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AACN Clinical Issues

Volume 16, Number 2, pp. 212231



C 2005, AACN

Management of Increased Intracranial


Pressure in the Critically Ill Child With
an Acute Neurological Injury
Kelly Keefe Marcoux, MSN, CPNP-AC, CCRN

mal blood due to a ruptured arteriovenous


malformation or aneurysm. The mechanism
Increased intracranial pressure reflects by which ICP increases varies depending on
the presence of mass effect in the brain the specific etiology (Table 1). The increased
and is associated with a poor outcome in ICP can be due to either an increase in tis-
children with acute neurological injury. If sue volume, cerebral blood volume, or cere-
sustained, it has a negative effect on brospinal fluid (CSF) volume. Examples of
cerebral blood flow and cerebral perfusion these are listed in Table 2. One or more of
pressure, can cause direct compression these factors occurring alone or simultane-
of vital cerebral structures, and can lead ously can increase ICP. The pathophysiology
to herniation. The management of the and management of increased ICP is based
patient with increased intracranial on the Monro-Kellie doctrine.
pressure involves the maintenance of an
adequate cerebral perfusion pressure,
 Normal Cerebral Physiology
prevention of intracranial hypertension,
and optimization of oxygen delivery. This
Intracranial pressure is defined as the total
article reviews the neurological
pressure exerted by the brain, blood, and CSF
assessment, pathophysiology, and
in the intracranial vault. The Monro-Kellie
management of increased intracranial
doctrine states that the cranium is a fixed
pressure in the critically ill child who has
vault made up of 3 components: the brain
sustained an acute neurological injury.
(80%), blood (10%), and CSF (10%).
(KEYWORDS: acute neurological injury,
When there is an increase in any one of these
critically ill child, ICP management,
components, one or more of the other com-
increased intracranial pressure,
ponents must decrease to keep the total vol-
neurological assessment)
ume the same. The blood and the CSF are
the only compartments that can compensate.
The CSF compensates by displacing CSF from
the ventricles and the cerebral subarachnoid
Children may have increased intracranial
pressure (ICP) for a variety of reasons. The
most common etiologies of increased ICP          

in the pediatric intensive care unit (PICU) From the Robert Wood Johnson Medical School, Uni-
are due to severe traumatic brain injury versity of Medicine & Dentistry of New Jersey, Piscat-
away, and the Bristol-Myers Squibb Childrens Hospital,
(TBI), hydrocephalus, brain tumors, infec- New Brunswick, NJ.
tions (ie, meningitis, encephalitis), metabolic Reprint requests to Kelly Keefe Marcoux, Clinical As-
encephalopathy, hypoxic/ischemic brain in- sistant Professor, 26 Covered Bridge Road, Neshanic Sta-
jury, cerebral infarction, and intraparenchy- tion, NJ 08853 (marcoukk@umdnj.edu).

212
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  213

18 months old), may be able to compensate


TABLE 1  Etiology of Increased
longer to chronic changes in the intracranial
Intracranial Pressure vault, but will still be susceptible to acute in-
Based on Acute creases in ICP. It is crucial to understand the
Neurological Insult Monro-Kellie doctrine because management
of increased ICP revolves around this basic
Acute principle.
Neurological Possible Etiology of Increased
Insult Intracranial Pressure Other key concepts of intracranial dynam-
ics include autoregulation, compliance, cere-
Traumatic brain Hematoma, cerebral edema, bral blood flow, cerebral metabolic rate, and
injury cerebral ischemia,
intraventricular or intracerebral
cerebral perfusion pressure (CPP). Autoreg-
hemorrhage ulation is the maintenance of a steady cere-
Hydrocephalus Obstruction or impairment of bral blood flow (CBF) by vasoconstriction
cerebrospinal fluid absorption, and vasodilatation of the cerebral vessels de-
cerebral edema spite fluctuations in systemic blood pressure.
Infections (eg, Meningeal scarring, inflammatory
meningitis, response, cerebral edema, If autoregulation is impaired, CBF and cere-
encephalitis) hydrocephalus, cerebral bral blood volume (CBV) will become depen-
hyperemia dent on changes in systemic blood pressure.
Brain tumor Mass effect of tumor, peritumoral Compliance is an indicator of the brains tol-
edema, hydrocephalus
Intraparenchymal Mass effect, cerebral edema
erance to increases in ICP. It is defined as a
bleed change in pressure resulting from a change
Intraventricular Hydrocephalus in volume. Each patient has varying degrees
bleed of compliance even with similar injuries. The
exact factors contributing to this are still un-
known. When the patients compliance is ex-
space through the foramen magnum to the
hausted, there is a dramatic increase in the
spinal subarachnoid space. The production
pressure/volume curve, leading to a rapid el-
of CSF can also be decreased, as well as the
evation in ICP.
absorption increased, to decrease the total
In an uninjured brain, cerebral blood flow
CSF. In addition, venous blood compensates
is regulated to supply the brain with adequate
by being displaced by the dural venous si-
oxygen and substrates to meet its demands.
nuses. For instance, if there is an intracranial
The main physiologic influences on CBF are
mass (eg, brain tumor), the brain and the
the partial pressure of arterial carbon diox-
arterial volume will remain static while the
ide (PaCO2 ), arterial oxygenation, pH, CPP,
CSF and the venous volumes will decrease
and cerebral metabolic rate. The PaCO2 is di-
until they can no longer compensate, at
rectly proportional to CBF and is the most po-
which point the ICP will increase (Figure 1).1
tent chemical mediator of CBF. An increase
However, infants and children with open
in PaCO2 will cause vasodilatation, which
fontanels and sutures (usually less than
will increase CBF and, thereby, potentially in-
crease ICP. Likewise, acidosis and hypoxemia
will also increase CBF by causing vasodilata-
TABLE 2  Etiology of Intracranial tion. CBF in excess of tissue demand will lead
Pressure Based on the to hyperemia. Normal CBF in an adult is ap-
Monro-Kellie Doctrine proximately 5070 mL/100 g/min, and CBF of
healthy children was found to be as high as
Increase in tissue volume
Cerebral edema
108 mL/100 g/min.2 CBF < 20 mL/100 g/min
Mass lesion is usually indicative of cerebral ischemia and
Increase in cerebral blood volume has been associated with a poor outcome in
Intracranial hemorrhage children with TBI.3
Hematoma formation Seizure activity and fever will increase
Decreased venous drainage CBF and cerebral metabolic rate. Methods
Increased arterial blood flow
to decrease the cerebral metabolic rate,
Increase in cerebrospinal fluid volume such as hypothermia and barbiturates, will
Hydrocephalus
also decrease CBF. Cerebral metabolism is
214  MARCOUX AACN Clinical Issues

