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AACN Clinical Issues

Volume 16, Number 2, pp. 212231C 2005, AACN

Management of Increased IntracranialPressure in the Critically Ill Child Withan Acute Neurological InjuryKelly Keefe Marcoux, MSN, CPNP-AC, CCRN

Increased intracranial pressure reflectsthe presence of mass effect in the brain

and is associated with a poor outcome in

children with acute neurological injury. If

sustained, it has a negative effect on

cerebral blood flow and cerebral perfusion

pressure, can cause direct compression

of vital cerebral structures, and can leadto herniation. The management of the

patient with increased intracranial

pressure involves the maintenance of an

adequate cerebral perfusion pressure,

prevention of intracranial hypertension,

and optimization of oxygen delivery. Thisarticle reviews the neurological

assessment, pathophysiology, and

management of increased intracranial

pressure in the critically ill child who has

sustained an acute neurological injury.(KEYWORDS: acute neurological injury,

critically ill child, ICP management,increased intracranial pressure,

neurological assessment)

Children may have increased intracranialpressure (ICP) for a variety of reasons. Themost common etiologies of increased ICP

in the pediatric intensive care unit (PICU)are due to severe traumatic brain injury(TBI), hydrocephalus, brain tumors, infec-tions (ie, meningitis, encephalitis), metabolicencephalopathy, hypoxic/ischemic brain in-jury, cerebral infarction, and intraparenchy-

mal blood due to a ruptured arteriovenousmalformation or aneurysm. The mechanismby which ICP increases varies depending onthe specific etiology (Table 1). The increasedICP can be due to either an increase in tis-sue volume, cerebral blood volume, or cere-brospinal fluid (CSF) volume. Examples ofthese are listed in Table 2. One or more ofthese factors occurring alone or simultane-ously can increase ICP. The pathophysiologyand management of increased ICP is basedon the Monro-Kellie doctrine.

Normal Cerebral Physiology

Intracranial pressure is defined as the totalpressure exerted by the brain, blood, and CSFin the intracranial vault. The Monro-Kelliedoctrine states that the cranium is a fixed

vault made up of 3 components: the brain(80%), blood (10%), and CSF (10%).When there is an increase in any one of thesecomponents, one or more of the other com-ponents must decrease to keep the total vol-ume the same. The blood and the CSF arethe only compartments that can compensate.The CSF compensates by displacing CSF fromthe ventricles and the cerebral subarachnoid

From the Robert Wood Johnson Medical School, Uni- versity of Medicine & Dentistry of New Jersey, Piscat-away, and the Bristol-Myers Squibb Childrens Hospital,New Brunswick, NJ.

Reprint requests to Kelly Keefe Marcoux, Clinical As-sistant Professor, 26 Covered Bridge Road, Neshanic Sta-tion, NJ 08853 ([email protected]).

212

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

TABLE 1 Etiology of IncreasedIntracranial Pressure

Based on AcuteNeurological Insult

AcuteNeurologicalInsult

Possible Etiology of IncreasedIntracranial Pressure

Traumatic braininjury

Hematoma, cerebral edema,cerebral ischemia,intraventricular or intracerebralhemorrhage

Hydrocephalus Obstruction or impairment ofcerebrospinal fluid absorption,cerebral edema

Infections (eg,meningitis,encephalitis)

Meningeal scarring, inflammatoryresponse, cerebral edema,hydrocephalus, cerebralhyperemia

Brain tumor Mass effect of tumor, peritumoraledema, hydrocephalus

Intraparenchymalbleed

Mass effect, cerebral edema

Intraventricularbleed

Hydrocephalus

space through the foramen magnum to the

spinal subarachnoid space. The productionof CSF can also be decreased, as well as theabsorption increased, to decrease the totalCSF. In addition, venous blood compensatesby being displaced by the dural venous si-nuses. For instance, if there is an intracranialmass (eg, brain tumor), the brain and thearterial volume will remain static while theCSF and the venous volumes will decreaseuntil they can no longer compensate, atwhich point the ICP will increase (Figure 1).1

However, infants and children with openfontanels and sutures (usually less than

TABLE 2 Etiology of IntracranialPressure Based on theMonro-Kellie Doctrine

Increase in tissue volume Cerebral edema Mass lesion

Increase in cerebral blood volume

Intracranial hemorrhage Hematoma formation Decreased venous drainage Increased arterial blood flow

Increase in cerebrospinal fluid volume Hydrocephalus

18 months old), may be able to compensatelonger to chronic changes in the intracranialvault, but will still be susceptible to acute in-

creases in ICP. It is crucial to understand theMonro-Kellie doctrine because managementof increased ICP revolves around this basicprinciple.

Other key concepts of intracranial dynam-ics include autoregulation, compliance, cere-bral blood flow, cerebral metabolic rate, andcerebral perfusion pressure (CPP). Autoreg-ulation is the maintenance of a steady cere-bral blood flow (CBF) by vasoconstrictionand vasodilatation of the cerebral vessels de-

spite fluctuations in systemic blood pressure.If autoregulation is impaired, CBF and cere-bral blood volume (CBV) will become depen-dent on changes in systemic blood pressure.Compliance is an indicator of the brains tol-erance to increases in ICP. It is defined as achange in pressure resulting from a changein volume. Each patient has varying degreesof compliance even with similar injuries. Theexact factors contributing to this are still un-known. When the patients compliance is ex-hausted, there is a dramatic increase in thepressure/volume curve, leading to a rapid el-evation in ICP.

