Head Trauma

Arabela Stock, MD, Consulting Staff, Department of Pediatrics, Divisions of Critical Care and Pulmonology, Florida Pediatric Association
Jagvir Singh, MD, Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge
Updated: Apr 14, 2010

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
o 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.
o Bleeding associated with scalp lacerations could be significant enough to cause hypotension and shock
in a small infant.
o 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
o 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.
o Location of the fracture is important because it may cross the path of a major vessel and be associated
with an intracranial bleed.
o 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
o 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.
o 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.
o 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/commotion
o 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.
o 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.
o 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
o 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.
o The typical presentation is of progressive neurologic deterioration secondary to local cerebral edema,
infarcts, and/or late-developing hematomas.
• Epidural hematoma (see images below)
 Epidural hematoma with midline shift.

Epidural hematoma with acute neurologic deterioration.

o 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.
o 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.
o 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)

Subdural hematoma.

o 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.
 o 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.
o 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).

Intraventricular hemorrhage.

• Subarachnoid hemorrhage
o 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.
o Common symptoms include nausea, vomiting, headache, restlessness, fever, and nuchal rigidity caused
by blood in the subarachnoid space.
• Diffuse axonal injury
o A result of rapid acceleration-deceleration forces, this type of injury causes disruption of the small axonal
pathways.
o 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.
o 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.
o 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)

o 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.
o 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)
o Cushing triad, bradycardia, hypertension, or alteration of respiration, if present, is a late manifestation
indicative of herniation.
o 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)
o 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.
o 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.
o 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

Score >1 Year 0-1 Year

4 Opens eyes spontaneously Opens eyes spontaneously

3 Opens eyes to a verbal command Opens eyes to a shout

2 Opens eyes in response to pain Opens eyes in response to pain

1 No response No response

Table 2. Best Motor Response

Score >1 Year 0-1 Year

6 Obeys command N/A

5 Localizes pain Localizes pain

4 Flexion withdrawal Flexion withdrawal

3 Flexion abnormal (decorticate) Flexion abnormal (decorticate)

2 Extension (decerebrate) Extension (decerebrate)

1 No response No response
Table 3. Best Verbal Response

Score > 5 Years 2-5 Years 0-2 Years

5 Oriented and able to converse Uses appropriate words Cries appropriately

4 Disoriented and able to converse Uses inappropriate words Cries

3 Uses inappropriate words Cries and/or screams Cries and/or screams inappropriately

2 Makes incomprehensible sounds Grunts Grunts

1 No response No response No response

• Head (secondary survey)

o 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.
o Lacerations and depressions, when present, require further exploration for foreign bodies and underlying
bone and dural disruption.
o 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.
o 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.
o 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.
o 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.
o Bulging of the fontanel is a sign of increased intracranial pressure (ICP).
• Respiratory patterns (secondary survey)
o 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.
o Hyperventilation is indicative of damage to the rostral brain stem or tegmentum.
o Apneustic respiration described as prolonged end-expiratory pauses is secondary to damage of mid or
caudal pontine level.
• Neurologic examination (secondary survey)
o 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.
o 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.
o 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.
o Nystagmus, when present, suggests cerebellar or vestibular injury.
o Tonic eye deviation is secondary to cortical lesions, cranial nerve dysfunction, or seizure activity. Retinal
hemorrhages suggest nonaccidental head trauma or sustained increased ICP.
o Papilledema, loss of venous pulsation, is observed with increased ICP.
o Reflexes such as corneal, gag, and oculovestibular and the presence of spontaneous respiratory effort
may help in locating the level of injury.
o Motor and sensory function should be assessed to determine the integrity of the spinal cord.
o Deep tendon reflexes that are symmetric and hyperactive indicate head or spinal cord injury, as
opposed to asymmetric reflexes, which indicate a unilateral lesion.
o 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%.
• In children younger than 3 years, the depth of head injury can be successfully used to determine injury causes and
mechanisms.[8 ]

Differential Diagnoses

Child Abuse & Neglect: Physical Abuse

Workup

Laboratory Studies
The following laboratory studies may be indicated in patients with head trauma:

• A CBC count, including platelets, provides a baseline hematocrit and should be monitored serially, especially when
bleeding is suspected in patients with head trauma.
• Blood chemistry, including an amylase and lipase, provides information regarding other organ injury.
• Coagulation profile, prothrombin time (PT)/activated partial thromboplastin time (aPTT), and fibrinogen should be
obtained in patients with head trauma because they may have an underlying or trauma-triggered coagulopathy.
• Type and cross is useful in anticipation of need for transfusion, especially in patients with multiple traumas.
• ABG provides information regarding oxygenation and ventilation, and results direct further treatment.
• A blood or urine toxicology screen should be obtained in addition to the routine panel, especially in patients who
have altered mental status, seizures, and an unclear history.
• Wound cultures from lacerations or open skull fractures should be taken; findings might help guide further therapy
when infection is suspected.

Imaging Studies
The following imaging studies may be indicated in patients with head trauma:

• CT scanning
o CT scanning of the head remains the most useful imaging study for patients with severe head trauma or
with unstable multiple organ injury.[9,10 ]
o Indications for CT scanning in a patient with a head injury include posttraumatic seizures, amnesia,
progressive headache, unreliable history or examination because of possible alcohol or drug ingestion,
loss of consciousness for longer than 5 minutes, physical signs of basilar skull fracture, repeated
vomiting or vomiting for more than 8 hours after injury, and instability following multiple traumas.
o A noncontrast study is useful in the immediate posttrauma period for rapid diagnosis of intracranial
pathology that requires prompt surgical intervention. A contrast-enhanced study should follow when the
patient is stable and IV contrast is no longer a contraindication.
o CT scanning provides information regarding the following:

The integrity of soft tissue and bone, the size of the fontanel and suture lines, and the
presence of foreign bodies

The appearance of the normal structures, the presence or absence of hemorrhage, and signs
of edema, infarct, or contusion

Mass effect as indicated by midline shift

The appearance of the ventricles and cisterns: Compression of the ventricles is suggestive of
mass effect. Ventricular enlargement may suggest development of hydrocephalus from
intraventricular hemorrhage or blockage by mass effect.

The presence of cerebral edema as indicated by loss of gray-white matter demarcation
• MRI
o MRI is a more sensitive imaging study providing more detailed information regarding the anatomic and
vascular structures, the myelination process, and detection of small hemorrhages in areas that might
escape CT scanning.
o MRI is not practical in emergency situations because the magnetic field precludes the use of monitors
and life-support equipment needed by unstable patients.
o MRI is useful for estimating the initial mechanism and extent of injury and predicting its outcome in the
neurologically stable patient.
• Skull radiography: This is not routinely indicated except in the following situations:
o Patients younger than 1 year
o Loss of consciousness for 3 minutes or longer
o Skull penetration
o Preexistent shunt
o Scalp hematoma and/or depression
o Otorrhea and/or rhinorrhea
o Hemotympanum
o Battle sign
o Raccoon eyes
o Altered mental status
o Focal neurologic examination
• Ultrasonography: This can be performed in neonates and small infants with open fontanel and could provide
information regarding intracranial bleed or obstruction of the ventricular system.
• Xenon CT scanning: This is a modality that may be useful in assessing the impact of medical management on the
cerebral perfusion of a patient with head trauma but is not widely available and requires special equipment.

Other Tests
Patients with head trauma are prone to developing dysrhythmias through a reentry mechanism. ST-T wave abnormalities
and prolonged QT interval could be present on ECG.