for more than 5 minutes, although a lower


number may be used for infants and young
children. One suggestion for pediatric pa-
tients has been to maintain the ICP < 20 mm
Hg for children aged 8 years to adults, < 18
mm Hg for children aged 18 years, and < 15
mm Hg for infants.5
An ICP > 20 mm Hg has been found to
be a powerful predictor of poor neurological
outcome in adults with TBI.9,10 ICP normally
increases with activities such as suctioning,
painful stimuli, and coughing and does not
Figure 1. Intracranial compensation for an expand- warrant intervention unless it does not return
ing mass lesion. CSF, cerebrospinal fluid; ICP, intracra- to baseline within about 5 minutes. However,
nial pressure. Reprinted with permission from Rogers interventions to minimize the ICP response
MC. Textbook of Pediatric Intensive Care. Baltimore, to these activities, such as lidocaine prior to
Md: Williams & Wilkins; 1996:646. suctioning, should be instituted. It is impor-
tant to distinguish normal or expected in-
dependent on glucose to meet the bodys creases in ICP versus intracranial hyperten-
energy demands. The brain functions via sion because the latter requires immediate
adenosine triphosphate (ATP) and the Krebs intervention based on a tiered management
cycle to maintain aerobic metabolism. If there approach.
is hypoxia, the Krebs cycle cannot be acti-
vated and anaerobic metabolism will ensue.
This will lead to the production of pyruvate  Pathophysiology Related to
and lactate, which will decrease the amount Increased ICP
of ATP available for the cells and, thereby,
decrease the amount of energy available.4 In addition to the primary injury caused by
Cerebral perfusion pressure (CPP) is the TBI, a space-occupying lesion, or an intra-
pressure at which cells are perfused and is cerebral bleed, etc., cerebral edema is often
an important indicator of CBF. Sufficient CPP a major cause of increased ICP. Cerebral
is necessary to prevent the development of edema can be categorized as vasogenic, cy-
secondary cerebral ischemia. CPP provides totoxic, or interstitial. However, rarely does
an indirect measurement of CBF and is cal- one occur in isolation; rather, the patient with
culated by measuring the difference between cerebral edema may have a combination of
the mean arterial pressure (MAP) and the ICP all 3 mechanisms. Vasogenic cerebral edema
as demonstrated by the following equation: is due to increased capillary permeability
CPP = MAP ICP. Normal CPP values for around the area of injury or inflammation.
children are not clearly established, but the It can be local or diffuse and occurs around
following values are generally accepted as mass lesions (eg, brain tumors, abscesses,
the minimal pressure necessary to prevent intracerebral hematomas) and inflammatory
ischemia: adults CPP > 70 mm Hg; chil- processes (eg, meningitis, encephalitis). Cy-
dren CPP > 5060 mm Hg; infants/toddlers totoxic cerebral edema is due to cerebral
CPP > 4050 mm Hg.5 Research has shown ischemia and hypoxia, causing irreversible
that a CPP < 40 mm Hg is a significant cell death. The cells affected may include
predictor of mortality in children with TBI.6 neurons and astrocytes, and occurs in dif-
Furthermore, in a study of 17 comatose fuse axonal injury, cerebral infarction, and
children with severe central nervous system near drowning. Interstitial cerebral edema
(CNS) infections, a CPP < 30 mm Hg was is often seen in patients with obstructive
associated with universal mortality.7 hydrocephalus or excessive CSF production
Normal ICP values are estimated at 26 and is due to an increase in the hydrostatic
mm Hg for infants and 37 mm Hg for young pressure of CSF. Cerebral edema begins to
children. The normal ICP for older children occur immediately after TBI, intracerebral
and adults is 010 mm Hg.8 Intracranial hy- hemorrhage, and other cerebral insults, and
pertension is defined as an ICP > 20 mm Hg increases for 72 hours post-insult.11
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  215

 Assessment and Monitoring compression. It is important to note earlier


signs of increased ICP (see Table 3) because
The initial assessment of the neurologi- Cushings triad is a very late sign in neurolog-
cally injured child consists of assessment of ically injured children and usually indicates
ABCs (airway, breathing, and circulation), impending herniation.
Glasgow Coma Scale (GCS) score, cranial
nerve function, signs and symptoms of in- Neurological Assessment
creased ICP, temperature, and cardiorespira-
tory assessment. Astute observation of any A thorough neurological assessment must be
abnormal respiratory patterns is crucial, since performed as soon as the child is clinically
this may be the first vital sign change in- stable because this will serve as the base-
dicating neurological dysfunction. Abnormal line for comparison of future examinations.
respiratory patterns that may be detected After the cardiorespiratory status has stabi-
include Cheyne-Stokes, central neurogenic lized, the GCS is determined. It is impor-
hyperventilation, apneustic, ataxic, and clus- tant to utilize a modified GCS for infants and
ter breathing. All, except for Cheyne-Stokes, young children in order to obtain the most
indicate brain stem abnormality. Cheyne- accurate score (Table 4). In a study of 151
Stokes is less specific and indicates a cere- children, a GCS < 8 twenty-four hours after
bral, cerebellar, or brainstem impairment. TBI, in addition to factors such as hypoxia
The most ominous cardiorespiratory ab- and cerebral edema, was associated with a
normality is Cushings triad. Cushings triad poor outcome.12 To obtain the best response,
occurs when there is cerebral ischemia caus- it is necessary to give the patient the max-
ing peripheral vasoconstriction. This vaso- imal stimulationthis may include giving
constriction leads to increased systolic blood painful stimuli such as mandibular pressure,
pressure to improve cerebral perfusion. Car- sternal rub, or supraorbital pressure. These
diac baroreceptors sense this increased blood tests are optimal because they assess the
pressure, resulting in a vagal response man- central nervous system response, whereas
ifested as bradycardia. Abnormal or irregu- fingerbed pressure assesses peripheral pain
lar respirations are the final component of response.
Cushings triad and occur due to brainstem Cranial nerve (CN) testing is next and be-
gins with an assessment of CN III to de-
termine direct and consensual pupillary re-
sponse including size, reactivity, and shape
TABLE 3  Signs and Symptoms of of each pupil. It is imperative to be aware
Increasing Intracranial of medications that were administered that
Pressure may affect pupil response (eg, atropine, nar-
cotics). At least 10 seconds should elapse
Early signs and symptoms between each eye exam to allow the consen-
Headache sual response to fade. Abnormal pupillary re-
Emesis
Change in level of consciousness sponses include pupils that are unequal, con-
Decrease in Glasgow Coma Scale score stricted, dilated, nonreactive, or have hippus
Irritability (Table 5). Hippus is the abnormal dilation
Sunsetting and constriction of the pupil in response to
Decreased eye contact (infants)
Pupil dysfunction
bright light. It may indicate pressure on CN III
Cranial nerve dysfunction and be associated with transtentorial hernia-
Seizures tion or it may be insignificant and represent
Late signs and symptoms a normal variant.
Further decrease in level of consciousness If the patient is awake, the 6 fields of gaze
Bulging fontanels are assessed to determine extra-ocular move-
Decreased spontaneous movements
Posturing
ments (EOMs). If the patient is unrespon-
Papilledema sive, EOMs can be assessed by oculocephalic
Pupil dilation with decreased or no response to light testing (Dolls eyes) and oculovestibular test-
Increased blood pressure ing (cold calorics). However, if the C-spine
Irregular respirations has not been cleared, the oculocephalic test
Cushings triad (late, ominous sign)
should be deferred. An abnormal response
216  MARCOUX AACN Clinical Issues

