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CRITICALCARENURSE Vol 24, No. 5, OCTOBER 2004 19

Richard Arbour is a staff nurse and clin-ical researcher in the medical intensivecare unit at Albert Einstein HealthcareNetwork, Philadelphia, Pa.

Intracranial hypertension canlead to potentially catastrophic con-sequences,1 including permanentneurological damage and disability.Intracranial hypertension may be dueto central nervous system infection,brain edema, cerebral hemorrhageor ischemic injury, or brain trauma.Traumatic brain injury is a majorcause of morbidity and mortality; itaccounted for 50 000 deaths in 1998.2

Fatality may not result from theimmediate traumatic or hemorrhagicinjury; rather, progressive damage tobrain tissue may develop over time.3

Brain damage becomes even moreprogressive if intracranial hyperten-sion is a consequence of injury.4

Astute nursing assessment and early,aggressive resuscitation of criticallyill patients may prolong life. Withbrain trauma, the initial injury canbe avoided only by using primaryprevention strategies.1,5 Rapid con-trol of fluctuations and elevations inintracranial pressure (ICP) mayincrease the potential for optimalfunctional recovery.6 In this article,

I provide an overview of intracranialphysiology and assessment findingsspecific to intracranial hypertension.Assessment findings reflect under-lying pathophysiology in response toinjury. These features are typicallythe first ones nurses consider in eval-uating patients. I also review ICPmonitoring and waveform analysisas central in caring for patients withintracranial hypertension.

BackgroundMonroe-Kellie Doctrine

The Monroe-Kellie doctrine pro-vides the framework for reviewingphysiology and treatment for eleva-tions in ICP. This concept holds thatthe skull is a rigid compartment thatcontains 3 components: brain tissue,arterial and venous blood, and cere-brospinal fluid (CSF). Under normalcircumstances, these components arebalanced in a state of dynamic equi-librium. If an increase occurs in therelative volume of one component,such as brain tissue, the volume ofone or more of the other components

CoverArticle

Author

* This article has been designated for CE credit.A closed-book, multiple-choice examination fol-lows this article, which tests your knowledge ofthe following objectives:

1. Identify the acute and chronic causes of intracranial hypertension

2. Describe the 4 methods of intracranial pressure monitoring

3. Discuss nursing assessment and monitoring of intracranial hypertension

Richard Arbour, RN, MSN, CCRN, CNRN

To purchase reprints, contact The InnoVision Group,101 Columbia, Aliso Viejo, CA 92656. Phone, (800)809-2273 or (949) 362-2050 (ext 532); fax, (949)362-2049; e-mail, [email protected].

CEContinuing Education

Intracranial HypertensionMonitoring and Nursing Assessment



must decrease or an elevation in ICPwill result.1,4,5,7-11 In a brain with diseaseor injury, small increases in volumemay result in large increases in ICP.In adults, normal ICP is less than 10to 15 mm Hg. Intracranial hyperten-sion is defined as ICP greater than20 mm Hg.6,7,11 Sustained intracranialhypertension is defined as an ICPgreater than 20 mm Hg that persistsfor 5 minutes or longer.1

PathophysiologyElevations in ICP are critical

because they can decrease cerebralperfusion and blood flow. The brainrequires 50 to 55 mL of blood per100 g of brain tissue to maintain anormal metabolic state. Cerebralperfusion pressure (CPP) is anapproximation of global cerebralblood flow. Patients with traumaticbrain injury or cerebral infection,edema, or ischemia are at risk formarked, sustained elevations in ICPthat if untreated may have devastat-ing consequences.

First, sustained elevations in ICPcompromise CPP, which is deter-mined by subtracting mean ICPfrom mean arterial blood pressure.Decreased CPP, whether from hemo-dynamic compromise (decreasedmean arterial blood pressure) or ele-vated ICP, can lead to global cere-bral ischemic injury and markedneurological changes.9 AdequateCPP is vital for supporting cerebralperfusion. Many clinicians1,2 advo-cate that CPP in adults should bemaintained at no lower than 70 mmHg. Robertson12 suggests that a CPPof 60 to 70 mm Hg is adequate aftertraumatic brain injury. Controlledclinical studies will be necessary tofirmly determine optimal CPP aftertraumatic brain injury.12

uncal, and subfalcine herniation.Central herniation, caused by brainswelling or an expanding space-occupying lesion, causes compres-sion and lengthening of thediencephalon. The medial temporallobes are displaced along the brainstem through the tentorial notch.13-15

Uncal herniation, caused by anexpanding mass lesion, for example,in a temporal lobe, results in dis-placement of the uncus of the tem-poral lobe through the tentorialnotch.13-15 Subfalcine herniation,caused by a unilateral mass lesionsuch as an expanding hematomaresults in displacement of the cingu-late gyrus under the falx cerebri.13-15

Infratentorial herniation includesbrain stem herniation and cerebellartonsillar herniation syndromes.