Procedures
Other procedures in patients with head trauma include the following:

• External ventricular drains

o The standard for intracranial pressure (ICP) monitoring, they are also used as a therapeutic modality
allowing for cerebrospinal fluid (CSF) removal during episodes of increased ICP or draining
hemorrhage-induced hydrocephalus.
o Placement is indicated for patients with severe head trauma and Glasgow Coma Scale (GCS) less than
8, abnormal CT scan findings on admission, and rapidly deteriorating neurologic examination results or
for patients in whom subsequent rises in the ICP are expected.
• Lumbar drains
o Lumbar drains are used for patients with refractory increased ICP, allowing further CSF removal.
o An external ventricular drain should be placed initially; basilar cisterns must be open on CT scan prior to
placement of a lumbar drain.
• Subarachnoid and epidural monitors
o Subarachnoid and epidural monitors have been used more often in the past, especially when an
intraventricular catheter could not be placed. Their use has decreased since the development of
fiberoptic transducers.
o The theoretical advantages, such as ease of placement, reduced risk of infection, and decreased risk of
hemorrhage should be weighed against the risk of inaccurate readings and inability to remove CSF.
 o Some other disadvantages include zero drift, hysteresis in measurement, and temperature sensitivity.

Treatment

Medical Care
The goal of medical care of patients with head trauma is to recognize and treat life-threatening conditions and to eliminate or
minimize the role of secondary injury. Guidelines for the treatment of patients with head trauma have been established.[11 ]

Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation
secondary to the increased intracranial pressure (ICP); therefore, frequent serial assessments of the neurologic status must
be performed.

The Brain Trauma Foundation has developed guidelines regarding the medical management of patients with severe head
injury. These guidelines suggest that cardiopulmonary resuscitation should be the foundation upon which treatment of
intracranial hypertension must be based. They also state that, in the absence of any obvious signs of increased ICP, no
prophylactic treatment should be initiated because this may directly interfere with the optimal resuscitation process.