In an uninjured brain, cerebral blood flowis regulated to supply the brain with adequateoxygen and substrates to meet its demands.The main physiologic influences on CBF arethe partial pressure of arterial carbon diox-ide (PaCO2), arterial oxygenation, pH, CPP,and cerebral metabolic rate. The PaCO2 is di-rectly proportional to CBF and is the most po-tent chemical mediator of CBF. An increase

in PaCO2 will cause vasodilatation, whichwill increase CBF and, thereby, potentially in-crease ICP. Likewise, acidosis and hypoxemiawill also increase CBF by causing vasodilata-tion. CBF in excess of tissue demand will leadto hyperemia. Normal CBF in an adult is ap-proximately 5070 mL/100 g/min, and CBF ofhealthy children was found to be as high as108 mL/100 g/min.2 CBF

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214 MARCOUX AACN Clinical Issues

Figure 1. Intracranial compensation for an expand-

ing mass lesion. CSF, cerebrospinal fluid; ICP, intracra-

nial pressure. Reprinted with permission from RogersMC. Textbook of Pediatric Intensive Care. Baltimore,

Md: Williams & Wilkins; 1996:646.

dependent on glucose to meet the bodysenergy demands. The brain functions viaadenosine triphosphate (ATP) and the Krebscycle to maintain aerobic metabolism. If thereis hypoxia, the Krebs cycle cannot be acti-vated and anaerobic metabolism will ensue.This will lead to the production of pyruvateand lactate, which will decrease the amountof ATP available for the cells and, thereby,decrease the amount of energy available.4

Cerebral perfusion pressure (CPP) is thepressure at which cells are perfused and isan important indicator of CBF. Sufficient CPPis necessary to prevent the development ofsecondary cerebral ischemia. CPP providesan indirect measurement of CBF and is cal-culated by measuring the difference betweenthe mean arterial pressure (MAP) and the ICPas demonstrated by the following equation:

CPP = MAP ICP. Normal CPP values forchildren are not clearly established, but thefollowing values are generally accepted asthe minimal pressure necessary to preventischemia: adults CPP > 70 mm Hg; chil-dren CPP > 5060 mm Hg; infants/toddlersCPP> 4050 mm Hg.5 Research has shownthat a CPP < 40 mm Hg is a significantpredictor of mortality in children with TBI.6

Furthermore, in a study of 17 comatosechildren with severe central nervous system

(CNS) infections, a CPP < 30 mm Hg wasassociated with universal mortality.7

Normal ICP values are estimated at 26mm Hg for infants and 37 mm Hg for youngchildren. The normal ICP for older childrenand adults is 010 mm Hg.8 Intracranial hy-pertension is defined as an ICP >20 mm Hg

for more than 5 minutes, although a lowernumber may be used for infants and youngchildren. One suggestion for pediatric pa-

tients has been to maintain the ICP < 20 mmHg for children aged 8 years to adults,

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Assessment and Monitoring

The initial assessment of the neurologi-

cally injured child consists of assessment of ABCs (airway, breathing, and circulation),Glasgow Coma Scale (GCS) score, cranialnerve function, signs and symptoms of in-creased ICP, temperature, and cardiorespira-tory assessment. Astute observation of anyabnormal respiratory patterns is crucial, sincethis may be the first vital sign change in-dicating neurological dysfunction. Abnormalrespiratory patterns that may be detectedinclude Cheyne-Stokes, central neurogenic

hyperventilation, apneustic, ataxic, and clus-ter breathing. All, except for Cheyne-Stokes,indicate brain stem abnormality. Cheyne-Stokes is less specific and indicates a cere-bral, cerebellar, or brainstem impairment.

The most ominous cardiorespiratory ab-normality is Cushings triad. Cushings triadoccurs when there is cerebral ischemia caus-ing peripheral vasoconstriction. This vaso-constriction leads to increased systolic bloodpressure to improve cerebral perfusion. Car-

diac baroreceptors sense this increased bloodpressure, resulting in a vagal response man-ifested as bradycardia. Abnormal or irregu-lar respirations are the final component ofCushings triad and occur due to brainstem

TABLE 3 Signs and Symptoms ofIncreasing IntracranialPressure

Early signs and symptoms Headache Emesis Change in level of consciousness Decrease in Glasgow Coma Scale score Irritability Sunsetting Decreased eye contact (infants) Pupil dysfunction Cranial nerve dysfunction Seizures

Late signs and symptoms Further decrease in level of consciousness

Bulging fontanels Decreased spontaneous movements Posturing Papilledema Pupil dilation with decreased or no response to light Increased blood pressure Irregular respirations Cushings triad (late, ominous sign)

compression. It is important to note earliersigns of increased ICP (see Table 3) becauseCushings triad is a very late sign in neurolog-

ically injured children and usually indicatesimpending herniation.

Neurological Assessment

A thorough neurological assessment must beperformed as soon as the child is clinicallystable because this will serve as the base-line for comparison of future examinations. After the cardiorespiratory status has stabi-lized, the GCS is determined. It is impor-

tant to utilize a modified GCS for infants andyoung children in order to obtain the mostaccurate score (Table 4). In a study of 151children, a GCS < 8 twenty-four hours afterTBI, in addition to factors such as hypoxiaand cerebral edema, was associated with apoor outcome.12 To obtain the best response,it is necessary to give the patient the max-imal stimulationthis may include givingpainful stimuli such as mandibular pressure,sternal rub, or supraorbital pressure. Thesetests are optimal because they assess thecentral nervous system response, whereasfingerbed pressure assesses peripheral painresponse.

