Pediatric Head Trauma

Updated: Apr 12, 2023
Author: Michael J Verive, MD, FAAP; Chief Editor: Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA 


Practice Essentials

Head trauma accounts for 80% or more of the traumatic injuries leading to death in US children older than 1 year. Most pediatric head trauma occurs secondary to motor vehicle accidents, falls, assaults, recreational activities, and child abuse. See the image below.

Pediatric Head Trauma. Epidural hematoma with acut Pediatric Head Trauma. Epidural hematoma with acute neurologic deterioration.

See Pediatric Concussion and Other Traumatic Brain Injuries, a Critical Images slideshow, to help identify the signs and symptoms of traumatic brain injury (TBI), determine the type and severity of injury, and initiate appropriate treatment.

Signs and symptoms

Patients with head trauma may experience one or a combination of primary injuries, including the following:

  • Scalp injury

  • Skull fracture (eg, basilar skull fracture)

  • Concussion

  • Contusion

  • Intracranial and/or subarachnoid hemorrhage

  • Epidural and/or subdural hematoma

  • Intraventricular hemorrhage (see the image below)

    Pediatric Head Trauma. Intraventricular hemorrhage Pediatric Head Trauma. Intraventricular hemorrhage.
  • Penetrating injuries

  • Diffuse axonal injury

Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation secondary to increased intracranial pressure.

See Presentation for more detail.


Patients with head trauma 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—thereby preventing secondary brain injury—and includes evaluation of the following:

  • Airway (eg, presence of foreign bodies, facial lacerations, bone instability, tracheal deviation, circumoral cyanosis), breathing (eg, apnea, hypoventilation), and circulatory status (eg, Cushing triad of bradycardia, hypertension, altered respiration)

  • Neurologic status (eg, alert, verbal, pain, unresponsive [AVPU] system; pediatric Glasgow Coma Scale [GCS])

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—and includes evaluation of the following:

  • Head (eg, cervical deformity, step-off, malalignment; lacerations; depressions; Battle sign or retroauricular/mastoid ecchymosis; raccoon eyes/periorbital ecchymosis; hemotympanum; cerebrospinal fluid otorrhea and rhinorrhea; bulging of fontanel)

  • Respiratory patterns (eg, apnea, Cheyne-Stokes, hyperventilation, apneustic respiration)

  • Neurologic status (eg, dilated/pinpoint pupil(s), Horner syndrome, eye deviation, retinal hemorrhage, motor/sensory dysfunction)


The following laboratory studies are used to assess children with head trauma:

  • Serial complete blood counts

  • Blood chemistries (eg, amylase and lipase levels)

  • Coagulation profile (including prothrombin time, international normalized ratio, activated partial thromboplastin time, fibrinogen level)

  • Type and crossmatch

  • Arterial blood gas

  • Blood or urine toxicology screening

Imaging studies

Radiologic studies used to evaluate pediatric head injuries include the following:

  • Computed tomography (CT) scanning of the head: Most useful imaging study for patients with severe head trauma or unstable multiple organ injury[1]

  • Magnetic resonance imaging (MRI) of the brain: More sensitive than CT scanning for intracranial evaluation of TBIs

  • Ultrasonography: For neonates and small infants with open fontanels; focused point-of-care ultrasonography has a high specificity for pediatric skull fractures[2]


Monitoring of intracranial pressure is indicated in the following patients:

  • Salvageable patients with severe TBI and an abnormal CT scan

  • Those with severe TBI and a normal CT scan in the presence of unilateral/bilateral motor posturing or a systolic blood pressure below the fifth percentile for age

  • Conscious patients with CT findings suggesting risk of neurologic deterioration

  • Inability to perform serial neurologic exams due to pharmacologic sedation/anesthesia

Removal of cerebrospinal fluid via external ventricular drains or lumbar drains may be necessary in patients with increased intracranial pressure.

See Workup for more detail.


The goal of medical care of pediatric patients with head trauma is to recognize and treat life-threatening conditions and to eliminate or minimize the role of secondary injury. Consult with a neurosurgeon. If child abuse is suspected, the mechanism of injury is unknown or unexplained, or the history is inconsistent, contact a child advocacy team or child protective services.

Resuscitation and treatment of life-threatening conditions

Treatment of children with severe head injury includes management of the following:

  • Airway

  • Cardiovascular and circulatory status

  • Intracranial pressure and cerebral perfusion

  • Bleeding

  • Seizure(s)

  • Temperature

  • Analgesia, sedation, and neuromuscular blockade


Surgical intervention in pediatric patients with head trauma may be required and includes the following:

  • Surgical decompression

  • Craniotomy and surgical drainage

  • Surgical debridement and evacuation

  • Surgical elevation

  • Decompressive craniotomy with duraplasty


Pharmacologic therapy in patients with head trauma is directed at controlling intracranial pressure through the administration of sedatives and neuromuscular blockers, diuretics, and anticonvulsants.

The following medications are used in the management of pediatric head trauma:

  • Nondepolarizing neuromuscular blockers (eg, vecuronium)

  • Barbiturate anticonvulsants (eg, thiopental, pentobarbital, phenobarbital)

  • Benzodiazepine anxiolytics (eg, midazolam, lorazepam)

  • Diuretics (eg, furosemide, mannitol)

  • Anesthetics (eg, fentanyl, propofol)

  • Anticonvulsants (eg, phenytoin, fosphenytoin)

See Treatment and Medication for more detail.


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 these 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.[3]

Most head injuries in children 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.

Patients with head trauma may experience one or a combination of primary injuries, including 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.

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. Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation secondary to increased intracranial pressure (ICP).

Brain Trauma Foundation guidelines suggest that cardiopulmonary resuscitation should be the foundation upon which treatment of intracranial hypertension must be based and that in the absence of any obvious signs of increased ICP, no prophylactic treatment should be initiated; if instituted, prophylactic treatment has the potential to interfere with optimal resuscitation.


