Crit Care Nurse-2011 - Traumatic Brain Injury - Advanced Multimodal Neuromonitoring From Theory to...

7/28/2019 Crit Care Nurse-2011 - Traumatic Brain Injury - Advanced Multimodal Neuromonitoring From Theory to Clinical Prac

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to poor neurological outcome and

mortality.1 Signs of secondary neu-

rological damage include brain

swelling (Figure 1), somnolence,

abnormal motor function, and

pupillary changes. Nevertheless, the

onset and extent of secondary injury

are still difficult to detect. Intensive

neuromonitoring is therefore criticalin improving neurological prognosis

in patients with TBI.

Changes in intracranial pressure

(ICP), cerebral perfusion pressure

(CPP), brain tissue partial pressure

Cover Article

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. Describe the interrelationships amongintracranial pressure, cerebral perfusionpressure, brain tissue partial pressure ofoxygen, blood pressure, and brain temperature

2. Identify aberrations in cerebral metabolitesindicative of cerebral ischemia

3. Discuss common neuromonitoring parametersand the threshold values and appropriatenursing interventions associated with each

Sandy Cecil, RN, BAPatrick M. ChenSarah E. Callaway, RN, BSNSusan M. Rowland, RN, BSN

David E. Adler, MDJefferson W. Chen, MD, PhD

CEContinuing Education

2010 American Association of Critical-

Care Nurses doi: 10.4037/ccn2010226

T

raumatic brain injury

(TBI) accounts for 1.4

million reported injuriesand 52000 deaths each

year in the United States.

TBI is the leading cause of death and

disability in patients from ages 1 to

44 years.1 The main causes of TBI

are motor vehicle crashes, falls, and

assaults. Secondary neurological

damage, the damage that occurs in

the ensuing hours and days after the

primary injury, contributes markedly

www.ccnonline.org CriticalCareNurse Vol 31, No. 2, APRIL 2011 25

Traumatic brain injury accounts for nearly 1.4 million injuries and 52 000 deaths

annually in the United States. Intensive bedside neuromonitoring is critical in pre-

venting secondary ischemic and hypoxic injury common to patients with traumatic

brain injury in the days following trauma. Advancements in multimodal neuromon-

itoring have allowed the evaluation of changes in markers of brain metabolism (eg,

glucose, lactate, pyruvate, and glycerol) and other physiological parameters such as

intracranial pressure, cerebral perfusion pressure, cerebral blood flow, partial pressure

of oxygen in brain tissue, blood pressure, and brain temperature. This article high-

lights the use of multimodal monitoring in the intensive care unit at a level I trauma

center in the Pacific Northwest. The trends in and significance of metabolic, physio-

logical, and hemodynamic factors in traumatic brain injury are reviewed, the tech-

nical aspects of the specific equipment used to monitor these parameters are

described, and how multimodal monitoring may guide therapy is demonstrated. As

a clinical practice, multimodal neuromonitoring shows great promise in improving

bedside therapy in patients with traumatic brain injury, ultimately leading to

improved neurological outcomes. (Critical Care Nurse. 2011;31:25-37)

TraumaticBrain InjuryAdvanced MultimodalNeuromonitoring FromTheory to Clinical Practice

Figure 1 Traumatic brain injury canresult in frontal intraparenchymalhematomas with contusion edema andtraumatic subarachnoid hemorrhage.


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of oxygen (PBTO2), blood pressure,

brain temperature, and, recently,

cerebral blood flow (CBF) are moni-

tored in the intensive care unit (ICU).2

Cerebral microdialysis is a technique

increasingly used as a bedside method

for measuring glucose, lactate, pyru-vate, and glycerol levels in the brain

of patients with severe head trauma.3-5

Cerebral ischemia may be detected

on the basis of aberrations in cerebral

metabolites. Similarly, minimizing

secondary ischemic injury common in

TBI may be possible with the manip-

ulation of ICP, CPP, CBF, blood pres-

sure, brain temperature, and PBTO2in brain parenchyma after acute brain

injury.2,4-7

In this article, we describe the suc-

cessful use of multimodal neuromon-

itoring to guide therapy in our ICU.

First, we provide an overview of the

significance of changes in glucose,

lactate, pyruvate, and glycerol levels

in traumatically injured brain and

review the importance and interrela-

tionships between ICP, CPP, CBF,

PBTO2, blood pressure, and braintemperature. We also describe the

background and important clinical

aspects of specific current equipment

used in our ICU to measure all the

changes. Finally, we indicate thresh-

old values that may change the treat-

ment of patients with severe braininjury. Our emphasis is on cerebral

microdialysis and CBF monitoring,

which are relatively new monitoring

techniques.

Metabolic and

Cellular EnergyMetabolic Trends of

Microdialysis Markers

Understanding the bioenergetics

of hypoxic and/or ischemic brain is

important.4-7 As brain tissue becomes

hypoxic, oxygen no longer functions

as the final electron carrier in the

electron transport chain. Nicoti-

namide adenine dinucleotide hydro-

gen therefore cannot deprotonate,

and cells must rely on anaerobic

respiration. Generation of adeno-

sine triphosphate (ATP) is compro-

mised; only 2 molecules of ATP

are produced in contrast to the aer-

obically generated 32 molecules

(Figure 2). During ischemia, a lack

of oxygen and glucose results in

anaerobic respiration. In ischemic

Sandy Cecil is the supervisor/educator and charge nurse in a 10-bed neurological trauma,neurosurgical, surgical intensive care unit at Legacy Emanuel Medical Center in Portland,Oregon.

Patrick M. Chen is an undergraduate biology student at Dartmouth College, Hanover,New Hampshire.

Sarah E. Callaway is a charge nurse in the neurological trauma, neurosurgical, surgicalintensive care unit at Legacy Emanuel Medical Center.

Susan M. Rowland is a relief charge nurse/preceptor coordinator at Legacy EmanuelMedical Center.

David E. Adler is a neurosurgeon at Legacy Emanuel Medical Center.

Jefferson W. Chen is the neurosurgical medical director at Legacy Emanuel Medical Center.

Corresponding author: Sandy Cecil, RN,2801 N Gantenbein Ave, Portland, OR 97227 (e-mail: [email protected] [email protected]).

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 8 99-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Authors

26 CriticalCareNurse Vol 31, No. 2, APRIL 2011 www.ccnonline.org

Figure 2 Flow chart of cellular metabolism. Under normal conditions, glucose is

turned to pyruvate and nicotinamide adenine dinucleotide hydrogen (NADH+) in aer-obic glycolysis. These products are used in the Krebs cycle and electron transportchain to generate 32 molecules of ATP (left side). In ischemia and hypoxia, glucoseand oxygen levels are reduced. Lack of oxygen disables the electron transport chain,causing cells to begin anaerobic respiration (right side), in which pyruvate is con-verted to lactate. Only 2 molecules of ATP are produced, resulting in brain tissuedeath and the release of glycerol.

