eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Head Trauma

Author: Arabela Stock, MD, Consulting Staff, Department of Pediatrics, Divisions of Critical Care and Pulmonology, Florida Pediatric Association
Coauthor(s): Jagvir Singh, MD, Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge
Contributor Information and Disclosures

Updated: Jun 1, 2009

Introduction

Background

Trauma is a leading cause of death in children older than 1 year in the United States, with head trauma representing 80% or more of the injuries. In approximately 5% of head trauma cases, patients die at the site of the accident. Head trauma has a high emotional, psychosocial, and economic impact because these patients often have comparatively long hospital stays, and 5-10% require discharge to a long-term care facility.¹

The anatomical differences of the child's brain render it more susceptible than the adult brain to certain types of injuries following head trauma. The head is larger in proportion to the body surface area, and stability is dependent on the ligamentous rather than bony structure. The pediatric brain has a higher water content, 88% versus 77% in adult, which makes the brain softer and more prone to acceleration-deceleration injury. The water content is inversely related to the myelinization process. The unmyelinated brain is more susceptible to shear injuries. Infants and young children tolerate intracranial pressure (ICP) increases better because of open sutures.

Pathophysiology

Primary and secondary injuries are described with head trauma, and the presence of these injuries affects the outcome of these patients.

The primary injury occurs at the time of impact, either by a direct injury to the brain parenchyma or by an injury to the long white matter tracts through acceleration-deceleration forces. Direct injury to the brain parenchyma occurs as the brain is impacted on the bony protuberances of the calvaria or by penetration of the brain by bony fragments or a foreign body. In children, the compliant skull is easily deformed, and impacts on the brain at the time of the insult result in a coup injury, as opposed to adults, in whom the brain is forced against the bony protuberances opposite the point of the impact, resulting in a countercoup injury. Intracranial hemorrhage may also result from shearing or laceration of vascular structures. Acceleration-deceleration forces cause shearing of the long white matter tracts, leading to axonal disruption and secondary cell death.

The secondary injury is represented by systemic and intracranial events that occur in response to the primary injury and further contribute to neuronal damage and cell death.

The systemic events are hypotension, hypoxia, and hypercapnia and may occur as a direct result of primary injury to the CNS or can result from associated injuries in a person with multiple traumas.

The intracranial events are a series of inflammatory changes and pathophysiologic perturbations that occur immediately after the primary injury and continue over time. Their presence adds to the adverse outcome of the head trauma patient. The inflammatory events are the result of a cascade of biomolecular changes triggered by the initial insult, leading to microcirculatory disruption and neuronal disintegration. A series of factors such as free radicals, free iron, and excitatory neurotransmitters (glutamate, aspartate) are the result of these inflammatory events, and their presence contributes to the negative outcome. The pathophysiologic events are cerebral edema, increased ICP, hyperemia, and ischemia.

The brain has minimal ability to store energy; thus, it depends on aerobic metabolism. The delivery of oxygen and metabolic substrate to the brain is maintained by a constant supply of blood known as cerebral blood flow (CBF). CBF, defined as the amount of blood in transit through the brain at one given point in time, is estimated to be 50 mL/100g/min in a healthy adult and is known to be much higher in children. However, the minimum amount necessary to prevent ischemia remains unknown. CBF is influenced by mean arterial blood pressure (MAP), ICP, viscosity of the blood, metabolic products, and the diameter of brain vessels. CBF should not be confused with cerebral blood volume (CBV), which represents the amount of blood present in the brain vasculature. CBV is the major contributor to the ICP and depends on the diameter of intracranial vessels. When CBV is increased, the pressure gradient across the compartment is decreased, and the CBF is decreased.

The brain has the capacity of maintaining constant blood flow through a mechanism known as autoregulation. This occurs over a wide range of blood pressures through changes in cerebral resistance in response to fluctuations in MAP pressure. The CBF is maintained at a MAP of 60-150 mm Hg. At 60 mm Hg, the cerebral vasculature is maximally dilated, and at 150 mm Hg, it is maximally constricted. Fluctuations past this range lead to alterations in CBF and contribute to ischemia or disruption of the blood-brain barrier. Several mechanisms are known to affect autoregulation of CBF, and they can be divided into metabolic products and ABG content and myogenic, neurogenic, and endothelium-dependent factors. Their effect is not fully known, and their mechanism of action is still under experimental investigation.

CBF is closely linked to cerebral metabolism. Although the mechanism of coupling is not clearly defined, it is suspected to involve vasodilators released from neurons. Several factors have been implicated such as adenosine and free radicals. Pathophysiologic states, such as fever and seizure activity, that are known to increase the metabolic activity lead to an increase in CBF.

CBF can be altered by changes in the partial pressure of oxygen or carbon dioxide. Alteration in the partial pressure of oxygen acts on the vascular smooth muscle through mechanisms that remain unclear. Hypoxia causes vasodilatation with significant increase in CBF. Increases in oxygen pressure cause vasoconstriction but to a lesser degree than hypoxia. Hypercarbia increases CBF up to 350% of normal; hypocapnia produces a decrease in blood flow. The mechanism appears to involve alteration in tissue pH that leads to changes in arteriolar diameter. This mechanism is preserved even when autoregulation is lost.