TABLE 4  Modified Glasgow Coma Scale for Infants and Children


Score Infant/Nonverbal Child Verbal Child/Adult
Eye opening 4 Spontaneously Spontaneously
3 To speech To verbal command
2 To pain To pain
1 No response No response
Best motor response 6 Normal spontaneous Obeys command
movement
5 Withdraws to touch Localizes pain
4 Withdraws to pain Flexion withdrawal
3 Abnormal flexion (decorticate) Abnormal flexion
2 Extension (decerebrate) Extension (decerebrate)
1 No response No response
25 Years > 5 Years
Best verbal response 5 Cries appropriately, coos Appropriate words Oriented
4 Irritable crying Inappropriate words Confused
3 Inappropriate screaming/ Screams Inappropriate
crying
2 Grunts Grunts Incomprehensible
1 No response No response No response

to oculocephalic testing (as you turn the manage their oropharyngeal secretions and
patients head side-to-side, the eyes remain protect their airway. Cranial nerves and their
fixed and do not rotate) may indicate injury functions are summarized in Table 6.
to the midbrain or pons, or that the patient Motor assessment includes recognition of
is in a deep coma. An abnormal response any abnormal posturing (eg, extension, flex-
to oculovestibular testing (after irrigating ion, flaccidity), muscle symmetry, strength,
each external auditory canal with iced wa- and tone. Flaccidity indicates severe dysfunc-
ter, the eyes do not deviate toward the tion of the lower brain stem. Deep tendon
side of irrigation with nystagmus) may indi- reflexes are elicited to assess for central and
cate injury to cranial nerves III, VI, or VIII, peripheral nervous system dysfunction.
or brain stem injury. The fundus is exam- Abnormalities that are detected in the
ined for papilledema. Although the presence neurological exam must be correlated with
of papilledema indicates increased ICP, its the patients previous examination, diagno-
absence does not indicate the absence of sis, and radiologic findings. The location of
increased ICP. The fundus is also examined a mass lesion or hemorrhage, or presence
for retinal hemorrhages, which may indicate of mass effect or hydrocephalus must be as-
child abuse, sagittal sinus thrombosis, or co- sessed immediately to accurately diagnose
agulation abnormalities. and respond to impending herniation.
Further cranial nerve testing in the unre-
sponsive or intubated child should include
Radiologic Assessment
eliciting a gag or cough reflex, and assess-
ment of swallowing. Impairment in CN IX The radiologic study of choice for imme-
and X can greatly affect the childs ability to diate assessment of the child with acute

TABLE 5  Abnormal Pupillary Responses


Pupillary Finding Possible Etiology
Bilateral fixed and dilated pupils Indicates inadequate CPP; may be irreversible
Bilateral constriction Injury to pons; early central herniation; opiod administration
Unilateral fixed and dilated Transtentorial herniation; traumatic optic nerve injury
Unilateral constriction Horners syndrome; unilateral brainstem injury
Hippus May indicate irritation to oculomotor nucleus; can be normal variant

CPP, cerebral perfusion pressure.


Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  217

have a neurodiagnostic test indicative of a


TABLE 6  Function of Cranial
high probability of increased ICP (ie, cerebral
Nerves edema, midline shift, cisternal compression,
Cranial Nerve Function
intracerebral hemorrhage).13,14 Children who
do not usually benefit from ICP monitoring
I: Olfactory Smell are children with hypoxic injuries (ie, near
II: Optic Vision drowning) and some central nervous system
III: Oculomotor Movement of eyeball;
pupillary constriction and
infections (ie, encephalitis).
accommodation Although ICP monitoring has never been
IV: Trochlear Downward/inward movement subjected to randomized controlled stud-
of eye ies to evaluate its effectiveness, its use has
V: Trigeminal Facial sensation; open/close been associated with decreased morbidity
mouth
VI: Abducens Lateral movement of eyeball and mortality, and improved outcome in pa-
VII: Facial Taste; facial movement; tients with TBI, intracerebral hemorrhages,
salivation and lacrimation and CNS infections.1517 It is not the moni-
VIII: Vestibulocochlear Hearing; equilibrium tor itself that improves outcome, but the in-
IX: Glossopharyngeal Tongue taste/sensation;
swallowing; salivation
formation gleaned from this modality that
X: Vagus Speech, swallowing; control guides appropriate interventions. ICP mon-
cardiac, respiratory, and itoring is crucial to identify rapidly increas-
gastrointestinal tracts ing pressure and to institute appropriate ther-
XI: Accessory Movement of head and apy to prevent intracerebral herniation and
shoulders
XII: Hypoglossal Movement of tongue preserve cerebral perfusion. It is also neces-
sary to monitor ICP in order to calculate the
CPP.
The current gold standard for ICP mon-
neurological impairment or deterioration is itoring is intraventricular catheter place-
a noncontrast CT scan. A contrast CT scan ment, preferably an implantable micro-
may be necessary for further diagnosis of transducer (fiberoptic or strain-gauge). This
space occupying and vascular lesions, and method allows simultaneous monitoring of
infections, but is not warranted in the ini- ICP and management of increased ICP by
tial assessment of the child with increased CSF drainage. Other methods of moni-
ICP. On a noncontrast CT, highly dense struc- toring ICP include intraparenchymal, sub-
tures, such as blood, will appear white, and dural, subarachnoid, and epidural catheter
low density areas, such as air, CSF, and placementalthough the latter locations are
edema, will appear black. Initial inspection very rarely used. Depending on the type of
of the CT scan should proceed with ob- catheter, care will vary. ICP monitors with in-
servation of any intracranial mass lesion, tracranial transducers are zeroed at the time
midline shift, skull fracture, presence of hem- of placement and therefore do not require
orrhage (extra-axial, intraparenchymal, or in- any further zeroing. However, extracranial
traventricular), ventricular size, symmetry, transducers require frequent zeroing and lev-
and patency of basal cisterns (Figure 2). eling because they must be adjusted with
CT findings consistent with increased ICP changes in patient position and recalibrated
include a mass lesion, intracerebral hem- to atmospheric pressure.
orrhage, midline shift, loss of sulci, ven- In the past, children at risk for increased
tricular effacement, and cerebral edema ICP were managed primarily with interven-
(Figure 3). tions to decrease their ICP and maintain an
adequate CPP. This remains true, but the role
of cerebral oxygenation and the ability to
Neurological Monitoring
monitor it has recently been incorporated
ICP monitoring is indicated for children with into the care of these children. Adjunct mon-
TBI whose GCS < 8 or for children with other itoring modalities utilized to prevent cere-
acute neurological injuries who have clinical bral ischemia and optimize the patients out-
signs of increasing ICP, are status post resec- come include transcranial doppler (TCD)
tion of acute traumatic intracranial hematoma ultrasonography, jugular venous oxygenation
or other major neurosurgical procedures, or saturation (SjvO2 ) monitoring, brain tissue
218  MARCOUX AACN Clinical Issues