Normal conditions

Brain tissuedeath

Glucose

Pyruvate (2)NADH+ LactateKrebs cycle

Electron transport chain(oxygen as final carrier inchain)

Decreased blood flow=Decreased oxygen=Switch to anaerobicrespiration

Ischemic and hypoxic conditions

32 ATP

2 ATP


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and hypoxic states, glucose is con-

verted primarily to lactate, resulting

in decreased levels of pyruvate.4,8-10

These alterations in the Krebs cycle

make lactate and pyruvate excellent

indicators of energy failure in the

brain. Because the levels of thesecompounds naturally fluctuate,

detecting the changes in lactate levels

in relation to pyruvate levels, a rela-

tionship known as the lactate to

pyruvate ratio (LPR), is desirable.

Extensive research has shown that

the LPR is a good indicator of

ischemic and hypoxic conditions as

well as possible mitochondrial dam-

age.5,7,8,11,12 Under anaerobic condi-

tions, the PBTO2 and glucose level

decrease while the LPR increases.8,9

Elevated glycerol levels also indi-

cate failure in cellular bioenergetics.

Glycerol levels increase when cells

do not have sufficient energy to

maintain homeostasis.11,12 Because

of a lack of ATP, calcium ion chan-

nels can no longer be maintained,

and cellular influx of calcium occurs.

The influx activates phospholipases,causing the phospholipids within

cellular membranes to be enzymati-

cally cleaved, yielding abnormally

high glycerol levels.7

Microdialysis Technology

Microdialysis enables measure-

ment of the metabolic markers

(glucose, pyruvate, lactate, and glyc-

erol). The technique was firstdescribed in 1966, when Bito and

colleagues successfully placed dex-

tran membrane-lined sacks in the

cerebral hemispheres of dogs to col-

lect amino acids. This technique was

refined to its present-day form in the

1970s by Tossman and Ungerstedt.7,11

Microdialysis involves a catheter

with a 10-mm semipermeable distal-

end membrane that is placed into

the brain parenchyma. The catheter

is pumped with fluid isotonic to tis-

sue interstitium. In short, the catheter

acts as an artificial blood capillary12

(Figure 3). Through diffusion, mole-cules related to the production of

ATP (glucose, pyruvate, lactate,

glycerol) are collected from the

interstitial fluid and are analyzed

hourly.3,7,13 The metabolites recovered

represent 70% of the true interstitial

fluid concentrations.3

Microdialysis

We use 2 devices to perform

cerebral microdialysis. The CMA

600 (CMA Microdialysis, Solna,

Sweden) is used for bedside analysis

of metabolic indicators. This device

was approved for use in the United

States by the Food and Drug Admin-

istration in 2005. A second type of

analyzer is the ISCUSflex (CMA

Microdialysis), which was approved

by the Food and Drug Administra-

tion in July 2009. At the time this

article was written, our facility was

the only one involved in beta tests

of the ISCUS in the United States.

We have clinical experience withmore than 100 patients with both

analyzers. The CMA 600 can be

used to monitor up to 3 patients

and 4 reagents. In contrast, the

ISCUSflex can be used to monitor

up to 8 patients simultaneously,

with a total of 16 catheters and 5

reagents. Calibration of both ana-

lyzers is performed automatically

every 6 hours, and controls are run

every 24 hours.

The microdialysis catheter is

placed through a bolt or burr hole or

is implanted during an open cran-

iotomy. The catheter is then attached

to a microdialysis syringe filled with

sterile perfusion fluid (artificial

CSF) and placed in the CMA 106

pump, which is precalibrated to


Figure 3 Microdialysis technique. The microdialysis catheter at the distal end actsas an artificial capillary. Extracellular substances diffuse from interstitial tissue toperfusion fluid inside the catheter membrane.

Courtesy of CMA Microdialysis, Solna, Sweden.

Cell

Extracellular fluid

Bloodcapillary

Microdialysiscathe

ter


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pump the perfusion fluid at a rate of

0.3 L/min. In TBI patients, the

catheter is ideally placed in the peri-

contusional penumbra of the injury,

and its position is verified by using

computed tomography.5 In addition,

we place a second microdialysiscatheter in an area of undamaged

tissue for comparison or reference.

Each metabolite marker has a separate

reagent for detection. The contents

of the buffer solution are mixed in

the reagent bottle.

We run samples every hour. Sam-

ples can be run every 20 minutes, as

indicated by changes in a patients

condition. Increased attention to a

patients catheters will decrease the

risk of dislodgement of the micro-

dialysis catheters. Of note, the Clini-

cal Laboratory Improvement Act

requires control testing for this

point-of-care device with low, normal,

and abnormally high concentrations

as controls. Known concentrations

along the linear range of each analyte

are run every 24 hours during moni-

toring and after a reagent change.8

Therapeutic Interventions for

Abnormal Levels of

Brain Metabolites

Normal brain glucose levels are

30.6 (SD, 16.2) mg/dL (to convert to

millimoles per liter, multiply by

0.0555).9,14 On the basis of the lowest

level within the standard deviation

(Table 1), the ischemic threshold for

brain glucose is 14.4 mg/dL. In our

patients, strict adherence to tight

glycemic control (blood glucose lev-

els 80-110 mg/dL) often leads to dan-

gerously low brain glucose levels that

can be detected only with cerebral

microdialysis.15 To avoid cerebral

hypoglycemia, we adjusted our blood

glucose ranges to 110 to 180 mg/dL,

resulting in brain glucose levels of

2.5 mg/dL or higher. This experi-

ence suggests that preventing sys-

temic hypoglycemia most likely is

key to preventing metabolic crisis

and, ultimately, secondary brain

injury.15 Therefore, earlier than

usual nutritional support as a

means of maintaining higher brain

glucose levels may be important.

The normal LPR is 23 (SD, 4).9

Normal glycerol levels are 184 to

460 mg/dL (to convert to mil-

limoles per liter, multiply by

0.1086). An LPR near a threshold

value of 30, in conjunction with alow glucose level, requires interven-

tion to prevent cellular energy fail-

ure. Similarly, glycerol levels near

921 mg/dL indicate cellular energy

failure9,14 (Table 1). Baseline LPR and

glycerol levels are recorded and

watched for changes and trends

toward threshold ischemic values.