The anatomic characteristics of the child's brain render it more susceptible than the adult brain to certain types of injuries following head trauma.[4] The head is larger in proportion to the body surface area, and stability is dependent on the ligamentous rather than bony structures. Due to their smaller stature, pediatric pedestrians are at significant risk of direct brain injury from automobile crashes, as their heads may be the site of initial impact and will absorb a higher percentage of the forces applied. Although infants and young children may tolerate intracranial pressure (ICP) increases better because of open sutures, the presence of open fontanelles and sutures does not preclude the presence of elevated intracranial pressure; ICP monitoring may be important in this population, as well as in older patients with traumatic brain injury.


Both primary and secondary injuries are described in pediatric patients with head trauma, and the presence of these injuries affects outcome.

In a prospective, multicenter study of 43,399 pediatric patients treated for head injuries in US emergency rooms, Quayle et al found that the most common mechanisms of injury in the overall population were the following[5] :

  • Falls from any distance (27%)

  • Falls while standing, walking, or running (11%)

  • Collisions with a stationary object when walking or running (6%)

  • Motor vehicle crashes (9%)

  • Bicycle crashes (4%)

Falls were the most frequent cause of traumatic brain injury (TBI) for children under age 12, whereas assaults, motor vehicle accidents, and sports activities were the most frequent cause of injuries for adolescents. Overall, 98% of head injuries were classified as mild.

A large proportion of injuries caused by motor vehicle or bicycle crashes occurred when the child was not using a seat belt (36%) or a helmet (72%).[5] Among the 16% of patients in a motor vehicle crash who were diagnosed with a TBI, 52% were not using a seat belt. Of the 4% of bicycle crash patients with a TBI, 93% were not wearing a helmet.

Among the 37% of children who underwent cranial computed tomography (CT) scanning, TBIs were identified in 7%, and 3% had skull fractures without intracranial findings. The most common injury identified on CT scan was subdural hematoma, followed by subarachnoid hemorrhage and cerebral contusion.

Primary injuries

The primary injury occurs at the time of impact, either via direct injury to the brain parenchyma or via injury to the long white-matter tracts through acceleration-deceleration forces.[6]

Direct injury to the brain parenchyma occurs as the brain makes forceful contact with the bony protuberances of the calvaria or is penetrated by bony fragments or a foreign body. Impact on the brain at the time of the insult results in a coup injury, whereas contrecoup injury occurs as the brain is forced against the bony protuberances opposite the point of the impact.

Intracranial hemorrhage (ICH) may also result from shearing or laceration of vascular structures. Although exceptions occur, epidural hematomas are usually secondary to arterial injury, while subdural hematomas are usually secondary to venous injury. Because of the higher arterial blood pressure, epidural hematomas may enlarge very rapidly, while subdural hematomas generally develop more gradually. However, subdural hematomas are typically associated with underlying direct tissue injury, which is less common with epidural hematomas.

Acceleration-deceleration forces cause shearing of the long white-matter tracts, leading to axonal disruption and secondary cell death.

Secondary injuries

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.[6]

The systemic events are hypotension, hypoxia, and hypercapnia and may occur either as a direct result of primary injury to the central nervous system (CNS) or as a consequence of associated injuries in a person with multiple traumas. Because of many factors (eg, higher brain metabolic activity, limited substrate availability, delay in seeking care), secondary brain injury commonly leads to greater morbidity than primary injury, while the reverse is true in adults.

The intracranial events are a series of inflammatory changes and pathophysiologic perturbations that occur immediately after the primary injury and continue over time. The nature of these events is poorly understood but has received greater attention due to the impact of secondary injury in pediatric traumatic brain injury.

Inflammatory changes are the result of a cascade of biomolecular alterations 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 negative outcomes. These pathophysiologic events include cerebral edema, increased ICP, hyperemia, and ischemia. Apoptotic neuronal cell death is more prevalent than necrotic neuronal cell death in pediatric patients, likely secondary to the role that apoptosis plays in the development of the pediatric brain.

Altered autoregulation of cerebral blood flow

Because the brain has minimal ability to store energy, it depends primarily on aerobic metabolism. The delivery of oxygen and metabolic substrate to the brain is maintained by a constant supply of blood, referred to as cerebral blood flow (CBF). CBF, defined as the amount of blood in transit through the brain at any given point in time, is estimated to be 50 mL/100 g/min in a healthy adult and is known to be much higher in children. However, the minimum amount necessary to prevent ischemic injury remains unknown.

CBF is influenced by mean arterial blood pressure (MAP), ICP, blood viscosity, metabolic products, and brain vessel diameter. CBF should not be confused with cerebral blood volume (CBV), which represents the amount of blood present in the brain vasculature. Because brain tissue and CSF volumes remain relatively stable, acute changes in CBV are mostly responsible for acute changes in ICP. CBV depends primarily on the diameter of intracranial vessels, so therapeutic interventions to reduce intracranial blood vessel diameter (vasoconstriction) are the most effective methods to acutely reduce elevated ICP. Hyperventilation, in the acute phase, decreases ICP by decreasing CBV via alkalosis-induced cerebral vasoconstriction.

The brain maintains constant blood flow through a mechanism known as autoregulation. This process occurs over a wide range of blood pressures through changes in cerebral resistance in response to fluctuations in MAP pressure. At a MAP of 60-150 mm Hg, CBF is maintained. At 60 mm Hg, the cerebral vasculature is maximally dilated. At 150 mm Hg, it is maximally constricted. (These are adult ranges; pediatric ranges are unknown but are likely age-dependent.) Fluctuations of MAP beyond either end of 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; they may be divided into the following categories:

  • Metabolic products

  • Arterial blood gas content

  • Myogenic factors

  • Neurogenic factors

  • Endothelium-dependent factors

The effects of these mechanisms are 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 thought to involve vasodilators released from neurons. Several factors have been implicated, such as adenosine and free radicals. Pathophysiologic states that are known to increase metabolic activity (eg, fever and seizure 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 result in dose-dependent vasoconstriction, although to a less pronounced degree than hypoxia-induced vasodilation.

