PART 7
Head and Brain Trauma in Children
250 Management of Head Injury: Special Considerations in
Children
Kristen Stabingas, Linda Wei Xu, Gerald A. Grant, and P. David Adelson
This chapter includes an accompanying lecture presentation
that has been prepared by the authors: Video 250.1.
KEY CONCEPTS
• Pediatric traumatic brain injury (TBI) is a leading cause
of disability in the United States.
• Management of pediatric head injury requires
understanding of the neurological development unique to
this population.
• Initial trauma resuscitation includes physiologic
stabilization with special attention to age-dependent
oxygen and volume status.
• If abusive trauma is suspected, patients should undergo a
comprehensive evaluation for additional systemic injuries
followed by a Child Protective Services referral.
• Routine computed tomography scans are not indicated
in children with a mild head injury and no evidence of
clinical decline.
• US law mandates that all youth athletes must be
removed from play if concussion is suspected and
may not return to play unless cleared by a medical
professional.
• The biomechanical properties of pediatric bone allow for
certain skull fractures that are unique to this population.
• Children are more susceptible to changes in carbon
dioxide levels, and alterations in autoregulation are
frequently seen in pediatric TBI.
• Pediatric patients have a preexisting lower seizure
threshold and thus are at increased risk of posttraumatic
seizure activity.
• There is no strong evidence to support the use of
therapeutic hypothermia in pediatric TBI.
EPIDEMIOLOGY
In the pediatric population, traumatic brain injury (TBI) is the
leading cause of mortality and morbidity in the United States.
According to the Centers for Disease Control and Prevention,
TBI causes nearly 500,000 emergency department visits per year
and results in more than 2000 deaths per year.1 Expanded media
coverage, political legislation, and recognition of TBI by profes-
sional sports organizations all could be factors contributing to
the heightened awareness of TBI in the pediatric population.
However, despite increased prevention and educational efforts,
pediatric TBI increased more than 30% from 2006 to 2013; this
1886
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was largely due to the increased recognition of mild TBI and
concussion.2
Falls are the leading cause of injury in children younger than
5 years of age, whereas motor vehicle collisions are the leading
cause in older (15–19 years old) youths.3 For infants and toddlers
(<2 years old), nonaccidental trauma is the most common cause
of injury.1,4 Both nonaccidental trauma, often with delay in
reporting, and motor vehicle collisions commonly results in more
severe injuries than those sustained from falls. Males have a 1.4
to 2 times higher risk of injury than females. The prevalence of
disability in patients who have sustained traumatic head injuries
is unknown but may be as high as 20% in hospitalized patients.3
Accordingly, mortality from TBI in children takes a bimodal
distribution: mortality rates are up to 5% in children younger
than 4 years, decrease in school-aged children to 2% to 3%,
and then increase to 19% in youths older than 15 years.1,5 The
specific management of pediatric patients is distinct from that
of adult patients because of different physiology in these age
groups. In this chapter, we aim to review unique considerations
for management of head injury in the pediatric population. 
TYPES OF HEAD INJURY
The clinical presentation of head injury in the pediatric popula-
tion is largely dependent on the severity and variability of the
initial trauma. Owing to the unique age-specific biomechanical
properties of pediatric neuroanatomy, namely, higher plasticity
and deformity, children are susceptible to a wide spectrum of
injuries, many of which are rare among adults.6
Head injuries can be classified generally into mild (Glasgow
Coma Scale [GCS] score of 13–15), moderate (GCS score of
9–12), and severe (GCS score of 3–8) categories after initial
resuscitation. Patients with GCS score of 14 or 15 are sometimes
grouped in a separate category from patients with GCS score
of 13 because the management is distinct in terms of initial
work-up and imaging. Mild head injuries are the most common;
yet despite the recognition of TBI as a public health concern,
injuries are still believed to be vastly underreported.7 A subset
of mild head injuries is classified as concussion, defined by a rapid-
onset, transient neurological impairment that resolves without
intervention. It is thought that these symptoms are due to a
transient disturbance in function rather than a true structural
injury. Commonly, patients experience loss of consciousness
(LOC), disorientation, headaches, amnesia, emotional lability,
and sleep disturbance. By convention, concussion is not
associated with any findings on computed tomography (CT),8,9
although in general findings such as a skull fracture or intracranial
abnormality are revealed on CT in 5% of patients with mild TBI.
Patients with concussion and CT findings are classified as having
complicated mild TBI.10-12 Achievement of an optimal outcome
starts with appropriate initial evaluation and assessment of the
type and severity of neurological injury. 
 CHAPTER 250  Management of Head Injury: Special Considerations in Children
TABLE 250.1   Age-Specific Hypotension140
Age Range (yr) Hypotension (mm Hg)
0–1 <65
2–5 <75
6–12 <80
13–16 <90
INITIAL EVALUATION
On presentation to the emergency department, a detailed and
focused history and physical examination can help with rapid
assessment and anticipation of potential injuries. Although at
times it may not be possible to obtain a complete history, impor-
tant factors to consider include the mechanism of injury, seizures,
LOC, headache, vomiting, history of bleeding disorders, history
of previous TBI, medications and whether medications were
given in the field, and whether symptoms or signs are currently
improving or worsening. When obtaining the history, it is impor-
tant to note inconsistencies in timing or events that would raise
suspicion of nonaccidental trauma or inflicted injury.
Advanced Trauma Life Support (ATLS) guidelines provide a
structured, systematic approach for emergency care of pediatric
trauma patients. The initial evaluation of patients who have
sustained severe head injury is based on physiologic stabilization
rather than targeted, diagnosis-based therapy.13 Evaluation of
airway, breathing, and circulation precedes the neurological
evaluation, and stabilization of these elements takes priority.