Routine interventions to lower the

LPR, by preventing anaerobic respi-

ration that leads to abnormally ele-

vated glycerol levels, include

increasing glucose levels by adjust-

ing insulin infusions for a permis-

sive blood glucose level of 110 to

180 mg/dL, elevating and adjusting

the patients head and position, and

augmenting CPP with vasopressors

(Figure 4).

Intracranial MonitoringPhysiology of ICP and CPP

Elevated ICP is a common neu-

rosurgical concern after trauma

because it impedes CBF and is

associated with ischemia and

hypoxia.16 Common causes of ele-

vated ICP include development of

mass lesions such as subdural

hematoma, epidural hematoma,

and intracerebral contusions.

Additionally, cerebral edema and

communicating and noncommuni-

cating hydrocephalus are treatable

causes of increased ICP.17,18 ICP is

the target parameter for manytreatment algorithms. ICP is used

to calculate CPP, the pressure gra-

dient for blood perfusion in the

brain measured in millimeters of

mercury and used to calculate CBF

(CPP/cerebral vascular resistance).2,18

High ICP, a source of energy

failure, is associated with a

decreased CPP and lower CBF, the

underlying cause of cellular energyfailure.19 Increased ICP and low

CPP often result in marked neuro-

logical morbidity and poor out-

come. The threshold values of ICP,

CPP, and CBF, which vary markedly

according to body position, age,

and body surface area, are widely

debated.16,18,20 Finally, ICP monitor-

ing is accepted in the Brain Trauma


Table 1 Normal and threshold values of metabolic parameters important inneuromonitoring of patients with traumatic brain injury

Parameter

Glucose, mean (SD), mg/dL

Pyruvate, mean (SD), mg/dL

Lactate mean (SD), mg/dL

Lactate to pyruvate ratio

Glycerol, mg/dL

Threshold value

14.4

0.27 (fatal)

80.2 (fatal)

30

21

Normal levels

30.6 (16.2)

1.46 (0.33)

26.1 (8.1)

23 (4)

184-460

SI conversion factors: To convert glucose to mmol/L, multiply by 0.0555; pyruvate to mol/L, multiply by113.56; lactate to mmol/L, multiply by 0.111; glycerol to mmol/L, multiply by 0.1086.


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Foundation guidelines1 as the gold

standard for TBI monitoring toguide intervention.

Cerebral Pressure and Perfusion

Monitoring Systems

Unlike microdialysis monitor-

ing, intracerebral technology and

monitors vary in concept and

design. Bedside physiological

monitors are used to measure ICP

and calculate CPP. Pressure trans-

duction varies between monitorsand involves different mechanisms,

including catheter-tip strain gauge,

external strain, and fiber optics.1

Pupillometers provide an alterna-

tive method of evaluating ICP lev-

els by giving quantitative evaluation

of pupillary function.2,21

Camino ICP Monitor. The

Camino ICP monitor (Integra

NeuroSciences, Plainsboro, NJ)consists of a patented fiber-optic

transducer-tipped pressure-

temperature catheter that is placed

via a burr hole and can be used to

measure ICP in the subdural,

parenchymal, and ventricular

spaces. The device measures ICP

and brain temperature and dis-

plays ICP waveforms and the cal-

can be used to measure ICP through

a tunneled catheter, a bolted catheter,or an intraventricular approach.

The ICP Express allows both contin-

uous readings and CSF drainage via

ventriculostomy. The ICP Express

can be implanted in the subdural

space or the intraparenchymal

space and then secured to the skull.

The Codman microsensor tip

is placed in sterile liquid to zero

the sensor before implantation. The

microsensors zero offset numberwill be displayed on the ICP Express

screen. This offset number is specific

to the transducer that was zeroed.

Recording the zero offset reference

number on the patients chart or on

the microsensor is important in

case of a disconnection. This device

is not compatible with magnetic

resonance imaging.

Ventriculostomy. A ventricu-lostomy catheter provides a method

for monitoring ICP while simultane-

ously reducing ICP through thera-

peutic CSF drainage. Using a

ventriculostomy is particularly help-

ful in treating obstructive hydro-

cephalus.23 If an excessive amount of

CSF accumulates in the ventricles

after TBI, the fluid can be externally

culated CPP. The Camino catheter

has a miniaturized transducer at thedistal end. The device has no fluid-

filled system, thus eliminating the

problems associated with an exter-

nal transducer, pressure dome, and

pressure tubing. The monitor pro-

vides continuous information and

does not require recalibration.22

The fiber-optic catheter, with its

integrated transducer, is inserted

through a burr hole space in the

subdural, parenchymal, and ven-tricular spaces. The transducer

must be zeroed before insertion

and disconnected from the pream-

plification connector when a

patient is moved. A red mark will

indicate correct placement in the

brain parenchyma. The subdural

and ventricular catheters do not

have a red line, rather they have

graduated lines to calculate thedepth of the catheter.22 The

catheter is visible on computed

tomography and is not compatible

with magnetic resonance imaging.

CODMAN ICP Express. The

CODMAN ICP Express (Codman &

Shurtleff Inc, Raynham, Massachu-

setts) is also used for measuring ICP

and calculating CPP. The ICP Express


Figure 4 Flow chart of metabolic related therapy integrates the possible responses to low blood glucose, elevated lactate topyruvate ratio, and glucose (left). Normothermic treatment is used to reduce brain metabolic demand (right).

Low blood

glucose

Enteral feedingInsulin Insulin infusion

Acetaminophen

or ibuprofen

Elevated braintemperature

Adjust head

positionVasopressors

Return aerobicrespiration and

glucose

Elevated

lactate to pyruvate

ratio and/or

high glycerol

Adjust capillaryblood glucose

Cooling blankets

or ice packs

Invasive cooling

Icycath

CoolGuard


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drained through a ventricular

catheter secured to the head.

ICP monitoring via a ventricular

drain is accomplished by using a

transducer system.2 Ventricu-

lostomies are leveled at the tragus

and open to drainage at the pre-scribed centimeters of water the

neurosurgeon orders. Documenting

the amount of CSF drained hourly is

important. Troubleshooting meas-

ures if drainage stops include lower-

ing the ventriculostomy, flushing

away from the head in case of clot

in the tubing, and flushing 0.1 mL

of preservative-free normal saline

toward the head. The stopcock to

the transducer must be turned in

the direction of flow for continuous

ICP monitoring or for drainage of

CSF. During repositioning of the

patient, the stopcock is turned to the

off position to prevent overdrainage

of CSF.