Hypercarbia increases CBF up to 350% of normal, while 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. However, renal compensation for respiratory alkalosis causes tissue pH levels to normalize, restoring CBF, which limits the effectiveness of prolonged hyperventilation for control of elevated ICP.

The myogenic mechanism was long considered to be the most important in the autoregulation process. Changes in the actin-myosin complex were thought to lead to rapid changes in the vasculature diameter, thus affecting the CBF. It has now been shown that changes in the actin-myosin complex mostly cause dampening of arterial pulsation and 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 toward higher pressures, whereas sympathetic blockade shifts it downward.

Studies have identified nitric oxide (NO) as one of the factors affecting cerebral autoregulation; it does so by producing relaxation of cerebral vessels. NO is present in several conditions, such as ischemia, hypoxia, and stroke. It is generated by different cells at rest but also under direct stimulation by factors such as cytokines.

Alterations in CBF during periods of hyperoxia, hypoxia, hypercarbia, and hypocarbia occur due to changes in local NO production. Vasodilation from somatosensory stimulation occurs through changes in neurogenic NO production, and impaired vasodilation associated with endothelial dysfunction appears to be due (at least in part) to the production of reactive oxygen species and reduced NO bioavailability.[7]

TBI may lead to loss of autoregulation through alteration of any of these mechanisms. One study found that mild TBIs are more likely than orthopedic injuries to cause transient or persistent increases in postconcussive symptoms during the first year after injury.[8] These mechanisms represent the foundation on which the medical management of increased ICP and cerebral perfusion pressure (CPP) is based in patients with TBI.


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 (eg, seizure disorder, attention deficit disorder, and alcohol and drug use) are known to enhance the vulnerability of the child or adolescent with respect to this type of trauma. Infants and young children are more vulnerable to abuse because of their dependency on adults and their inability to defend themselves.

Motor vehicle accidents account for 27-37% of all pediatric head injuries. In most 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 involved in motor vehicle accidents, and alcohol is often a contributing factor.

Falls are the most common cause of injury and the leading cause of traumatic brain injury in children aged 0-4 years.[9]

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 accounts for 10% of all pediatric brain injuries, and firearm-related injuries account for 2%. 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%. The risk of abusive head trauma (AHT) appears to decrease with increasing maternal age and increasing gestational age at birth.[10] Factors that appear to associated with AHT include lack of or poor prenatal care, maternal single status, documented social concerns, as well as missing maternal prenatal data for antenatal care, partner status, social concerns, and substance abuse.[10]

In children younger than 3 years, the depth of head injury can be successfully used to determine injury causes and mechanisms.[11]


In the United States, the estimated annual incidence of pediatric head injury is approximately 200 per 100,000 population. This number includes all head injuries that result in hospitalization, death, or both in persons aged 0-19 years.

Age-, sex-, and race-related demographics

The distribution of head trauma is relatively stable throughout childhood. An increase in the incidence of head trauma was identified in two 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 also have an elevated incidence of head trauma, which is attributed to falls and child abuse.[12]

Males are twice as likely to sustain head injuries as females and have four times the risk of fatal trauma. Black adolescent males account for most of the firearms-related CNS injuries in the pediatric population.


The overall outcome for children with head injuries is better than that for adults with the same injury scores.[13, 14, 15] Time to maximum recovery after injury is longer in children (months to years) than in adults (typically about 6 months). Patients with multiple organ injuries, including head trauma, generally have a far worse outcome than those with head injury alone.

Outcome assessment based on the Pediatric Glasgow Coma Scale (PGCS) can be used as an early predictor, but this scale has limitations regarding long-term outcome. Mechanism of injury appears to be a significant predictor of clinical and functional outcomes at discharge for equivalently injured patients.[16]

According to the National Center for Health Statistics, mortality from head trauma is 29% in the pediatric population.[17] 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.

Patients with severe head trauma and a PGCS score of 3-5 have a mortality of 6-35%; this figure increases to 50-60% for those with a PGCS score of 3. Of those with a PGCS score of 3-5 who survive, 90% require rehabilitation after hospital discharge, and most of them eventually return to school.

Risk factors associated with increased mortality for children suffering from abusive, non-accidental head trauma include, not surprisingly, low GCS (3 or 4-5), retinal hemorrhage, intraparenchymal hemorrhage and cerebral edema. Surprisingly, presence of a chronic subdural hematoma is associated with survival.[18]

Short-term memory problems and delayed response times are reported in 10-20% of children with moderate-to-severe head injury (PGCS score, 6-8), especially if the coma lasts longer than 3 weeks. Patients with a PGCS score 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.[19]

More than half of children with a PGCS score of 3-5 have permanent neurologic deficits. Patients with a PGCS score of 3 have particularly poor neurologic outcomes.

A study that primarily investigated adult TBI patients revealed that diabetic TBI victims had an unfavorable mortality odds ratio (1.5), with the trend being worse for insulin-dependent diabetes patients than for noninsulin-dependent ones.[20] The study raises the question of whether insulin deficiency may contribute to TBI mortality, either along with or independent of glucose changes after TBI.

At the very least, this study points out that meticulous insulin and glucose management of diabetic TBI patients, matching insulin to carbohydrate administration as needed, may help reduce TBI mortality in this population. Care must still be taken not to induce hypoglycemic events in these critically ill patients while trying to avoid potentially harmful insulin deficiency.[20]


Long-term complications of head injury are common in children, and they are related to both primary and secondary injuries.[21, 22]

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,[23] penetrating injury, or other injuries that cause disruption of the dura mater.