Neurosurgeons require an understanding of how the basic trauma
evaluation differs in children compared with adults and of the
implication for any operative intervention that may be needed.
Although evaluation for airway and breathing management
is typically similar to the evaluation in adults, evaluation of
circulatory status and blood loss in children can be quite different.
Thus a physiology-driven approach should be used for fluid
resuscitation in pediatric patients, while still respecting the age-
related differences within this population, keeping in mind that
excessive fluid may be harmful.14
Among pediatric patients, 39% of traumatic deaths can be
attributed to exsanguination,15 and several factors contribute to
why children are particularly more at risk. In general, children
have higher oxygen requirements but a lower blood volume than
adults. However, children also have increased physiologic reserve
and can easily conceal common signs of hypovolemia. A child
can typically maintain a normal blood pressure despite a 25%
to 30% blood volume loss.16 Thus by the time hypotension is
noted, the patient is likely very close to cardiovascular collapse,
which is highly associated with morbidity and mortality.17,18
Furthermore, many practitioners are not familiar with normal
blood pressure ranges in this population. Normal blood pressure
ranges are outlined in Table 250.1 and can be estimated by the
following equation: 90 + (2 × age). Hypotension is defined as 20
points below normal.19 Blood volume can be estimated at 80 mL/
kg.20,21 Because hypotension can be a late presenting symptom
of hypovolemia, it is particularly important to note clinical signs
of hypovolemia. Symptoms such as decreased pulse pressure
(<20 mm Hg), mottled skin, hypothermia, lethargy, metabolic
acidosis, decrease in palpable pulses, decrease in urine output,
and increased capillary filling time all can give important clues
before reaching the point of cardiovascular instability.16
Because hypovolemia is such a high risk in pediatric patients,
venous access is key to initial resuscitation. If two attempts
at peripheral access have been tried, interosseous access is
indicated.22 According to the pediatric guidelines, resuscitation
should proceed as described in Box 250.1. When evaluating for
the source of hemorrhage, whereas in adults the primary sources
of massive bleeding are typically long bones, abdominal cavity,
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1887
BOX 250.1  Resuscitation Protocol142 250
Warm crystalloid boluses in 20-mg/kg units × 3
Administer type-specific or O-negative packed red blood cells in
10-mg/kg boluses and locate source of bleeding as soon as
possible
Monitor urine output to gauge success of resuscitation with goal
urine output of >2 mL/kg per hour in infants and 1–1.5 mL/kg
per hour in older children
and external hemorrhaging, in children it is important to keep in
mind that head trauma itself can be a source of significant blood
loss. Although at times trivial in adults, blood loss from scalp
lacerations and hematomas can be a significant portion of blood
volume in children. Furthermore, head injury in infants with
open sutures can expand the cranial vault and mask a significant
amount of internal bleeding.21
Damage control resuscitation, a military-derived concept of
traumatology, is an attempt to limit the use of crystalloid products
during rapid transfusions; this concept applies to both adult and
pediatric patients.23 According to the most recent edition of
ATLS, an initial fluid bolus of 20 mL/kg is followed by 10 to
20 mL/kg of packed red blood cells and 10 to 20 mL/kg of fresh
frozen plasma and platelets in patients at risk of needing a massive
transfusion.
Coagulopathy also develops in 40% of children with severe
TBI, likely owing to consumption of clotting factors from bleeding
and dilution from resuscitation. Children with head injury are at
particular risk for disseminated intravascular coagulopathy.24 It is
thought that damaged brain tissue releases tissue thromboplastin
and elevates risk for disseminated intravascular coagulopathy, as
demonstrated by thrombocytopenia, increase in prothrombin
time and partial thromboplastin time, increase in D-dimer, and
reduction in fibrinogen.21,24,25 Early coagulopathy increases
mortality fourfold in pediatric patients with TBI,26 and platelet
transfusion is associated with improved overall survival.27 In the
setting of massive blood loss, especially in children, transfusion of
platelets and plasma should accompany transfusion of packed red
blood cells. Tranexamic acid, a pharmaceutical hemostatic agent,
was implemented as standard practice in adult trauma after a large
randomized controlled trial demonstrated its safety, efficacy, and
statistically significant reduction in mortality. Tranexamic acid
has been studied in the perioperative setting of various pediatric
surgery subspecialties; however, its role in pediatric trauma
remains unclear.28
After initial resuscitation and stabilization of a patient
with severe trauma, a detailed neurological examination can
be undertaken. Standard cervical spine precautions should
be maintained for patients in whom head injury is suspected
because concomitant cervical injuries are common. Important
aspects of the primary survey in all patients with suspected head
injury include inspection for scalp hematomas or lacerations,
palpable skull fractures or evidence of basilar skull fractures,
and focal neurological signs. In infants a bulging fontanelle may
be indicative of elevated intracranial pressure (ICP). The GCS
score is a useful tool for older children and has been modified
for younger children (Table 250.2). If abusive head trauma is
suspected, evidence of other systemic injuries such as concomitant
fractures (old or new), abdominal injuries, or retinal hemorrhages
may be important to note. Any pediatric patient with suspected
inflicted trauma should undergo all or a combination of a skeletal
survey, magnetic resonance imaging (MRI) of the brain, MRI
of the spine, and ophthalmologic examination, followed by a
referral to Child Protective Services. In addition to level of
consciousness (via the GCS score), careful evaluation of pupillary
size and reaction and recognition of lateralizing signs are vital
1888 SECTION 8  Pediatrics

TABLE 250.2   Glasgow Coma Scale Score

Original Modified for Infants141
Best eye response 1—Does not open eyes 1—None
2—Opens eyes to painful stimuli 2—To pain
3—Opens eyes to verbal command 3—To shout/loud noise
4−Opens eyes spontaneously 4—Spontaneously
Best verbal response 1—No response 1—None
2—Incomprehensible sounds 2—Grunt, agitated
3—Inappropriate words 3—Inconsolable screams
4—Disoriented and converses 4—Consolable, cries
5—Fully oriented and converses 5—Smiles, coos
Best motor response 1—No motor response 1—None
2—Extension (decerebrate posturing) 2—Extension to pain (decerebrate posturing)
3—Flexion (decorticate posturing) 3—Flexion to pain (decorticate posturing)
4—Withdraws purposefully from painful stimuli 4—Withdraws to pain
5—Localizes painful stimuli 5—Localizes pain
6—Follows verbal commands 6—Normal movement

to identification of intracranial injuries, which may require

neurosurgical or neuroprotective interventions.