Second, sustained ICP elevationscan also lead to herniation syndromes,which are due to a shifting of braintissue from an area of high pressure,such as occurs with a unilateral lesionwithin one cerebral hemisphere, toan area of lower pressure.13-15

Assessment FindingsAssessment findings associated

with intracranial hypertension(Table 1) and herniation syndromes(Table 2) are classified as early andlate. Sustained elevations in ICP dra-matically increase mortality andmorbidity. Herniation syndromescan be further classified into supra-tentorial and infratentorial (Figure 1).Supratentorial herniations occurabove the meningeal layer of the ten-torium cerebelli and include central,

20 CRITICALCARENURSE Vol 24, No. 5, OCTOBER 2004

Table 1 Assessment findings associated with intracranial hypertension14,15

Early findingsDecreased level of consciousnessChanges in mental statusConfusionLethargyAbnormal findings on eye examination

Unequal and/or sluggish pupillary responsesPapilledema: swelling of optic disc because of venous congestionCranial nerve deficit: ptosis

Seizure activitySensory changes

Later findingsContinued decrease in level of consciousness

StuporComa states

HeadacheHemiplegiaDecorticate (flexion) posturingDecerebrate (extensor) posturingVomiting (without nausea)Brain stem pressure

Decrease or loss of protective reflexes: cough, gag, corneal reflexesChanges in vital signs

Bradycardia, hypertension (initially)Respiratory changes (rate, depth, pattern)Cheyne-Stokes respirations, ataxic respirations.

Terminal findingsUnstable blood pressure, heart rateProfound hypotension



Depending on location of the lesion,upward displacement of structures inthe posterior fossa may also occur.13-15

EtiologyThe causes of intracranial hyper-

tension are classified as acute orchronic. Acute causes include braintrauma, ischemic injury, and intra-cerebral hemorrhage. Infections suchas encephalitis or meningitis may also

lead to intracranial hypertension.Chronic causes include many intracra-nial tumors, such as ependymomas,that may gradually impinge on CSFpathways and interfere with CSF out-flow and circulation. Chronic subduralhematomas also may cause intracra-nial hypertension. Intracerebralhemorrhage is the result of arterialbleeding directly into brain tissue.Localized injury occurs at the source

of the bleeding, and the hemorrhagemay directly damage the brain tissueas well as cause global injury due tobrain edema and elevations in ICP.Intracerebral hemorrhage may alsolead to obstructive hydrocephalusdue to compression or occlusion ofthe CSF pathways. As the ICP con-tinues to increase, the brain tissuebecomes distorted, leading to herni-ation and additional vascular injury.10

In severe head trauma, in additionto the localized, direct tissue damageand hemorrhage5 associated with theinjury, edema within brain tissuecommonly occurs, resulting in ICPelevation and further brain injury.8

Meningitis is an inflammation of themeninges. It can lead to localized orglobal cerebral ischemia, cerebraledema, and hydrocephalus due todecreased CSF reabsorption andincreased CSF production.16-18

These acute and chronic causesof intracranial hypertension can, ifnot managed aggressively, lead todevastating consequences. Figure 2shows a catastrophic elevation in ICPwith associated early hemodynamicconsequences of a hyperdynamicstate. Figure 3 shows hemodynamicchanges that occur in response tocatastrophic intracranial hyperten-sion and brain stem herniation.

SignificanceThe significance of the onset of

intracranial hypertension is not lim-ited to the initial traumatic or hemor-rhagic event. The initial event causesa physical distortion of and damageto neural tissue or an increase inpressure within a single compartment.Additional vascular and tissue injurymay then occur. This phenomenon,known as secondary brain injury,occurs over hours to days after the


Table 2 Assessment findings associated with supratentorial herniation syndromes13-15

Cingulate/subfalcine herniationDetected by using neuroimaging such as head computed tomography or magneticresonance imaging. Often an indication of brain decompensation and poor intracranial compliance. This herniation syndrome does not have a specific set ofassessment findings but may lead to further injury related to localized compromisein blood flow and tissue distortion.

Central herniationEarly findings

Pupils constricted and reactive to lightLimitations on upward gaze and eye movementsConfusion, progressive decrease in level of consciousnessWeakness followed by paralysis contralateral to lesionNo Babinski reflex (An object such as a key is used to stroke the lateral aspect of

the sole of the foot. Dorsiflexion or “fanning” of the toes in response is a Babinski reflex and generally indicates a lesion in the central nervous system.)