Cranial nerve injury may develop secondary to basilar skull fracture, mass effect, or herniation. 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. Postconcussion symptoms may be more prevalent that previously reported, involve neurologic and nonneurologic components, and require attention to physical, cognitive, and emotional symptoms (especially for patients with persistent symptoms).[24]

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 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.

Patient Education

Children should be referred for early intervention and rehabilitation services. Both children and their families should be referred for psychosocial counseling. Children should be referred for neuropsychiatric testing, especially when learning difficulties are present.

Unfortunately, postnatal parental intervention does not appear to reduce the incidence of abusive head trauma (AHT) in infants and young children. In a study that compared AHT hospitalization rates in Pennsylvania before and during such intervention to that of five other states without universal parental AHT education over the same period (2003-2013), Pennsylvania incidence rate ratios for AHT hospitalizations increased 2.5% per 100,000 children aged 0-23 months, a nonsignificant difference from the 0.4% aggregate changes seen in the other five states.[25] The interventions included a brochure, an 8-minute video regarding infant crying and AHT, questions/answers with a nurse, and a signed participation commitment statement affirmation; however, only a little over one fifth (20.6%) of parents saw the brochure and video, and 5.7% had exposure to the entire intervention—out of 16,111 parents who completed the postnatal survey and 1,180,291 parents who signed the commitment statement. Of the 143 respondents who subsequently completed the 7-month survey, over three quarters (76.2%) self-reported gains in parental knowledge.[25]




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 (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 can 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 often crosses the suture lines, whereas cephalohematoma involves sub-periosteal 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 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

Basilar skull fracture is present in 6-14% of pediatric patients with head trauma[23] 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.[26]


Concussion is a transient alteration of consciousness and occurs as the result of head trauma. Patients often have normal findings on neurologic examination and computed tomography scanning; 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.


In 2014, comprehensive guidelines for the assessment and management of pediatric concussion were developed by an expert panel assembled by the Children's Hospital of Eastern Ontario and the Ontario Neurotrauma Foundation.[27] The guidelines include evidence-based recommendations for health care professionals, schools and/or community sports organizations, and parents and/or caregivers.

The guidelines were updated in 2019 and include tools and instructions for all user levels, such as an algorithm to help guide assessment in the emergency room, a pocket tool for recognizing concussion on the sidelines at games, examples of discharge handouts for patients and families, and an example of a policy statement on pediatric concussion for use by school boards.[27, 28, 29]


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.

Pediatric Head Trauma. Epidural hematoma with midl Pediatric Head Trauma. Epidural hematoma with midline shift.

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).

Pediatric Head Trauma. Epidural hematoma with acut Pediatric Head Trauma. Epidural hematoma with acute neurologic deterioration.

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.

Pediatric Head Trauma. Subdural hematoma. Pediatric Head Trauma. Subdural hematoma.

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.

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.

Pediatric Head Trauma. Intraventricular hemorrhage Pediatric Head Trauma. Intraventricular hemorrhage.

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. Although common, subarachnoid hemorrhages are only infrequently the cause of acute neurological deterioration in pediatric head trauma, and they rarely require neurosurgical intervention unless associated with vascular malformations or injuries.[30]

Penetrating injuries

Penetrating injuries derive from a variety of sources, and they make up only a small proportion of pediatric traumatic head injury cases. They should be considered neurosurgical emergencies because rapid deterioration and fatal hemorrhages may ensue. See Penetrating Head Trauma for a more thorough discussion on penetrating head injuries.

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.

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, especially in patients with higher diffuse axonal injury scores.[31]

Physical Examination

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 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.


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, taking care to maintain cervical spine stabilization in patients with known or suspected cervical spine injury.


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 intracranial hemorrhage (ICH). Several other causes may lead to this finding, including but not limited to, internal hemorrhages, spinal cord injury, cardiac contusion, chest trauma with pneumothorax and/or hemothorax, drug or alcohol effect, 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)


≥1 Year

0-1 Year


Opens eyes spontaneously

Opens eyes spontaneously


Opens eyes to a verbal command

Opens eyes to a shout


Opens eyes in response to pain

Opens eyes in response to pain


No response

No response

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


≥1 Year

0-1 Year


Obeys command



Localizes pain

Localizes pain


Flexion withdrawal

Flexion withdrawal


Flexion abnormal (decorticate)

Flexion abnormal (decorticate)


Extension (decerebrate)

Extension (decerebrate)


No response

No response

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


> 5 Years

2-5 Years

0-2 Years


Oriented and able to converse

Uses appropriate words

Cries appropriately


Disoriented and able to converse

Uses inappropriate words



Uses inappropriate words

Cries and/or screams

Cries and/or screams inappropriately


Makes incomprehensible sounds




No response

No response

No response

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, taking care not to misinterpret spinal reflexes as appropriate responses). 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


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, 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 the 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.

Cerebrospinal fluid (CSF) otorrhea and rhinorrhea may be 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.



Diagnostic Considerations

The following diagnostic pitfalls are associated with head trauma:

  • Failure to recognize or suspect child abuse: One study suggests that certain combinations of clinical features may be suggestive of abusive head trauma, though a larger-scale prospective study would be required to develop a more refined tool[32]

  • Failure to recognize associated life-threatening injuries

  • Failure to recognize severe head injury that may initially seem less serious in a patient with multiple trauma: An example is the Waddell triad for a child pedestrian hit by a motor vehicle, which involves chest-abdomen trauma, leg injury, and a countercoup head injury

Differential Diagnoses



Laboratory Studies

A complete blood count (CBC) should be monitored serially, especially when bleeding is suspected in patients with head trauma. Blood chemistry studies, including amylase and lipase levels, provide information regarding other organ injuries.

A coagulation profile; a prothrombin time (PT), with international normalized ratio (INR); activated partial thromboplastin time (aPTT); and a fibrinogen level should be obtained in patients with head trauma because these patients may have an underlying or trauma-triggered coagulopathy.

