Cover Article

Traumatic
Brain Injury
Advanced Multimodal
Neuromonitoring From
Theory to Clinical Practice
Sandy Cecil, RN, BA
Patrick M. Chen
Sarah E. Callaway, RN, BSN
Susan M. Rowland, RN, BSN
David E. Adler, MD
Jefferson W. Chen, MD, PhD

Traumatic brain injury accounts for nearly 1.4 million injuries and 52 000 deaths to poor neurological outcome and
annually in the United States. Intensive bedside neuromonitoring is critical in pre- mortality.1 Signs of secondary neu-
venting secondary ischemic and hypoxic injury common to patients with traumatic rological damage include brain
brain injury in the days following trauma. Advancements in multimodal neuromon- swelling (Figure 1), somnolence,
itoring have allowed the evaluation of changes in markers of brain metabolism (eg, abnormal motor function, and
glucose, lactate, pyruvate, and glycerol) and other physiological parameters such as
pupillary changes. Nevertheless, the
intracranial pressure, cerebral perfusion pressure, cerebral blood flow, partial pressure
onset and extent of secondary injury
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
are still difficult to detect. Intensive
center in the Pacific Northwest. The trends in and significance of metabolic, physio- neuromonitoring is therefore critical
logical, and hemodynamic factors in traumatic brain injury are reviewed, the tech- in improving neurological prognosis
nical aspects of the specific equipment used to monitor these parameters are in patients with TBI.
described, and how multimodal monitoring may guide therapy is demonstrated. As Changes in intracranial pressure
a clinical practice, multimodal neuromonitoring shows great promise in improving (ICP), cerebral perfusion pressure
bedside therapy in patients with traumatic brain injury, ultimately leading to (CPP), brain tissue partial pressure
improved neurological outcomes. (Critical Care Nurse. 2011;31:25-37)

CEContinuing Education
This article has been designated for CE credit.
A closed-book, multiple-choice examination fol-
lows this article, which tests your knowledge of
the following objectives:
1. Describe the interrelationships among
intracranial pressure, cerebral perfusion
pressure, brain tissue partial pressure of
oxygen, blood pressure, and brain temperature
2. Identify aberrations in cerebral metabolites
indicative of cerebral ischemia
3. Discuss common neuromonitoring parameters
and the threshold values and appropriate
nursing interventions associated with each
2010 American Association of Critical-
Care Nurses doi: 10.4037/ccn2010226
T
raumatic brain injury
(TBI) accounts for 1.4
million reported injuries
and 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
Figure 1 Traumatic brain injury can
damage, the damage that occurs in result in frontal intraparenchymal
the ensuing hours and days after the hematomas with contusion edema and
traumatic subarachnoid hemorrhage.
primary injury, contributes markedly

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

of oxygen (PBTO2), blood pressure,
brain temperature, and, recently, Normal conditions Glucose Ischemic and hypoxic conditions
cerebral blood flow (CBF) are moni-
tored in the intensive care unit (ICU).2
Cerebral microdialysis is a technique 2 ATP
increasingly used as a bedside method
for measuring glucose, lactate, pyru- Krebs cycle Pyruvate (2)
NADH+ Lactate
vate, and glycerol levels in the brain
of patients with severe head trauma.3-5
Brain tissue
Cerebral ischemia may be detected
death
on the basis of aberrations in cerebral Electron transport chain
metabolites. Similarly, minimizing (oxygen as final carrier in Decreased blood flow=
chain) Decreased oxygen=
secondary ischemic injury common in Switch to anaerobic
TBI may be possible with the manip- 32 ATP respiration
ulation of ICP, CPP, CBF, blood pres-
sure, brain temperature, and PBTO2
in brain parenchyma after acute brain Figure 2 Flow chart of cellular metabolism. Under normal conditions, glucose is
injury.2,4-7 turned to pyruvate and nicotinamide adenine dinucleotide hydrogen (NADH+) in aer-
obic glycolysis. These products are used in the Krebs cycle and electron transport
In this article, we describe the suc- chain to generate 32 molecules of ATP (left side). In ischemia and hypoxia, glucose
cessful use of multimodal neuromon- and 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-
itoring to guide therapy in our ICU. verted to lactate. Only 2 molecules of ATP are produced, resulting in brain tissue
First, we provide an overview of the death and the release of glycerol.
significance of changes in glucose,
lactate, pyruvate, and glycerol levels aspects of specific current equipment which are relatively new monitoring
in traumatically injured brain and used in our ICU to measure all the techniques.
review the importance and interrela- changes. Finally, we indicate thresh-
tionships between ICP, CPP, CBF, old values that may change the treat- Metabolic and
PBTO2, blood pressure, and brain ment of patients with severe brain Cellular Energy
temperature. We also describe the injury. Our emphasis is on cerebral Metabolic Trends of
background and important clinical microdialysis and CBF monitoring, Microdialysis Markers
Understanding the bioenergetics
of hypoxic and/or ischemic brain is
Authors important.4-7 As brain tissue becomes
hypoxic, oxygen no longer functions
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, as the final electron carrier in the
Oregon. electron transport chain. Nicoti-
Patrick M. Chen is an undergraduate biology student at Dartmouth College, Hanover, namide adenine dinucleotide hydro-
New Hampshire. gen therefore cannot deprotonate,
Sarah E. Callaway is a charge nurse in the neurological trauma, neurosurgical, surgical and cells must rely on anaerobic
intensive care unit at Legacy Emanuel Medical Center.
respiration. Generation of adeno-
Susan M. Rowland is a relief charge nurse/preceptor coordinator at Legacy Emanuel
Medical Center. sine triphosphate (ATP) is compro-
David E. Adler is a neurosurgeon at Legacy Emanuel Medical Center. mised; only 2 molecules of ATP
Jefferson W. Chen is the neurosurgical medical director at Legacy Emanuel Medical Center.
are produced in contrast to the aer-
obically generated 32 molecules
Corresponding author: Sandy Cecil, RN, 2801 N Gantenbein Ave, Portland, OR 97227 (e-mail: scecil@lhs.org or (Figure 2). During ischemia, a lack
cecilsandy@hotmail.com).
of oxygen and glucose results in
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org. anaerobic respiration. In ischemic