Pupillometry. The pupil check

with a flashlight has always been a

standard subjective measurement

of pupil reactivity and status of thenervous system and brain. Now

changes in constriction and dilata-

tion of pupils to light can be quanti-

tatively assessed. The Neuroptics

ForeSite pupillometer (Medtronic,

Minneapolis, Minnesota) is a non-

invasive, battery-operated, hand-

held device that uses light stimulus

and rapid live photography to meas-

ure maximum and minimum aper-

ture and constriction velocity of

pupils.2 Although the pupillometer

is a relatively new device, preliminary

testing suggests that constriction

velocities less than 0.8 mm/s indicate

increased brain volume and veloci-

ties less than 0.6 mm/s suggest ele-

vated and problematic ICP. Similarly,

pupil reactivity less than 10% after

light stimulus suggests elevated ICP

and should be considered in con-

junction with the results of other

monitoring systems for ICP.21 We

have found that using the pupil-

lometer is an easy and quick

adjunct to assessing neurological

changes of patients with TBI.

In order to use the pupillometer,

the head rest of the device must be

fitted correctly. The head rest is dis-

posable and should be changed for

each patient. Awake patients are

instructed to look straight ahead

and focus their untested eye on a

distant object. Manually and gently

holding the patients eye open maybe necessary. The green pupil

boundary circle must be centered

on the pupil for measurement. Exact

measurement of each pupil and

constriction is then obtained. This

measurement is more reliable and

consistent than the subjective assess-

ment of a health care provider.21

ICP monitoring and catheters

have become the standard of care

for measuring ICP.5 Baseline normal

ICP levels range from 0 to 10 mm

Hg; treatment threshold values are

usually 20 to 25 mm Hg.1,16,18,24,25 Ideal

CPP is approximately 60 mm Hg;

the treatment threshold value is

about 50 mm Hg1,24,25 (Table 2).

Current TBI guidelines include

first- and second-tier interventions

to reduce ICP if it increases beyond

the threshold value. First-tier inter-

ventions may involve draining CSF,

increasing PaO2 and PaCO2 levels,

administering diuretics, or elevating

the head of the bed to an optimal

30 angle. Second-tier interventions

involve administering medications,

such as mannitol, furosemide (to

reduce intravascular volume),

hypertonic saline, or barbiturates,

to reduce ICP. Patients who do not

respond to these therapeutic inter-

ventions require computed tomog-

raphy and, possibly, craniotomy or

craniectomy.1,24,25 Finally, a brief trial

of hyperventilation may be used asa temporary measure to control

high ICP1 (Figure 5).

Cerebral Blood Flow

CBF is a complex and essential

variable in determining whether the

brain experiences posttraumatic

secondary damage. Acute brain

trauma causes a decrease in CBF

while increasing the demand for

blood and oxygen.2,26 Many variables

affect blood flow in the brain, includ-

ing metabolic regulation, PaCO2,

PaO2, and autoregulation.18,26

Increases in CPP can increase CBF

during ischemic conditions. Autoreg-

ulation of this change in CPP and

CBF includes vasodilatation and

vasoconstriction (Figure 6). The


Table 2 Normal and threshold values of hemodynamic parameters importantin neuromonitoring of patients with traumatic brain injury

Parameter

Intracranial pressure, mm Hg

Cerebral perfusion pressure, mm Hg

Mean arterial pressure, mm Hg

Cerebral blood flow, mL/100 g per minute

Threshold value

20-25

50

15

Normal levels

0-10

>60

Augmented to keep

cerebral perfusionpressure >60 mm Hg

18-35


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vasodilatation cascade occurs when

CPP decreases, cyclically increasing

vasodilatation. In response, ICP

and cerebral vascular resistance

increase, aggravating brain edema.

In contrast, the vasoconstriction

cascade occurs when CPP increases,

causing constriction of vessels to

reduce cerebral blood volume and

CBF. If autoregulation is ineffective,CBF is determined by blood pres-

sure. Hypotension may then cause

ischemia. Similarly, hypertension

may cause hyperemia.26-28

CBF Monitoring Systems

Direct measurement of CBF is

relatively new in neurointensive care.

Accordingly, real-time perfusion

per 100 grams per minute) with an

attached probe. The probe is mini-

mally invasive and includes a

heated distal thermister and a prox-

imal thermister to track baseline

temperature. The monitor and

probe measure tissue perfusion by

measuring the ability of the tissue to

carry heat through thermal conduc-

tion, represented as the K value bythermal convection from blood

flow. The monitoring system calcu-

lates tissue perfusion by calculating

thermal convection and total dissi-

pated initial power. The probe can

be viewed on computed tomogra-

phy and radiography. It is not com-

patible with magnetic resonance

imaging.30

measuring devices and technology

are still being developed and refined.

Monitoring CBF could play an

important role in neurological care,

because the brain depends on con-

tinuous blood flow to supply glucose

and oxygen. Regional CBF is consid-

ered an important upstream moni-

toring parameter indicative of

tissue viability.

29

Hemedex System. The Hemedex

CBF monitoring system (Codman &

Shurtleff, Inc) is approved by the

Food and Drug Administration for

the bedside monitoring of tissue

blood flow and circulation. With

this device, CBF is measured by cal-

culating real-time tissue perfusion

at the capillary level (in milliliters


Figure 5 Flow chart of hemodynamic related therapy integrates the possible responses to elevated ICP, low CPP, and low or highbrain oxygen level.

Abbreviations: CPP, cerebral perfusion pressure; CSF, cerebral spinal fluid; CT, computed tomography; ICP, intracranial pressure; P BTO2, brain tissue partial pressure ofoxygen.

Low cerebral

blood flow

Brain

oxygen

(PBTO2)

Adjust blood

pressure

Maximize

CPP

Low blood pressure: phenylephrine,norepinephrine, vasopressins,

dopamineCT scan

Mannitol

hypotonic

saline

Barbiturates vs craniotomy/craniectomy30 anglehead

Diuretics

+ PaO2+ PCO2

Drain CSF

High blood pressure: metoprolol,

nicardipine, enalapril,

nitroglycerin, sodium nitroprusside

Reduce ICP to

maximize CPP

and cerebral

blood flow

Elevated

ICP, low

CPP

Medication,

sedation, anti-

inflammatory

cooling

devices

Reduce ICP

Increase

CPP

Treat

hypovolemia,hypotension,

hypoxia

Hyperventi-

lation

Increase

body

tempera-ture

anesthesia,

sedatives

Increase

demand

Reduce

delivery

High PBTO2luxury perfusion

Low PBTO2

Reduce

increased

demand

Increased

deliveryTier 2Tier 1


8/13

The probe is inserted through a

burr hole or is placed 2 to 2.5 cm

below the dura into brain white

matter (Figure 7). The probe is

secured via fixation disc or a single-

or double-lumen bolt. In patients

with TBI, the probe is placed either

in noninjured brain white matter

ipsilateral or contralateral to the

injury or in the ischemic penumbrasurrounding injured brain tissue.