An admission INR measurement of 1.3 or higher appears to be a strong independent prognostic factor for death in children who have suffered abusive head trauma.[33] A retrospective study (2005-2014) of 101 level 1 pediatric (age, 0-17 years) trauma patients with abusive head trauma noted an overall mortality of 24.8%, of which 60% were in children with an INR of 1.3 or greater. Elevated INR was also associated with more early packed RBC transfusions and neurosurgical intervention.[33]

Typing and cross-matching of blood is useful in anticipation of a possible need for transfusion, especially in patients with multiple trauma.

Arterial blood gas values provide information regarding oxygenation, ventilation, and acid-base status and can be used to help 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.

S100β and Glial fibrillary acidic protein

Serum levels of S100β (S100β) protein appear to be a useful adjunct diagnostic tool for detecting intracranial injury in children with mild head trauma, having a high degree of sensitivity (all children, 95%; those aged >2 years, 100%) but poor specificity (all children, 34%; those aged >2 years, 37%).[34]

Glial fibrillary acidic protein (GFAP) appears to outperform S100β as a marker for detecting intracranial lesions on computed tomography (CT) scanning not only in adults but also in children and youth with mild traumatic brain injury.[35] In one study, the area under the receiver operating characteristic curve (AUC) for distinguishing head trauma from no head trauma for GFAP was 0.84 but 0.64 for S100β, and the AUC for predicting intracranial lesions on CT scanning for GFAP was 0.85 versus 0.67 for S100β. In children 10 years or younger, the AUC for predicting intracranial lesions was 0.96 for GFAP and 0.72 for S100β, whereas in those younger than 5 years, the AUC was 1.00 for GFAP and 0.62 for S100β.[35]

Computed Tomography

Computed tomography (CT) scanning of the head remains the most useful imaging study for patients with severe head trauma or unstable multiple organ injury.[1]

Indications for CT scanning in a patient with a head injury include anisocoria, Glasgow Coma Scale (GCS) score less than 12 (some studies suggest CT scanning in any pediatric patient with a GCS score of < 15), posttraumatic seizures, amnesia, progressive headache, an 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 after multiple trauma. Various studies and prediction algorithms (eg, National Emergency X-Radiography Utilization Study II [NEXUS II], Canadian Assessment of Tomography for Childhood Head Injury [CATCH], among others) have attempted to assess the ability of clinical characteristics to predict the utility of neuroimaging for patients with mild head injury, but there remains considerable variation in clinical practice.

The application of Pediatric Emergency Care Applied Research Network (PECARN) rule successfully identified all patients with clinically-important traumatic brain injuries, with a limited use of CT scanning.[36] The implementation of this assessment tool also showed a reduction of head CT use in a nonpediatric emergency departments.[37] The PECARN study noted that CT scanning may be unnecessary for children who are at very low risk for clinically important traumatic brain injury (TBI) after closed head trauma. In this study, the prediction rules for children younger than 2 years were normal mental status, no scalp hematoma except frontal, no loss of consciousness or loss of consciousness for less than 5 seconds, nonsevere injury mechanism, no palpable skull fracture, and normal behavior as deemed by the parents. The prediction rules for children older than 2 years were normal mental status, no loss of consciousness, no vomiting, nonsevere injury mechanism, no signs of basilar skull fracture, and no severe headache.[38]

A retrospective study (2014-2016) indicated that a subset of pediatric patients up to age 24 months whose presentation to an emergency department was delayed (>24 hours) after minor head trauma and who had scalp swelling with otherwise nonfocal neurologic findings did not need surgical intervention nor experienced any neurologic decline.[39] Neurosurgical management in these patients was not affected with findings from further radiographic studies. The investigators noted that CT scan findings might have influenced workup for child abuse and social care and suggested further work needs to be done to determine how to safely avoid CT scanning in the setting of delayed presentation after minor head trauma with scalp swelling.[39]

A noncontrast study is useful in the immediate posttrauma period for rapid diagnosis of intracranial pathology that calls for prompt surgical intervention.

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

In the absence of neurologic deterioration or increasing intracranial pressure (ICP), obtaining a repeat CT scan more than 24 hours after the admission and initial follow-up study may not be indicated for decisions about neurosurgical intervention.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is a more sensitive imaging study than computed tomography (CT) scanning in the setting of traumatic brain injury, providing more detailed information regarding the anatomic and vascular structures and the myelination process as well as allowing the detection of small hemorrhages in areas that might escape CT scanning.

MRI is useful for estimating the initial mechanism and extent of injury and predicting its outcome in the neurologically stable patient. It is not practical in emergency situations, because the magnetic field precludes the use of the monitors and life-support equipment needed by unstable patients. In addition, the time required for obtaining the appropriate MRI studies can cause unacceptable delays in the management of patients with severe traumatic brain injury.

Although MRI sensitivity is understood to be superior to CT scanning for intracranial evaluation, it is not as easily obtained acutely after injury and has not been as widely validated in large studies, particularly regarding influence on management decisions. In current practice, little evidence supports the use of MRI in influencing management of patients with severe traumatic brain injury.[40]

Ultrafast MRI appears to have limited use in pediatric patients for the evaluation of abusive head trauma. In a prospective study that compared nonsedated ultrafast MRI, noncontrast head CT scanning, and standard MRI for identifying intracranial trauma in 24 children with potential abusive head trauma (AHT), interreader agreement between two pediatric neuroradiologists were almost perfect for standard MRI and substantial for noncontrast CT scanning but only moderate for ultrafast MRI.[41] There was a high discrepancy rate between standard MRI and ultrafast MRI (42% of patients). The specificity and positive predictive values were 100% each for noncontrast CT scanning, ultrafast MRI, and a combination of the two; however, noncontrast CT scanning had a 25% sensitivity and 21% negative predictive value versus 50% and 31%, respectively, for ultrafast MRI. Sensitivity for detecting intraparenchymal hemorrhage was greater for ultrafast MRI than noncontrast CT scanning, and the combination of both was more sensitive for intracranial trauma than noncontrast CT scanning alone.[41]


Ultrasonography can be performed in neonates and small infants with open fontanel and may provide information regarding intracranial bleeding or obstruction of the ventricular system.