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 shapeof each pupil. It is imperative to be awareof medications that were administered thatmay affect pupil response (eg, atropine, nar-cotics). At least 10 seconds should elapse

between each eye exam to allow the consen-sual response to fade. Abnormal pupillary re-sponses include pupils that are unequal, con-stricted, dilated, nonreactive, or have hippus(Table 5). Hippus is the abnormal dilationand constriction of the pupil in response tobright light. It may indicate pressure on CN IIIand be associated with transtentorial hernia-tion or it may be insignificant and representa normal variant.

If the patient is awake, the 6 fields of gaze

are assessed to determine extra-ocular move-ments (EOMs). If the patient is unrespon-sive, EOMs can be assessed by oculocephalictesting (Dolls eyes) and oculovestibular test-ing (cold calorics). However, if the C-spinehas not been cleared, the oculocephalic testshould be deferred. An abnormal response

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TABLE 4 Modified Glasgow Coma Scale for Infants and Children

Score Infant/Nonverbal Child Verbal Child/Adult

Eye opening 4 Spontaneously Spontaneously3 To speech To verbal command2 To pain To pain1 No response No response

Best motor response 6 Normal spontaneousmovement

Obeys command

5 Withdraws to touch Localizes pain4 Withdraws to pain Flexion withdrawal3 Abnormal flexion (decorticate) Abnormal flexion2 Extension (decerebrate) Extension (decerebrate)1 No response No response

25 Years > 5 YearsBest verbal response 5 Cries appropriately, coos Appropriate words Oriented

4 Irritable crying Inappropriate words Confused3 Inappropriate screaming/

cryingScreams Inappropriate

2 Grunts Grunts Incomprehensible1 No response No response No response

to oculocephalic testing (as you turn thepatients head side-to-side, the eyes remainfixed and do not rotate) may indicate injuryto the midbrain or pons, or that the patientis in a deep coma. An abnormal response

to oculovestibular testing (after irrigatingeach external auditory canal with iced wa-ter, the eyes do not deviate toward theside of irrigation with nystagmus) may indi-cate injury to cranial nerves III, VI, or VIII,or brain stem injury. The fundus is exam-ined for papilledema. Although the presenceof papilledema indicates increased ICP, itsabsence does not indicate the absence ofincreased ICP. The fundus is also examinedfor retinal hemorrhages, which may indicate

child abuse, sagittal sinus thrombosis, or co-agulation abnormalities.Further cranial nerve testing in the unre-

sponsive or intubated child should includeeliciting a gag or cough reflex, and assess-ment of swallowing. Impairment in CN IXand X can greatly affect the childs ability to

TABLE 5 Abnormal Pupillary Responses

Pupillary Finding Possible Etiology

Bilateral fixed and dilated pupils Indicates inadequate CPP; may be irreversibleBilateral constriction Injury to pons; early central herniation; opiod administrationUnilateral fixed and dilated Transtentorial herniation; traumatic optic nerve injuryUnilateral constriction Horners syndrome; unilateral brainstem injuryHippus May indicate irritation to oculomotor nucleus; can be normal variant

CPP, cerebral perfusion pressure.

manage their oropharyngeal secretions andprotect their airway. Cranial nerves and theirfunctions are summarized in Table 6.

Motor assessment includes recognition ofany abnormal posturing (eg, extension, flex-

ion, flaccidity), muscle symmetry, strength,and tone. Flaccidity indicates severe dysfunc-tion of the lower brain stem. Deep tendonreflexes are elicited to assess for central andperipheral nervous system dysfunction.

Abnormalities that are detected in theneurological exam must be correlated withthe patients previous examination, diagno-sis, and radiologic findings. The location ofa mass lesion or hemorrhage, or presenceof mass effect or hydrocephalus must be as-

sessed immediately to accurately diagnoseand respond to impending herniation.

Radiologic Assessment

The radiologic study of choice for imme-diate assessment of the child with acute

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TABLE 6 Function of CranialNerves

Cranial Nerve Function

I: Olfactory SmellII: Optic VisionIII: Oculomotor Movement of eyeball;

pupillary constriction andaccommodation

IV: Trochlear Downward/inward movementof eye

V: Trigeminal Facial sensation; open/closemouth

VI: Abducens Lateral movement of eyeballVII: Facial Taste; facial movement;

salivation and lacrimationVIII: Vestibulocochlear Hearing; equilibriumIX: Glossopharyngeal Tongue taste/sensation;

swallowing; salivationX: Vagus Speech, swallowing; control

cardiac, respiratory, andgastrointestinal tracts

XI: Accessory Movement of head andshoulders

XII: Hypoglossal Movement of tongue

neurological impairment or deterioration isa noncontrast CT scan. A contrast CT scanmay be necessary for further diagnosis ofspace occupying and vascular lesions, andinfections, but is not warranted in the ini-tial assessment of the child with increasedICP. On a noncontrast CT, highly dense struc-tures, such as blood, will appear white, andlow density areas, such as air, CSF, andedema, will appear black. Initial inspectionof the CT scan should proceed with ob-servation of any intracranial mass lesion,

midline shift, skull fracture, presence of hem-orrhage (extra-axial, intraparenchymal, or in-traventricular), ventricular size, symmetry,and patency of basal cisterns (Figure 2).CT findings consistent with increased ICPinclude a mass lesion, intracerebral hem-orrhage, midline shift, loss of sulci, ven-tricular effacement, and cerebral edema(Figure 3).

Neurological Monitoring

ICP monitoring is indicated for children withTBI whose GCS < 8 or for children with otheracute neurological injuries who have clinicalsigns of increasing ICP, are status post resec-tion of acute traumatic intracranial hematomaor other major neurosurgical procedures, or

have a neurodiagnostic test indicative of ahigh probability of increased ICP (ie, cerebraledema, midline shift, cisternal compression,

intracerebral hemorrhage).13,14 Children whodo not usually benefit from ICP monitoringare children with hypoxic injuries (ie, neardrowning) and some central nervous systeminfections (ie, encephalitis).