For comparison, a probe can be

placed in uninjured brain tissue.

Once the probe is placed by a neu-

rosurgeon, a nurse attaches the

probe to an umbilical cord and

monitor to begin calibration. The

proper K value for white brain mat-

ter is 4.9 to 5.8 mW/cm per degree

Celsius. The probe can be retractedor advanced accordingly if the K

value is not within range.

The monitor provides CBF

parameters within a temperature

range of 25C to 39.5C. Cooling the

patient should be considered if brain

temperature is greater than 38.5C.

The monitor does not run on

battery power, so the probe must be

disconnected from the umbilical cord

before the patient is transported to

other departments for procedures

or tests. The probe should be secured

to the patients head dressing to pre-

vent dislodging the probe. If the

probe is used in conjunction with a

microdialysis catheter, the 2 catheters

must be separated by 2.0 mm for

accurate results.Transcranial

Doppler Sonog-

raphy. Although

we do not rou-

tinely use tran-

scranial Doppler

sonography for

patients who do

not have an

aneurysm, thistechnique is

being investi-

gated in patients

with TBI. With

this technique, a

probe with a

low-frequency

ultrasonic signal

is used on thin

areas of cranium to measure veloc-

ity and direction of blood flow in

the intracranial arteries.31,32

Although most commonly used to

detect vasospasm after cerebral

aneurysms, Doppler imaging can be

used to detect posttraumatic cere-

bral hemodynamic changes and

complications such as hyperemia,


Figure 6 Vasodilatation (left) and vasoconstriction (right) cascades protect the brain. The dynamics of cerebral blood flow arebest encompassed by the patterns of intact autoregulation. The vasodilatation cascade occurs when cerebral perfusion pressure(CPP) decreases, leading to increases in cerebral blood volume (CBV) and intracranial pressure (ICP), which can lead to edema. IfCPP increases, vasoconstriction occurs, reducing CBV and decreasing edema by decreasing ICP.

Edema+CSF

Reduceedema

Blood viscosity

Hyperemia

Hypocapnia

+ Blood viscosity

Hypoxia

Hypercapnia CPP + CPP

+ ICP ICP+ CBV CBV

+ Vasodi-latation

+ Vasocon-striction

Figure 7 Hemedex catheter. Probe can be tunneled or bolted.Probe is embedded 2 to 2.5 cm below the dura.

Courtesy Hemedex Inc, Cambridge, Massachusetts.


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vasospasm, decreased CBF, and

intracranial hypertension.31,32 Tran-

scranial Doppler sonography pro-

vides a real-time assessment of

changes in flow velocity that reflect

changes in CBF when cardiac out-

put and blood pressure remainconstant.32-34

Blood Pressure

Mean arterial pressure (MAP)

and ICP are important in calculat-

ing CPP (CPP= ICP MAP). CPP is

directly proportional to CBF. Drastic

decreases in CPP result in decreased

CBF. Autoregulation (Figure 6) pro-

tects the brain from variation in

blood pressure. When autoregula-

tion is functional, large changes in

MAP do not lead to significant

changes in CBF.35 If autoregulation

is impaired, uncontrolled blood

pressure directly causes changes in

ICP, CPP, and CBF. In patients with

impaired autoregulation, reducing

blood pressure reduces CBF and

aggravates ischemia. In contrast, in

patients with impaired cerebralautoregulation, hypertension can

cause increases in ICP and CBF.35

Blood pressure is measured by

using a cuff or an arterial catheter.

Normal CBF is 18 to 35 mL/100 g

per minute.30 The threshold value is

15 mL/100 g per minute36 (Table 2).

Because of the synergistic relation-

ship between CBF and arterial blood

pressure, both parameters must beconsidered in therapeutic decision

making.26 MAP is monitored at least

hourly; the goal is to maintain an

optimal MAP to achieve a CPP

greater than 60 mm Hg (Table 2).

MAP can be controlled by using flu-

ids and vasoactive agents. Medica-

tions that decrease MAP include

metoprolol, nicardipine, enalapril,

such as near-infrared spectroscopy

and more invasive fiber-optic

catheter technology1; however, a

direct monitoring system has

recently been introduced.

The Licox PBTO2 monitoring sys-

tem (Integra NeuroSciences, Plains-boro, New Jersey) measures PO2 and

temperature in the brain. PO2 is an

established marker of cerebral

ischemia and secondary brain injury.

The triple-lumen introducer kit,

with a 7-mmlong oxygen-sensing

area at the distal tip, measures

regional oxygenation, with separate

probes to measure ICP and temper-

ature. The most recent device pro-

vides the option to bolt or tunnel

the catheter and has a sensor that

measures temperature and oxygen

integrated into the same catheter.

The Licox catheter uses Clark-type

electrode technology to measure

PO2 in blood of tissue.38

The catheter is placed 25 to

35 mm into the brain. The oxygen

sensor is located in the white matter

of the brain, preferably in thepenumbra of the injured area. The

catheter is inserted via the triple- or

double-lumen bolt. The optimal

location for normal brain measure-

ments is uninjured brain. Setup

and calibration are minimal. After

the brain has adjusted to the new

catheter, an oxygen challenge test

should be performed by setting the

ventilator fraction of inspired oxy-gen at 100% for 2 to 5 minutes. PBTO2should increase. A neurosurgeon

can adjust the probe as needed.

Although measuring ICP and

CPP is key in patients with TBI,

monitoring cerebral oxygenation

can indicate hypoxic events earlier

than monitoring ICP and CPP can

and thus may improve neurological

nitroglycerin, and nitropresside. Sub-

optimal MAP can be increased by

using phenylephrine, norepinephrine,

vasopressin, or dopamine. Maintain-

ing optimal CPP in order to maximize

CBF may also require interventions

that decrease ICP (Figure 5).

Brain Tissue OxygenationMechanisms

Maintaining appropriate oxygen

flow to satisfy the metabolic demands

of the brain is critical to ensuring

good neurological outcome. This

concept is emphasized more generally

in the overall physiological resuscita-

tion of injured patients.1,17 Establish-

ing a patent airway and restoring

circulating blood volume and oxy-

genation are all attempts to maintain

normal oxygenation of brain tissue.