ICP Monitoring and CSF Drainage

Intracranial pressure (ICP) should be monitored in all salvageable patients with severe traumatic brain injury (TBI) (GCS score of 3-8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns.

ICP monitoring is also indicated in patients with severe TBI with a normal CT scan in the presence of unilateral or bilateral motor posturing or a systolic blood pressure less than the fifth percentile for age.

In certain conscious patients with CT findings suggesting risk of neurologic deterioration (hematomas, contusions, swelling, herniation, or compressed basal cisterns), however, monitoring may be considered based on the opinion of the treating physician. Inability to perform serial neurologic examinations, because of pharmacologic sedation or anesthesia, may also influence a clinician's decision to monitor ICP in an individual patient.

External ventricular drains are often used as a therapeutic modality, especially when the removal of cerebrospinal fluid (CSF) during episodes of increased ICP or drainage of hemorrhage-induced hydrocephalus may be required.

Lumbar drains may also used for patients with refractory increased ICP, allowing further CSF removal. An external ventricular drain should be placed initially; basilar cisterns must be open on CT scan before placement of a lumbar drain.

ICP can also be monitored by transducers placed via small burr holes, especially when an intraventricular catheter cannot be placed. The theoretical advantages (eg, ease of placement, reduced risk of infection, and decreased risk of hemorrhage) should be weighed against the inability to remove CSF. The recent introduction of tissue partial pressure of oxygen monitoring allows direct measurement of brain tissue oxygenation. If brain oxygenation monitoring is used, maintenance of partial pressure of brain tissue oxygen greater than 15 mm Hg may be considered.[40]



Approach Considerations

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.[6] Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents, previously published in 2003, were updated in 2012 and provide an excellent basis for treatment decisions.[40]

Consultation with a neurosurgeon should be obtained. 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 also been established and were updated in 2015.[42]

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

Admission to an intensive care unit (ICU) should be based on the severity of the trauma and associated injuries. Transfer to a hospital where consultation with a neurosurgeon is available may be required, especially when surgical intervention is necessary.

The results from one study note that children with minor blunt head trauma (defined by initial Pediatric Glasgow Coma Scale [PGCS] scores of 14 or 15) and normal cranial computed tomography (CT) scans are at very low risk for subsequent abnormal CT scans or magnetic resonance imaging (MRI) studies and are highly unlikely to require neurosurgical intervention; hospitalization of these children is generally not necessary.[43]

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 neurologic status must be performed.

In all patients, tetanus immunization status should be checked and updated, especially when lacerations or contaminated wounds are present. Anticonvulsants may be needed to control or provide prophylaxis for seizure activity. Routine seizure prophylaxis is not recommended; prophylaxis should be provided for patients on an individual basis with consultation with neurosurgery. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used for minor pain control, but may be contraindicated with DIC or severe head trauma. Beta-blockers can be prescribed for patients with trauma-induced migraines.

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

Patients who sustained a loss of consciousness lasting less than 5 minutes and have normal findings on neurologic examination, no symptoms of increased ICP (eg, 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.


Elevation of the head to 30° and maintaining midline position continues to be recommended because it improves the venous drainage and decreases the intracranial pressure without affecting the cerebral blood flow. A cervical spine collar should be used until clearance of the spine is achieved.

Athletes with concussion injuries should not be cleared to return to sports activities until all residual symptoms from their original head injury are no longer occurring. For more information, see Repetitive Head Injury Syndrome and Postconcussive Syndrome in Emergency Medicine.

The frequency of “second impact syndrome” among head-injured children participating in sporting activities has been documented.[44] Several states have now passed or are considering legislation to mandate education of youth coaches, athletes, and parents regarding how to recognize participants who have had a concussion and the importance of not letting the athlete return to play until all symptoms have resolved and (in many cases) the athlete has been cleared by appropriate medical personnel.

Resuscitation and Treatment of Life-Threatening Conditions

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 on which treatment of intracranial hypertension must be based. They also state that, in the absence of any obvious signs of increased intracranial pressure (ICP), no prophylactic treatment should be initiated, because this may directly interfere with optimal resuscitation.

Airway management

A stable airway should be obtained to provide adequate oxygenation and ventilation. If endotracheal intubation is required, adequate sedation and paralysis must be ensured to prevent further increases in ICP. Rapid-sequence induction (RSI) 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 when basilar skull fracture is suspected.

Breathing may be impaired because of neurologic or thoracic injuries. Patients with significant head injury and altered mentation should receive 100% oxygen supplementation and should be supported with positive-pressure ventilation. Endotracheal intubation should be performed in cases where the patient has difficulty maintaining the airway because of copious secretions, poor gag reflex, coma, or the need for prolonged ventilatory support.

Premedication for RSI includes atropine (0.02 mg/kg for children younger than 8 years) to blunt the effect of vagal stimulation and decrease the secretions (controversial and not supported by high-level evidence). Lidocaine (1-2 mg/kg) may decrease airway stimulation during intubation and prevent an increase in ICP; however, although lidocaine has been widely used in the past to blunt transient increases in ICP during endotracheal intubation, there is no high-level evidence to support its continued use for this purpose.[45] Etomidate (0.3 mg/kg), and 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 (controversial) 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 has a short duration of action. Succinylcholine is contraindicated in neuromuscular disorders, patients with penetrating eye injury, glaucoma, upper motor neuron injury, and history of malignant hyperthermia in patient or family, among other conditions. Nondepolarizing agents, including rocuronium, pancuronium, and vecuronium, are commonly used in young children.

