptomeninges and the cribriform plate. A glucose oxidase tape may be used to differentiate between rhinorrhea and CSF leakage.

Bulging of the fontanel is a sign of increased intracranial pressure (ICP).

Respiratory patterns

Apnea secondary to diaphragmatic paralysis indicates high spinal cord injury. Cheyne-Stokes respiration or alternating periods of hyperpnea with apnea indicates injury to the cerebral hemispheres or diencephalon. Hyperventilation is indicative of damage to the rostral brain stem or tegmentum. Apneustic respiration, described as prolonged end-expiratory pauses, is secondary to damage of the midpontine or caudal pontine level.

Neurologic examination

A unilateral dilated pupil is due to compression of cranial nerve III and usually indicates ipsilateral herniation. Initially, the light reflex is preserved, but as herniation progresses and cranial nerve III is compressed by the temporal lobe, the pupil becomes unresponsive to light stimulus.

Pupillary size may suggest the level of the injury. Pinpoint pupils are present in pontine lesions. Pupils that are in midposition and nonreactive to light but maintain hippus and response to accommodation indicate midbrain tectum injury.

Horner syndrome or ipsilateral pupillary constriction, ptosis, and anhydrosis accompany damage of the hypothalamus and disruption of the sympathetic pathways. This may also be an early sign of transtentorial herniation. Nystagmus, when present, suggests cerebellar or vestibular injury.

Tonic eye deviation is secondary to cortical lesions, cranial nerve dysfunction, or seizure activity. Retinal hemorrhages suggest nonaccidental head trauma or sustained increased ICP. Papilledema, loss of venous pulsation, is observed with increased ICP.

Reflexes (eg, corneal, gag, and oculovestibular) and the presence of spontaneous respiratory effort may help in locating the level of injury.

Motor and sensory function should be assessed to determine the integrity of the spinal cord. Deep tendon reflexes that are symmetric and hyperactive indicate head or spinal cord injury, as opposed to asymmetric reflexes, which indicate a unilateral lesion. Babinski reflex, dorsiflexion of the great toe at plantar stimulation, suggests pyramidal tract involvement. Infants might have a positive sign normally, and the value of this sign in this age group is limited.

Seizures are more commonly observed with contusions (more so with subdural hematoma than with epidural hematoma), depressed skull fracture, and severe head injury (PGCS score, 3-5).

Leptomeningeal cyst or growing fracture represents extrusion of leptomeninges and brain tissue through a dural defect. Meningitis may develop secondary to basilar skull fracture.

Cranial nerve injury may develop secondary to basilar skull fracture. Oculomotor palsy is due to injury of cranial nerves VI, III, or IV. Trauma to nerve VII leads to facial nerve palsy. Hearing loss may occur because of injury of cranial nerve VIII.

Posttraumatic syndrome may develop after mild-to-moderate head trauma and consists of irritability, inability to concentrate, nervousness, and occasionally behavioral or cognitive impairment.

Cortical blindness, described as an acute loss of vision after head trauma, usually resolves spontaneously within 24 hours. Several mechanisms have been implicated, including acute cerebral edema and transient vasospasm. Cortical blindness is now considered to result from minor transient alterations in the brain function triggered by the traumatic event.

Trauma-induced migraine may begin from minutes to hours after the injury and may last from hours to days. Beta-blockers are the drugs of choice for this complication.

Hydrocephalus results from either an obstruction caused by an intraventricular hemorrhage or decreased reabsorption of CSF due to proteinaceous obstruction of the arachnoid villi.

Neurogenic pulmonary edema is thought to be due to medullary ischemia that leads to increased sympathetic tone with subsequent increase in pulmonary vascular pressure and a shift in blood distribution from the systemic to the pulmonary circulation.

Pulmonary infections are often present in patients with head trauma because of either an initial aspiration process or prolonged mechanical ventilation.