The myogenic mechanism was considered for a long time to be the most important in the autoregulation process. The changes in the actin-myosin complex were thought to lead to rapid changes in the vasculature diameter, thus affecting the CBF. Currently, changes in the actin-myosin complex have been shown to mostly cause dampening of arterial pulsation and to have little direct effect on cerebral autoregulation.

The neurogenic mechanism is represented by the effect of the sympathetic system on the cerebral vasculature. The sympathetic nervous system shifts autoregulation towards higher pressures, whereas sympathetic blockade shifts it downwards.

Studies have identified nitric oxide as one of the factors affecting cerebral autoregulation by producing relaxation of cerebral vessels. It is present in several conditions such as ischemia, hypoxia, and stroke. Nitric oxide has been shown to be generated by different cells at rest but also under direct stimulation by factors such as cytokines.

Traumatic brain injury may lead to loss of autoregulation through alterations of the described mechanisms. A recent study revealed that mild traumatic brain injuries are more likely than orthopedic injuries to cause transient or persistent increases in postconcussive symptoms during the first year after injury.² These mechanisms represent the foundation upon which the medical management of increased ICP and cerebral perfusion pressure (CPP) is based in patients with traumatic brain injury.

Frequency

United States

Head injury is estimated to occur in approximately 200 per 100,000 population per year. The number includes all head injuries that resulted in hospitalization, death, or both in persons aged 0-19 years.

Mortality/Morbidity

The overall outcome for children with head injuries is better than that of adults with the same injury score.^3,4,5 Recovery in children takes longer, from months to sometimes years, whereas adults reach maximum recovery by about 6 months following the injury. Outcome assessment based on the Glasgow Coma Scale (GCS) could be used as an early predictor, but it has limitations regarding long-term outcome. Patients with multiple organ injuries, including head trauma, generally have a far worse outcome than those with head injury alone.

• Mortality: According to the National Center for Health Statistics, the mortality rate from head trauma is 29% in the pediatric population. These data are based on death certificate information, and 29% could be an underestimation of the actual rate. Data reported by studies in trauma centers show that head injury represents 75-97% of pediatric trauma deaths.
• Neurologic deficits: Short-term memory problems and delayed response times are reported in 10-20% of children with moderate-to-severe head injury (GCS of 6-8), especially if the coma lasts longer than 3 weeks. More than half of children with GCS of 3-5 have permanent neurologic deficits.

Race

Black adolescent boys account for most of the firearms-related CNS injuries in the pediatric population.

Sex

Males are twice as likely to sustain head injuries as females and have 4 times the risk of fatal trauma.

Age

The distribution of head trauma is relatively stable throughout childhood. An increase in the incidence of head trauma was identified in 2 age groups. At approximately age 15 years, a dramatic increase occurs, mainly in males, related to their involvement in sports and driving activities. Infants younger than 1 year have also been identified by several studies as having an elevated incidence of head trauma, which is attributed to falls and child abuse.⁶

Clinical

History

Patients with head trauma may experience one 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, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, intraventricular hemorrhage, penetrating injuries, and diffuse axonal injury.

• Scalp injury
  • Often observed with traumatic brain injuries, scalp injury can overlie other intracranial pathology; therefore, it requires 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.
  • Location of the fracture is important because it may cross the path of a major vessel and be associated with an intracranial bleed.
  • Depressed skull fracture is defined as displacement of the inner table of the skull by more than one 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
  • This 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.⁷
• Concussion
  • A transient loss of consciousness, concussion 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
  • Caused by a direct injury to the head, a contusion is an area of bruising or tearing of the brain tissue. The temporal and frontal lobes are the most vulnerable areas because of their anatomical relationship with the bony protuberances of calvaria.
  • The typical presentation is of progressive neurologic deterioration secondary to local cerebral edema, infarcts, and/or late-developing hematomas.
• Epidural hematoma (see images below)
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    Epidural hematoma with midline shift.

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    Epidural hematoma with midline shift.

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    Epidural hematoma with acute neurologic deterioration.

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    Epidural hematoma with acute neurologic deterioration.

  • Developing between the skull and the dura and secondary to the laceration of an artery or vein, epidural hematomas of arterial origin peak in size 6-8 hours after the injury. Epidural hematomas 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 and/or brain stem.
• Subdural hematoma (see image below)
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    Subdural hematoma.

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    Subdural hematoma.

  • Located between the dura and the cortex, subdural hematoma results from tearing of the bridging veins across the dura or laceration of the cortical arteries during 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.
  • Subdural hematoma is also a feature of shaken baby syndrome; the usual presentation is of new-onset seizures, increased head circumference, poorly thriving infant, and tense fontanel. Focal neurologic deficits are usually absent.
• Penetrating injuries: Resulting from various sources, penetrating injuries should be considered neurosurgical emergencies because rapid deterioration and fatal hemorrhages may ensue.
• Intraventricular hemorrhage: This type of hemorrhage is usually the result of minor trauma and resolves spontaneously. Large hemorrhages could 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 (see image below).
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    Intraventricular hemorrhage.