Cardiovascular management

Achieving normotension and euvolemia is the goal in cardiovascular management unless there is evidence of increased ICP requiring supraphysiologic blood pressure to drive cerebral perfusion pressure (CPP). Cerebral perfusion pressure is defined as mean arterial blood pressure (MAP) minus ICP (ie, CPP = MAP – ICP) and is the physiologic variable that defines the pressure gradient driving cerebral blood flow (CBF) and metabolite delivery; it is therefore closely related to ischemia. CPP should be determined in a standard fashion, with ICP zeroed to the tragus (as an indicator of the foramen of Monro and midventricular level) and MAP zeroed to the right atrium with the head of the bed elevated 30°.

Several clinical studies suggest that 70-80 mm Hg may be the critical threshold for CPP in adults. Recent guidelines suggest that a CPP threshold 40-50 mm Hg may be considered in children, with age-specific thresholds with infants at the lower end and adolescents at the upper end of this range.[40]

Adequate volume resuscitation with isotonic solutions is indicated to maintain adequate filling pressures, normal cardiac output, and, ultimately, normotension (MAP >90 mm Hg in adults; pediatric values vary with age and height, but MAP for children at the 50th percentile for height can be estimated using the formula MAP = (1.5 × age in years) + 55).[46]

Several adult and pediatric studies have found hypertonic solutions to be superior to lactated Ringer solution or isotonic sodium chloride for resuscitation. The use of hypertonic solutions is associated with improved blood pressure response, overall decreased fluid requirements, fewer interventions employed to control ICP, fewer complications, and improved survival.

Hypertension, if present, could represent a compensatory mechanism responding to the increased ICP; thus, reflex treatment of it may significantly compromise cerebral perfusion. When normotension is desired in the presence of intracranial or intracerebral hemorrhage after surgical evacuation, calcium channel blockers or beta-blockers should be given instead of direct vasodilators to prevent sudden hypotension.

Continuous cardiac monitoring should be performed because of the high incidence of ventricular dysrhythmias in patients with head trauma and patients in whom cardiac contusion is suspected.

ICP and cerebral perfusion management

Little evidence supports any specific threshold for the treatment of intracranial hypertension in children. Pooled studies suggest that prolonged elevations of ICP greater than 20 mm Hg are associated with poorer outcomes in children with traumatic brain injury (TBI), thus a threshold of 20 mm Hg is typically used to guide medical management.

Osmotic therapy is a key component of medical management of intracranial hypertension. Hypertonic saline should be considered for the treatment of severe pediatric TBI associated with intracranial hypertension. Effective doses as a continuous infusion of 3% saline range from 0.1-1 mL/kg of body weight per hour administered on a sliding scale. The minimum dose needed to maintain ICP at less than 20 mm Hg should be used. Serum osmolarity should be maintained less than 360 mOsm/L.

Although mannitol is commonly used in the management of elevated ICP in adult and pediatric TBI, the evidence supporting its use in pediatric patients is inconclusive and did not meet the standards for inclusion in the 2012 guidelines.[40] However, hypertonic saline solution is another osmotic agent that may be used to manage high ICP.

CBF is known to be diminished in the first 24 hours in patients who have sustained severe TBI, with absolute values close to those seen in ischemia.

Hyperventilation reduces ICP by producing hypocapnia-induced cerebral vasoconstriction and a reduction in CBF and cerebral blood volume, resulting in a decrease in ICP. However, hyperventilation may decrease cerebral oxygenation and may induce brain ischemia. In addition, after TBI, the CBF response to changes in PaCO2 can be unpredictable.

Avoidance of prophylactic severe hyperventilation to a PaCO2 of less than 30 mm Hg may be considered in the initial 48 hours after injury. If hyperventilation is used in the management of refractory intracranial hypertension, advanced neuromonitoring for evaluation of cerebral ischemia may be considered.[40] The opposite, hypoventilation, must also be avoided; eucapnia should be the upper limit of the PaCO2 (partial pressure of carbon dioxide) goal.

Removal of CSF via extraventricular drains improves the ICP in these patients and provides continuous ICP monitoring.

Corticosteroids do not decrease the cerebral edema associated with head trauma and are not currently recommended.[40]

Bleeding management

Disseminated intravascular coagulopathy (DIC) is present in one third of head trauma patients. Aggressive management of DIC and correction with replacement factors (including fresh frozen plasma, cryoprecipitate, and/or platelets) are required to decrease the risk of further intracranial bleeding and allow surgical intervention when necessary. The administration of recombinant factor VIIa in patients with severe coagulopathy secondary to traumatic brain injury may allow more rapid correction of DIC and may reduce mortality.[47]

Seizure management

Posttraumatic seizures, which occur in 10% of pediatric patients with head trauma, may affect the outcome adversely by raising the ICP, increasing the metabolic demands of the brain, and causing hypoxia or hypoventilation in a spontaneously breathing patient. Benzodiazepines (eg, lorazepam and diazepam) or phenytoin/fosphenytoin may be used for initial seizure control, and phenytoin or phenobarbital may be used for maintenance anticonvulsant therapy.

While not indicated in all patients, prophylactic treatment with phenytoin or fosphenytoin may be considered to reduce the incidence of early posttraumatic seizures (PTS) in pediatric patients with severe TBI.[40]

Temperature control

In general, hyperthermia in patients with TBI and increased ICP should be avoided and treated promptly, as hyperthermia increases intracranial blood volume and pressure and is implicated in increased secondary posttraumatic injury.

However, the use of therapeutic hypothermia remains controversial. Although initial studies suggested reduced ICP in patients with TBI who had been treated with moderate hypothermia (core body temperature 32-33°C, beginning within 8 hours, and continued for up to 48 hours), the “Cool Kids” trial of hypothermia in pediatric TBI was halted secondary to futility.[40]

Analgesia, sedation, and neuromuscular blockade

Sedation and paralysis are used to prevent agitation and increased muscular activity, which may increase ICP. If neuromuscular blockers are used, monitoring the ICP and having an electroencephalograph (EEG) in place are necessary, as neuromuscular blockade eliminates the motor signs of seizures.

