semirigid cervical collar or inline manual stabilization. If intubation is
determined to be necessary, endotracheal intubation is the preferred method.
Evaluation by a neurosurgeon is preferred prior to intubation with
neuromuscular blockade, but there should not be any delay in obtaining an
advanced airway. Patients should be preoxygenated, and lidocaine should
be utilized as a pretreatment medication. Atropine is no longer considered
to be standard of care for pediatric rapid sequence intubation, and special
consideration must be taken with this population as it can mask bradycardia
secondary to increased ICP. Lidocaine at 1 to 2 mg/kg of weight with a
maximum of 100 mg is used to prevent potential increased ICP by blunting
airway reflexes. Rapid sequence intubation includes administration of
medications for sedation and paralysis. Sedative medications should be
used to decrease airway responses and keep the patient comfortable. (Refer
to Chapter 8 Airway .) Preferred medications for the child in whom a head
injury is suspected include etomidate and midazolam. Etomidate has
minimal cardiovascular effects and is used effectively in patients with
hemodynamic instability, thus providing neuroprotection. The typical dose
of etomidate is 0.3 mg/kg of weight. Midazolam has minimal effects on
systemic arterial pressure with typical dosage of 0.1 to 0.3 mg/kg of weight.
Neuromuscular blockade and paralysis may be achieved with rocuronium at
doses of 0.6 to 1.2 mg/kg of weight or succinylcholine at doses of 1 to 2
mg/kg of weight. There is no available outcome data regarding the use of
sedatives and paralytic medications in children with ciTBI, and their use
should be tailored to the individual patient.
Noninvasive maneuvers also should be standard management to decrease
ICP. The head of the bed should be elevated to 30 degrees, the head should
be kept in a neutral position while maintaining cervical spine
immobilization, ventilation to maintain PaCO2 at 35 to 40 mm Hg,
continuous sedation infusion to prevent complications after intubation and
agitation. There is no evidence to support or refute the use of brain
oxygenation monitoring, transcranial Doppler, cerebral microdialysis or

near-infrared spectroscopy (NIRS) in conjunction with ICP monitoring.
Aggressive hyperventilation should not be the standard as an initial therapy;
however, it may be necessary acutely for refractory intracranial
hypertension and to prevent cerebral herniation.


If the above measures are not adequate to control ICP, hyperosmolar
therapy may be necessary to control cerebral perfusion pressure. Hypertonic
(3%) saline may be used in the acute setting with bolus doses of 6 to 10
mL/kg of weight. Continuous infusions of hypertonic saline may be
necessary to maintain ICP less than 20 mm Hg with doses starting at 0.1
mL/kg of weight that may need to be increased incrementally to 1.0 mL/kg
of weight per hour, titrated to keep target serum sodium levels between 145
and 155 mEq/L. Serum osmolarity should be monitored and maintained at
less than 360 mOsm/L. In conjunction with hyperosmolar therapy,
externalization of CSF drainage by placement of a ventricular catheter may
be necessary to monitor and adjust ICP to maintain ICP <20 mm Hg.
Depending on the stability of the patient, decompressive craniectomy may
be necessary, especially for the evacuation of intracranial hematomas.
Craniectomy is necessary for large hematomas associated with neurologic
compromise or impending cerebral herniation. The timing of surgical
intervention depends on the severity of the injury and stability of the patient
and should be executed in collaboration with neurosurgery.
Other therapeutic adjuncts include the routine use of acetaminophen to
maintain a core temperature of 36°C to 37°C and the initiation of
antiseizure prophylaxis with levetiracetam at loading doses of 60 mg/kg of
weight (maximum of 4,500 mg) and continuing maintenance therapy within
12 hours at 30 mg/kg/day.
Medications that are not routinely recommended in children with ciTBI
include steroids. The use of corticosteroids has not been shown to either

improve neurologic outcome or decrease ICP. When used in spinal cord
injuries, there is anecdotal evidence that it may worsen outcomes for
patients with ciTBI.
Head trauma has been recognized as a common cause of posttraumatic
hydrocephalus. As management schemes for neurotrauma have improved
over recent years, more patients are surviving severe head traumas with
hydrocephalus occurring as a delayed complication. About 4% of patients
develop posttraumatic hydrocephalus requiring surgical CSF diversion.
Specific Brain Injury Patterns
The spectrum of brain injury patterns ranges in severity from mild and
isolated to diffuse with associated hemorrhages. The continuum of injury is


based upon mechanism; however, neurologic outcome is related to degree
of neurologic impairment at time of presentation.
Diffuse Injury. These injury patterns include DAI, cerebral edema, hypoxic
ischemia, and diffuse vascular injuries. DAI is due to shear injuries of axons
and blood vessels involving the white matter of the brain. The shear occurs
with acceleration and deceleration or rotational forces involving the brain
matter. The degree of tissue disruption is indicative of the amount of energy
dissipation. DAI may not be seen on CT scan, as the severity of injury
typically has DAI with associated intracerebral hemorrhages, especially
multiple petechial hemorrhages in the deep white matter. MRI is more
sensitive in delineating transient signal changes along white matter tracts.
Cerebral edema may be caused by a multitude of factors. Not only is
edema due to direct insult to the neurons with local release of inflammatory
mediators and vascular leakage, but may progress as secondary injury due
to hypoxemia and changes in cerebral blood flow. On CT scan, brain edema
appears as an area of decreased density associated with brain shift,
especially pronounced with loss of gray–white matter interface

differentiation. Both DAI and cerebral edema are commonly associated
with intracerebral hemorrhage and/or contusion and may lead to herniation.
The component of hemorrhage or significant mass effect resulting from
edema becomes a neurosurgical emergency.
Focal Injury. These injury patterns include contusions, lacerations,
hemorrhage, and midline shifts. Cerebral contusions are typically due to
direct impact of the brain along dural edges or intracranial bony surfaces.
The presentation may be benign or symptomatic with a focal neurologic
deficit or seizure. Isolated contusions with minimal localized swelling
without midline shift are injuries that may be managed nonsurgically.
Subdural hemorrhage occurs when bridging vessels rupture into the
potential space between the dura and the arachnoid. This anatomic location
allows the blood to transverse cranial sutures and accounts for the typical
crescent-shaped or convex appearance ( Fig. 113.1 ). Subdural hematomas
in children under the age of 2 years are more likely to be associated with
child abuse than other injury patterns. Please refer to Chapter 87 Child
Abuse/Assault for further discussion.


FIGURE 113.1 Traumatic subdural hemorrhage. Axial noncontrast CT shows a
significant 6-mm SDH over the left hemispheric convexity with approximately 9 mm of
midline shift.

In contrast, the vascular injury causing epidural hemorrhage, typically the
middle meningeal artery or dural venous sinus, allows blood to transverse
the space between the dura and overlying bony surface. The accumulating
epidural blood is not able to transverse the dural attachments at the sutures
accounting for the lens-shaped biconvex appearance on radiographic
imaging ( Fig. 113.2 ). Venous bleeding may accumulate slowly and
account for the classic presentation of patients with epidural hematomas

with a period of lucidity followed by rapid clinical deterioration.