Decreased responses to stimulation (tactile, auditory)Alterations in respiratory pattern: Cheyne-Stokes respirations

Late findingsPupils unequal and nonreactive progressing to pupils fixed and dilatedDysconjugate gaze progressing to eyes fixedComa stateDecortication progressing to decerebration progressing to flaccidityVariations in body temperature (hyperthermia)Changes in vital signsUnstable vital signs progressing to cardiopulmonary arrestPotentially, diabetes insipidus

Uncal herniationEarly findings

Unilateral dilated, slow-reactive pupilsWeakness of extraocular movementsRestlessness progressing to confusionSlight weakness on affected sideDecreased ability to respond to stimulationNo Babinski reflex

Late findingsUnilateral fixed, dilated pupils progressing to bilateral fixed or dilated pupilsParalysis of eye movementsRapid decrease in level of consciousness progressing to comaDecerebrate posturing progressing to flaccidityBabinski reflex progressing to flaccidityAltered respiratory patterns progressing to apneaChanges in vital signs progressing to cardiopulmonary arrest



initial brain injury. Secondary injuryis progressive and often begins shortlyafter brain injury. Contributing fac-tors to secondary brain injury include

leading to multiple stages of progres-sive neuronal damage. From the pointof injury, disruption of cell mem-branes leads to loss of electrical sta-

hypotension, cerebral edema, hypox-emia, and intracranial hyperten-sion.9,19 Primary and secondary injurymay then begin a “vicious cycle”


Figure 1 Coronal views of supratentorial and infratentorial compartments with associated changes caused by specific herniationsyndromes. A, Normal relationship of the compartments. B, Central transtentorial herniation. The brain is swollen, the diencephalon is compressed and elongated, and the medial temporal lobes are forced along the brain stem through the tentorialnotch. C, Uncal and transtentorial herniation. The cingulate gyrus is herniated under the falx cerebri, the uncus herniates throughthe tentorial notch, and the brain stem is compressed and shifted laterally and downward.Adapted from Stubgen and Caronna,13 with permission from Elsevier.

A B C

Figure 2 ICP waveforms show catastrophic elevation in ICP and associated early hemodynamic consequences of a hyperdynamicstate. Devastating ICP elevation with hemodynamic surges leads to arterialization of ICP waveform and lethal cerebral perfusionpressure.

Abbreviations: ABP, arterial blood pressure; CPP, cerebral perfusion pressure; HR, heart rate; ICP, intracranial pressure; PAWP, pulmonary artery wedge pressure; RESP,respirations; SaO2, oxygen saturation; VENT TACHY, ventricular tachycardia.



bility and depolarization. Throughthe effects of the inflammatoryresponse, generation of free radicalsand calcium-mediated damage, mem-brane integrity is further degraded,leading to increased tissue edemaand ICP elevation.20-22 The initialbrain injury plus secondary eventsresults in a cumulative process thatis life threatening.19 Ultimately, phys-iological stability becomes disturbedand compromising tissue damageoccurs, advancing the cycle of sec-ondary injury.5,9,10,20,22-24 The resultingchange in cerebral physiology mayproduce dramatic, potentially cata-strophic ICP elevations in excess of

20 mm Hg. If significant ICP eleva-tions are not aggressively treated,severe, permanent neurologicaldeficits or death will occur.

Intracranial hypertension cancause additional ischemic injury andhighlights the need for early ICPmonitoring and optimal hemody-namic management to maintain ade-quate global cerebral perfusion.21,25

Cerebral ischemia is an importantsecondary event after brain injury.Cerebral ischemia may occur for 2reasons: (1) an already compromisedcerebral blood flow near mass lesionscaused by compression of localizedblood vessels26 or (2) the presence of

vasospasm after traumatic injury26

or subarachnoid hemorrhage. Lossof autoregulation, the brain’s abilityto maintain consistent cerebral bloodflow despite variations in systemicarterial pressure, may also occurafter traumatic brain injury.27 Loss ofautoregulation increases the risk forsecondary brain injuries such ascerebral ischemia and intracranialhypertension.27

Rationale for ICP MonitoringThe Monroe-Kellie doctrine

describes pressure-volume relation-ships within the intracranial cavity.Secondary brain injury may be a


Figure 3 Hemodynamic changes in a patient in response to catastrophic intracranial hypertension and brain stem herniation.Hemodynamic changes began shortly after 5 AM and were accompanied by a decline in the patient’s neurological status. The “gap”in data coincides with transport of the patient for a neuroimaging study. Severe hemodynamic surges at approximately 8:10 AMindicate total loss of cardiovascular stability. This loss was accompanied by loss of all signs of neurological activity. Progressivedepletion in catecholamine stores between 9 AM and 12:30 PM is indicated by decreases in blood pressure and heart rate. Care waswithdrawn (appropriately) at approximately 12:30 PM. The patient was unsuitable for organ donation.