Etomidate may be considered to control severe intracranial hypertension; however, the risks resulting from adrenal suppression must be considered.

In the absence of outcome data, the specific indications and the choice and dosing of analgesics, sedatives, and neuromuscular-blocking agents used in the management of infants and children with severe TBI should be left to the treating physician. In addition, as stated by the Food and Drug Administration, continuous infusion of propofol for either sedation or refractory intracranial hypertension in infants and children with severe TBI is not recommended.[40]

Barbiturate therapy lowers the ICP and exerts cerebral protection through the following 3 mechanisms:

  • Alterations in vascular tone

  • Inhibition of free radical–mediated lipid peroxidation

  • Suppression of metabolism

By lowering metabolic demands, barbiturate therapy decreases CBF and cerebral blood volume, exerting beneficial effects on ICP and global cerebral perfusion.

High-dose barbiturate therapy may be considered in hemodynamically stable patients with refractory intracranial hypertension despite maximal medical and surgical management. When high-dose barbiturate therapy is used to treat refractory intracranial hypertension, continuous arterial blood pressure monitoring and cardiovascular support to maintain adequate cerebral perfusion pressure are required.[40]

Continuous EEG (to achieve burst-suppression pattern) or bispectral index (BIS) monitoring (target range, 6-20) are required to allow titration of barbiturate therapy.

Surgical Decompression and Elevation

Surgical decompression is required in the presence of a rapidly expanding epidural or subdural hematoma that causes an increase in intracranial pressure (ICP) and focal compression. Surgical decompression should also be considered in patients with focal traumatic brain injury (TBI) and refractory intracranial hypertension with a potentially salvageable brain.

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 mental status, or pressure effects with midline shift are present and if the hematoma is smaller than 2 cm.

A subdural hematoma with midline shift or altered mental status should be emergently drained. A 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.

Decompressive craniectomy (DC) with duraplasty, leaving the bone flap out, may be considered for pediatric patients with TBI who are showing early signs of neurologic deterioration or herniation or are developing intracranial hypertension refractory to medical management during the early stages of their treatment.[40]



Medication Summary

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

Neuromuscular Blockers, Nondepolarizing

Class Summary

Nondepolarizing neuromuscular blockers are used in combination with a sedative as part of the rapid-sequence intubation process or as a means of controlling ICP.


Vecuronium is used to facilitate endotracheal intubation and provide neuromuscular relaxation during intubation and mechanical ventilation. It is given as an adjunct to a sedative or hypnotic agent.

Anticonvulsants, Barbiturates

Class Summary

Barbiturates are used as adjuncts for intubation in patients with head trauma and in the management of elevated ICP. They may also be used as anticonvulsants. Their use must be accompanied by appropriate hemodynamic monitoring, as they may cause profound hypotension and apnea/hypopnea.

Pentobarbital (Nembutal)

Pentobarbital is a short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties. It may be used in high dosages to induce barbiturate coma for treatment of refractory increased ICP.


Phenobarbital is used for seizure control in patients with head trauma.

Anxiolytics, Benzodiazepines

Class Summary

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


Midazolam is a short-acting benzodiazepine with a rapid onset of action. It is useful in treating increased ICP.

Lorazepam (Ativan)

Lorazepam is a long-acting benzodiazepine used as an anticonvulsant for the immediate control of seizure activity.


Class Summary

Diuretics may have a beneficial effect in lowering ICP by decreasing cerebrospinal fluid (CSF) production, preferentially excreting water over solute, and decreasing blood viscosity, with subsequent improvement of cerebral blood flow (CBF).

Furosemide (Lasix)

Furosemide is a loop diuretic that helps decrease ICP via 2 separate mechanisms. One mechanism influences CSF formation by affecting sodium-water movement across the blood-brain barrier; the other mechanism is the preferential excretion of water over solute in the distal tubule.

Mannitol (Osmitrol)

Mannitol is an osmotic diuretic that lowers blood viscosity and produces cerebral vasoconstriction with normal CBF. A decrease in ICP occurs subsequent to a decrease in cerebral blood volume (CBV).


Class Summary

These agents may be used to control ICP by decreasing the effect of noxious stimuli (eg, endotracheal intubation, suctioning, pain from traumatic injury itself). Although lidocaine has been widely used in the past to blunt transient increases in ICP during endotracheal intubation, there is no high-level evidence to support its continued use for this purpose.[45]

Fentanyl (Sublimaze)

Fentanyl is a potent synthetic opioid with a rapid onset and short duration of action. Although an opioid, fentanyl produces only mild sedation at usual doses, and it is commonly used in combination with a benzodiazepine.

Propofol (Diprivan)

Propofol is an oil-soluble hypnotic agent with a rapid onset and short duration of action. Because propofol has limited anesthetic action, it is usually used with an opioid such as fentanyl for painful procedures. Propofol use is associated with hypotension, bradycardia, and apnea, especially when boluses are given for induction of anesthesia. Because of its short duration of action, propofol infusions may be discontinued briefly to allow neurologic testing, and then restarted (with or without bolus) to resume sedation.


Class Summary

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

Phenytoin (Dilantin, Phenytek)

Phenytoin may act in the motor cortex, where it may inhibit the spread of seizure activity. It may also inhibit the activity of the brainstem centers responsible for the tonic phase of grand mal seizures. Phenytoin is preferred to phenobarbital for controlling seizures because it does not cause as much central nervous system (CNS) depression.

Fosphenytoin (Cerebyx, ProEpanutin)

Fosphenytoin is a diphosphate ester salt of phenytoin that acts as a water-soluble pro-drug of phenytoin. Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.

To avoid the need to perform molecular weight–based adjustments when converting between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents (PE). Although fosphenytoin can be administered IV and IM, the IV route is the route of choice and should be used in emergency situations.