• Airway management
o A stable airway should be obtained to provide adequate oxygenation and ventilation. If endotracheal
intubation is required, adequate sedation and paralysis must be assured to avoid further increase in ICP.
Rapid sequence induction and endotracheal intubation are generally recommended. Stabilization of the
cervical spine should be achieved in every patient with severe head trauma. Nasal intubation or
nasogastric tube placement should be avoided, especially for patients in whom basilar skull fracture is
suspected.
o Breathing may be impaired because of neurological or thoracic injuries. Patients with significant head
injury and altered mentation should be supplemented with 100% oxygen and should be supported with
positive pressure ventilation.
o Endotracheal intubation should be performed in cases in which the patient has difficulty maintaining the
airway because of large secretions, poor gag reflex, coma, or the need prolonged ventilatory support.
o Premedication for rapid sequence induction (RSI) includes atropine (0.02 mg/kg for children younger
than 8 y) to blunt the effect of vagal stimulation and decrease the secretions. Lidocaine (1-2 mg/kg) may
be used to decrease airway stimulation during intubation and prevent an increase in ICP. Thiopental (4-
7 mg/kg), etomidate (0.3 mg/kg), or midazolam (0.1 mg/kg) have been successfully used to sedate the
patient for intubation. Ketamine is contraindicated in patients with significant head and eye injuries
because it may increase ICP and intraocular pressure (IOP). Succinylcholine, a depolarizing paralytic
agent, may be used in older children in doses of 1-1.5 mg/kg. It acts rapidly and lasts for a short
duration. Succinylcholine is contraindicated in neuromuscular disorders. Nondepolarizing agents
including rocuronium, pancuronium, and vecuronium are commonly used in young children.
• Cardiovascular management
o Achieving normotension and euvolemia is the goal in cardiovascular management. Cerebral perfusion
pressure (CPP), defined as the mean arterial blood pressure (MAP) minus the ICP (CPP = MAP - ICP),
is the physiologic variable that defines the pressure gradient driving the cerebral blood flow (CBF) and
metabolite delivery; it is therefore closely related to ischemia. Several clinical studies suggest that
maintaining CPP at 70-80 mm Hg may be the critical threshold.
o Adequate volume resuscitation with isotonic solutions should be conducted to maintain adequate filling
pressures, normal cardiac output, and ultimately normotension (MAP >90 mm Hg). More recent adult
and pediatric studies have shown that the use of hypertonic solution in the resuscitation process is
superior to that of lactated Ringer solution or isotonic sodium chloride solution. Patients who have
received hypertonic sodium chloride solution have improved blood pressure response, overall
decreased fluid requirement, fewer interventions in controlling the ICP, fewer complications, and
improved survival.
o Hypertension, if present, could represent a compensatory mechanism in response to the increased ICP;
thus, reflex treatment of it may significantly compromise the cerebral perfusion. When normotension is
desired in the presence of intracranial or intracerebral hemorrhage following surgical evacuation,
calcium channel blockers or beta-blockers are the drugs of choice instead of direct vasodilators to avoid
sudden hypotension.
o Continuous cardiac monitoring should be performed because of the high incidence of ventricular
dysrhythmias present in patients with head trauma and in those in whom cardiac contusion is suspected.
• Increased ICP and cerebral perfusion management
 o Medical management of increased ICP includes elevating the head end of the bed to 30° and
maintaining head and neck in midline position. Sedation and paralysis are used to prevent agitation and
increased muscular activity that may increase the ICP. If neuromuscular blockers are used, monitoring
the ICP and having an electroencephalogram in place is necessary.
o The use of loop or osmotic diuretics (eg, furosemide, mannitol) is directed mostly at decreasing CSF
production and improving cerebral compliance and CBF by decreasing the cerebral blood volume
(CBV). The effect on the reduction of cerebral edema remains unproved. They are also used to maintain
euvolemia.
o Hyperventilation should be used carefully for treating acute ICP elevations. Studies have shown that
prolonged prophylactic use of hyperventilation in head trauma patients is associated with negative
outcome. CBF is known to be diminished in the first 24 hours in patients with severe traumatic brain
injury, with absolute values close to those of ischemia. Hyperventilation decreases CBF. It also
potentially leads to the loss of autoregulation. This may cause further ischemic injury and does not
produce a consistent reduction in ICP. Therefore, mild hyperventilation with PaCO2 level of 30-35 mm
Hg is tolerated better over a longer period with less deleterious effect.
o CSF drainage by extraventricular drains improves the ICP in these patients and provides continuous ICP
monitoring.
o Corticosteroids have no effect in decreasing the cerebral edema associated with head trauma and are
not currently recommended. However, in the presence of head trauma and spinal cord injury, prompt
use of methylprednisolone as a continuous infusion may improve the outcome of spinal injury.
o Barbiturate therapy lowers the ICP and exerts cerebral protection through several mechanisms:
alterations in vascular tone, inhibition of free radical–mediated lipid peroxidation, and suppression of
metabolism. By lowering the metabolic demands, it decreases the CBF and related CBV, providing
beneficial effects on the ICP and global cerebral perfusion. However, several studies have shown that
barbiturate therapy does not improve outcome when compared to mannitol as empiric coma therapy or
when used as prophylactic treatment of ICP.
o The only patients to respond favorably to barbiturate ICP control seem to be those in whom the
cerebrovascular autoregulatory response is preserved. Therefore, their use should be reserved only for
intractable increased ICP when all conventional medical therapies have failed. The goal of barbiturate
therapy should be directed to achieve electroencephalographic burst suppression because maximal
reduction in CBF and metabolism occurs at this level. The main side effect remains hypotension and
cardiovascular toxicity. Hence, when used, invasive hemodynamic monitoring is generally
recommended.
• Bleeding management: Disseminated intravascular coagulopathy is present in one third of head trauma patients
and requires aggressive management and correction with replacement factors in order to decrease the risk of
further intracranial bleeding and allow surgical intervention when necessary.
• Seizure management: Posttraumatic seizures present in 10% of pediatric patients with head trauma may affect the
outcome adversely by increasing the ICP, increasing the metabolic demands of the brain, and causing hypoxia
and/or hypoventilation in a spontaneously breathing patient. Short-acting benzodiazepines (eg, lorazepam,
diazepam) may be used to control the seizure, and phenytoin or phenobarbital should be used for maintenance
anticonvulsant.