Although ICP monitoring has never beensubjected to randomized controlled stud-ies to evaluate its effectiveness, its use hasbeen associated with decreased morbidityand mortality, and improved outcome in pa-tients with TBI, intracerebral hemorrhages,

and CNS infections.1517

It is not the moni-tor itself that improves outcome, but the in-formation gleaned from this modality thatguides appropriate interventions. ICP mon-itoring is crucial to identify rapidly increas-ing pressure and to institute appropriate ther-apy to prevent intracerebral herniation andpreserve cerebral perfusion. It is also neces-sary to monitor ICP in order to calculate theCPP.

The current gold standard for ICP mon-itoring is intraventricular catheter place-ment, preferably an implantable micro-transducer (fiberoptic or strain-gauge). Thismethod allows simultaneous monitoring ofICP and management of increased ICP byCSF drainage. Other methods of moni-toring ICP include intraparenchymal, sub-dural, subarachnoid, and epidural catheterplacementalthough the latter locations are very rarely used. Depending on the type ofcatheter, care will vary. ICP monitors with in-tracranial transducers are zeroed at the time

of placement and therefore do not requireany further zeroing. However, extracranialtransducers require frequent zeroing and lev-eling because they must be adjusted withchanges in patient position and recalibratedto atmospheric pressure.

In the past, children at risk for increasedICP were managed primarily with interven-tions to decrease their ICP and maintain anadequate CPP. This remains true, but the roleof cerebral oxygenation and the ability to

monitor it has recently been incorporatedinto the care of these children. Adjunct mon-itoring modalities utilized to prevent cere-bral ischemia and optimize the patients out-come include transcranial doppler (TCD)ultrasonography, jugular venous oxygenationsaturation (SjvO2) monitoring, brain tissue

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Figure 2. Normal brain computed tomography scan.

partial pressure oxygen monitoring (PbtO2),non-invasive cerebral oxygenation monitor-ing, and brain metabolism monitoring.

As mentioned previously, CPP monitor-ing involves calculating the difference be-tween MAP and ICP. CPP can also be as-sessed via xenon computed tomography (CT)

scan, perfusion CT, perfusion magnetic reso-nance imaging (MRI), and positron emissiontomography (PET) scanning. These modali-ties offer excellent information regarding re-gional CBF but are limited to one point intime. Continuous monitoring of CBF wouldbe ideal and allow for interventions aimed atoptimizing cerebral perfusion. For instance,if CBF were low, interventions would be di-rected at increasing vasopressor support orfluid therapy, or by decreasing cerebral de-

mand by increasing sedation. If the patient were hyperemic, then methods to decreasethe CBF, such as hyperventilation, would beinstituted.18

CBF can also be evaluated via TCD ul-trasonography, which non-invasively deter-

mines CBF velocity in the proximal vessels ofthe Circle of Willis. This is particularly helpfulwhen assessing for vasospasm and stenosis ina child with a stroke. The adequacy of CBFrelated to cerebral metabolic demand can beassessed by SjvO2 and PbtO2. SjvO2 is a con-tinuous measurement of the oxygen satura-

tion in the jugular vein after cerebral perfu-sion has occurred. The jugular mixed venoussaturation is compared to the arterial oxy-gen saturation, and the arteriovenous oxy-gen content difference (AVDO2) is then cal-culated. Normal SjvO2 is 55% to 70%; 75% in-dicates luxury perfusion and possible cellulardeath. Although SjvO2 is helpful in assessingcerebral oxygenation, a more direct approach

is the measurement of partial pressure braintissue oxygenation.PbtO2 is a more specific method of mea-

suring cerebral oxygenation via a microprobeinserted directly into parenchymal tissue orthe penumbra of an intracerebral lesion.

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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 optimalinsertion area. Some advocate for placementin uninjured brain tissue to assess global cere-bral oxygenation, while others opt for place-ment in the penumbra of an intracerebral

lesion to obtain information of cerebral oxy-genation for the area most at risk.19 Ideally,either method allows for continuous monitor-ing of cerebral oxygenation and early recog-nition of cerebral ischemia. The various typesof catheters currently available (eg, Neu-rotrend [Diametrics Medical Limited, St. Paul,MN], LICOX [Integra Life Sciences, Plains-boro, NJ]) may yield different values and in-terventions should be adjusted accordingly.PbtO2 is a more specific method of measur-

ing cerebral oxygenation via a microprobe in-serted directly into parenchymal tissue or thepenumbra of an intracerebral lesion. There iscontroversy regarding the optimal insertionarea. Some advocate for placement in unin-jured brain tissue to assess global cerebral

oxygenation, while others opt for placementin the penumbra of an intracerebral lesionto obtain information of cerebral oxygena-tion for the area most at risk.19 Ideally, eithermethod allows for continuous monitoring of

cerebral oxygenation and early recognitionof cerebral ischemia. The various types ofcatheters currently available (eg, Neurotrend,[Diametrics Medical Limited, St. Paul, MN],LICOX [Integra Life Sciences, Plainsboro, NJ])may yield different values, and interventionsshould be adjusted accordingly. Using theLICOX catheter, normal PbtO2 values in un-injured parenchyma are 20 mm Hg and in-terventions to improve cerebral oxygenationare indicated if the value is < 15 mm Hg.20

For non-injured brain tissue, normal valuesare between 20 to 35 mm Hg. A decrease inpartial pressure of brain tissue oxygen canbe seen with decreased PaCO2, hypoxemia,increased ICP, and decreased CPP. Most ofthe available research on the utility of brain