The principal cause of secondary

brain damage and poor neurological

outcome is cerebral hypoxia triggered

during the ischemic cascade.17,37 Sys-

temic hypoxia, hypotension, and

intracranial hypertension can lead to

oxygen deprivation. If autoregulationis functional, low PO2 can be resolved

by vasodilatation. When autoregula-

tion is impaired, low oxygen flow eas-

ily disrupts brain metabolism.17,28 The

effects of manipulations of ICP, CPP,

and PCO2 on PBTO2 have been reviewed

extensively, stressing that high ICP

and low CPP correlate with low PBTO2and poor neurological outcome.37

Monitoring Systems

The Brain Trauma Foundation

recommends oxygen monitoring

because a significant number of

patients with TBI have hypoxemia

and hypotension. As with ICP tech-

nology, various techniques for PBTO2monitoring have been developed.

Examples include indirect systems



10/13

outcome. The goal PBTO2 value is

greater than 20 mm Hg; the ideal is

30 mm Hg. Lower values may indi-

cate impending hypoxia.1 A PBTO2of 55 mm Hg suggests a threshold

value defined as luxury perfusion.39

In order to improve PBTO2 duringischemic conditions, CBF can be

maximized by decreasing ICP via

barbiturates, CSF drainage, and/or

craniotomy. If the decreased PBTO2is due to lower oxygen delivery,

increasing CPP and avoiding hypoten-

sion, hypovolemia, and hypoxia will

be important. Common interven-

tions to improve cerebral oxygen

delivery include administration of

isotonic solutions, vasopressors,

and blood transfusions and increases

in the fraction of inspired oxygen.

Because pain, shivering, agitation,

and fever further increase cerebral

metabolism, sedatives, anti-

inflammatory agents, and cooling

devices are used. In contrast, PBTO2may reach luxury perfusion levels

because of hyperemia or excessive

cerebral blood flow, which increasesICP. High PBTO2 and hyperemia can

be temporarily reduced with care-

fully guided prophylactic hyperven-

tilation, although this intervention

may cause secondary injury. If hyper-

ventilation is used, brain oxygena-

tion should be monitored with either

a tissue oxygenation monitor or a

jugular bulb catheter. Decreasing

body temperature and inducingheavy sedation can further decrease

the demand of the brain tissue and

in turn increase PBTO21 (Figure 5).

Brain Temperature andHypothermiaReduction of Brain Temperature

In humans, brain temperature

is an important marker of brain

Monitoring Brain Temperature

Monitoring brain temperature

is relatively easy because it is an

integral part of multiple systems.

In our ICU, the Camino bolt system

and the Hemedex and Licox systems

can all be used to monitor braintemperature.

Brain hyperthermia, a tempera-

ture of 38.5C or greater, can be pre-

vented by multiple methods. Of

note, brain hyperthermia must be

monitored simultaneously with

body temperature to ensure that

cooling interventions are adequately

affecting the temperature of the

injured brain tissue. Administration

of antipyretics such as acetamino-

phen or ibuprofen is a common ini-

tial therapeutic intervention. Passive

cooling measures such as cooling

blankets and/or ice packs can be

used.43 Invasive cooling measures

are considered if the noninvasive

methods are ineffective. We use the

Thermogard XP system (Zoll Med-

ical Corporation, Chelmsford, Mas-

sachusetts), an intravascular,multilumen catheter. We prevent

hyperthermia in patients with TBI

by starting use of the Thermogard

XP system if brain temperature is

greater than 38.5C. The Hemedex

monitor for CBF functions within

the temperature ranges of 25C to

39.5C.1 The goal of using the Ther-

mogard XP system is to reduce

brain temperature to a normother-

mic range of 36C to 37C. Our

hyperthermia orders require fre-

quent laboratory tests for levels of

potassium, phosphates, and magne-

sium; prothrombin and partial

thromboplastin times, and platelet

counts to prevent coagulopathies.43

Treatment with the Thermogard

may cause shivering, a normal

metabolism and cellular injury. In

initial studies on ischemic brain in

animals, slight changes in brain

temperature accounted for fluctua-

tions in histological changes in brain

tissue. Normothermia and moder-

ate hypothermia in rats (33C)resulted in a marked decrease in

brain glutamate levels, the metabo-

lite uncontrollably released during

tissue energy failure. Although low-

ering brain temperature in humans

with TBI is still debated and scien-

tifically unproved, the intervention

is a neuroprotective strategy that in

theory reduces the metabolic demand

of the brain, possibly decreasing

secondary neuronal injury and

improving behavioral outcomes.40-42

The mechanisms of moderate

hypothermia (32C-33C) and nor-

mothermia (36C-37C) on postis-

chemic tissue, although complex,

are multifunctional. At the cellular

level, hypothermia and reduction

of brain temperature in general can

block excitatory neurotransmitters.

Prevention of toxic calcium overloadallows continued proper amino acid

folding by replacing ubiquitin and

results in improved oxygen delivery

and CBF and depresses the immune

response. Increased brain tempera-

ture has been associated with longer

ICU stays and thus extended inten-

sive care, as well as higher mortal-

ity.42 Finally, smaller nonrandom

and class 2 clinical studies haveindicated the successful use of

hypothermia in neuroprotection.42

Similarly the Brain Trauma Founda-

tion1 has recommended that induced

hypothermia within the first 48

hours of injury may reduce mortal-

ity, further stressing the importance

and merit of temperature monitor-

ing in TBI.



11/13

thermoregulatory response to hypo-

thermia. Shivering increases oxygen

consumption in skeletal muscles,

diverting valuable oxygen away from

the injured brain. Refractory shiver-

ing may require deep sedation and/

or the administration of paralyticagents to facilitate the induction and

maintenance of hypothermia and

minimize oxygen consumption.43-45

ConclusionAdvancements in neuromonitor-

ing have improved the bedside care

of patients with TBI. These develop-

ments have provided the possibility

of true multimodal monitoring for

effective therapy. As described in

this article, we have taken steps to

turn this possibility into a routine

standard of practice. Neuromonitor-

ing traditionally has been used as a

method of detecting problems as

the problems emerge. Yet, many of

these technologies can be used to

detect problems before the problems

become major, thus creating the

opportunity for more timely inter-ventions. The nursing staff in our

ICU realize that caring for patients

with complex brain injuries requires

vigilant monitoring of multiple

parameters in hopes of preventing

secondary injury. In addition to the

conventional placement of a ven-

triculostomy in a patient with TBI,

we routinely use microdialysis to

evaluate metabolic changes (glucose,

pyruvate, lactate, glycerol) and vari-

ous monitoring systems to assess

ICP, CPP, CBF, blood pressure, and

brain temperature. Figure 8 showsplacement of the devices in a typical

patient in our ICU. In this article,

we have detailed our practice by

explaining the background of the

parameters monitored in TBI

patients, the technical aspects of

each machine or device used, and

related therapeutic interventions.