Abbreviations: ABP, arterial blood pressure; D, diastolic; HR, heart rate; M, mean; S, systolic.



direct consequence of intracranialhypertension. Therefore, monitoringICP and CPP should be an immediateobjective in the care of patients withsevere traumatic or hemorrhagic braininjury. Vigilant assessment and mon-itoring of intracranial hypertensionis the standard of care.1,3,5,21 ICP mon-itoring is appropriate in patients withsevere head injury if 2 or more of thefollowing are present: age greater than40 years, unilateral or bilateral motorposturing (decortication or decere-bration), or systolic blood pressureless than 90 mm Hg.6 Evidence ofdistortion, swelling, or hydrocephaluson imaging studies such as head com-puted tomography is an additionalindication for ICP monitoring.10

Before ICP monitoring is started,the initial evaluation of patients withpotential neurological injury includesa physical examination and an imag-ing study such as head computedtomography. This workup yields vitalinformation on the state of the brainbefore invasive monitoring is started.1

Continuous monitoring of ICP andCPP, a determining factor for clinicaloutcome,28 provides effective guidancein managing ICP elevations and hemo-dynamic status. Further interventionscan be based on these clinical findings.The goal of ICP and hemodynamicmonitoring is to augment and main-tain stability of CPP and cerebralblood flow to prevent further cerebralischemic injury.5,9,21,26,29

Significance of ICP Pulse Waveforms

ICP pulse waveforms are gener-ated from a pressure wave transmit-ted through the cardiovascular systeminto the tissues within the intracranialcavity,30 including the choroid plexus,where CSF is produced. The pulse

fluid such as preservative-free saline(in 1-mL increments) is instilled intothe intracranial space and the ICPresponse is measured (volume-pressure curve). An increase in ICPgreater than 2 mm Hg for each milli-liter of fluid added to the systemindicates compromised intracranialcompliance.7,14,15 In another method,ICP is measured before and after astimulus such as endotracheal suc-tioning. An ICP that returns to nor-mal or baseline values quickly (within5 minutes) indicates adequateintracranial compliance. An ICP thattakes 20 to 25 minutes to return tonormal or baseline values may indi-cate poor intracranial compliance.In a third method, intracranial com-pliance is assessed by directly exam-ining the ICP pulse waveform. Ahigher than normal or baselineamplitude of the P-2 component ofthe pulse waveform is associatedwith compromised intracranial com-pliance,7,14,15 particularly if P-2 is thehighest-amplitude component of thepulse waveform. Figure 5 shows ICPpulse waveforms associated withnormal and compromised intracra-nial compliance.

waveform con-sists of 3 com-ponents: P-1,P-2, and P-3(Figure 4). Thepercussionwave, P-1,reflects pulsa-tions of thechoroid plexusas transmittedfrom the cardio-vascular systemat systole. Undernormal condi-tions, P-1 is thehighest of the 3 waveform compo-nents. The tidal wave, P-2, has amore variable shape and reflects rel-ative brain volume. The P-2 compo-nent is often elevated in response toa rapidly expanding mass lesionsuch as a hematoma or an intracra-nial tumor.7,11,30,31 The dicrotic wave,P-3, follows the dicrotic notch on thedownslope of the individual ICPpulse waveform. Additional wavesthat may represent pulsations withinthe cerebral venous system mayoccur before the next P-1.14,15 Nor-mally, the segments of the ICP pulsewaveform progress in a descendingstaircase pattern; P-1 is the highestwaveform segment, and P-3 is thelowest.14,15,30,32

Intracranial ComplianceIntracranial compliance refers to

the ability of the brain to toleratestimulation such as endotrachealsuctioning or increases in volume of1 or more of the brain’s 3 compo-nents (brain tissue, blood, and CSF)without a corresponding increase inICP.4,7,14,15 Several methods are usedto assess intracranial compliance. Inone method, a limited volume of


Figure 4 Components of an intracranial pressure pulse wave-form illustrating compromised intracranial compliance withelevated P-2 waveform component: P-1, percussion wave; P-2,tidal wave; and P-3, dicrotic wave.



ICP Monitoring TechniquesSeveral methods are used to

monitor ICP. These methodsinclude insertion of an intraventric-ular catheter, a subarachnoid bolt orscrew, or a subdural or epiduralcatheter and intraparenchymalinsertion of a fiberoptic transducer-tipped catheter (Figure 6).33 Eachmethod has specific advantages, dis-advantages, and nursing considera-tions (Table 3).7,14,34,35

Ventriculostomy/Intraventricular Catheter

Currently, ventriculostomy isthe most accurate, cost-effective,and reliable method of monitoringICP.31 It is the standard for ICP meas-urement.3,36,37 The ventriculostomycatheter is part of a system thatincludes an external drainage system

and a transducer. The drainage systemand transducer are primed on inser-tion with preservative-free saline. Thetransducer can easily be calibrated

or zeroed against a known pressure.This calibration ensures the consis-tency and accuracy of the pressuremeasurements obtained.


Figure 5 ICP pulse waveforms associated with normal (A) and compromised (B) intracranial compliance. A, Mean ICP is 6-7 mmHg. The components of the ICP pulse waveform proceed in a descending staircase pattern; P-1 is the highest component. B, ICPis elevated, and P-2 is the highest waveform component, indicating poor intracranial compliance.

Abbreviations: ABP, arterial blood pressure; ICP, intracranial pressure.