Based on the findings in the history and physical examination,
the next step in the evaluation is determining which children are
most appropriate for imaging of acute injuries. Historically, in
the absence of high-quality clinical algorithms, skull x-ray was
used as the initial imaging modality; this was later replaced
with more sensitive and specific alternatives.13 Given its ready
availability and ability to detect most acute injuries, CT scan of
the head with brain and bone windows that may include three-
dimensional reconstructions is the mainstay of trauma evaluations.
Particularly with children, most modern imaging protocols allow
for reduction in radiation dose without reducing image quality. In
general, if the patient presents with focal neurological findings,
clinical concern for skull fracture, altered mental status (GCS
score of <14), bulging fontanelle, persistent vomiting, seizures,
or prolonged LOC, or if there is any concern for abusive head
trauma, the patient should undergo diagnostic imaging.29-31
Although determining when to image patients with moderate
to severe head injuries is less controversial, there is debate about
whether imaging in warrants in patients who present with mild
head trauma. In studies of patients with a GCS score of 14 or 15
and no focal findings, CT scan revealed a clinically significant
finding (defined as requiring neurosurgical intervention,
intubation for more than 24 hours, or hospital admission for
more than 2 days or as having brain injury on CT or dying
from the injury) in only 1% of patients.11,29 If these cases are
further stratified to patients with normal mental status, no scalp
hematoma, no LOC, no clinical evidence of skull fractures, and a
low-risk mechanism, the chances of having a clinically significant
finding on CT decrease to 0.05% to 0.2%. This set of guidelines
for when to obtain CT, defined by the Pediatric Emergency Care
Applied Research Network (PECARN), has been subsequently
validated by other groups as an efficient and useful way to identify
patients who do not need imaging.11,32,33 Indications for CT after
pediatric TBI are summarized in the 2014 recommendations
produced by the National Institute for Health and Care
Excellence (Box 250.2).34 Although the PECARN guidelines
recommend imaging if the patient experienced LOC or a high-
impact mechanism, newer findings suggest that isolated LOC
or isolated severe injury mechanism in the absence of other risk
factors is associated with a low risk for clinically important TBI
and does not require CT.35,36 For low-risk patients, observation
without CT can be considered. Alternatively, a fast brain MRI
scan (usually a shortened MRI scan lasting 2 minutes with limited
sequences) has been developed to screen children with head
and neck trauma. Repeat imaging in patients with severe TBI
with subsequent CT scans can be considered in settings of no
neurological improvement, increasing ICP, or inability to obtain
BOX 250.2  Indications for Screening Computed
Tomography in Pediatric Traumatic Brain Injury34,40
Head injury and any of the following risk factors:
• Inflicted trauma
• Posttraumatic seizure
• GCS score of <14 or for children <1 year old, GCS score of
<15
• GCS score of <15 after 2 hours
• Suspected open or depressed skull fracture
• Tense fontanelle
• Signs of basilar skull fracture
• Focal neurological deficit
• If <1 year old, bruising, swelling, or laceration >5 cm on the
head
Head injury and more than one of the following risk factors:
• Loss of consciousness for >5 minutes
• Abnormal drowsiness
• More than three episodes of vomiting
• Dangerous mechanism of injury
• Amnesia for >5 minutes
GCS, Glasgow Coma Scale.
adequate neurological examinations such as in patients with
severe facial injuries or pharmacologic coma. Otherwise, routine
repeat CT scans are not necessarily needed.37 
MANAGEMENT OF TRAUMATIC BRAIN INJURY
Mild Traumatic Brain Injury
Only 0.1% to 1% of children presenting with mild TBI will even-
tually require some type of surgical intervention.11,12,30 Because
most of these patients do well overall, there are no clear rules
about how to best manage these patients when presenting to the
emergency department. According to the 2016 update of the
American Academy of Pediatrics “Choosing Wisely” campaign,
clinical observation is an effective alternative to CT imaging in
children with minor head trauma.38 If there is any suspicion of
injury that may lead to further decline, intracranial injury on CT,
depressed skull fractures, persistent vomiting, other serious con-
comitant injuries, high-risk medical comorbidities, or suspicion
of nonaccidental trauma, patients should be admitted for obser-
vation. For patients who do not have any of these risk factors,
routine observation for 6 to 8 hours in the emergency depart-
ment is adequate to ensure the patient remains intact without

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 CHAPTER 250  Management of Head Injury: Special Considerations in Children
TABLE 250.3   Concussion Grading and Return to Play Guidelines8,47,49,52
Grade I Grade II
ImPACT Mental status changes Mental status Any LOC
(disorientation, changes for
amnesia) for <15 >15 min
min
Colorado Medical Confusion Confusion and LOC
Society Guidelines amnesia
American Academy No LOC and <15 min No LOC and
of Neurology confusion >15 min
Guidelines confusion
Fourth International No grading guidelines
Congress of
Concussion
LOC, Loss of consciousness; RTP, return to play.
postconcussive symptoms or signs and is able to tolerate an oral
diet without emesis. Delayed deterioration in patients with mild
TBI and no findings on initial CT is uncommon.39,40 Thus rou-
tine repeat CT scans are not indicated in children with mild injury
and no evidence of clinical decline.41 These patients may be dis-
charged home with instructions to follow up with a qualified pro-
vider who has experience or training in concussion management.
