Brain Tissue Oxygen Monitoring in Severe Brain Injury, I: Research and Usefulness

in Critical Care
Linda R. Littlejohns, Mary Kay Bader and Karen March

Crit Care Nurse 2003, 23:17-25.

© 2003 American Association of Critical-Care Nurses
Published online http://www.cconline.org

Subscription Information
http://ccn.aacnjournals.org/subscriptions
Information for authors
http://ccn.aacnjournals.org/misc/ifora.xhtml

Submit Manuscript
www.editorialmanager.com/ccn

E-mail alerts
http://ccn.aacnjournals.org/subscriptions/etoc.xhtml

Critical Care Nurse is the official peer-reviewed clinical journal of the

American Association ofCritical-Care Nurses, published bi-monthly by
The InnoVision Group 101 Columbia, Aliso Viejo, CA 92656.
Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949)
362-2049. Copyright © 2011 by AACN. All rights reserved.

Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014

 CoverArticle
Brain Tissue
Oxygen Monitoring
in Severe Brain Injury, I
Research and Usefulness
in Critical Care
Linda R. Littlejohns, RN, MSN, CCRN, CNRN
Mary Kay Bader, RN, MSN, CCRN, CNRN
Karen March, RN, MN, CCRN, CNRN
S evere traumatic brain
injury has challenged the medical
community for decades. According
to the Centers for Disease Control and
Prevention,1 a traumatic brain injury
is “an injury to the head that disrupts
the normal function of the brain.”
Almost 1.5 million cases of traumatic
brain injury—some mild, some
severe—are reported each year in
the United States. Approximately
50 000 of the persons who have a
traumatic brain injury die, and
80 000 leave the hospital with some
disability. Currently, about 5.3 mil-
lion persons in the United States live
with a disability caused by a traumatic
brain injury.1 The primary injury,
which happens at the time of the
event, causes the disruption of axons,
cell bodies, and the integrity of the
cell membrane, resulting in an accel-
erated disintegration of cell struc-
ture and function and, eventually,
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
CE Continuing Education
cell death.2 Secondary injury occurs
in response to unchecked cerebral
edema, ischemia, and the chemical
changes associated with direct trauma CE This article has been designated for
CE credit. A closed-book, multiple-choice
to or systemic effects on the brain. examination follows this article, which tests your
Historically, the management of knowledge of the following objectives:
1. Discuss the dynamics of brain injury
traumatic brain injury focused on the related to oxygen
management of intracranial pressure 2. Identify the influence of interventions on
brain tissue oxygen
(ICP) and cerebral perfusion pressure 3. Describe the use of brain tissue oxygen
monitoring in severe brain injury
(CPP) via a variety of technologies.
Authors
Linda R. Littlejohns has 20 years of experience as a neuroscience critical care nurse and 6
years of experience as a neuroscience clinical nurse specialist. She is currently vice president
of clinical development at Integra NeuroSciences, San Diego, Calif.
Mary Kay Bader has 22 years of experience as a neuroscience critical care nurse and 11
years of experience as a neuroscience clinical nurse specialist. She is currently the neuro-
science clinical nurse specialist at Mission Hospital Regional Medical Center, Mission
Viejo, Calif.
Karen March has 29 years of experience as a neuroscience critical care nurse and 11 1⁄2
years of experience as a neuroscience clinical nurse specialist. She is currently the director of
clinical development at Integra NeuroSciences, San Diego, Calif.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-
2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.
CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003 17
ICP monitoring has never been scru-
tinized in a prospective randomized
study. However, most clinicians agree
that monitoring provides information
that can improve patients’ outcomes
when targeted interventions are used
to control ICP and CPP. This agree-
ment was indicated by the acceptance
of the Guidelines for the Management
of Severe Brain Injury, published in
2000 by the Brain Trauma Founda-
tion, and guideline-compliant care.3,4
The concept of managing and
treating only ICP in brain injury lim-
its the ability to assess perhaps one of
the most important parameters: oxy-
genation. The delivery and use of oxy-
gen at the cellular level, in addition to
control of the excitatory amino acids,
can directly affect tissue survival.
Technological advances in brain tis-
sue oxygen monitoring provide infor-
mation on the cellular dynamics of
oxygenation and a better understand-
ing of the impact of low oxygen states
in the brain on patients’ outcome.
This technology enables practitioners
to assess levels of brain tissue oxygen
associated with secondary injury and
with treatment interventions.5 In this
article, we provide an overview and
historical perspective of the latest
technology in brain tissue oxygen
monitoring, present research find-
ings on factors that affect the levels
of brain tissue oxygen, and suggest
interventions to maintain adequate
brain oxygenation.
Dynamics of Brain Injury
Related to Oxygen
The Monro-Kellie doctrine states
that the cranium is a closed box with
essentially noncompressible contents
of approximately 80% brain tissue,
10% blood, and 10% cerebrospinal
fluid. These percentages remain con-
18 CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
stant through intrinsic regulatory
mechanisms, but an increase in any
one or more of the contents requires
compensation and a decrease in the