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tissue oxygenation is from adult TBI pa-tients. There are a few studies from adultpatients with brain tumors, arteriovenous

malformations, and stroke demonstrating thatthe additional information obtained from thismodality is beneficial.19 A decrease in par-tial pressure of brain tissue oxygen can beseen with decreased PaCO2, hypoxemia, in-creased ICP, and decreased CPP. Most of theavailable research on the utility of brain tis-sue oxygenation is from adult TBI patients.There are a few studies from adult patientswith brain tumors, arteriovenous malforma-tions, and stroke demonstrating that the addi-

tional information obtained from this modal-ity is beneficial.19

Noninvasive measurement of cerebraloxygenation can be done by near-infraredspectroscopy, which measures cerebral oxy-gen saturation via oximetry. This methodhas the advantage of being noninvasive andportable, but it is not commonly used inpediatrics.

Brain metabolism monitoring provides anindividual assessment of brain chemistry af-ter injury to guide treatment accordingly. Cur-rently, it is not routinely used in most PICUs,but would allow for measurement of neu-rochemicals (ie, lactate, pyruvate, glucose,glutamate, urea, and glycerol) via an intra-parenchymal microdialysis catheter.

Management of Increased ICP

Despite the etiology of the primary neuro-logical injury, the main focus of management

is to prevent and minimize secondary injury.Although primary injury and secondary in-jury most commonly refer to children withTBI, this terminology can also be applied tochildren with metabolic or hypoxic-ischemicencephalopathy and children with nontrau-matic primary brain lesions, infections, andintracranial hemorrhage. The primary injuryrefers to the initial insult regardless of themechanism of injury or illness. The sec-ondary brain injury refers to the processes

that occur within hours to days after theprimary injury that can be prevented orminimizedsuch as cerebral ischemia, cere-bral edema, and neurochemical alterations.Mitigating factors known to worsen sec-ondary injury are hypoxia and hypotension.21

Other factors that may worsen secondarybrain injury after TBI include the release ofexcitatory neurotransmitters, the formation of

free radicals, and increased levels of intra-cellular calcium and potassium.4 The neuro-logical devastation caused by the secondaryinjury is often worse than the underlying pri-mary disorder. Therefore, management is di-rected at prevention of secondary injury.

Recently, recommendations on the man-agement of increased ICP in children withTBI have been published.13,22 These recom-mendations are based on pediatric studiesand extrapolated from adult TBI research.

Since there are limited outcome studies tosupport the current management of childrenwith increased ICP from etiologies other thanTBI, this management is often instituted forthese children also. A schematic of increasedICP management is provided in Figure 4.The reader is also referred to the Guidelinesfor the Acute Medical Management of SevereTraumatic Brain Injury in Infants, Children,and Adolescents13 for an algorithm detailingescalation of therapy.

ICP management based on the Monro-Kellie doctrine includes interventions to de-crease cerebral volume, control CSF volume,control CBV, and decrease cerebral metabolicrate (Table 7). The goal of these therapies isto maintain an age-appropriate CPP and anICP 70 mm Hg is used in some centers basedon research demonstrating that increasing theCPP, rather than decreasing the ICP, improvespatient outcomes.23However, there are lim-

ited data on the benefits of CPP-driven man-agement in pediatrics,24 and it is not routinelyimplemented.

Airway, Breathing, and Circulation

The initial management of the child with sus-pected increased ICP is assessment of air-way, breathing, and circulation (ABCs). Evenprior to a thorough neurological exam, ifthe patient is unarousable or having diffi-

culty maintaining a patent airway, rapid se-quence intubation should occur. Endotra-cheal intubation should also be considered ifthe child has a GCS < 8, a CT scan consistentwith diffuse cerebral edema, neurological in-jury at risk for decompensation, chest wall

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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 escalatingtherapies. 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.

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TABLE 7 Management ofIncreased Intracranial

PressureGoals ofManagement Interventions

Decrease Evacuation of mass lesioncerebral Maintain euvolemiavolume Hyperosmolar therapy

Decrease CSF Ventriculostomy to drain CSFvolume +/ lumbar drain

Decreasecerebral

Maintain head midline withhead of bed 30

blood volume Maintain normocarbia Consider mild hyperventilation

if refractory intracranialhypertension

Decrease Normothermiametabolic rate Sedation and analgesia

Seizure management andprophylaxis

For refractory intracranialhypertension

barbiturate therapymild/moderate hypothermia

CSF, cerebrospinal fluid.

instability, abnormal respiratory pattern, lossof protective airway reflexes, or upper airwayobstruction. Intubation should proceed withadministration of medications to blunt theICP during the procedure. Suggested med-ications to facilitate the intubation withoutincreasing the ICP are thiopental, lidocaine,and a short-acting, nondepolarizing neuro-muscular blockade agent (eg, vecuronium,atracurium).