Surgical Care
Surgical treatment in patients with head trauma includes the following:

• Surgical decompression is required in the presence of a rapidly expanding epidural or subdural hematoma that
causes an increase in ICP and focal compression.
• The craniotomy and surgical drainage of an epidural hematoma and repair of vessels should be done immediately
if signs of increased ICP, altered mentation, focal neurologic signs, pupillary changes, or a midline shift are
present.
• Conservative management with close monitoring in a pediatric ICU (PICU) is acceptable if no focal neurologic
signs, altered mentation, or pressure effects with midline shift are present and the hematoma is less than 2 cm.
• Patients with subdural hematoma with midline shift or altered mental status should have the hematoma emergently
drained.
• Patients with small subdural hematoma with no midline shift or pressure effects should be managed conservatively
with close monitoring.
• Surgical drainage of subdural hematoma is not required in most cases.
 • Most patients with penetrating injuries require surgical debridement and evacuation of the hematoma and receive
prophylactic antibiotics, as well as anticonvulsants.
• Depressed skull fractures require surgical elevation if the depth of the depression is thicker than the calvaria, if the
depression is greater than 1 cm, and if bony fragments are causing the compression against the brain tissue.

Consultations
The following consultations may be indicated:

• Consult a neurosurgeon.
• A child advocacy team or child protective services should be contacted if child abuse is suspected, the mechanism
of injury is unknown or unexplained, or the history is inconsistent. Guidelines for the evaluation of suspected child
physical abuse have been established.[12 ]

Diet
Aspects of diet in patients with head trauma include the following:

• Nutritional support is directed at avoiding hypoglycemia or hyperglycemia and providing enough calories to prevent
catabolism and a negative nitrogen balance.
• Either the enteral or the parenteral route can be used, depending on the clinical status of the patient.

Activity
Aspects of activity in patients with head trauma include the following:

• Elevation of the head to 30° and maintaining midlin e position continues to be recommended because it improves
the venous drainage and decreases the ICP without affecting the CBF.
• A cervical spine collar should be used until clearance of the spine is achieved.

Medication

Medical therapy is directed at controlling the intracranial pressure (ICP) with sedatives and neuromuscular blockers,
diuretics, lidocaine, and anticonvulsants.

Nondepolarizing neuromuscular blockers

These are used in combination with a sedative as part of the rapid sequence intubation process or to achieve control of the
ICP.

Vecuronium (Norcuron)

Used to facilitate endotracheal intubation and provide neuromuscular relaxation during intubation and mechanical ventilation.
Used as an adjunct to a sedative or hypnotic agent.

Dosing

Adult

0.1 mg/kg/dose IV

Pediatric

Loading dose: 0.08-0.1 mg/kg/dose IV

Maintenance: 0.05-0.1 mg/kg/dose IV q1h prn; alternatively, 0.1 mg/kg/h IV as continuous infusion

Interactions

When vecuronium is used concurrently with inhalational anesthetics, neuromuscular blockade is enhanced; renal or hepatic
failure as well as concomitant administration of steroids may result in prolonged blockade despite withdrawal of the agent
Contraindications

Documented hypersensitivity; myasthenia gravis or related syndromes

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to
fetus

Precautions

Smaller dose should be used in patients with myasthenia gravis, and the effect should be titrated with a peripheral nerve
stimulator

Barbiturates
These are used as an adjunct for intubation in patients with head trauma and in the management of elevated ICP. They may
also be used as anticonvulsants.

Thiopental (Pentothal Sodium)

DOC for endotracheal intubation of patients with head injury. Also decreases the ICP.
Facilitates transmission of impulses from thalamus to cortex of brain, resulting in an imbalance in central inhibitory and
facilitatory mechanisms.

Dosing

Adult

75-250 mg/dose IV, repeat prn

Pediatric

Induction: 4-7 mg/kg/dose IV

Maintenance: 1 mg/kg IV prn
Acute rises in ICP: 1.5-5 mg/kg/dose IV

Interactions

Coadministration with CNS depressants, salicylates, and sulfisoxazole increases toxicity

Contraindications

Documented hypersensitivity; porphyria; severe hypovolemia; unstable hemodynamics; lack of familiarity with drug; inability
to manage airway

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to
fetus

Precautions

May cause myocardial depression, decreased cardiac output, and hypotension; caution in hepatic or renal insufficiency,
asthma, severe cardiovascular disease, unstable aneurysm, hypotension, and laryngospasm or bronchospasm

Pentobarbital (Nembutal)

Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties. May be used in high dosage to induce
barbiturate coma for treatment of refractory increased ICP.