Figure 2. Normal brain computed tomography scan.

partial pressure oxygen monitoring (PbtO2 ), mines CBF velocity in the proximal vessels of
non-invasive cerebral oxygenation monitor- the Circle of Willis. This is particularly helpful
ing, and brain metabolism monitoring. when assessing for vasospasm and stenosis in
As mentioned previously, CPP monitor- a child with a stroke. The adequacy of CBF
ing involves calculating the difference be- related to cerebral metabolic demand can be
tween MAP and ICP. CPP can also be as- assessed by SjvO2 and PbtO2 . SjvO2 is a con-
sessed via xenon computed tomography (CT) tinuous measurement of the oxygen satura-
scan, perfusion CT, perfusion magnetic reso- tion in the jugular vein after cerebral perfu-
nance imaging (MRI), and positron emission sion has occurred. The jugular mixed venous
tomography (PET) scanning. These modali- saturation is compared to the arterial oxy-
ties offer excellent information regarding re- gen saturation, and the arteriovenous oxy-
gional CBF but are limited to one point in gen content difference (AVDO2 ) is then cal-
time. Continuous monitoring of CBF would culated. Normal SjvO2 is 55% to 70%; < 55%
be ideal and allow for interventions aimed at indicates cerebral hypoperfusion; < 40% in-
optimizing cerebral perfusion. For instance, dicates cerebral ischemia, whereas > 75% in-
if CBF were low, interventions would be di- dicates luxury perfusion and possible cellular
rected at increasing vasopressor support or death. Although SjvO2 is helpful in assessing
fluid therapy, or by decreasing cerebral de- cerebral oxygenation, a more direct approach
mand by increasing sedation. If the patient is the measurement of partial pressure brain
were hyperemic, then methods to decrease tissue oxygenation.
the CBF, such as hyperventilation, would be PbtO2 is a more specific method of mea-
instituted.18 suring cerebral oxygenation via a microprobe
CBF can also be evaluated via TCD ul- inserted directly into parenchymal tissue or
trasonography, which non-invasively deter- the penumbra of an intracerebral lesion.
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  219

Figure 3. Abnormal brain computed tomograph scan. A16-year-old status/post MVA; note right occipital EDH;
mass effect with right to left shift, uncal herniation; multiple parenchymal hemorrhagic contusions. MVA, motor
vehicle accident; EDH, epidural hematoma.

There is controversy regarding the optimal oxygenation, while others opt for placement
insertion area. Some advocate for placement in the penumbra of an intracerebral lesion
in uninjured brain tissue to assess global cere- to obtain information of cerebral oxygena-
bral oxygenation, while others opt for place- tion for the area most at risk.19 Ideally, either
ment in the penumbra of an intracerebral method allows for continuous monitoring of
lesion to obtain information of cerebral oxy- cerebral oxygenation and early recognition
genation for the area most at risk.19 Ideally, of cerebral ischemia. The various types of
either method allows for continuous monitor- catheters currently available (eg, Neurotrend,
ing of cerebral oxygenation and early recog- [Diametrics Medical Limited, St. Paul, MN],
nition of cerebral ischemia. The various types LICOX [Integra Life Sciences, Plainsboro, NJ])
of catheters currently available (eg, Neu- may yield different values, and interventions
rotrend [Diametrics Medical Limited, St. Paul, should be adjusted accordingly. Using the
MN], LICOX [Integra Life Sciences, Plains- LICOX catheter, normal PbtO2 values in un-
boro, NJ]) may yield different values and in- injured parenchyma are 20 mm Hg and in-
terventions should be adjusted accordingly. terventions to improve cerebral oxygenation
PbtO2 is a more specific method of measur- are indicated if the value is < 15 mm Hg.20
ing cerebral oxygenation via a microprobe in- For non-injured brain tissue, normal values
serted directly into parenchymal tissue or the are between 20 to 35 mm Hg. A decrease in
penumbra of an intracerebral lesion. There is partial pressure of brain tissue oxygen can
controversy regarding the optimal insertion be seen with decreased PaCO2 , hypoxemia,
area. Some advocate for placement in unin- increased ICP, and decreased CPP. Most of
jured brain tissue to assess global cerebral the available research on the utility of brain
220  MARCOUX AACN Clinical Issues