Adequate oxygenation is necessary to

prevent the sequelae of secondary insultsand should be maintained with a PaO2 >60 mm Hg, an oxygen saturation > 90%, andphysiologic positive end expiratory pressure(PEEP) of 5 cm H2O. Increasing the PEEPto 10 cmH2O has not been associated witha worse neurological outcome. The deleteri-ous effects of hypoxemia are more significantthan the possible venous congestion causedby PEEP > 5 cm H2O.25,26

Age-appropriate blood pressure must also

be maintained or restored to ensure ade-quate CPP and prevent further ischemia. Theavoidance of hypotension is crucial sinceit has been associated with increased mor-tality in children with TBI.21,2730 Hypoten-

sion in children is defined as systolic bloodpressure below the fifth percentile for ageor by clinical signs of shock.13 Median sys-

tolic blood pressure (50th percentile) canbe estimated by using the following for-mula for children greater than 1 year ofage: 90 + (2 age in years).31 Children inhypovolemic shock can compensate fairlywell and may not become hypotensive untilthey become profoundly hypovolemic. Othersigns of decreased perfusion and shock in-clude tachycardia, decreased urine output(< 1 mL/kg/hr), weak/thready/absent periph-eral pulses, prolonged capillary refill time (>2

seconds), and/or decreased mentation. Fluidboluses are administered as needed to thehypotensive child. The neurologically injuredchild must be fluid resuscitated the same asany other child presenting in shock. Thereis no indication for fluid restriction. Vaso-pressor support is initiated if the child re-mains hypotensive despite appropriate fluidresuscitation.

Positioning

The patients head is positioned midline toencourage jugular venous drainage and thehead of the bed is elevated to 15 to 30.These methods have been found to be effec-tive in decreasing intracranial pressure andoptimizing CPP in adult patients with TBI.3234

Both increasing the head of the bed beyond30 and decreasing the head of the bed below15 have been associated with increased ICPand/or decreased CPP.33,35 In another study,36

CPP was found to be optimal with the bed

in a flat position; however, ICP increased. Astudy of adult patients with cerebral lesions(ie, tumors, infections) recommended supineflat position due to a linear decrease in CBF with head of bed increased to 45.37 How-ever, if ICP was elevated and CBF was nor-mal or increased, positioning the head of bed30 was recommended.37

Based on the available literature, thechilds head should be maintained midlineto prevent impairment in drainage from the

external jugular veins and the head of bedshould be maintained at 30 with alterationsbased on the childs response. The child mustbe euvolemic prior to placing in this positionto avoid orthostatic hypotension.

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ICP50 and renal insufficiency.44 In addition todecreasing cerebral edema, advantages of HSmay include improved hemodynamic status

by expansion of plasma volume, as well asvasoregulatory effects and immune modula-tion that may contribute to prevention of sec-ondary injury.49

Regardless of which osmotic therapy isinstituted, the patient must be maintained eu-volemic with an indwelling catheter measur-ing urine output throughout therapy. Main-tenance and bolus intravenous fluids areadministered to maintain euvolemia. Serumosmolality must also be monitored to pre-

vent renal tubular dysfunction. With manni-tol, the maximum recommended serum os-molality is 320 mOsm/L. However, a serumosmolality of 365 mOsm/L has been well tol-erated in children receiving HS.44,45 It is un-clear whether this disparity is due to inherentdifferences between mannitol and HS, cur-rent management aimed at euvolemia ver-sus fluid restriction, or differences betweenadults and children with regard to nephro-toxicity susceptibility.13 Recently, some con-cern was expressed regarding increased re-nal dysfunction when serum sodium is >160meq/L in euvolemic children with intracranialhypertension;51however, these findings havenot been reported in randomized controlledtrials.

Ventilation

In the past, prophylactic hyperventilation was a mainstay of therapy for increasedICP management. It was thought that chil-

dren after TBI were hyperemic, which led tocerebral edema and increased ICP and thathyperventilation decreased CBF and im-proved outcome.52 However, the role ofhyperemia was challenged when a study2 revealed that children normally have higherresting CBF than adults, not just children afterTBI. Further studies3,53 revealed that childrenmay actually have decreased CBF after TBI.

Hyperventilation was employed to de-crease ICP by causing vasoconstriction,

which decreased CBF and CBV. However, re-cent studies have demonstrated that aggres-sive hyperventilation dramatically decreasesCBF, which may give rise to or exacerbatecerebral ischemia, thus enhancing rather thandecreasing secondary injury.5457 Patients that

have received hyperventilation have alsobeen found to have a worse outcome.58,59

Hyperventilation is currently only recom-

mended in the initial management of in-creased ICP for acute, significant increases inICP.60,61 It is not recommended for prophylac-tic treatment of increased ICP because of thepotential for worsening cerebral ischemia.Furthermore, it depletes the brain tissue inter-stitial bicarbonate buffering capacity, whichmay lead to a loss of local vasoconstrictoreffects.62 Normally, alkalosis causes arterio-lar constriction, but with loss of this buffersystem, it can no longer respond appropri-

ately and may not cause vasoconstriction todecrease CBF. Mild hyperventilation (PaCO230 to 35 mm Hg) may be implemented if in-creased ICP continues despite CSF drainage,appropriate sedation and analgesia, head po-sition, and osmolar therapy. Significant hy-perventilation (PaCO2 < 30 mm Hg) shouldbe reserved for patients with refractory in-tracranial hypertension unresponsive to ini-tial therapies.58 Intermittent hyperventilationshould be instituted for acute, sharp increasesin ICP or signs of impending herniation.63,64

Temperature Regulation

Maintaining the patient normothermic (T =37C) is the goal to prevent complications ofboth hypothermia (T 38.5C). Patients who have acuteneurological injury may have temperaturefluctuations due to infection, sepsis, intracra-nial blood, and hypothalamic disturbances. Acore temperature greater than 37.5C is as-

sociated with increased ICP and increasedcerebral metabolic rate of oxygen. In exper-imental models of brain injury, hypothermiahas been found to be neuroprotective bydecreasing cerebral metabolism, extracellularglutamate release, mobilization of calcium,production of free radicals, and nitric ox-ide synthesis.65 However, in studies of adults with TBI, hypothermia has been associated with increased systemic complications andno improvement in patient outcomes.6668 Po-

tential side effects of hypothermia include in-creased risk of pneumonia, skin breakdown,electrolyte imbalances, hypotension, coagu-lopathy, and shivering.