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    Intraventricular hemorrhage.

• Subarachnoid hemorrhage
  • The most common form of hemorrhage associated with head trauma, subarachnoid hemorrhage, 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
  • A result of rapid acceleration-deceleration forces, this type of injury causes disruption of the small axonal pathways.
  • The most commonly affected areas are the basal ganglia, thalamus, deep hemispheric nuclei, and corpus callosum. Their increased vulnerability to shear injuries is attributed to a different momentum of these structures 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 CT scanning is observed. Occasionally, small petechial hemorrhages may be present.
  • Prognosis for full recovery is often poor.

Physical

Head trauma patients often have multiple organ injuries. Assessment of patients with severe head injuries involves a primary 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 by this, preventing secondary brain injury. The secondary survey of patients with head trauma is a detailed examination and assessment of the system with the goal of identifying all traumatic injuries and directing further treatment.

• Airway (primary survey)
  • 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 airway may suggest the presence of upper airway obstruction, especially when a turbulent flow pattern is noted.
• Breathing (primary survey): Apnea and hypoventilation secondary to pulmonary or neurologic causes are common findings in patients with head trauma. When present, they require immediate intervention and endotracheal intubation.
• Circulation (primary survey)
  • Cushing triad, bradycardia, hypertension, or alteration of respiration, if present, is a late manifestation indicative of herniation.
  • When present, hypotension should not solely be attributed to intracranial hemorrhage. 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 highly suspicious of spinal cord injury.
• Neurologic examination (primary survey)
  • Responsiveness is assessed with the alert, verbal, pain, unresponsive (AVPU) system and with the Glasgow Coma Scale (GCS) and its modified Pediatric Glasgow Coma Scale (PGCS). The PGCS was developed for children younger than 5 years of age as a more accurate tool to avoid errors that occur when the GCS is applied to children and infants with limited verbal skills. A PGCS of 13-15 represents minor injury, 8-12 is moderate injury, and less than 8 is severe injury. The GCS and its pediatric modification do not include a pupillary examination. For this reason, pupillary assessment should be performed each time a neurologic assessment is conducted.
  • Pupillary size and response to light may include the following: (1) Ipsilateral pupillary dilatation with no response to direct or consensual stimulation to light is caused by transtentorial herniation and compression of the parasympathetic fibers of cranial nerve III. (2) Bilateral, dilated, and unresponsive pupils constitute an ominous sign indicative of either bilaterally compressed cranial nerve III or global cerebral anoxia and ischemia.
  • Motor ability is assessed by direct observation of spontaneous and symmetric movement, by pressure applied to the nail bed, or by centrally applied painful stimuli such as a sternal rub. Findings may include the following: (1) Decreased spontaneous movement and/or flaccidity may indicate local or spinal cord injury. (2) Decerebrate posturing suggests damage to the midbrain. (3) Decorticate posturing indicates damage to the cerebral cortex, white matter, or basal ganglia.

Table 1. Eye Opening

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Table 2. Best Motor Response

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Table 3. Best Verbal Response

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• Head (secondary survey)
  • Cervical deformity, swelling, pain with palpation, step-off, 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, require 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 (secondary survey)
  • 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 mid or caudal pontine level.
• Neurologic examination (secondary survey)
  • 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 the cranial nerve III is compressed by the temporal lobe, the pupil becomes unresponsive to light stimulus.
  • Pupillary size could suggest the level of the injury. Pinpoint pupils are present in pontine lesions. Pupils that are mid position 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 such as 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.

Causes

Most head injuries occur secondary to motor vehicle accidents, falls, assaults, recreational activities, and child abuse. The percentage of each contributing factor differs between studies, and the distribution varies according to age, group, and sex. A few factors such as seizure disorder, attention deficit disorder, and alcohol and drug use enhance the vulnerability of the child or adolescent to this type of trauma. Infants and young children are more vulnerable to abuse because of their dependency on adults.

• Motor vehicle accidents account for 27-37% of all pediatric head injuries. In most of the cases involving children younger than 15 years, the victim is a pedestrian or a bicyclist; pedestrian accidents in children aged 5-9 years are the second most frequent cause of death. Young adults aged 15-19 years tend to be passengers in the accidents, and alcohol is often a contributing factor.
• Falls are the largest cause of injury in children younger than 4 years, contributing to 24% of all cases of head trauma.
• Recreational activities have a seasonal distribution, with peaks during spring and summer months. They represent 21% of all pediatric brain injuries, with the largest vulnerable group aged 10-14 years.
• Assault represents 10% and firearm-related injuries are 2% of all pediatric brain injuries.
• Child abuse has been identified as the cause of brain injury in 24% of pediatric patients younger than 2 years; it was suspected in another 32%.

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