Dosing
Adult

Pediatric

Pentobarbital coma:
Loading dose: 10-15 mg/kg/dose IV over 1-2 h
Maintenance: 1 mg/kg/h IV; may increase to 2-3 mg/kg/h until burst suppression is shown on EEG

Interactions

Concomitant use with alcohol may produce additive CNS effects and fatality; chloramphenicol may inhibit pentobarbital
metabolism; pentobarbital may enhance chloramphenicol metabolism; MAOIs may enhance sedative effects of barbiturates;
valproic acid appears to decrease barbiturate metabolism, increasing toxicity; barbiturates can decrease effects of
anticoagulants (patients may require dosage adjustments if barbiturates are added to or withdrawn from the regimen);
barbiturates may decrease corticosteroid and digitoxin effects through induction of hepatic microsomal enzymes, which
increase metabolism; barbiturates decrease theophylline levels and may decrease effects; pentobarbital may decrease
verapamil bioavailability

Contraindications

Documented hypersensitivity; liver failure

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Rapid and prolonged IV administration may cause hypotension, respiratory depression, apnea, bronchospasm, and
laryngospasm; caution in hypovolemic shock, respiratory dysfunction, renal dysfunction, and congestive heart failure

Phenobarbital (Luminal, Solfoton)

Used for seizure control in patients with head trauma.

Dosing

Adult

300-800 mg, followed by 120-240 mg/dose at 20-min intervals until seizures are controlled or total dose of 1-2 g is
administered

Pediatric

Loading dose: 15-20 mg/kg/dose IV in single or divided doses

Maintenance: 5 mg/kg/d PO/IV divided bid

Interactions

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole,
and anticoagulants (patients stabilized with anticoagulants may require dosage adjustments if medications are added to or
withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol,
valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects

Contraindications

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions
Monitor respiratory and cardiac function during loading dose; may cause drowsiness and impaired ability to perform tasks
requiring alertness; caution in myasthenia gravis and myxedema

Benzodiazepines
These agents may be used to obtain immediate control of seizure activity or as adjuncts to narcotics and neuromuscular
blockers to control the ICP. Prolonged use of these drugs may alter neurologic examination findings.

Midazolam (Versed)

Short-acting benzodiazepine with rapid onset of action. Useful in treating increased ICP.

Dosing

Adult

Pediatric

0.05-0.1 mg/kg/dose IV; dose may be repeated prn; not to exceed a cumulative dose of 6 mg for infants and 10 mg for
children

Interactions

Sedative effects of midazolam may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative
effects of midazolam because of decreased clearance

Contraindications

Documented hypersensitivity; uncontrolled pain; preexisting hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Careful monitoring of cardiorespiratory status during administration; caution in congestive heart failure, pulmonary disease,
renal impairment, and hepatic failure

Lorazepam (Ativan)

Long-acting benzodiazepine, used as anticonvulsant for immediate control of seizure activity.

Dosing

Adult

4 mg/dose IV slowly over 2-5 min and repeat in 10-15 min prn; not to exceed a cumulative dose of 8 mg/12 h

Pediatric

0.05-0.1 mg/kg/dose IV over 2-5 min; may be repeated in 10-15 min

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and
MAOIs

Contraindications

Documented hypersensitivity; CNS depression; hypotension; narrow-angle glaucoma; uncontrolled pain

Precautions

Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Cardiorespiratory monitoring during administration is required; long-term use requires liver function and CBC monitoring;
caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Anticonvulsants
These agents are recommended as a prophylactic measure for patients at increased risk for seizure activity following head
trauma. No proof exists of a beneficial effect in seizure prevention after 1 week following head trauma. They are also used
for immediate control of seizures.