A

B

Figure 6 Major types of intracranial pressure monitoring. Coronal section of thebrain shows potential sites for placement of the monitoring devices.Adapted from Kerr and Crago,33 with permission from Elsevier.

Epidural

Intraparenchymal

Subarachnoid

Ventricular

Subdural




Table 3 Advantages, disadvantages, and nursing considerations of ICP monitoring techniques

Monitoring device

Intraventricular catheter (ventriculostomy)

Subarachnoid bolt or screw

Subdural or epidural catheter orsensor

Fiberoptic transducer-tipped catheter

Advantages

Allows accurate ICP measurementProvides access to CSF for drainage or samplingProvides access for instillation of contrast mediaAllows reliable evaluation of intracranial

compliance (volume-pressure relationships)

Is associated with lower infection rates than isventriculostomy

Is quickly and easily placedCan be used with small or collapsed ventriclesRequires no penetration of brain tissue

Is least invasiveIs associated with decreased risk of infectionIs easily and quickly placed

Can be placed in subdural or subarachnoid space,in a ventricle, or directly within brain tissue

Is easily transportedRequires zeroing only once (during insertion)Has baseline drift of up to 1 mm Hg per dayIs associated with decreased risk for infection

when brain tissue is not penetratedProvides good quality ICP waveforms (less arti-

fact than with other devices)Requires no adjustment in level of transducer

with patient’s change of position

Disadvantages

Provides an additional site for infectionIs most invasive ICP monitoring techniqueRequires frequent transducer balancing or

recalibrationCatheter may become occluded by blood clot

or tissue debrisInsertion is difficult if ventricles are small,

compressed, or displacedIs associated with risk for CSF leakage around

insertion siteIs associated with increased risk for infection

Has potential for dampened waveform (cerebral edema, blood or tissue debris)

Is less accurate at high ICP elevationsRequires frequent balancing/recalibration (and

with position changes)Provides no access for CSF sampling

Increase in baseline drift over time meanspossible loss of reliability or accuracy

Provides no access for CSF drainage/sampling

Provides no access for CSF sampling/drainageCannot be recalibrated after placementRequires periodic replacement of probeIs easily damaged

*Fluid-filled ICP monitoring systems not maintained with continuous flush or pressure bag. Abbreviations: CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; ICP, intracranial pressure.

Adapted from Shpritz,34 with permission from Elsevier. Added material based on information in March,7 Hickey,14 Kerr and Crago,33 and American Association of Neuroscience Nurses.15,35



A ventriculostomy is most com-monly placed in the nondominantlateral ventricle via a twist drill holein the skull. The dura is incised orpunctured, and the catheter ispassed through the cerebral tissueinto the ventricle. The catheter isthen typically tunneled under thescalp and sutured to the skin surfacea few centimeters from the initialinsertion site.

Advantages of using an indwellingventricular catheter include allowingCSF drainage to effectively decreaseICP and using the catheter as a meansto instill medications.3,15 Access toCSF drainage allows serial laboratorytests of CSF and determination ofvolume-pressure relationships.14,15

Disadvantages of ventriculostomyinclude risk of infection, which ishigher than that associated withother ICP monitoring techniques. Inaddition, the catheter may becomeoccluded with blood or tissue debris,interfering with CSF drainage or ICPmonitoring. Also, if significant cere-bral edema is present, locating thelateral ventricle for insertion of theventriculostomy catheter may be dif-ficult. Last, bleeding or ventricularcollapse may occur if CSF is drainedtoo rapidly.11,14,15 For this last reason,many clinicians set the ventricu-lostomy drainage system to drainCSF when the ICP is greater than 15to 20 mm Hg by adjusting the heightof the drip chamber. In addition, alimit of ventricular drainage such as5 to 10 mL/h has been used to avoidexcessively rapid CSF drainage. Usinga ventriculostomy may allow lifesav-ing CSF drainage and control ofintracranial hypertension.3-5,14,15,36,37

Subarachnoid Bolt or ScrewThe subarachnoid bolt or screw

is inserted via a twist drill hole to the


Nursing considerations*

Provide appropriate sedatives or analgesics during catheter insertionDo baseline and serial neurological assessmentsMeasure patient’s temperature at least every 4 hoursNote character, amount, and turbidity of CSF drainageDocument ICP/CPP measurements, response to stimulation, nursing care activities per

hospital/unit protocolMonitor quality of ICP waveformMonitor system/tubing for air bubbles and flush or purge system as appropriateDrain CSF as indicated for treatment of ICP elevationNotify physician if CSF drainage is not within prescribed parametersMonitor insertion site for bleeding, drainage, swelling, CSF leakageZero or calibrate device per hospital/unit protocolLevel transducer at the foramen of Monro; external landmarks include the tragus of the

patient’s ear and the external auditory canal, among others; all ICP measurementsshould be made with the transducer at a consistent level relative to external landmarks

Administer sedatives or analgesics as appropriate to decrease risk of catheter being dislodged by patient’s movements

