Professional Documents
Culture Documents
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
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
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
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
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
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:
with refractory intracranial hypertension. The Pathophysiology and management. Crit Care
best neurological outcome is associated with Med. 1993;21:15911603.
control of ICP < 20 mmHg (or age appro- 12. Ong L, Selladurai BM, Dhillon MK, Atan M,
priate) and a CPP > 50 (or age appropriate), Lye, MS. The prognostic value of the Glas-
as well as prevention of hypoxia and hy- gow Coma Scale, hypoxia and computerized
potension. Much research is still needed to tomography in outcome prediction of pediatric
head injury. Pediatric Neurosurg. 1996;24:285
optimize management strategies for children
291.
with acute increased intracranial hyperten- 13. Guidelines for the acute medical manage-
sion, particularly nursing interventions that ment of severe traumatic brain injury in in-
may ultimately improve patient outcomes. fants, children, and adolescents. Crit Care Med.
2003;31:S417S491.
14. Hammer GB, Andrews BT. Physiological mon-
itoring in the pediatric intensive care unit. In:
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