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

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

Microdialysis catheter
brain. Because the levels of these

Blood capillary
compounds naturally fluctuate,
detecting the changes in lactate levels Cell
in relation to pyruvate levels, a rela-
tionship known as the lactate to
pyruvate ratio (LPR), is desirable.
Extensive research has shown that Extracellular fluid

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 first
described 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-
Figure 3 Microdialysis technique. The microdialysis catheter at the distal end acts
as an artificial capillary. Extracellular substances diffuse from interstitial tissue to
perfusion fluid inside the catheter membrane.
Courtesy of CMA Microdialysis, Solna, Sweden.
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 with
more 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

www.ccnonline.org CriticalCareNurse Vol 31, No. 2, APRIL 2011 27

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 microdialysis
catheter 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,
28 CriticalCareNurse Vol 31, No. 2, APRIL 2011
Table 1 Normal and threshold values of metabolic parameters important in
neuromonitoring 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
SI conversion factors: To convert glucose to mmol/L, multiply by 0.0555; pyruvate to mol/L, multiply by
113.56; lactate to mmol/L, multiply by 0.111; glycerol to mmol/L, multiply by 0.1086.
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 a
low 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).
Normal levels Threshold value
30.6 (16.2) 14.4
1.46 (0.33) 0.27 (fatal)
26.1 (8.1) 80.2 (fatal)
23 (4) 30
184-460 21
Intracranial Monitoring
Physiology 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 many
treatment 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 energy
failure.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
www.ccnonline.org

Low blood
glucose
Adjust capillary
blood glucose
Insulin Enteral feeding
Figure 4 Flow chart of metabolic related therapy integrates the possible responses to low blood glucose, elevated lactate to
pyruvate ratio, and glucose (left). Normothermic treatment is used to reduce brain metabolic demand (right).
Foundation guidelines1 as the gold
standard for TBI monitoring to
guide 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 monitors
and 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-
www.ccnonline.org
Elevated
lactate to pyruvate
ratio and/or
high glycerol
Acetaminophen
Return aerobic
respiration and
glucose
Adjust head
Insulin infusion Vasopressors
position
culated CPP. The Camino catheter
has a miniaturized transducer at the
distal 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 the
depth 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
CriticalCareNurse Vol 31, No. 2, APRIL 2011 29
Elevated brain
temperature
Cooling blankets
or ibuprofen or ice packs
Invasive cooling
Icycath
CoolGuard
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 number
will 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
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 the
nervous 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
30 CriticalCareNurse Vol 31, No. 2, APRIL 2011
Table 2 Normal and threshold values of hemodynamic parameters important
in 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
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 may
be 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
Normal levels Threshold value
0-10 20-25
>60 50
Augmented to keep
cerebral perfusion
pressure >60 mm Hg
18-35 15
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 as
a 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
www.ccnonline.org
 Elevated Brain
Low cerebral
ICP, low oxygen
blood flow
CPP (PBTO2)