Our use of multimodal monitoring

to provide comprehensive care has

great potential to improve the out-

comes of our patients who have

marked neurological injury. CCN

AcknowledgmentsThis manuscript would not have been possible

without the editorial guidance of Christine SmithSchulman, RN, CNS, CCRN, the clinical nurse special-ist at Legacy Emanuel Medical Center. In addi-tion, we thank Dan Jones, RN, and KimberlySkaale, RN, staff nurses in ICU East at LegacyEmanuel Medical Center, for their review of themanuscript.

Financial DisclosuresNone reported.

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ciation of Neurological Surgeons; Congressof Neurological Surgeons; Joint Section on

Neurotrauma and Critical Care, AANS/CNS;Bratton SL, Chestnut RM, Ghajar J, et al.

Guidelines for the management of severehead injury [published correction appearsinJ Neurotrauma. 2008;25(3):276-278] .J Neurotrauma. 2007;24 (suppl 1):S1-S106.

2. Bader M. Gizmos and gadgets for the neu-roscience intensive care unit.J Neurosci Nurs.2006;38(4):248-260.

3. Bellander B, Cantais E, Enblad P, et al.Consensus meeting on microdialysis inneurointensive care.Intensive Care Med.2004;30(12): 2166-2169.

4. Goodman JC, Robertson CS. Microdialysis:is it prime time? Curr Opin Crit Care. 2009;15(2):110-117.

5. Presciutti M, Schmidt JM, Alexander S.Neuromonitoring in intensive care: focuson microdialysis and its nursing implica-

tions.J Neurosci Nurs. 2009;41(3):131-139.6. Persson L, Hillered L. Chemical monitoringof neurosurgical intensive care patients usingintracerebral microdialysis.J Neurosurg.1992;76:72-80.

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9. Johnston AJ, Gupta AK. Advanced monitor-ing in the neurology intensive care unit: micro-dialysis. Curr Opin Crit Care. 2002;8:121-127.

10. Zauner A, Daugherty WP, Bullock MR,

Warner DS. Brain oxygenation and energymetabolism, I: biological function andpathophysiology.Neurosurgery. 2002;51(2):289-301.

11. Peerdeman SM, Girbes AR, Vandertop WP.Cerebral microdialysis as a new tool forneurometabolic monitoring.Intensive CareMed. 2000;26:662-669.

12. Ungerstedt U, Rostami E. Microdialysis inneurointensive care. Curr Pharm Des. 2004;10(18):2145-2152.

13. Peerdeman S, Tulder MW, Vandertop W.Cerebral microdialysis as a monitoringmethod in subarachnoid hemorrhagepatients, and correlation with clinicalevents.J Neurol. 2003;250:797-805.

Figure 8 Placement of multimodal catheters and monitoring probes. Computedtomography scans of 24-year-old woman with severe traumatic brain injury showplacement of catheter for microdialysis and probes for monitoring brain tissue partialpressure of oxygen, blood flow, and intracranial pressure.

Microdialysis

Hemedex

HemedexLicox

To learn more about traumatic brain injury,read Functional and Cognitive Recovery ofPatients With Traumatic Brain Injury: Pre-diction Tree Model Versus General Modelin Critical Care Nurse, 2009;29(4):12-22.Available at www.ccnonline.org.

Now that youve read the article, create or contributeto an online discussion about this topic using eLetters.

Just visit www.ccnonline.org and click Respond toThis Article in either the full-text or PDF view ofthe article.



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14. Reinstrup P, Stahl N, Mellergard P, Uski T,Ungerstedt U, Nordstrom CH. Intracerebralmicrodialysis in clinical practice: baselinevalues for chemical markers during wake-fulness, anesthesia, and neurosurgery.Neu-rosurgery. 2000;47:701-709.

15. Oddo M, Schmidt JM, Carrera E, et al.Impact of tight glycemic control of cerebralglucose metabolism after severe braininjury: a microdialysis study. Crit Care Med.

2008;36(12):3233-3238.16. Chang JJ, Youn TS, Benson D, et al. Physio-logic and functional outcome correlates ofbrain tissue hypoxia in traumatic braininjury. Crit Care Med. 2009;37(1):283-290.

17. Meixensberger J, Jaeger M, Vth A, Dings J,Kunze E, Roosen K. Brain tissue oxygenguided treatment supplementing ICP/CPPtherapy after traumatic brain injury.J Neu-rol Neurosurg Psychiatry. 2003;74(6):760-764.

18. Steiner LA, Andrews PJ. Monitoring theinjured brain: ICP and CBF.Br J Anaesth.2006;97(1):26-38.

19. Reinert M, Barth A, Rothen HU, Schaller B,Takala J, Seiler RW. Effects of cerebral per-fusion pressure and increased fraction ofinspired oxygen on brain tissue, oxygen,

lactate and glucose in patients with severehead injury.Acta Neurochir (Wein).2003;145(5):341-349.

20. Carter BG, Butt W, Taylor A. ICP and CPP:excellent predictors of long term outcomein severely brain injured children. ChildsNerv Syst. 2008;24(2):245-251.

21. Taylor WR, Chen JW, Meltzer H, et al.Quantitative pupillometry, a new technol-ogy: normative data and preliminary obser-vations of patients with acute head injury.J Neurosurg. 2003;98(1):205-213.

22. Camino User Manual. Plainsboro, NJ: Inte-gra NeuroSciences; 2004.

23. Jenkinson MD, Hayhurst C, Al-Jumaily M,Kandasamy J, Clark S, Mallucci CL. Therole of endoscopic third ventriculostomy inadult patients with hydrocephalus.J Neuro-surg. 2009;110(5):861-866.

24. Chesnut R. The implications of the guide-lines for the management of severe headinjury for the practicing neurosurgeon.Surg Neurol. 1998;50:87-193.

25. Wolfe T, Torbey M. Management of intracra-nialpressure. Curr Neurol Neurosci Rep. 2009;9:477-485.

26. Shardlow E, Jackson A. Cerebral blood flowand intracranial pressure.Anesth IntensiveCare Med. 2008;9:222-225.

27. Gwinnutt CL, Saha B. Cerebral blood flowand intracranial pressure.Anesth IntensiveCare Med. 2005;6:153-156.

28. Walters FJ. Intracranial pressure and cere-bral blood flow. Update Anaesth. 1998;8.http://www.nda.ox.ac.uk/wfsa/html/u08

/u08_013.htm. Accessed May 30, 2010.29. Vajkoczy P, Schomacher M, Czabanka M,

Horn P. Monitoring cerebral blood flow inneurosurgical intensive care.Eur Neurol Dis.2007;7:6-10. http://www.touchneurology.com/articles/monitoring-cerebral-blood-flow-neurosurgical-intensive-care?page=0%2C4. Accessed June 7, 2010.