Concussion can often be evaluated outside of an emergency
department setting, either in the field or in an outpatient setting
after the initial injury. After a diagnosis of concussion is confirmed,
the patient should not be left alone in the first hours of injury in
case of neurological decline and should be evaluated by a medical
provider. If the injury occurred in the setting of a sports event,
the patient should not return to play because same-day return to
play is associated with delayed onset of neurological symptoms
and worse postconcussive symptoms.42 It is important to note
that ongoing clinical symptoms, history of prior concussion, and
younger age all are associated risk factors of future impairments.
As such, current recommendations emphasize the importance of
a more conservative approach to the management concussions in
youths.43
A second injury in the postconcussive period puts the patient
at risk for second impact syndrome, whereby a mild second head
injury with close proximity in time to the first injury can trigger
much more severe repercussions than two isolated head injuries
that are separated in time.44 The most severe cases of second
impact syndrome have been reported with sudden collapse,
pupillary dilation, loss of eye movement, respiratory failure, and
death. The severe effects of second impact syndrome are often
attributed to a sudden loss of vascular autoregulation with rapid
elevation in ICP within a matter of minutes, and nearly one-
third of pediatric patients have been found to have alterations
in vascular autoregulation after head injury.45 Because of
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1889
250
Grade III RTP
ImPACT testing—computerized testing of:
• Verbal memory
• Visual memory
• Reaction time
• Processing speech
• Impulse control
• Postconcussion symptom scale
No return to play until values return to baseline
Grade I:
• First time—15 min
• Second time—1 wk
Grade II:
• First time—1 wk
• Second time—2 wk with physician approval
Grade III:
• First time—1 to 6 mo, based on severity of LOC
• Second time—6 mo to 1 yr with physician approval
LOC As summarized in Colorado Medical Society
Guidelines
Summary of how to progress Stepwise RTP:
through stepwise RTP: • Stage 1: No activity—rest with goal of recovery
Must be asymptomatic for 24 h • Stage 2: Light aerobic exercise—goal of
in each step increasing heart rate
If any symptoms occur, • Stage 3: Sport-specific exercise—training drills
drop back to previous with no head impact
step at which patient was • Stage 4: Noncontact training drills—complex
asymptomatic training drills with resistive training
At least 1 wk to progress • Stage 5: Full-contact practice—medical
through entire protocol clearance to participate in normal training with
Absolutely no same-day RTP goal of restoring functional skills
if any concussion occurs • Stage 6: RTP
concern for second impact syndrome, Washington state passed
the Zackery Lystedt Law (2009), which dictates that all youth
athletes must be removed from play if concussion is suspected and
may not return to play unless cleared by a medical professional.46
This law has since been adopted by all 50 states. To help
guide medical professionals assessing these patients, there have
been many postulated ways to grade concussions and different
recommendations for return to play. Several concussion grading
systems are outlined in Table 250.3 with their recommendations
for return to play. In general, most recommend an assessment of
severity of the concussion based on duration and type of mental
status change including amnestic symptoms and LOC. Most
agree with a graduated return-to-play strategy whereby activities
are gradually increased in a stepwise fashion if the patient remains
asymptomatic.8,9,47 If symptoms occur, the patient needs to step
down to a previous level of activity until symptoms resolve.
The recommended return-to-play guidelines are limited in that
timelines provided are generally for adults and do not provide
an objective measure of suitability for return to play, but
rather the patient’s own perception of symptoms and recovery.
When adolescents were tested for neurocognitive changes after
concussion, many who reported no symptoms showed delays
and memory deficits on objective testing.48 One such objective
test is ImPACT, a computerized test that quantifies six different
neurocognitive factors, as summarized in Table 250.3. Athletes
can be tested with this tool before initiating sports, and return
to play can be held until the athlete returns to the preconcussion
baseline.49-52
Although the immediate risk of repeated injury can cause
a physician to ask the patient to delay return to play, a serious
discussion needs to be held about long-term effects and long-term
risks of repeated concussions. Postconcussion syndrome is described
as headaches, dizziness, neuropsychiatric symptoms, or cognitive
1890 SECTION 8  Pediatrics
impairment in the first week following a concussion.9 Of these
patients, 10% to 15% will have more prolonged symptoms after
1 week and can be inclined to develop depression and other
mental health issues, sleep disturbance, and anxiety.47 Any child
experiencing extended symptoms should undergo comprehensive
neuropsychological testing to assess symptoms, cognitive
function, and other residual injury and should be considered for
further imaging, including MRI with susceptibility-weighted
imaging,53,54 diffusion tensor imaging,55 blood oxygen level–
dependent signal sequences,56 or other modern assessments
for extent of injury.57 Similarly, if there are visual or vestibular
symptoms, more extended testing may be required for these
areas. Although some of these symptoms can be managed with
medications, most recommendations are for significant periods of
uninterrupted rest and decreased stimulation or brain activation,
including reduced electronics or television use or even reduced
focused time in school. In a study of children with mild head
injury, the children who continued with all normal school and out-
of-school cognitive activities or had the most limited reduction
(continuing to read, do homework, sending text messages, and
participating in other stimulating activities) had the longest
duration of postconcussive symptoms.58 Some physicians believe
that a child who is still experiencing postconcussive symptoms or
requires medication to suppress these symptoms should continue
to refrain from high-risk athletic activities. It is still controversial
how many concussions it takes before developing irreversible
neuropsychological sequelae, although it has been postulated
that repeated concussions in childhood and young adulthood
may predispose to the development of chronic traumatic
encephalopathy.42,59  growing bony defect. Thus the dural defect is greater than the
Moderate and Severe Traumatic Brain Injury
The first published guideline for acute medical management of
severe TBI in children was published in 2003 and later updated
in 2012.19,37 Because management of TBI in pediatric patients
differs from management in adults, better outcomes have been
noted in children who can be managed in a specialized pediatric
trauma center.60-63 As many as 39% of severe TBIs are associated
with other traumatic injuries, so initial management relies pri-
marily on resuscitation efforts as outlined earlier.54 In the follow-
ing sections, we focus specifically on neurosurgical management
after initial stabilization.  with 86% of pediatric patients with a score of less than 9 having an
SURGICAL INDICATIONS AND PREOPERATIVE
CONSIDERATIONS
At the time of initial evaluation, the neurosurgeon often makes
a clinical decision about whether the patient requires immedi-
ate surgical intervention. Surgical intervention is indicated to
ensure stabilization physiologically, to treat a secondary insult, or
to treat intracranial hypertension from secondary injury. In the
most severe TBI cases, the decision to proceed with surgery often
carries a high probability of an unfavorable outcome. Recent
literature demonstrates that patient age and pupillary response
are the strongest predictors of outcomes in children with poor
postresuscitation neurological examinations (GCS score 3 or 4).64
Physiologically, in this population, hemostasis from the scalp
flap is particularly important because it can be a significant cause
of blood loss during surgery. In children younger than 2 years,
it may be beneficial to keep the periosteum intact over the bone
to minimize blood loss along the line of the planned bone flap.