Reduce ICP to Adjust blood Maximize High PBTO2

Low PBTO2
maximize CPP pressure CPP luxury perfusion
and cerebral
blood flow

Reduce Increased Reduce Increase

Tier 1 Tier 2 High blood pressure: metoprolol, increased delivery delivery demand
nicardipine, enalapril, demand
Drain CSF nitroglycerin, sodium nitroprusside Increase Hyperventi-
Reduce ICP CPP lation
Mannitol
hypotonic
+ PaO2 saline Increase
Medication,
+ PCO2 Treat body
sedation, anti-
Low blood pressure: phenylephrine, hypovolemia, tempera-
inflammatory
norepinephrine, vasopressins, hypotension, ture
cooling
dopamine hypoxia anesthesia,
Diuretics CT scan devices
sedatives

30 angle Barbiturates vs craniotomy/craniectomy

head

Figure 5 Flow chart of hemodynamic related therapy integrates the possible responses to elevated ICP, low CPP, and low or high
brain oxygen level.
Abbreviations: CPP, cerebral perfusion pressure; CSF, cerebral spinal fluid; CT, computed tomography; ICP, intracranial pressure; PBTO2, brain tissue partial pressure of
oxygen.

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
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
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 by
thermal 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

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

 + Blood viscosity Blood viscosity
Hypoxia Hyperemia
Hypercapnia Hypocapnia
+ Vasodi- + CPP + Vasocon-
CPP
latation striction

+ CBV ICP CBV

+ ICP

Edema Reduce
+CSF edema

Figure 6 Vasodilatation (left) and vasoconstriction (right) cascades protect the brain. The dynamics of cerebral blood flow are
best 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. If
CPP increases, vasoconstriction occurs, reducing CBV and decreasing edema by decreasing ICP.

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 penumbra
surrounding 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 retracted
or 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 areas of cranium to measure veloc-
before the patient is transported to ity and direction of blood flow in
other departments for procedures the intracranial arteries.31,32
or tests. The probe should be secured Although most commonly used to
to the patients head dressing to pre- detect vasospasm after cerebral
vent dislodging the probe. If the aneurysms, Doppler imaging can be
probe is used in conjunction with a used to detect posttraumatic cere-
microdialysis catheter, the 2 catheters bral hemodynamic changes and
must be separated by 2.0 mm for complications such as hyperemia,
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, this
technique is
being investi-
gated in patients
with TBI. With
this technique, a
probe with a
low-frequency Figure 7 Hemedex catheter. Probe can be tunneled or bolted.
Probe is embedded 2 to 2.5 cm below the dura.
ultrasonic signal Courtesy Hemedex Inc, Cambridge, Massachusetts.
is used on thin

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

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 remain
constant.32-34
Blood Pressure
Mean arterial pressure (MAP)
and ICP are important in calculat-
ing CPP (CPP=ICPMAP). 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 cerebral
autoregulation, 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 be
considered 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,
www.ccnonline.org
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 Oxygenation
Mechanisms
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 autoregulation
is 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 PBTO2
and 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 PBTO2
monitoring have been developed.
Examples include indirect systems
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 the
penumbra 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. PBTO2
should increase. A neurosurgeon
can adjust the probe as needed.
N
Although measuring ICP and to
Ju
CPP is key in patients with TBI, T
th
monitoring cerebral oxygenation
can indicate hypoxic events earlier
than monitoring ICP and CPP can
and thus may improve neurological
CriticalCareNurse Vol 31, No. 2, APRIL 2011 33
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 PBTO2
of 55 mm Hg suggests a threshold
value defined as luxury perfusion.39
In order to improve PBTO2 during
ischemic conditions, CBF can be
maximized by decreasing ICP via
barbiturates, CSF drainage, and/or
craniotomy. If the decreased PBTO2
is 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, PBTO2
may reach luxury perfusion levels
because of hyperemia or excessive
cerebral blood flow, which increases
ICP. 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 inducing
heavy sedation can further decrease
the demand of the brain tissue and
in turn increase PBTO21 (Figure 5).
Brain Temperature and
Hypothermia
Reduction of Brain Temperature
In humans, brain temperature
is an important marker of brain
34 CriticalCareNurse Vol 31, No. 2, APRIL 2011
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 overload
allows 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 have
indicated 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.
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 brain
temperature.
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
www.ccnonline.org
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 paralytic
agents to facilitate the induction and
maintenance of hypothermia and
minimize oxygen consumption.43-45
Conclusion
Advancements 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
To learn more about traumatic brain injury,
read Functional and Cognitive Recovery of
Patients With Traumatic Brain Injury: Pre-
diction Tree Model Versus General Model
in Critical Care Nurse, 2009;29(4):12-22.
Available at www.ccnonline.org.
www.ccnonline.org
Licox Hemedex
Figure 8 Placement of multimodal catheters and monitoring probes. Computed
tomography scans of 24-year-old woman with severe traumatic brain injury show
placement of catheter for microdialysis and probes for monitoring brain tissue partial
pressure of oxygen, blood flow, and intracranial pressure.
ICP, CPP, CBF, blood pressure, and
brain temperature. Figure 8 shows
placement 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
Now that youve read the article, create or contribute
to an online discussion about this topic using eLetters.
Just visit www.ccnonline.org and click Respond to
This Article in either the full-text or PDF view of
the article.
Acknowledgments
This manuscript would not have been possible
without the editorial guidance of Christine Smith
Schulman, RN, CNS, CCRN, the clinical nurse special-
ist at Legacy Emanuel Medical Center. In addi-
tion, we thank Dan Jones, RN, and Kimberly
Skaale, RN, staff nurses in ICU East at Legacy
Emanuel Medical Center, for their review of the
manuscript.
Financial Disclosures
None reported.
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www.ccnonline.org
CE Test Test ID C112: Traumatic Brain Injury: Advanced Multimodal Neuromonitoring From Theory to Clinical Practice
Learning objectives: 1. Describe the interrelationships among intracranial pressure, cerebral perfusion pressure, brain tissue partial pressure of oxygen, blood
pressure, and brain temperature 2. Identify aberrations in cerebral metabolites indicative of cerebral ischemia 3. Discuss common neuromonitoring parameters
and the threshold values and appropriate nursing interventions associated with each