30. HEMEDEX Pocket Reference Guide. Rayn-ham, MA: Codman & Shurtleff Inc; 2008.

31. Doberstein C, Martin NA. TranscranialDoppler ultrasonography in head injury.In: Narayan RK, Wilberger JE, PovlishockJT, eds.Neurotrauma.New York, NY:McGraw-Hill Co; 1996:539-552.

32. Saqqur M, Zygun D, Demchuk A. Role oftranscranial Doppler in neurocritical care.Crit Care Med. 2007;35:216-223.

33. Molina CA, Barreto AD, Taivgoulis G, et al.Transcranial ultrasound in clinical sono-brombolysis (TUCSON) trial.Ann Neurol.2009;66(1):28-38.

34. Czosnyka M, Brady K, Reinhard M,Smielewski P, Steiner LA. Monitoring ofcerebrovascular autoregulation: facts, myths

and missing links.Neurocrit Care. 2009;10(3):373-386.35. Phan N, Rosenthal G, Manley G. Bedside

assessment of cerebral pressure autoregula-tion and vasoreactivity in severe traumaticbrain injury: insight in arterial vs. venouscontrol [abstract].J Neurotrauma. 2009;26(8):A66. Abstract 255.

36. Botteri M, Bandera E, Minelli C, LatronicoN. Cerebral blood flow thresholds for cere-bral ischemia in traumatic brain injury: asystematic review. Crit Care Med. 2008;36:3089-3092.

37. Narotam PK, Burjonrappa SC, Raynor SC,Rao M, Taylon C. Cerebral oxygenation inmajor pediatric trauma: its relevance totrauma severity and outcome.J Pediatr

Surg. 2006;41(3):505-513.38. Licox IMC Complete Neuromonitoring:Directions for Use (Model IP2.P). Plains-boro, NJ: Integra NeuroSciences; 2004.

39. Wilensky EM, Bloom S, Leicter D, et al.Brain tissue oxygen practice guidelinesusing the LICOX CMP monitoring system2005.J Neurosci Nurs. 2005;37:278-288.

40. Gallangher C, Tyson R, Sutherland G. Dif-ferential neuronal and glial metabolicresponse during hypothermia in an experi-mental animal model.Neurosurgery. 2009;64:555-561.

41. Zhao H, Steinberg G, Sapolsky R. Generalversus specific actions of mild-moderatehypothermia in attenuating cerebralischemic damage.J Cereb Blood Flow Metab.2007;27:1879-1894.

42. Sahuquillo J, Mena MP, Vilalta A, Poca MA.Moderate hypothermia in management ofsevere traumatic brain injury: a good ideaproved ineffective? Curr Pharm Design.2004;10:2193-2204.

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CE Test Test ID C112: Traumatic Brain Injury: Advanced Multimodal Neuromonitoring From Theory to Clinical PracticeLearning objectives: 1. Describe the interrelationships among intracranial pressure, cerebral perfusion pressure, brain tissue partial pressure of oxygen, bloodpressure, and brain temperature 2. Identify aberrations in cerebral metabolites indicative of cerebral ischemia 3. Discuss common neuromonitoring parametersand the threshold values and appropriate nursing interventions associated with each

Program evaluationYes No

Objective 1 was met K KObjective 2 was met K KObjective 3 was met K KContent was relevant to my

nursing practice K KMy expectations were met K KThis method of CE is effective

for this content K KThe level of difficulty of this test was:

K easy K medium K difficultTo complete this program,

it took me hours/minutes.

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. Which of these changes in cerebral metabolite levels is expected in brain tissueunder anaerobic conditions?a. Increased glucose and glycerol levels and increased lactate to pyruvate ratio (LPR)b. Decreased glucose and glycerol levels and decreased LPRc. Increased LPR and decreased brain tissue partial pressure of oxygen and glycerol leveld. Decreased glucose level and increased glycerol level and LPR

2. Cellular influx of calcium occurs as a result of a lack of which of the following?a. Pyruvateb. Glucosec. Adenosine triphosphated. Nicotinamide adenine dinucleotide hydrogen

3. Cerebral microdialysis enables measurement of which of the following metabolicmarkers?a. Phospholipases c. Calciumb. Amino acids d. Pyruvate

4. Which of the following did the authors do to avoid cerebral hypoglycemia inpatients with traumatic brain injury?a. Maintain blood glucose levels between 80-110 mg/dLb. Maintain blood glucose levels between 110-180 mg/dL

c. Prevent systemic hyperglycemiad. Strictly adhere to tight glycemic control

5. The metabolites recovered for cerebral microdialysis measurement representwhat percentage of the true interstitial fluid concentrations?a. 70% c. 80%b. 75% d. 85%

6. The Clinical Laboratory Improvement Act requires control testing of the point-of-care devices used in which type of monitoring?a. Intracranial pressure measurementb. Cerebral blood flow measurementc. Microdialysis measurementd. Pupillometer measurement

7. Which of the following parameters is accepted in the Brain Trauma Foundation

guidelines as the gold standard for traumatic brain injury monitoring to guideintervention?a. Intracranial pressureb. Cerebral blood flowc. Cerebral perfusion pressured. Mean arterial pressure

8. A pupillary constriction velocity measurement of less than 0.8 mm/s suggestswhich of the following?a. Normal brain volumeb. Increased brain volumec. Decreased brain volumed. Problematic and elevated intracranial pressure

9. The stopcock on a ventricular drain should be turned to the off positionduring patient repositioning to prevent which of the following?a. Formation of clots in the tubingb. Falsely elevated intracranial pressure measurementsc. Damage to the transducerd. Overdrainage of cerebral spinal fluid

10. The vasodilatation cascade occurs in response to which of the following?a. Decreased PaCO2b. Increased PaO2c. Decreased cerebral perfusion pressured. Increased intracranial pressure

11. Which of the following is a second-tier intervention to reduce intracranialpressure if it increases beyond the threshold value?

a. Elevating the head of the bed to a 30 angleb. Draining cerebral spinal fluidc. Increasing PaO2d. Administering mannitol

12. Measurement of brain tissue ability to carry heat through thermal conduc-tion is used in calculations for assessment of what other parameter?a. Autoregulationb. Cerebral blood flowc. LPRd. Brain tissue partial pressure of oxygen

13. Which of the following would be the expected result of hypertension in apatient with impaired cerebral autoregulation?a. Increased cerebral blood flowb. Reduced cerebral blood flow

c. Increased PaCO2d. Decreased intracranial pressure

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