Other indications may include complex skull fractures resulting
in open depressed fractures, cerebrospinal fluid leaks, or gross
contamination.
Urgent surgical intervention should be considered in cases of
elevated ICP that is due to diffuse swelling and/or an intracranial
mass lesion such as intracranial or intracerebral hematoma.
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Later in the posttraumatic course, cranioplasty and “growing
skull fracture” repair may also need to be considered in pediatric
patients. These procedures are discussed subsequently, with
special considerations for pediatric patients.
Skull Fracture
Skull fractures can generally be categorized into open versus
closed fractures and structurally as linear, displaced, depressed,
or comminuted. Most fractures in children are treated conserva-
tively without operative management; however, open fractures,
significantly depressed fractures, and fractures that involve the
posterior wall of the frontal sinus with dural disruption and cere-
brospinal fluid leak may require surgical repair. Uniquely, the
cranial bones in children remodel quickly. Furthermore, the
frontal sinuses typically do not start to aerate until age 4 to 5
years, and thus frontal fractures in young children can be man-
aged conservatively, as sinuses are often not involved.65
Young children with thinner and softer bone can have a small
area of depressed bone referred to as a ping-pong fracture. A burr
hole can often be placed adjacent to the fracture allowing the
surgeon to slide an instrument underneath the bone to elevate
the fracture from inside; an alternative method involves inserting
a temporary screw into the depressed bone and percutaneously
applying outward pressure.
In a small subset (0.1%) of patients with linear fractures, the
defect can expand in size over time and cause noticeable cosmetic
deformity.65 These growing skull fractures are always associated
with a dural tear, with the dural edges retracting under the
observed bony pathology. It is important to locate these edges to
repair them, with or without a patch. The skull can be repaired
using calvarial split-thickness grafts, various commercial rapid-
setting cranioplastic materials, or morcellized bone.66 
Placement of Intracranial Pressure Monitors and
External Ventricular Drains
Elevated ICP is independently associated with increased morbid-
ity and mortality; aggressive management of elevated ICP is para-
mount in the setting of significant head trauma. Clinically the
presence of elevated ICP is best predicated based on GCS scores,
ICP of more than 20 mm Hg in one study.67 Thus based on GCS
score, overall clinical status, and suspicious radiographic findings,
an ICP monitor may be warranted.68 Monitoring and lowering
ICP after severe TBI have been shown to improve overall out-
comes and survival.37,69 Of note, an open fontanelle in an infant is
not an adequate replacement of definitive ICP monitoring.
Strain gauge–type or “wire” ICP monitors can be used
without concern of using a “bolt” and can be considered for
younger children. Ventriculostomies are also viable options in
children with severe TBI. Some patients with refractory ICP
have experienced further ICP decrease with a lumbar drain in
addition to an external ventricular drain. A lumbar drain should
be considered only if there is a functioning external ventricular
drain, open basal cisterns, and no mass lesion.37 
Hematoma Evacuation
In the presence of an identifiable hematoma causing either
focal neurological symptoms or decreased level of conscious-
ness, most surgeons proceed to operative intervention for
evacuation. Middle fossa and posterior fossa epidural hema-
tomas are most concerning because of the increased risk for
herniation.70 However, several series have suggested that neu-
rologically intact patients with epidural hematomas can be
managed with observation and serial imaging. In one study of
 CHAPTER 250  Management of Head Injury: Special Considerations in Children
BOX 250.3  Indications for Decompressive
Hemicraniectomy74,75,79,143
1. Diffuse swelling on CT scan
2. Patient within 48 hours of initial injury
3. No episodes of sustained intracranial pressure of >40 mm Hg
before surgery
4. GCS score of >3 at some point after injury
5. Secondary deterioration after initial good clinical presentation
6. Evidence of herniation
CT, Computed tomography; GCS, Glasgow Coma Scale.
13 pediatric patients, 12 patients were successfully managed
with observation alone, and all made a full recovery at their
4-month follow-up visit with no residual hematoma on CT
scan.71 Conversely, others argue that although it is possible
to avoid surgery in select cases, patients typically experience
prolonged headache, nausea, and vomiting, which may actually
result in longer hospital stays.
Subdural hematomas are typically the result of venous
bleeding from a cortical or bridging vessel with brain imaging
demonstrating layered blood products crossing cranial sutures.