Educate patient’s family as indicatedNotify physician if ICP/CPP not within specified parameters

Administer appropriate sedatives or analgesics during insertionDo baseline and serial neurological assessmentsMeasure patient’s temperature at least every 4 hoursMonitor insertion site for bleeding, drainage, swelling, CSF leakageMonitor quality of ICP waveformDocument ICP/CPP measurements, response to stimulation per hospital/unit protocolAdminister sedatives or analgesics as appropriate to decrease risk of catheter being

dislodged by patient’s movementsZero or calibrate device per hospital/unit protocolLevel transducer at the foramen of Monro; external landmarks include the tragus of the

patient’s ear and the external auditory canal, among others; all ICP measurementsshould be made with the transducer at a consistent level relative to external landmarks

Educate patient’s family as indicatedNotify physician if ICP/CPP is not within specified parameters

Administer appropriate sedatives or analgesics during insertionDo baseline and serial neurological assessmentsMeasure patient’s temperature at least every 4 hoursMonitor insertion site for bleeding, drainage, swellingMonitor quality of ICP waveform, drift over timeDocument ICP/CPP measurements, response to stimulation per hospital/unit protocolAdminister sedatives or analgesics as appropriate to decrease risk of catheter being

dislodged or damaged by patient’s movementsEducate patient’s family as indicatedNotify physician if ICP/CPP is not within specified parameters

Administer appropriate sedatives or analgesics during insertionDo baseline and serial neurological assessmentsMeasure patient’s temperature at least every 4 hoursMonitor insertion site for bleeding, drainage, swelling, CSF leakageMonitor quality of ICP waveform, drift over timeDocument ICP/CPP measurements, response to stimulation per hospital/unit protocolAdminister sedatives or analgesics as appropriate to decrease risk of catheter being

dislodged or damaged by patient’s movementsEducate patient’s family as indicatedNotify physician if ICP/CPP is not within specified parameters



level of the subarachnoid space overthe nondominant cerebral hemi-sphere. The dura is then opened, andthe device (filled with preservative-free saline) is placed in contact withthe subarachnoid space. The bolt isthen secured to pressure tubing anda transducer system also primedwith preservative-free saline.14,15,34,35

This technique of ICP monitoringis easier to initiate than is a ventricu-lostomy, a characteristic that is anadvantage. Locating the ventricles isnot necessary, facilitating ease ofinsertion and ICP monitoring evenin patients who have mass effect orbrain edema. Because the cerebraltissue is not violated, the infectionrate for the procedure is lower thanthe rates for other ICP monitoringmethods that penetrate cerebral tis-sue.7,11,14,15,34

Disadvantages of a subarachnoidbolt or screw include the following.The bolt can be occluded by debris,blood clots, or herniation of braintissue into the device. This blockagemay dampen the ICP waveform andmake the pressure measurement inac-curate. As with any invasive monitor-ing technique, leakage of CSF andinfection may still occur. Last, bleed-ing and intracranial hematoma for-mation may occur, possibly causingfurther brain injury.7,11,14,15

Subdural or Epidural CatheterPlacement of a subdural or

epidural fiberoptic transducer-tippedcatheter is accomplished via a smalltwist drill hole through the skull. Thismonitoring technique does notrequire penetration of the cerebraltissue, and the risk of infection is lessthan that associated with other ICPmonitoring techniques that penetratecerebral tissue. Catheter insertion

inability to assess intracranial com-pliance by determining volume-pressure relationships. In addition,the fiberoptic cable may be fragile,and manipulation of the cathetermay damage optical fibers, affectingICP readings.7,11,14,15,34,35 Last, althoughICP measurements obtained at thetime of insertion are accurate, baselinedrift can occur, which may result inan error in ICP measurements afterseveral days of use.3

Nursing ConsiderationsThe Monroe-Kellie doctrine dic-

tates that the 3 components of theskull (blood, brain tissue, and CSF)interact with one another for stabil-ity of ICP and intracranial physiol-ogy. Treatment of elevations in ICPinvolves selectively manipulating ordecreasing the relative volume ofone or more of these components.Interventions for ICP elevation mustdo more than address the specificderangement in intracranial physiol-ogy such as elevated cerebral bloodflow, edema, or hydrocephalus; theymust also be tailored to the specificphysiological changes at a givenmoment.

The interactions between the 3components of the skull are a dynamicprocess. How the brain responds toinjury over time is similarly dynamic.For example, an intervention thatprovides effective management ofintracranial hypertension the firstday after injury, such as using osmoticdiuresis to treat cerebral edema, maynot be as effective for intracranialhypertension related to an increasein cerebral blood flow that occurs 3days after injury.12 This change inthe effectiveness of interventionsunderscores the need for continualneurological assessment and ICP

and initiation of monitoring are alsoeasier, and recalibration of the systemis not necessary.