Given the potential benefits of hypother-mia, moderate hypothermia (33C) has been

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researched for its role in the managementof increased ICP. Adult studies have shownthat moderate hypothermia may improve

outcome.69,70 Recently, very mild hypother-mia (3535.5C) was studied65 in adult headinjured patients and was found to decreaseintracranial hypertension and maintain suffi-cient CPP. This study65 also found that de-creasing the body temperature below 35Cdid not improve intracranial hypertensionand actually decreased CPP. A recent pedi-atric study71 instituted moderate hypothermiawithin 6 hours of TBI and continued it for 48hours. This study71 demonstrated a decrease

in the severity of intracranial hypertensionand was tolerated without any side effects,although there was no significant differencein mean ICP and CPP.

Children with increased ICP should benormothermic with interventions aimed atprevention of fever and shivering. Ideally,core or brain temperature is measured. Coretemperatures can be measured via a SwanGanz catheter or a bladder or rectal probe.Brain temperature can be monitored viaSjvO2 or PbtO2 catheters. Moderate hypother-mia is reserved for children with refractoryintracranial hypertension not responsive toinitial therapies. Upon discontinuation of hy-pothermia treatment, the patient must berewarmed slowly to prevent complications,such as electrolyte imbalances (particularlypotassium), an increase in cerebral edema,acidosis, and hypotension.

Sedation, Analgesia, Neuromuscular Blockade

Children with acute brain injury who are me-chanically ventilated should be appropriatelysedated and receive adequate pain manage-ment to prevent pain and anxiety, which willincrease the cerebral metabolic rate and ICP.There are no randomized controlled studiescomparing sedation methods in children withacute neurological injury. The most commonagents used are opiods, benzodiazepines,and/or barbiturates. Administration of neu-romuscular blockade agents (NMB) may be

necessary to facilitate mechanical ventilationand control PaCO2, prevent shivering, andprevent movement that may increase ICP.Use of NMB will limit physical examinationfindings of increased ICP to assessment of thepupillary response; no other assessments will

be accurate while the patient is pharmaco-logically paralyzed. An ICP monitor is usu-ally necessary in these patients. Additional

monitoring may include the Bispectral Index(BIS) to provide an objective measure ofcerebral electrical activity and assign a nu-merical value to the level of sedation.

Since the use of NMB will eliminate motoractivity associated with seizures, but notbrain epileptiform activity, children at highrisk for seizures may require continuous elec-troencephalograph (EEG) monitoring. Indi-cations for NMB must be weighed againstobscuring the neurological examination, as

well as a possible increase in patient compli-cations. In a study of adults with TBI,72 theuse of NMB was associated with increasedintensive care unit (ICU) length of stay andnosocomial pneumonia.

Seizure Prevention and Management

Children who have sustained a significanthead injury are more likely than adults tohave seizures, possibly due to their lowerseizure threshold.13 Patients with GCS

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brain injury. Studies in adults have shownthat anti-epileptic medications for long-termprophylaxis did not improve outcome74 and

are only effective in the first week afterTBI to decrease the incidence of early on-set seizures.75 In children, anti-epileptic med-ications are recommended for short-termuse, unless deemed otherwise by the childsseizure activity.

Barbiturate Therapy

The administration of high dose barbiturates(eg, pentobarbital) is reserved for intracra-nial hypertension refractory to the afore-

mentioned interventions. Barbiturates de-crease ICP by decreasing cerebral metabolicrate, which decreases glucose utilization andoxygen demand, but may cause significanthemodynamic instability. Although there arelimited pediatric studies examining barbi-turate effectiveness and role in outcome,some studies have shown that intractableICP may improve and in some lead to agood outcome.76 However, many patients re-quire vasopressor support during therapy.77

Adult studies have also reported pentobarbi-tal as an effective treatment to decrease ICP.78

However, some have shown no benefit inoutcome,79 while others have shown an asso-ciation with worse neurological outcome dueto jugular venous desaturation.80

Monitoring of the child in a barbituratecoma should include burst suppression viaEEG, invasive hemodynamic monitoring (eg,arterial blood pressure, central venous pres-sure, SjvO2), and frequent assessment of oxy-

genation status. Because of the significantside effects of barbiturate therapy and thelimited data supporting its use, barbituratetherapy is only recommended for childrenwith refractory intracranial hypertension.

Surgical Management

Initial surgical management includes the im-mediate evacuation of a mass lesion (eg,brain tumor, epidural hematoma) and place-ment of ICP monitor as indicated, preferably

a ventriculostomy. Decompressive craniec-tomy to increase intracranial compliance isreserved for patients with refractory intracra-nial hypertension, although some studies81,82

have advocated its use early after TBI beforesecondary injury occurs.

Steroids

The use of corticosteroids is not indicated

in the management of increased ICP afterTBI. However, steroids may be indicated indecreasing swelling and stabilizing the cellmembrane in patients with increased ICP dueto mass lesions, such as brain tumors and ab-scesses, inflammation, and infections.

Fluids, Electrolytes, and Nutrition

The main goals of fluid therapy are to main-tain the patient euvolemic, normoglycemic,

and prevent hyponatremia. In a recent pe-diatric study83 of 170 children with TBI,mean serum glucose > 200 mg/dL was asso-ciated with poor neurological outcome, andserum glucose > 300 mg/dL on admission wasassociated with 100% mortality. Althoughthe exact mechanism of hyperglycemia af-ter TBI is multifactorial and not completelyunderstood, the detrimental effects of hy-perglycemia on the injured brain have beenrepeatedly demonstrated.8386 Current treat-ment in adults with TBI includes stringentglycemic control with insulin therapy.