Phenytoin (Dilantin)

May act in motor cortex where may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase
of grand mal seizures may also be inhibited. Is preferred to phenobarbital to control seizures because it does not cause as
much CNS depression.

Dosing

Adult

Loading dose for status epilepticus: 15-20 mg/kg PO/IV once or in divided doses, followed by 100-150 mg/dose at 30-min
intervals
Initial maintenance dose (administered 12 h after loading dose): 100 mg (if administering oral susp, use dose of 125 mg)
PO/IV tid
Maintenance: 300-400 mg/d PO/IV divided tid or qd/bid if using ER; increase to 600 mg/d (625 mg/d for PO susp) may be
necessary; not to exceed 1500 mg/24 h
Rate of IV infusion must not exceed 50 mg/min to avoid hypotension and arrhythmias

Pediatric

Loading dose: 15-20 mg/kg PO/IV once or in divided doses

Initial maintenance dose (administered 12 h after loading dose): 5 mg/kg/d PO/IV divided bid/tid
Maintenance: 4-8 mg/kg PO/IV divided bid/tid; children > 6 y may require minimum adult dose (300 mg/d); not to exceed 300
mg/d

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole,

phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim,
and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with
barbiturates, diazoxide, ethanol (long-term ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and
sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline,
estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone,
mexiletine, PO contraceptives, and valproic acid; continuous tube feeding decreases the bioavailability of phenytoin

Contraindications

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes
syndrome

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalyses when therapy is initiated; discontinue use if a rash appears and do not resume use if
rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening;
caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction
occurs
Diuretics
These may have a beneficial effect in lowering the ICP by decreasing the CSF production, excreting more water over solute
and decreasing blood viscosity, with subsequent improvement of CBF.

Furosemide (Lasix)

A loop diuretic helpful in decreasing the ICP via 2 mechanisms. One influences CSF formation by affecting the sodium-water
movement across the blood-brain barrier; the other mechanism is the preferential excretion of water over solute in the distal
tubule.
Mostly useful when used in combination with mannitol, especially when the latter is administered 15 min before furosemide.

Dosing

Adult

20-80 mg/d IV/IM; may increase dose; not to exceed 600 mg/d

Pediatric

1-2 mg/kg/dose IV q6-12h

Interactions

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and
antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of
aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be
enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when
taken concurrently with this medication

Contraindications

Documented hypersensitivity; hepatic coma, anuria, and severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to
fetus

Precautions

Avoid hypotension due to large-volume depletion; requires serum electrolyte monitoring

Mannitol (Osmitrol)

Osmotic diuretic, which lowers the blood viscosity and produces cerebral vasoconstriction with normal CBF. ICP decrease
occurs subsequent to a decrease in CBV.

Dosing

Adult

1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

0.5-1 g/kg/dose IV initial dose

0.25-0.5 g/kg/dose IV q4-6h

Interactions

May decrease serum lithium levels

Contraindications
Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active
intracranial bleeding; progressive heart failure

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to
fetus

Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol because a sudden increase in extracellular
fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood is administered simultaneously, add at least 20
mEq of sodium chloride to each liter of mannitol solution; do not administer electrolyte-free mannitol solutions with blood; If
used every 4-6 h, serum osmolarity should be monitored and dose held if osmolarity exceeds 320 mOsm/kg

Anesthetics
These agents may be used to blunt ICP elevation during endotracheal intubation process or during airway manipulation such
as suctioning.

Lidocaine 1% (Xylocaine)

Used with good results in controlling the ICP in patients with head trauma.

Dosing

Adult

Pediatric

1-1.5 mg/kg/dose IV

Interactions

Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and
tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Contraindications

Documented hypersensitivity; Adams-Stokes syndrome (avoid); Wolf-Parkinson-White syndrome (avoid); severe sinoatrial,
(AV), or intraventricular block if artificial pacemaker not in place (avoid)

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may
increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, heart
block, and AV conduction abnormalities

Follow-up

Further Inpatient Care

Criteria for hospitalization in patients with head trauma should be directed on an individual basis. Usual indications for
admission include the following:

• Documented loss of consciousness longer than 5 minutes

• Coma, altered mental status, or seizures
• Focal neurologic deficit
• Protracted vomiting, severe and persistent headache
 • Intoxication with substances such as alcohol or drugs that interfere with the neurologic examination
• Suspected child abuse
• Unreliable caregiver
• Underlying pathology such as coagulopathy or hydrocephalus

ICU admission should be based upon the severity of the trauma and associated injuries.