Disadvantages of this techniqueare multiple. First, access to CSF isnot possible. Second, a wedge effectmay occur from pressure betweenthe catheter tip and the adjacentdura. This effect may compromisethe accuracy of the ICP measure-ments and waveform quality. Third,volume-pressure relationships can-not be determined as an indicationof intracranial compliance. Last, ICPwaveforms may be of poor quality,limiting the amount of useful infor-mation obtained with this monitor-ing technique.7,11,14,15,34,35 Becauseepidural or subdural monitoringtends to be less accurate than othermonitoring techniques, it is used farless frequently.

Intraparenchymal SensorIntraparenchymal sensors are

typically placed via a small twistdrill hole and passed through a boltdevice placed in contact with thesubarachnoid space. The fiberoptictransducer-tipped catheter is placedthrough the bolt into the brain tis-sue. This ICP monitoring device iseasy to insert and maintains excel-lent quality waveforms even inpatients with cerebral edema.

An advantage to using this tech-nique is the minimal risk of tissueherniation and the accuracy of ICPmeasurements despite variations inhead positioning. Because head posi-tioning has minimal influence on theaccuracy of ICP measurements, ICPmonitoring can also be maintainedduring patients’ transport.7,11,14,15

Disadvantages of this techniqueinclude lack of access to CSF fordrainage or laboratory tests and an




measurement and the need todetermine the cause of elevated ICPin order to tailor therapy specificallyto the physiological disturbance at agiven time.4,12

The need for vigilance in ICP mon-itoring and patients’ assessment is fur-ther underscored by the ICP responseto medical and nursing interventions.Cervical spine immobilization bymeans of rigid cervical collars mayalso result in ICP elevations by com-pressing the jugular vein.38 Prone posi-tioning of patients who have acuterespiratory distress syndrome aftersubarachnoid hemorrhage can alsoresult in increased ICP.39 In theseinstances, clearly, measures to immo-bilize the cervical spine and optimizeoxygenation are appropriate; however,the potential effects of these interven-tions on ICP necessitate vigilance andappropriate attention.

Optimal assessment of intracra-nial compliance is tremendouslyimportant for favorable outcomes.Recognition of even subtle changesin intracranial compliance can havefar-reaching implications in overallmanagement, including nursingconsiderations. One example is pul-monary care and endotracheal suc-tioning. A patient with compromisedintracranial compliance is at higherrisk than a patient without compro-mise for potentially dangerous, acuteelevations in ICP and further neuro-logical injury related to the coughreflex, noxious stimulation, and dra-matic increases in intrathoracic pres-sure.4,7,14 Under these circumstances,measures such as administration ofanalgesics or intratracheal lidocaineto attenuate the cough reflex and theresponse to noxious stimuli may beappropriate considerations in high-risk patients. An arousal response to

endotracheal suctioning can bedetected by clinical assessment andcan be documented by using elec-troencephalography-based monitor-ing.25,26 The arousal response can beblunted by giving patients intravenousopioids40 or intratracheal lidocaine41

before the airway is suctioned.Patients with poor intracranial

compliance are more sensitive tostimuli that can increase ICP. Thesestimuli include nursing care activi-ties, peripheral venipuncture, andrepositioning, among others. Asclinically appropriate, interventionsshould be spaced over time to limit acumulative effect on increasing ICP.4

Patients experiencing intracra-nial hypertension are among themost challenging in critical carepractice. Rapid initiation of treat-ment to protect them from a devas-tating outcome depends onaggressive and thorough clinicalassessment.

Changes in the level of conscious-ness are the most important measureof cerebral stability. Consciousness

reflects physiological stability andcoordination between and amongmultiple brain areas. Consequently,any change in level of consciousness,cognition, or responsiveness, even ifsubtle, can have great significance.Decreases in the level of consciousnesscan be caused by brain compressiondue to hemorrhage, edema, hema-toma formation, and expanding solidtumors. Monitoring of consciousnessand arousal by using the GlasgowComa Scale14,42 (Table 4) is vital.

Monitoring changes in pupil sizeand reactivity and alterations in vitalsigns is also imperative. ICP elevationsand localized space-occupying lesionsmay result in compression or displace-ment of the optic or oculomotornerves, causing changes in pupil sizeand reactivity. Changes in vital signsmay be an early or late indication ofintracranial hypertension. Nursesshould also be alert for changes inrespiratory rate, depth, or pattern,which may indicate brain stem com-pression. Clinical assessment, partic-ularly of unconscious patients or


Table 4 Glasgow Coma Scale14,41

Response

Eye openingOpens eyes spontaneouslyOpens eyes in response to speechOpen eyes in response to painful stimulation (eg, endotracheal suctioning)Does not open eyes in response to any stimulation

Motor responseFollows commandsMakes localized movement in response to painful stimulationMakes nonpurposeful movement in response to noxious stimulationFlexes upper extremities/extends lower extremities in response to painExtends all extremities in response to painMakes no response to noxious stimuli

Verbal responseIs oriented to person, place, and timeConverses, may be confusedReplies with inappropriate wordsMakes incomprehensible soundsMakes no response

Score

4321

654321

54321



patients receiving sedatives, anal-gesics, or neuromuscular blockingagents, may not be optimal fordetecting intracranial hypertension.For this reason, ICP monitoring willremain essential in patients’ man-agement. Intracranial pressure ele-vations and diminished compliancecan be quickly detected, facilitatingoptimal treatment.