Parenteral dextrose is avoided for at least48 hours after acute neurological injury dueto the increased risk of lactic acidosis, unlessthe patient is hypoglycemicwhich requiresprompt treatment. Enteral feedings may andshould be instituted within 72 hours after in-jury. Early enteral feeding in adult patientswith TBI has been associated with a dramaticdecrease in ICU days and complications.87

Children with TBI have been found to have

caloric needs 30%60% greater than theirbasal metabolic expenditure88,89and shouldbe supplemented accordingly with the ap-propriate formula and rate. Unless con-traindicated, the preferred method of deliv-ering nutrition is via the enteral route. Dueto potential impairments in the protective air-way reflexes, it may be prudent to administerfeedings via a postpyloric feeding tube to de-crease the risk of aspiration.

Children with increased ICP should re-

ceive fluids at a daily maintenance rate, aswell as fluid boluses as indicated for hypov-olemia, hypotension, or decreased urine out-put. Since dextrose is usually avoided for thefirst 48 to 72 hours after injury, maintenancefluids usually consist of normal saline with

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the daily requirements of potassium chloridebased on body weight. All fluids adminis-tered must be isotonic or hypertonic (eg, hy-

pertonic saline) and hypotonic fluids mustbe avoided. In addition, hyponatremia mustbe prevented since it will worsen cerebraledema. If hyponatremia occurs, it must becorrected slowly to prevent central pontinemyelinosis that can occur with rapid correc-tion of sodium.

Nursing Care

In addition to the nursing and medical in-

terventions outlined above, care of the childand family is an important component inproviding optimal patient care. In pediatrics,the child is cared for within the context ofthe family, and the child with increased ICPis no exception. It is important to encour-age the caregivers and siblings (as appropri-ate) to touch and speak to the child. Stud-ies in children and adults have found thatICP did not increase significantly or actuallydecreased with family presence90,91or withphysical touch.92,93 During these interactions,the childs ICP and hemodynamic status aremonitored and care modified accordingly forany significant change.

There is limited research on whether clus-tering patient care activities (ie, bathing, suc-tioning, procedures, etc.) or providing restperiods in between activities is more bene-ficial to the patient.91,93,94It is recommendedto monitor the patients ICP, MAP, heart rate,central venous pressure, and CPP and con-tinue or abort care accordingly. Additional

sedation and analgesia should also be pro-vided prior to any procedure that may causepain, anxiety, or increased ICP, although theresearch in this area is lacking.

Research on the use of lidocaine priorto endotracheal suctioning to attenuate theICP response in pediatric patients is scantand dated. Based on the available research,lidocaine (via endotracheal tube or intra- venously) is usually recommended prior tosuctioning to blunt the ICP response.9597 One

study95 demonstrated a more significant sup-pression of ICP elevation with 2 mL of 4%lidocaine administered intratracheally due toits anesthetic effect on the tracheobronchialmucosa. Lidocaine 1.5 mg/kg is the recom-mended dose for IV administration prior to

suctioning.97,98 Regardless of the method ofadministration, the patients response mustbe monitored and care adjusted accordingly.

Summary

Neuro-critical care of children with increasedICP revolves around the basic tenet ofthe Monro-Kellie doctrine and aims to de-crease one or more of the intracranial com-partments. The goal of management is tocontrol CSF volume, brain volume, andblood volume. This control is achieved by

TABLE 8 Summary of IntracranialPressure Management

Maintain adequate oxygenation: PaO2 > 60; SpO2> 90%

Maintain adequate systemic perfusionpreventhypotension and hypoxia

Maintain age appropriate ICP and CPP; or ICP < 20and CPP > 5070

Drain CSF as indicated Positioning: maintain supine with head of bed 30

and head midline Review CT scan and neurodiagnostic results as

indicated No indication for prophylactic hyperventilation Hyperventilationonly for acute ICP elevations or

impending herniation Order lidocaine prior to suctioning Mannitol q4h for ICP > 20 mm Hg; maintain serum

osmo < 320 mOsm Consider hypertonic saline; maintain serum osmo< 360 mOsm/L

Maintain euvolemia Monitor electrolytes; prevent hyponatremia Monitor glucoseprevent hyperglycemia and

hypoglycemia Maintain normothermiafor every change by 1C,

ICP increases several mm Hg Provide adequate sedation and analgesia;

consider neuromuscular blockade Monitor for seizure activity; order anti-epileptics as

indicated Institute enteral feedings within 72 hours after injury Frequent neurological assessment: Glasgow Coma

Scale, pupil reactivity, extraoccular movements,motor function, vital signs

Minimize auditory and visual stimulation Encourage family touch and patient contact Provide patient and family support and education Consider 2nd-tier therapy for refractory intracranial

hypertension

SpO2,continuous arterial oxygen saturation; ICP,intracranial pressure; CPP, cerebral perfusionpressure; CSF, cerebrospinal fluid; CT, computedtomography.

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proper patient positioning, normocarbia, CSFdrainage, euvolemic osmolar therapy, seda-tion and analgesia, optimal cardiorespiratory

status, normothermia, and seizure prophy-laxis based on the patients condition andresponse (Table 8). Implementation of hy-perventilation, moderate hypothermia, andbarbiturate therapy is reserved for patientswith refractory intracranial hypertension. Thebest neurological outcome is associated withcontrol of ICP 50 (or age appropriate),as well as prevention of hypoxia and hy-potension. Much research is still needed to

optimize management strategies for children with acute increased intracranial hyperten-sion, particularly nursing interventions thatmay ultimately improve patient outcomes.

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