When acute, they necessitate a full craniotomy; a chronic
subdural hematoma may be successfully evacuated with burr
holes. Subdural hematomas are common in abusive head
trauma.72
Principles for trauma craniotomies use the general principles
outlined previously for operating in a pediatric population. If
significant edema is seen on preoperative imaging or during the
case, the bone flap should be left off.  the strongest regulators of blood flow in adults, and studies
Decompressive Craniectomy
Determining which patients will benefit from a decompressive
craniectomy for the treatment of elevated ICP in the absence
of a focal hematoma is more controversial. It is well known
that decompression can reduce ICP significantly.73,74 However,
some argue that patients who develop diffuse brain edema are
so severely injured that expected outcomes are poor regardless
of decompression. Decompressive craniectomies carry risk of
additional morbidity including intraoperative blood loss, devel-
opment of hygromas, hydrocephalus, and resorption of reim-
planted bone after cranioplasty.75-77 Some studies suggest that
pediatric patients are more likely to have better outcomes from
decompression if done early enough compared with their adult
counterparts.73,74,78,79 Box 250.3 lists some of the criteria to con-
sider when determining whether a patient would benefit from
decompression.
The technique for decompression can be similar to the
hemicraniectomy described earlier for hematoma evacuation, or
bifrontal craniotomy can be performed based on the location of
the edema and injury. Additionally, evidence shows significantly
lower ICP in patients who have had a duraplasty.80,81  of patients with TBI is centered on preventing intracranial
Cranioplasty
When the brain edema has subsided, the bone flap can be
replaced, usually at least 6 weeks to 3 months after the injury. If
there is any concern that the patient continues to have ongoing
medical issues, this can be delayed, and the patient can continue
to proceed with the rehabilitation course while wearing a helmet
for safety. In young patients, the autologous bone should be used
whenever possible rather than an artificial plate owing to contin-
ued skull growth. However, 50% of children will develop bone
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1891
resorption after cranioplasty, and rigid fixation is prudent.75,77,82
250
Graft failure is strongly correlated with larger defects (especially
defects greater than 75 cm2) and timing of reconstruction, with
significantly greater resorption rates when delayed beyond 6
weeks.83 
INTENSIVE CARE UNIT MANAGEMENT
Although the management of the full spectrum of trauma-asso-
ciated complications in a patient with TBI is beyond the scope of
this chapter, intensive care unit teams generally rely on neurosur-
geons to help guide management of ICP, posttraumatic seizures,
and need for repeat cranial imaging. Repeat imaging in patients
with severe TBI can be considered in the setting of no neuro-
logical improvement, increasing ICP, or inability to obtain an
adequate neurological examination owing to injuries or pharma-
cologic coma. Otherwise, routine repeat CT scans are not nec-
essarily needed.37 Management of ICP and seizures is discussed
later. 
PHYSIOLOGY
Cerebral metabolism, oxygen requirements, and glucose require-
ments are lower at birth but increase to a maximum at 3 to 9 years
of age. Consequently, cerebral blood flow increases in children
until a maximum at about 5 years of age, then gradually decreases
to adult levels. This time period correlates with the development
of vascular resistance, which is lowest in this age range and subse-
quently increases with age.84,85
These factors are important in understanding how
regulation of blood flow, metabolism, and oxygen levels
can differ in the pediatric brain. Carbon dioxide is one of
show an even stronger effect in children, with an up to 14%
change in velocity of blood flow for every 1 mm Hg change
in carbon dioxide. Children most effectively regulate cerebral
blood flow at mean arterial pressures between 60 and 160 mm
Hg.85 In TBI, autoregulation can become problematic and
can cause dangerous sequelae with ischemia, hyperemia, or
ICP elevations. Both an increase and a decrease in blood flow
can cause secondary injury. Decreases in overall blood flow
can cause ischemia, whereas increases in blood flow can cause
elevated ICP, brain edema, and hemorrhage. As many as 17%
to 28% of pediatric patients with mild TBI have been found to
have alterations in autoregulation. In children with severe TBI,
this rate increases to 42%.45,85
ICP can change in a biphasic way after a severe head trauma in
a child. Secondary cellular cascades from the initial inflammatory
episode can cause a delayed elevation in ICP.85-87 Because this
suspended ICP elevation is more common in children, one can
consider a longer duration for ICP monitoring than in adults.88
Prevention of secondary injury should be initiated as early
as possible with a focus on maintaining normal oxygenation,
temperature, and ventilation.89
The primary focus of neurocritical care management
hypertension. Cerebral perfusion pressure (CPP) likely provides
the best guidance for ICP management in infants and children.
CPP is calculated by subtracting ICP from the mean arterial
pressure. In correlative studies, young children 2 to 6 years old
have the best outcomes when their CPP is in the range of 40
to 60 mm Hg, whereas children 7 to 16 years old have the best
outcomes when their CPP is in the range of 50 to 70 mm Hg.90,91
However, no definitive studies have demonstrated improved
outcome by adherence to these CPP goals.37,92-94
To attain these ICP and CPP goals, several strategies can
be employed. A tiered management strategy is depicted in
1892 SECTION 8  Pediatrics
Suspected or confirmed
ICP elevation
Basic management of
head trauma
Figure 250.1. Tiered management
of intracranial hypertension.19 CSF,
Cerebrospinal fluid; ICP, intracranial pressure.