tissue oxygenation is from adult TBI pa- Other factors that may worsen secondary
tients. There are a few studies from adult brain injury after TBI include the release of
patients with brain tumors, arteriovenous excitatory neurotransmitters, the formation of
malformations, and stroke demonstrating that free radicals, and increased levels of intra-
the additional information obtained from this cellular calcium and potassium.4 The neuro-
modality is beneficial.19 A decrease in par- logical devastation caused by the secondary
tial pressure of brain tissue oxygen can be injury is often worse than the underlying pri-
seen with decreased PaCO2 , hypoxemia, in- mary disorder. Therefore, management is di-
creased ICP, and decreased CPP. Most of the rected at prevention of secondary injury.
available research on the utility of brain tis- Recently, recommendations on the man-
sue oxygenation is from adult TBI patients. agement of increased ICP in children with
There are a few studies from adult patients TBI have been published.13,22 These recom-
with brain tumors, arteriovenous malforma- mendations are based on pediatric studies
tions, and stroke demonstrating that the addi- and extrapolated from adult TBI research.
tional information obtained from this modal- Since there are limited outcome studies to
ity is beneficial.19 support the current management of children
Noninvasive measurement of cerebral with increased ICP from etiologies other than
oxygenation can be done by near-infrared TBI, this management is often instituted for
spectroscopy, which measures cerebral oxy- these children also. A schematic of increased
gen saturation via oximetry. This method ICP management is provided in Figure 4.
has the advantage of being noninvasive and The reader is also referred to the Guidelines
portable, but it is not commonly used in for the Acute Medical Management of Severe
pediatrics. Traumatic Brain Injury in Infants, Children,
Brain metabolism monitoring provides an and Adolescents13 for an algorithm detailing
individual assessment of brain chemistry af- escalation of therapy.
ter injury to guide treatment accordingly. Cur- ICP management based on the Monro-
rently, it is not routinely used in most PICUs, Kellie doctrine includes interventions to de-
but would allow for measurement of neu- crease cerebral volume, control CSF volume,
rochemicals (ie, lactate, pyruvate, glucose, control CBV, and decrease cerebral metabolic
glutamate, urea, and glycerol) via an intra- rate (Table 7). The goal of these therapies is
parenchymal microdialysis catheter. to maintain an age-appropriate CPP and an
ICP < 20 mm Hg or as appropriate for age.
In adults with TBI, the maintenance of CPP
 Management of Increased ICP > 70 mm Hg is used in some centers based
on research demonstrating that increasing the
Despite the etiology of the primary neuro- CPP, rather than decreasing the ICP, improves
logical injury, the main focus of management patient outcomes.23 However, there are lim-
is to prevent and minimize secondary injury. ited data on the benefits of CPP-driven man-
Although primary injury and secondary in- agement in pediatrics,24 and it is not routinely
jury most commonly refer to children with implemented.
TBI, this terminology can also be applied to
children with metabolic or hypoxic-ischemic
Airway, Breathing, and Circulation
encephalopathy and children with nontrau-
matic primary brain lesions, infections, and The initial management of the child with sus-
intracranial hemorrhage. The primary injury pected increased ICP is assessment of air-
refers to the initial insult regardless of the way, breathing, and circulation (ABCs). Even
mechanism of injury or illness. The sec- prior to a thorough neurological exam, if
ondary brain injury refers to the processes the patient is unarousable or having diffi-
that occur within hours to days after the culty maintaining a patent airway, rapid se-
primary injury that can be prevented or quence intubation should occur. Endotra-
minimizedsuch as cerebral ischemia, cere- cheal intubation should also be considered if
bral edema, and neurochemical alterations. the child has a GCS < 8, a CT scan consistent
Mitigating factors known to worsen sec- with diffuse cerebral edema, neurological in-
ondary injury are hypoxia and hypotension.21 jury at risk for decompensation, chest wall
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  221

Figure 4. Increased intracranial pressure (ICP) algorithm. Continual assessment of neurological and cardiorespi-
ratory status is imperative. Obtain head computed tomography (CT) if ICP continues to increase despite escalating
therapies. GCS, Glasgow Coma Scale score; HOB, head of bed; NMB, neuromuscular blockade; PaCO2 , partial
pressure of arterial carbon dioxide; SjvO2 , jugular venous oxygen saturation; CSF, cerebrospinal fluid; PbtO2 , partial
pressure of brain tissue oxygen.
222  MARCOUX AACN Clinical Issues

sion in children is defined as systolic blood


TABLE 7  Management of
pressure below the fifth percentile for age
Increased Intracranial or by clinical signs of shock.13 Median sys-
Pressure tolic blood pressure (50th percentile) can
be estimated by using the following for-
Goals of
Management Interventions mula for children greater than 1 year of
age: 90 + (2 age in years).31 Children in
Decrease
Evacuation of mass lesion hypovolemic shock can compensate fairly
cerebral
Maintain euvolemia well and may not become hypotensive until
volume
Hyperosmolar therapy
Decrease CSF
Ventriculostomy to drain CSF they become profoundly hypovolemic. Other
volume
+/ lumbar drain signs of decreased perfusion and shock in-
Decrease
Maintain head midline with clude tachycardia, decreased urine output
cerebral head of bed 30 (< 1 mL/kg/hr), weak/thready/absent periph-
blood volume Maintain normocarbia
Consider mild hyperventilation
eral pulses, prolonged capillary refill time (>2
if refractory intracranial seconds), and/or decreased mentation. Fluid
hypertension boluses are administered as needed to the
Decrease Normothermia hypotensive child. The neurologically injured
metabolic rate Sedation and analgesia child must be fluid resuscitated the same as
Seizure management and
prophylaxis any other child presenting in shock. There
For refractory intracranial is no indication for fluid restriction. Vaso-
hypertension pressor support is initiated if the child re-
barbiturate therapy mains hypotensive despite appropriate fluid
mild/moderate hypothermia
resuscitation.
CSF, cerebrospinal fluid.
Positioning
instability, abnormal respiratory pattern, loss The patients head is positioned midline to
of protective airway reflexes, or upper airway encourage jugular venous drainage and the
obstruction. Intubation should proceed with head of the bed is elevated to 15 to 30 .
administration of medications to blunt the These methods have been found to be effec-
ICP during the procedure. Suggested med- tive in decreasing intracranial pressure and
ications to facilitate the intubation without optimizing CPP in adult patients with TBI.3234
increasing the ICP are thiopental, lidocaine, Both increasing the head of the bed beyond
and a short-acting, nondepolarizing neuro- 30 and decreasing the head of the bed below
muscular blockade agent (eg, vecuronium, 15 have been associated with increased ICP
atracurium). and/or decreased CPP.33,35 In another study,36
Adequate oxygenation is necessary to CPP was found to be optimal with the bed
prevent the sequelae of secondary insults in a flat position; however, ICP increased. A
and should be maintained with a PaO2 > study of adult patients with cerebral lesions
60 mm Hg, an oxygen saturation > 90%, and (ie, tumors, infections) recommended supine
physiologic positive end expiratory pressure flat position due to a linear decrease in CBF
(PEEP) of 5 cm H2 O. Increasing the PEEP with head of bed increased to 45 .37 How-
to 10 cmH2 O has not been associated with ever, if ICP was elevated and CBF was nor-
a worse neurological outcome. The deleteri- mal or increased, positioning the head of bed
ous effects of hypoxemia are more significant 30 was recommended.37
than the possible venous congestion caused Based on the available literature, the
by PEEP > 5 cm H2 O.25,26 childs head should be maintained midline
Age-appropriate blood pressure must also to prevent impairment in drainage from the
be maintained or restored to ensure ade- external jugular veins and the head of bed
quate CPP and prevent further ischemia. The should be maintained at 30 with alterations
avoidance of hypotension is crucial since based on the childs response. The child must
it has been associated with increased mor- be euvolemic prior to placing in this position
tality in children with TBI.21,2730 Hypoten- to avoid orthostatic hypotension.
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  223