1. Which of these changes in cerebral metabolite levels is expected in brain tissue 8. A pupillary constriction velocity measurement of less than 0.8 mm/s suggests
under anaerobic conditions? which of the following?
a. Increased glucose and glycerol levels and increased lactate to pyruvate ratio (LPR) a. Normal brain volume
b. Decreased glucose and glycerol levels and decreased LPR b. Increased brain volume
c. Increased LPR and decreased brain tissue partial pressure of oxygen and glycerol level c. Decreased brain volume
d. Decreased glucose level and increased glycerol level and LPR d. Problematic and elevated intracranial pressure

2. Cellular influx of calcium occurs as a result of a lack of which of the following? 9. The stopcock on a ventricular drain should be turned to the off position
a. Pyruvate during patient repositioning to prevent which of the following?
b. Glucose a. Formation of clots in the tubing
c. Adenosine triphosphate b. Falsely elevated intracranial pressure measurements
d. Nicotinamide adenine dinucleotide hydrogen c. Damage to the transducer
d. Overdrainage of cerebral spinal fluid
3. Cerebral microdialysis enables measurement of which of the following metabolic
markers? 10. The vasodilatation cascade occurs in response to which of the following?
a. Phospholipases c. Calcium a. Decreased PaCO2
b. Amino acids d. Pyruvate b. Increased PaO2
c. Decreased cerebral perfusion pressure
4. Which of the following did the authors do to avoid cerebral hypoglycemia in d. Increased intracranial pressure
patients with traumatic brain injury?
a. Maintain blood glucose levels between 80-110 mg/dL 11. Which of the following is a second-tier intervention to reduce intracranial
b. Maintain blood glucose levels between 110-180 mg/dL pressure if it increases beyond the threshold value?
c. Prevent systemic hyperglycemia a. Elevating the head of the bed to a 30 angle
d. Strictly adhere to tight glycemic control b. Draining cerebral spinal fluid
c. Increasing PaO2
5. The metabolites recovered for cerebral microdialysis measurement represent d. Administering mannitol
what percentage of the true interstitial fluid concentrations?
a. 70% c. 80% 12. Measurement of brain tissue ability to carry heat through thermal conduc-
b. 75% d. 85% tion is used in calculations for assessment of what other parameter?
a. Autoregulation
6. The Clinical Laboratory Improvement Act requires control testing of the point- b. Cerebral blood flow
of-care devices used in which type of monitoring? c. LPR
a. Intracranial pressure measurement d. Brain tissue partial pressure of oxygen
b. Cerebral blood flow measurement
c. Microdialysis measurement 13. Which of the following would be the expected result of hypertension in a
d. Pupillometer measurement patient with impaired cerebral autoregulation?
a. Increased cerebral blood flow
7. Which of the following parameters is accepted in the Brain Trauma Foundation b. Reduced cerebral blood flow
guidelines as the gold standard for traumatic brain injury monitoring to guide c. Increased PaCO2
intervention? d. Decreased intracranial pressure
a. Intracranial pressure
b. Cerebral blood flow
c. Cerebral perfusion pressure
d. Mean arterial pressure

Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. a 2. a 3. a 4. a 5. a 6. a 7. a 8. a 9. a 10. a 11. a 12. a 13. a
b b b b b b b b b b b b b
c c c c c c c c c c c c c
d d d d d d d d d d d d d
Test ID: C112 Form expires: April 1, 2013 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 10 correct (77%) Synergy CERP: Category A
Test writer: Ann Lystrup, RRN, BSN, CEN, CFRN, CCRN
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