Further Outpatient Care

Patients with minor head injury (ie, Pediatric Glasgow Coma Scale [PGCS] of 14-15) can be discharged with observation
instructions in the care of a reliable adult.

Patients who sustained loss of consciousness less than 5 minutes and have normal findings on neurologic examination, no
symptoms of increased intracranial pressure (ICP) such as vomiting or headache, no signs of basilar skull fracture, and
normal findings on CT scanning or skull radiography can also be discharged with close observation by a reliable adult.

Inpatient & Outpatient Medications

Tetanus immunization status should be checked and updated for any patient, especially when lacerations or contaminated
wounds are present. Anticonvulsants may be needed to control or provide prophylaxis for seizure activity. Nonsteroidal anti-
inflammatory drugs (NSAIDs) may be used for minor pain control. Beta-blockers can be prescribed for patients with trauma-
induced migraines.

Transfer
Transfer may be required to hospitals where consultation with a neurosurgeon is available, especially when surgical
intervention is necessary.

Deterrence/Prevention
Passenger seat belts and airbags may be useful in preventing head injury. Helmet use by children and adolescents during
certain sport activities may reduce head trauma risk. Education regarding avoidance of alcohol and drug use may also help
in decreasing the incidence of alcohol-related and drug-related accidents. Children younger than 12 years should ride in the
back seat of the car away from the airbag.

Complications
Complications in head trauma may include the following:

• Seizures are more commonly observed with contusions (subdural hematoma more so than epidural hematoma),
depressed skull fracture, and severe head injury (PGCS of 3-5).
• Leptomeningeal cyst or growing fracture represents extrusion of leptomeninges and brain tissue through a dural
defect.
• Meningitis could 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 following 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 following 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 following 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 cerebrospinal fluid (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
pulmonary bed.
• Pulmonary infections are often present in patients with head trauma because of either an initial aspiration process
or prolonged mechanical ventilation.
Prognosis
The prognosis is as follows:

• Patients with severe head trauma and a PGCS of 3-5 have a mortality rate of 6-35%; the rate increases to 50-60%
for those with a PGCS of 3.
• Of those with a PGCS of 3-5 who survive, 90% require rehabilitation following hospital discharge and most of them
eventually return to school.
• Patients with a PGCS of 3 have poor neurologic outcomes.
• Patients with a PGCS of 6-8 are most likely to regain consciousness within 3 weeks, but one third are left with
focal neurologic deficits and learning difficulties, especially when coma persists beyond 3 weeks.[13 ]

Patient Education
The following patient education is indicated:

• Refer children for early intervention and rehabilitation services.

• Refer the family and the child for psychosocial counseling.
• Children should be referred for neuropsychiatric testing, especially when learning difficulties are present.
• For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center, Back, Neck, and
Head Injury Center, and Eye and Vision Center. Also, see eMedicine's patient education articles Concussion,
Bicycle and Motorcycle Helmets, Black Eye, and Child Passenger Safety.

Miscellaneous

Medicolegal Pitfalls
The following pitfalls are associated with head trauma:

• Failure to recognize or suspect child abuse

• Failure to recognize associated life-threatening injuries
• Failure to recognize severe head injury that may initially seem less serious in a patient with multiple traumas (An
example is the Waddell triad for a child pedestrian hit by motor vehicle, involving chest-abdomen trauma, leg
injury, and a countercoup head injury.)

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Keywords

head trauma, head injury, brain trauma, brain injury, primary head trauma, secondary head trauma, intracranial pressure,
traumatic brain injury, scalp injury, skull fracture, treatment, diagnosis