Fig. 250.1. If ICP remains elevated with basic maneuvers, second-
tier management strategies with cerebrospinal fluid drainage,
sedation and pain control, and hyperosmolar therapy can be
used. If ICP remains refractory, third-tier management strategies
include consideration of decompressive craniectomy, barbiturate
coma, hypothermia, and short-term hyperventilation.19 Of note,
steroids, which are commonly used in other situations in which
there is concern for elevated ICP owing to vasogenic edema (i.e.,
brain tumors), are contraindicated in trauma. Studies have shown
that steroids confer no improvement in outcomes following TBI
but do increase general rates of infections.24,95-98 Specifics on
medical management of intracranial hypertension are outlined in
the following sections.  the ICP remains refractory. If dropping the Paco2 to below 30
MEDICAL TREATMENT OF INTRACRANIAL
HYPERTENSION
Hyperosmolar Therapy
Both mannitol and hypertonic saline have been used as com-
mon hyperosmolar therapies to manage intracranial hyperten-
sion.87,99-102 Administration of mannitol generally entails boluses
of 0.25 to 1 g/kg, with goal serum osmolarity of 320 mOsm/L.19
Studies show a 10% decrease in ICP for 3 hours before return-
ing to baseline.99 Mannitol may cause a brisk diuresis in a patient
who is likely already at risk for hypovolemia because of traumatic
injury. Particularly, in a child with small overall blood volume,
volume status can be difficult to regulate with mannitol.
Although there are no published studies comparing
hypertonic saline to mannitol, the 2012 Guidelines for the
Acute Management of Severe TBI in Children, Second Edition,
favor the use of 3% hypertonic saline over mannitol.89 This
has been shown to be effective in children, with no significant
renal complications noted.103-106 The 3% hypertonic infusions
are administered as 0.1 to 1.0 mL/kg per hour, with goal serum
osmolarity of up to 360 mOsm/L.19,104 Hypertonic saline has not
been associated with a brisk diuresis and can help with overall
volume status. For patients with existing hypervolemia, more
concentrated hypertonic saline, such as 23.4%, has been studied
in trials as well, without significant complications in the pediatric
population.107  reserved for when other ways to address refractory ICP have
Hyperventilation
As discussed earlier, regulation of blood flow in children is partic-
ularly sensitive to serum carbon dioxide levels.85 Hyperventilation
decreases serum Pco2 and at extreme levels can put the patient
at risk for decreased overall cerebral perfusion.108 Continued
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Refractory elevated Barbiturate
ICP coma
Decompressive
craniotomy
Obtain ICP monitor
CSF drainage
Sedation and pain control
Hyperosmolar therapy
Surgical evacuation of mass lesion
Elevate head of bed
Maintain oxygenation
Eucapnia
Avoid hypotension
Avoid fever
Maintain adequate venous return
hyperventilation and hypocapnia can eventually decrease overall
bicarbonate levels and cause a left shift of the hemoglobin oxy-
gen affinity curve, decreasing oxygen release in brain tissue and
causing brain ischemia in addition to the overall restriction in
blood flow.109-112 Because of this, hyperventilation is meant to
be a short-term mechanism of decreasing ICP in patients with
an acute ICP elevation or herniation as a bridging therapy until
a more definitive method to lower ICP can be obtained, such as
decompressive craniotomy or barbiturate coma. There is no indi-
cation for using hyperventilation as a preventive therapy if ICP is
not currently elevated.37 Goals for hyperventilation can be using
a respiratory rate to obtain a Paco2 of 30 mm Hg or lower if
mm Hg, one can consider using brain tissue oxygen monitors or
venous oxygen monitors to ensure that the patient is not experi-
encing cerebral ischemia.19 
Sedation and Paralysis
Sedation has been noted to decrease ICP and likely works
through several different mechanisms. Propofol (2,6-diisopro-
pylphenol) is a commonly employed sedative to reduce ICP
owing to its vasoconstrictive properties. However, propofol-
related infusion syndrome is of particular concern in children,
and the drug should not be used for prolonged sedation (>12
hours) in pediatric patients with TBI.113 In this syndrome,
patients develop metabolic acidosis, hyperkalemia, hypertri-
glyceridemia, and hepatomegaly, which can rapidly lead to
multiorgan failure.114-117 Long-term propofol use in pediatric
TBI is generally avoided for this reason and is discouraged by
the US Food and Drug Administration.37 Sedative agents are
compared in Table 250.4. For further decrease in ICP, neuro-
muscular blockade can be added. Paralysis can decrease shiver-
ing, posturing, working against the ventilator, and airway and
thoracic pressures.118 Although this can successfully decrease
ICP, paralysis is also associated with increased rates of pneu-
monia, cardiovascular instability, and myopathy. Intensive care
unit stays tend to be longer when paralysis is used, and it also
compromises the ability to obtain a neurological examination
to assess change.19,119 Thus neuromuscular blockade should be
failed. 
Barbiturate Coma
Barbiturates are the sedatives associated with the most signifi-
cant ICP decreases and with improved outcomes. Barbiturates
control ICP by suppressing metabolism, changing vascular tone,
 CHAPTER 250  Management of Head Injury: Special Considerations in Children
TABLE 250.4   Sedatives for Intracranial Pressure Management114-117
Agents Pros
Benzodiazepines Less hypotension
Raises seizure threshold
Reduces cerebral metabolism and ICP
Narcotics Pain control
Little effect on blood pressure
Dexmedetomidine No respiratory depression
Can be used in patients who are not intubated
Decreases delirium
ICP, Intracranial pressure.