Cerebrospinal Fluid Drainage CBF and cerebral oxygen delivery that leads
to vasoconstriction and decreased ICP. The
CSF drainage provides an immediate, but
osmotic diuresis develops more slowly and
transient, decrease in ICP due to reduction
lasts up to 6 to 8 hours. As such, mannitol is
in CSF.38 Depending on the patients status,
usually given as a bolus every 4 to 6 hours
it can be done either continuously or inter-
since its osmotic effect occurs 15 to 30 min-
mittently. The optimal method of continu-
utes after administration and its duration of
ously monitoring ICP and draining CSF simul-
action is 2 to 8 hours. Autoregulation of CBF
taneously is via a ventriculostomy catheter.
must be intact for the effects of mannitol to
There is limited research on the effect of CSF
work; however, autoregulation is often dis-
drainage on ICP, CPP, CBF, and metabolic
rupted in brain injured patients.
rate. One pediatric study39 revealed that chil-
Recently hypertonic saline (HS) admin-
dren undergoing ventricular drainage had
istration has been shown to decrease ICP
decreased ICP and improved outcome. An-
and improve outcome in pediatric TBI
other study40 in adults compared ventricu-
patients.4447 Hypertonic solutions have the
lar drainage to mannitol and found that both
advantage of decreasing ICP and decreas-
treatments decreased ICP.
ing cerebral volume by producing an
For refractory intracranial hypertension,
osmotic gradient in the brain, while also sup-
lumbar drainage may be considered if the
porting intravascular volume. Pediatric stud-
basal cisterns are open, and there is no ev-
ies in children with TBI have found that
idence of midline shift or a significant mass
HS is effective in decreasing ICP and im-
lesion on neuroimaging.41
proving CPP with no adverse reactions, in-
cluding children with refractory intracranial
hypertension.4447 Hypertonic saline has also
Osmotic Therapy
been reviewed in children with diabetic ke-
Mannitol has been a cornerstone of intracra- toacidosis and presumed cerebral edema.
nial hypertension management for decades, The use of 10 mL/kg bolus dosing of HS was
but has not been compared to a placebo found to correlate with an improvement in
in randomized controlled studies. Its effi- the childs GCS and level of consciousness.48
cacy has been evaluated by comparison to HS is usually administered as a continu-
other existing therapies for intracranial hy- ous infusion, starting at 0.1 to 1.0 mL/kg/hr.
pertension. When mannitol was compared to Serum sodium and neurological status must
CSF drainage, it was found to be more ef- be closely monitored during therapy due to
fective in the management of increased ICP the possibility of osmotic demyelination syn-
in adults with TBI.40 Boluses of mannitol drome (central pontine myelinosis), which
were also found to be more effective than a can occur with a rapid increase in serum
continuous drip.42 Some have argued that ad- sodium.49 This destruction of the white mat-
ministration of mannitol on a standard dos- ter, often to the pons, can cause significant
ing regimen (eg, every 2 hours), instead of as neurological devastation due to rapid os-
needed for ICP > 25 mm Hg, provides better motic shifts. In addition, the formation of or-
ICP control.43 ganic osmolytes (idiogenic osmoles), which
Mannitol has two mechanisms of action: are osmotically active molecules that accu-
(1) an osmotic diuretic that produces an os- mulate intracellularly in the brain during hy-
motic gradient, drawing fluid from the brain perosmolar states to maintain cerebral vol-
tissue into the vascular space to be excreted ume and prevent cellular dehydration, may
via kidneys and (2) a rheological effect that contribute to cerebral edema upon abrupt
decreases blood viscosity and hematocrit and discontinuation of hyperosmolar therapy. As
increases CBF and cerebral O2 delivery.22 The such, when HS therapy is no longer indi-
rheologic effect occurs immediately and is cated, serum sodium should be slowly cor-
responsible for decreased ICP within min- rected to normal values (0.5 to 1.0 meq/L/
utes of administration. This occurs due to hour) to avoid complications associated with
increased plasma volume, which decreases osmotic shifts. Other potential complications
blood viscosity and hematocrit, and increases of HS therapy include rebound increase in
224  MARCOUX AACN Clinical Issues

ICP50 and renal insufficiency.44 In addition to have received hyperventilation have also
decreasing cerebral edema, advantages of HS been found to have a worse outcome.58,59
may include improved hemodynamic status Hyperventilation is currently only recom-
by expansion of plasma volume, as well as mended in the initial management of in-
vasoregulatory effects and immune modula- creased ICP for acute, significant increases in
tion that may contribute to prevention of sec- ICP.60,61 It is not recommended for prophylac-
ondary injury.49 tic treatment of increased ICP because of the
Regardless of which osmotic therapy is potential for worsening cerebral ischemia.
instituted, the patient must be maintained eu- Furthermore, it depletes the brain tissue inter-
volemic with an indwelling catheter measur- stitial bicarbonate buffering capacity, which
ing urine output throughout therapy. Main- may lead to a loss of local vasoconstrictor
tenance and bolus intravenous fluids are effects.62 Normally, alkalosis causes arterio-
administered to maintain euvolemia. Serum lar constriction, but with loss of this buffer
osmolality must also be monitored to pre- system, it can no longer respond appropri-
vent renal tubular dysfunction. With manni- ately and may not cause vasoconstriction to
tol, the maximum recommended serum os- decrease CBF. Mild hyperventilation (PaCO2
molality is 320 mOsm/L. However, a serum 30 to 35 mm Hg) may be implemented if in-
osmolality of 365 mOsm/L has been well tol- creased ICP continues despite CSF drainage,
erated in children receiving HS.44,45 It is un- appropriate sedation and analgesia, head po-
clear whether this disparity is due to inherent sition, and osmolar therapy. Significant hy-
differences between mannitol and HS, cur- perventilation (PaCO2 < 30 mm Hg) should
rent management aimed at euvolemia ver- be reserved for patients with refractory in-
sus fluid restriction, or differences between tracranial hypertension unresponsive to ini-
adults and children with regard to nephro- tial therapies.58 Intermittent hyperventilation
toxicity susceptibility.13 Recently, some con- should be instituted for acute, sharp increases
cern was expressed regarding increased re- in ICP or signs of impending herniation.63,64
nal dysfunction when serum sodium is >160
meq/L in euvolemic children with intracranial Temperature Regulation
hypertension;51 however, these findings have
not been reported in randomized controlled Maintaining the patient normothermic (T =
trials. 37 C) is the goal to prevent complications of
both hypothermia (T < 35 C) and hyperther-
mia (T > 38.5 C). Patients who have acute
Ventilation
neurological injury may have temperature
In the past, prophylactic hyperventilation fluctuations due to infection, sepsis, intracra-
was a mainstay of therapy for increased nial blood, and hypothalamic disturbances. A
ICP management. It was thought that chil- core temperature greater than 37.5 C is as-
dren after TBI were hyperemic, which led to sociated with increased ICP and increased
cerebral edema and increased ICP and that cerebral metabolic rate of oxygen. In exper-
hyperventilation decreased CBF and im- imental models of brain injury, hypothermia
proved outcome.52 However, the role of has been found to be neuroprotective by
hyperemia was challenged when a study2 re- decreasing cerebral metabolism, extracellular
vealed that children normally have higher glutamate release, mobilization of calcium,
resting CBF than adults, not just children after production of free radicals, and nitric ox-
TBI. Further studies3,53 revealed that children ide synthesis.65 However, in studies of adults
may actually have decreased CBF after TBI. with TBI, hypothermia has been associated
Hyperventilation was employed to de- with increased systemic complications and
crease ICP by causing vasoconstriction, no improvement in patient outcomes.6668 Po-
which decreased CBF and CBV. However, re- tential side effects of hypothermia include in-
cent studies have demonstrated that aggres- creased risk of pneumonia, skin breakdown,
sive hyperventilation dramatically decreases electrolyte imbalances, hypotension, coagu-
CBF, which may give rise to or exacerbate lopathy, and shivering.
cerebral ischemia, thus enhancing rather than Given the potential benefits of hypother-
decreasing secondary injury.5457 Patients that mia, moderate hypothermia (33 C) has been
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  225