AcknowledgmentsThe author thanks Cathy McDeed-Breault, RN, MSN, CANP,

at the Veterans Administration Medical Center, SanDiego, Calif, for her editorial assistance as a publishingpartner in the preparation of this manuscript.

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Management of increased intracranial pres-sure: a review for clinicians. J Emerg Med.1999;17:711-719.

2. Tolias C, Sgouros S. Initial evaluation andmanagement of CNS injury. eMed J. Lastupdated January 17, 2003. Available at:http://www.emedicine.com/med/topic3216.htm. Accessed July 2, 2004.

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14. Hickey JV. The Clinical Practice of Neurologi-cal and Neurosurgical Nursing. 4th ed.

Nursing: Assessment and Management ofClinical Problems. St Louis, Mo: CV MosbyInc; 2004: 1491-1524.

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38. Ho AMH, Fung KY, Joynt GM, KarmakarMK, Peng Z. Rigid cervical collar andintracranial pressure of patients with severehead injury. J Trauma. 2002;53:1185-1188.

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40. Brocas E, Dupont H, Paugham-Burtz C,Servin F, Mantz J, Desmonts JM. Briefreport: bispectral index variations duringtracheal suction in mechanically ventilatedcritically ill patients: effect of an alfentanilbolus. Intensive Care Med. 2002;28:211-213.

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CE Test Form

Intracranial Hypertension: Monitoring and Nursing Assessment

Objectives:

1. Identify the acute and chronic causes of intracranial hypertension

2. Describe the 4 methods of intracranial pressure monitoring

3. Discuss nursing assessment and monitoring of intracranial hypertension

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This continuing education program is provided by AACN, which is accredited as a provider of continuing education in nursing by theAmerican Nurses Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuing educa-tion by the State Boards of Nursing of Alabama (#ABNP0062), California (01036), Florida (#FBN2464), Iowa (#332), Louisiana(#ABN12), and Nevada. AACN programming meets the standards for most other states requiring mandatory continuing educationcredit for relicensure.

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7. Which of the following is the most accurate, cost-effective, and reliable method of monitoring ICP?a. Subarachnoid bolt or screwb. Subdural or epidural catheterc. Intraparenchymal sensord. Ventriculostomy catheter

8. Which complication of ventriculostomy is higherthan that associated with other ICP monitoringtechniques?a. Cerebral bleedingb. Cerebral ischemiac. Cerebral infection d. Cerebral edema

9. Which of the following interventions does notresult in ICP elevation?a. Supine positionb. Rigid cervical collar c. Suctioningd. Venipuncture

10. Acute elevations in ICP can be prevented by blunting the arousal response to endotracheal suctioning through administration of which medication?a. Intratracheal lavage with salineb. Intratracheal lidocainec. Intratracheal opioidsd. Intratracheal bronchodilators

11. Which is the most important measure of cerebralstability?a. Motor functionb. Sensory functionc. Pupil sized. Level of consciousness

12. Which of the following scales is vital in monitoringarousal and consciousness?a. Glasgow Coma Scaleb. Ramsay Sedation Scalec. Motor Activity Assessment Scaled. Glasgow Outcome Scale

1. According to the Monroe-Kellie doctrine, which 3components contained in the skull are balanced ina state of dynamic equilibrium?a. Bone, brain tissue, and cerebral bloodb. Brain tissue, cerebral blood, and

cerebrospinal fluidc. Cerebral blood, cerebrospinal fluid, and boned. Cerebrospinal fluid, bone, and brain tissue

2. Which intracranial pressure (ICP) is indicative ofintracranial hypertension?a. 12 mm Hgb. 15 mm Hgc. 18 mm Hgd. 21 mm Hg

3. Which of the following conditions is not an acutecause of intracranial hypertension?a. Cerebral traumab. Ischemic injuryc. Intracranial tumord. Cerebral hemorrhage

4. Which of the following factors does not contributeto secondary brain injury?a. Hypertensionb. Cerebral edemac. Hypoxemiad. Intracranial hypertension

5. Before ICP monitoring is started, the initial evalua-tion of patients should include a physical examina-tion and which of the following studies?a. Electroencephalogram b. Carotid ultrasoundc. Computed tomography of the headd. Carotid arteriogram

6. Which component of the ICP pulse waveform iselevated in response to a rapidly expanding lesionsuch as a hematoma?a. P-1b. P-2c. P-3d. P-4

CE Test QuestionsIntracranial Hypertension: Monitoring and Nursing Assessment



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