and decreasing free radicals and stabilizing cell membranes in
the brain.120,121 Barbiturate coma is commonly induced with
pentobarbital. Continuous electroencephalography is needed
to help titrate the maintenance dose because serum levels have
been shown to be inconsistently correlated with true treatment
effect.37 The dosing for pentobarbital includes a loading dose of
10 mg/kg and a maintenance dosage of 1 mg/kg per hour, with
adjustments for burst suppression.122
Barbiturates can cause concomitant hemodynamic instability
and may require the simultaneous use of vasopressors to
maintain an adequate blood pressure. In some pediatric studies,
the improvement in ICP is counterbalanced by mortality from
hemodynamic problems and may not actually result in improved
overall outcomes.123,124 Thus barbiturates should be used with
caution and should never be used unless other methods of ICP
control have failed.  isolated, mild TBI with no CT findings, quality of life 1 year
Seizures
Seizures are common after trauma and can increase cerebral
metabolism and ICP, contributing to secondary brain injury.89
Children have a preexisting lower seizure threshold than adults,
and 20% to 39% of children with severe TBI have seizures in the
early posttraumatic period.125-127 Seizure prophylaxis should also
be considered in high-risk populations, including TBI patients
younger than 3 years old, with cerebral edema, with intrapa-
renchymal injuries, with acute subdural hematomas, and with
depressed skull fractures.89 Anticonvulsants can decrease the inci-
dence of seizures and have been associated with improved overall
survival.19,125-127 Levetiracetam has been shown to be a safe and
efficacious agent in children.128 Subclinical seizures are common,
and an increasing number of pediatric centers have employed the
use of continuous electroencephalography in children with severe
TBI.129 Late posttraumatic seizures, defined as seizures occurring
more than 1 week after injury, can occur in 7% to 12% of patients
with TBI.19 Although long-term neurological sequelae of post-
traumatic seizures remain unclear, patients with TBI are twice as
likely to develop epilepsy as children without TBI.89,130  capabilities and family environment, including demographics,
Temperature and Hypothermia
Elevated body temperature is associated with increased over-
all metabolism, inflammation, excitotoxicity, seizures, and cell
death.6 In an initial pediatric study, improved outcomes were
seen after hypothermia compared with historical controls.131
However, several subsequent studies have failed to demonstrate
overall benefit. Although ICP may improve, overall outcome
can include increased mortality and worse functional outcome
because of other factors associated with hypothermia such as
increased coagulopathy, cardiovascular problems, and hemody-
namic instability.132 In a review of seven randomized controlled
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1893
250
Cons Use
Slow wakeup due to buildup of metabolites Induction: 0.1 mg/kg
Withdrawal Maintenance: 0.01–0.2
Delirium mg/kg/h
Respiratory depression
Plateau with no increase in ICP control at high doses
Could possibly increase ICP in high-dose boluses Adjunct to other
sedatives
Hypotension Induction: 1 μg/kg
Bradycardia Infusion: 0.42–1 μg/kg/h
Arrhythmia
trials, mortality and arrhythmia were increased in the hypother-
mic cohort.133 At this time, there is no strong evidence to support
the use of therapeutic hypothermia in pediatric TBI, although
avoidance of hyperthermia is maintained in many pediatric
trauma centers. 
OUTCOMES
Much attention recently has been given to previously unrecog-
nized cognitive and psychological sequelae of isolated mild TBI
and especially repeated mild TBI or concussions. Concussion
typically results in short-lived, transient neurological impair-
ment that resolves spontaneously. However, approximately
25% to 35% of children may experience physical, cognitive,
emotional, or behavioral postconcussive symptoms.13 Even in
after original injury can be diminished in as many as 10% of
pediatric patients.134 In adolescents, there is a twofold increased
risk for developing a new mood disorder in the 5 years follow-
ing a TBI.135
Some studies suggest that patients with complicated mild
TBI have outcomes similar to patients with moderate head
injuries,136 whereas other studies suggest that there are eventually
no functional differences for patients with complicated injuries
compared with patients with uncomplicated mild TBI.10 When
evaluating children with multiple concussive injuries, risks for
chronic headaches and cognitive and behavioral deterioration
should be discussed in detail with both the patients and the parents
to help inform decisions about further and future participation in
sports with increased risk for concussive injuries.
With advancements in neurocritical care, overall outcomes
for children with moderate and severe TBI continue to improve,
with more recent studies reporting less than 25% mortality.69
With rehabilitation efforts, the greatest functional improvements
are observed in basic activity participation, while communication
and independent self-care are the least likely to recover.136,137
Predictors of poor long-term overall outcome are preinjury
parenting style, and socioeconomic status.27,138,139 
CONCLUSION
The scope of pediatric TBI ranges from evaluating an athlete
who wishes to return to sports after a concussion to a child
who has severe systemic injuries from a motor vehicle collision.
Management of pediatric head injuries requires rapid and effec-
tive stabilization techniques while simultaneously identifying and
correcting modifiable risk factors for secondary injury. Specific
knowledge of how the pediatric brain responds to trauma and
understanding differences in physiology are key to optimizing
overall outcome.
1894 SECTION 8  Pediatrics

SUGGESTED READINGS Kuppermann N, et al. Identification of children at very low risk of clini-
Adelson PD, et al. Phase II clinical trial of moderate hypothermia after se- cally-important brain injuries after head trauma: a prospective cohort
vere traumatic brain injury in children. Neurosurgery. 2005;56:740–754; study. Lancet. 2009;374:1160–1170.
discussion 740–754. Pechmann A, et al. Decompressive craniectomy after severe traumatic
Guskiewicz KM, et al. Cumulative effects associated with recurrent con- brain injury in children: complications and outcome. Neuropediatrics.
cussion in collegiate football players: the NCAA Concussion Study. J 2015;46:5–12.
Am Med Assoc. 2003;290:2549–2555.
Khanna S, et al. Use of hypertonic saline in the treatment of severe re- See a full reference list on ExpertConsult.com
fractory posttraumatic intracranial hypertension in pediatric traumatic
brain injury. Crit Care Med. 2000;28:1144–1151.
Kochanek PM, et al. Guidelines for the acute medical management of se-
vere traumatic brain injury in infants, children, and adolescents–second
edition. Pediatr Crit Care Med. 2012;13(suppl 1):S1–S82.

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