researched for its role in the management be accurate while the patient is pharmaco-
of increased ICP. Adult studies have shown logically paralyzed. An ICP monitor is usu-
that moderate hypothermia may improve ally necessary in these patients. Additional
outcome.69,70 Recently, very mild hypother- monitoring may include the Bispectral Index
mia (3535.5 C) was studied65 in adult head (BIS) to provide an objective measure of
injured patients and was found to decrease cerebral electrical activity and assign a nu-
intracranial hypertension and maintain suffi- merical value to the level of sedation.
cient CPP. This study65 also found that de- Since the use of NMB will eliminate motor
creasing the body temperature below 35 C activity associated with seizures, but not
did not improve intracranial hypertension brain epileptiform activity, children at high
and actually decreased CPP. A recent pedi- risk for seizures may require continuous elec-
atric study71 instituted moderate hypothermia troencephalograph (EEG) monitoring. Indi-
within 6 hours of TBI and continued it for 48 cations for NMB must be weighed against
hours. This study71 demonstrated a decrease obscuring the neurological examination, as
in the severity of intracranial hypertension well as a possible increase in patient compli-
and was tolerated without any side effects, cations. In a study of adults with TBI,72 the
although there was no significant difference use of NMB was associated with increased
in mean ICP and CPP. intensive care unit (ICU) length of stay and
Children with increased ICP should be nosocomial pneumonia.
normothermic with interventions aimed at
prevention of fever and shivering. Ideally,
Seizure Prevention and Management
core or brain temperature is measured. Core
temperatures can be measured via a Swan Children who have sustained a significant
Ganz catheter or a bladder or rectal probe. head injury are more likely than adults to
Brain temperature can be monitored via have seizures, possibly due to their lower
SjvO2 or PbtO2 catheters. Moderate hypother- seizure threshold.13 Patients with GCS < 8
mia is reserved for children with refractory have an increased risk of early seizures after
intracranial hypertension not responsive to TBI.73 If the child presents with seizure activ-
initial therapies. Upon discontinuation of hy- ity, initial treatment with a benzodiazepine
pothermia treatment, the patient must be (eg, lorazepam) and/or phenytoin (or fos-
rewarmed slowly to prevent complications, phenytoin) should be instituted, followed
such as electrolyte imbalances (particularly by anti-epileptic medication (eg, phenytoin,
potassium), an increase in cerebral edema, fosphenytoin) for at least 2 weeks. The etiol-
acidosis, and hypotension. ogy of the seizure (ie, temporal lobe tumor,
intraparenchymal bleed) and the patients
clinical status will ultimately determine the
Sedation, Analgesia, Neuromuscular Blockade
duration of antiepileptic treatment.
Children with acute brain injury who are me- Children who have significant parenchy-
chanically ventilated should be appropriately mal injury after TBI or are less than one
sedated and receive adequate pain manage- year old are at increased risk of seizure ac-
ment to prevent pain and anxiety, which will tivity and should be considered for seizure
increase the cerebral metabolic rate and ICP. prophylaxis to prevent early posttraumatic
There are no randomized controlled studies seizures.13 In children with TBI, seizures most
comparing sedation methods in children with commonly occur within the first 24 hours af-
acute neurological injury. The most common ter injury.5 Regardless of the seizure etiology,
agents used are opiods, benzodiazepines, seizure activity must be terminated immedi-
and/or barbiturates. Administration of neu- ately in the child with increased ICP. Seizures
romuscular blockade agents (NMB) may be increase the metabolic rate, which will in-
necessary to facilitate mechanical ventilation crease CBF and CBV leading to an increase
and control PaCO2 , prevent shivering, and in ICP. If the metabolic demands exceed the
prevent movement that may increase ICP. supply, cerebral ischemia will ensue, leading
Use of NMB will limit physical examination to irreversible neurological damage.
findings of increased ICP to assessment of the There is limited research on the use
pupillary response; no other assessments will of anti-epileptic medications after traumatic
226  MARCOUX AACN Clinical Issues

brain injury. Studies in adults have shown Steroids


that anti-epileptic medications for long-term
The use of corticosteroids is not indicated
prophylaxis did not improve outcome74 and
in the management of increased ICP after
are only effective in the first week after
TBI. However, steroids may be indicated in
TBI to decrease the incidence of early on-
decreasing swelling and stabilizing the cell
set seizures.75 In children, anti-epileptic med-
membrane in patients with increased ICP due
ications are recommended for short-term
to mass lesions, such as brain tumors and ab-
use, unless deemed otherwise by the childs
scesses, inflammation, and infections.
seizure activity.

Barbiturate Therapy
Fluids, Electrolytes, and Nutrition
The administration of high dose barbiturates
The main goals of fluid therapy are to main-
(eg, pentobarbital) is reserved for intracra-
tain the patient euvolemic, normoglycemic,
nial hypertension refractory to the afore-
and prevent hyponatremia. In a recent pe-
mentioned interventions. Barbiturates de-
diatric study83 of 170 children with TBI,
crease ICP by decreasing cerebral metabolic
mean serum glucose > 200 mg/dL was asso-
rate, which decreases glucose utilization and
ciated with poor neurological outcome, and
oxygen demand, but may cause significant
serum glucose > 300 mg/dL on admission was
hemodynamic instability. Although there are
associated with 100% mortality. Although
limited pediatric studies examining barbi-
the exact mechanism of hyperglycemia af-
turate effectiveness and role in outcome,
ter TBI is multifactorial and not completely
some studies have shown that intractable
understood, the detrimental effects of hy-
ICP may improve and in some lead to a
perglycemia on the injured brain have been
good outcome.76 However, many patients re-
repeatedly demonstrated.8386 Current treat-
quire vasopressor support during therapy.77
ment in adults with TBI includes stringent
Adult studies have also reported pentobarbi-
glycemic control with insulin therapy.
tal as an effective treatment to decrease ICP.78
Parenteral dextrose is avoided for at least
However, some have shown no benefit in
48 hours after acute neurological injury due
outcome,79 while others have shown an asso-
to the increased risk of lactic acidosis, unless
ciation with worse neurological outcome due
the patient is hypoglycemicwhich requires
to jugular venous desaturation.80
prompt treatment. Enteral feedings may and
Monitoring of the child in a barbiturate
should be instituted within 72 hours after in-
coma should include burst suppression via
jury. Early enteral feeding in adult patients
EEG, invasive hemodynamic monitoring (eg,
with TBI has been associated with a dramatic
arterial blood pressure, central venous pres-
decrease in ICU days and complications.87
sure, SjvO2 ), and frequent assessment of oxy-
Children with TBI have been found to have
genation status. Because of the significant
caloric needs 30%60% greater than their
side effects of barbiturate therapy and the
basal metabolic expenditure88,89 and should
limited data supporting its use, barbiturate
be supplemented accordingly with the ap-
therapy is only recommended for children
propriate formula and rate. Unless con-
with refractory intracranial hypertension.
traindicated, the preferred method of deliv-
ering nutrition is via the enteral route. Due
Surgical Management
to potential impairments in the protective air-
Initial surgical management includes the im- way reflexes, it may be prudent to administer
mediate evacuation of a mass lesion (eg, feedings via a postpyloric feeding tube to de-
brain tumor, epidural hematoma) and place- crease the risk of aspiration.
ment of ICP monitor as indicated, preferably Children with increased ICP should re-
a ventriculostomy. Decompressive craniec- ceive fluids at a daily maintenance rate, as
tomy to increase intracranial compliance is well as fluid boluses as indicated for hypov-
reserved for patients with refractory intracra- olemia, hypotension, or decreased urine out-
nial hypertension, although some studies81,82 put. Since dextrose is usually avoided for the
have advocated its use early after TBI before first 48 to 72 hours after injury, maintenance
secondary injury occurs. fluids usually consist of normal saline with
Vol. 16, No. 2, Apr-Jun 2005 MANAGEMENT OF INCREASED ICP  227

the daily requirements of potassium chloride suctioning.97,98 Regardless of the method of


based on body weight. All fluids adminis- administration, the patients response must
tered must be isotonic or hypertonic (eg, hy- be monitored and care adjusted accordingly.
pertonic saline) and hypotonic fluids must
be avoided. In addition, hyponatremia must
be prevented since it will worsen cerebral  Summary
edema. If hyponatremia occurs, it must be
corrected slowly to prevent central pontine Neuro-critical care of children with increased
myelinosis that can occur with rapid correc- ICP revolves around the basic tenet of
tion of sodium. the Monro-Kellie doctrine and aims to de-
crease one or more of the intracranial com-
Nursing Care
partments. The goal of management is to
control CSF volume, brain volume, and
In addition to the nursing and medical in- blood volume. This control is achieved by
terventions outlined above, care of the child
and family is an important component in
providing optimal patient care. In pediatrics, TABLE 8  Summary of Intracranial
the child is cared for within the context of Pressure Management
the family, and the child with increased ICP
is no exception. It is important to encour- Maintain adequate oxygenation: PaO2 > 60; SpO2
> 90%
age the caregivers and siblings (as appropri- Maintain adequate systemic perfusionprevent
ate) to touch and speak to the child. Stud- hypotension and hypoxia
ies in children and adults have found that Maintain age appropriate ICP and CPP; or ICP < 20
ICP did not increase significantly or actually and CPP > 5070
decreased with family presence90,91 or with Drain CSF as indicated
Positioning: maintain supine with head of bed 30
physical touch.92,93 During these interactions, and head midline
the childs ICP and hemodynamic status are Review CT scan and neurodiagnostic results as
monitored and care modified accordingly for indicated
any significant change. No indication for prophylactic hyperventilation
Hyperventilationonly for acute ICP elevations or
There is limited research on whether clus- impending herniation
tering patient care activities (ie, bathing, suc- Order lidocaine prior to suctioning
tioning, procedures, etc.) or providing rest Mannitol q4h for ICP > 20 mm Hg; maintain serum
periods in between activities is more bene- osmo < 320 mOsm
ficial to the patient.91,93,94 It is recommended Consider hypertonic saline; maintain serum osmo
< 360 mOsm/L
to monitor the patients ICP, MAP, heart rate, Maintain euvolemia
central venous pressure, and CPP and con- Monitor electrolytes; prevent hyponatremia
tinue or abort care accordingly. Additional Monitor glucoseprevent hyperglycemia and
sedation and analgesia should also be pro- hypoglycemia
Maintain normothermiafor every change by 1 C,
vided prior to any procedure that may cause ICP increases several mm Hg
pain, anxiety, or increased ICP, although the Provide adequate sedation and analgesia;
research in this area is lacking. consider neuromuscular blockade
Research on the use of lidocaine prior Monitor for seizure activity; order anti-epileptics as
to endotracheal suctioning to attenuate the indicated
Institute enteral feedings within 72 hours after injury
ICP response in pediatric patients is scant Frequent neurological assessment: Glasgow Coma
and dated. Based on the available research, Scale, pupil reactivity, extraoccular movements,
lidocaine (via endotracheal tube or intra- motor function, vital signs
venously) is usually recommended prior to Minimize auditory and visual stimulation
Encourage family touch and patient contact
suctioning to blunt the ICP response.9597 One Provide patient and family support and education
study95 demonstrated a more significant sup- Consider 2nd-tier therapy for refractory intracranial
pression of ICP elevation with 2 mL of 4% hypertension
lidocaine administered intratracheally due to
its anesthetic effect on the tracheobronchial SpO2 ,continuous arterial oxygen saturation; ICP,
intracranial pressure; CPP, cerebral perfusion
mucosa. Lidocaine 1.5 mg/kg is the recom- pressure; CSF, cerebrospinal fluid; CT, computed
mended dose for IV administration prior to tomography.
228  MARCOUX AACN Clinical Issues

proper patient positioning, normocarbia, CSF Intracranial hypertension and cerebral perfu-
drainage, euvolemic osmolar therapy, seda- sion pressure: influence on neurological dete-
tion and analgesia, optimal cardiorespiratory rioration and outcome in severe head injury. J
status, normothermia, and seizure prophy- Neurosurg. 2000;92:16.
10. Marmarou A, Anderson RL, Ward JD, et al. Im-
laxis based on the patients condition and
pact of ICP instability and hypotension on out-
response (Table 8). Implementation of hy- come in patients with severe head trauma. J
perventilation, moderate hypothermia, and Neurosurg. 1991;75:S59S66.
barbiturate therapy is reserved for patients 11. Diringer MN. Intracerebral hemorrhage:
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as well as prevention of hypoxia and hy- gow Coma Scale, hypoxia and computerized
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291.
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2003;31:S417S491.
14. Hammer GB, Andrews BT. Physiological mon-
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