others. Under normal circumstances,
the brain compensates to some degree
through autoregulation, shunting of
cerebrospinal fluid, and compliance.
Once these compensatory mecha-
nisms are exhausted, increases in ICP
occur. If the pressure increases
markedly, the amount of blood flow
to brain tissue is reduced, thus com-
promising cerebral tissue oxygena-
tion. The causes of tissue hypoxia and
ischemia may be related to intracra-
nial events (eg, edema, structural
damage, intracranial hypertension,
seizures, vasospasm), systemic events
(eg, hypoxemia, hypotension, hypo-
capnia, anemia, hyperthermia), or a
combination of the two.
The brain depends on the con-
stant uninterrupted delivery of oxy-
gen and glucose to prevent secondary
ischemic injury. Any decrease in per-
fusion in the brain causes additional
secondary ischemia and injury and
results in poor outcomes.6 Because
failure to deliver oxygenated blood to
injured brain tissue is thought to be
detrimental, Meixensberger et al7 sug-
gest that monitoring the partial pres-
sure of brain tissue oxygen (PbtO2)
may help prevent hypoxic events and
improve patients’ outcomes. Studies
in Europe indicated that measure-
ment of ICP and CPP alone does not
accurately reflect the tissue oxygena-
tion in injured brain.8 The develop-
ment of PbtO2 monitoring adds to
the information needed to target
therapy in patients as they respond
to the changes in blood flow, decrease
in energy production, alteration in
cellular response, and potential
ischemia.9
Historical Perspectives in
Brain Tissue Oxygen Monitoring
Because the interest of many
practitioners is the sufficient deliv-
ery and use of oxygen in brain tis-
sues for necessary cellular function,
brain tissue oxygen monitoring
should enable clinicians to measure
the difference between delivery and
consumption of oxygen. Developing
an accurate and reliable method for
measuring brain tissue oxygenation
has been the priority of researchers
during the past 15 to 20 years.
Tissue oxygenation is heteroge-
neous in animal and human models
and has been well defined since the
1960s by using the Clark cell method
of measurement.10 A Clark cell polaro-
graphic probe is a semipermeable
membrane covering 2 electrodes, 1
silver and 1 gold. In the presence of
dissolved oxygen crossing the mem-
brane, an electrical current is generat-
ed and is transferred to a monitor for
interpretation. Early trials of tissue
oxygen measurement were done in an
animal model to ensure the useful-
ness and validity of the information
derived from placement of the probe
in both cerebrospinal fluid and
tissue.11 In both animals and humans,
accurate placement of the probe in
the lateral ventricle is easily accom-
plished.12 Values obtained reflect the
expected and appropriate changes
during manipulation of the blood
pressure and oxygenation and corre-
late with measurements taken in the
deep white matter of the brain. A dis-
tinct drawback in measuring oxygen
in the cerebrospinal fluid of the ven-
tricles, however, is the condition of
the ventricles in head injury. They are
often slitlike because of secondary
swelling, and monitoring in this cir-
cumstance does not provide an accu-
rate measure of oxygenation in the tis-
sue of the brain. Therefore, measur-
ing the oxygen level in the tissue is
obviously more useful. Further testing
of probe placement revealed that
measurements taken from the deep
white matter of the brain are the most
valuable and stable because oxygen
consumption is most stable in that
area.11 Placement of the probe in a bolt
with a predetermined depth allows
access to the white matter of the brain.
Early evaluations of the measure-
ment of oxygen in tissue included
measurement of tissue temperature,
because the temperature coefficient
Planning interventions at the bedside
to enhance tissue oxygenation can
affect patients’ outcomes.
is needed to calculate the oxygen
value. Several studies indicated that
gradients exist between brain tem-
perature and body temperature in
the bladder, rectum, and jugular
bulb. Although researchers have
assumed that rectal temperature
reflects brain temperature, Rumana
et al13 found that brain temperature
was consistently and significantly
higher than the core body tempera-
ture after brain injury. Thirty
patients were evaluated and moni-
tored by using a LICOX oxygen/tem-
perature probe placed in the
parenchyma, a rectal temperature
probe, and a jugular bulb catheter.
In the initial 5 days after admission,
mean brain temperature was 38.9°C
(SD 1.0°C), and mean rectal temper-
ature was 37.8°C (SD 0.4°C); both
rectal and jugular venous oximetric
(SjvO2) temperatures were 1.1°C (SD
0.6°C) lower than mean brain tem-
perature. The difference was more
than 1°C in 18 patients and more
than 2°C in 3; brain temperatures
were lower than rectal temperatures
in 2 patients. The temperature in the
brain was also measured before and
after the induction of barbiturate
coma; values before and after induc-
tion did not differ significantly.
In a small sample of 8 patients,
Henker et al14 found that brain tissue
temperature was underrepresented
(ie, higher than bladder and rectal
temperatures); mean brain tempera-
ture was 0.32°C to 1.9°C higher
than bladder and rectal tempera-
tures. In most patients, when the
bladder and rectal temperatures were
outside the normal range, the differ-
ence was even greater.
Several studies indicated the
importance of controlling fever in
Figure 1 LICOX catheter system. Left, The brain tissue oxygen catheter and
monitor. Right, Placement of the catheter in brain white matter.
Reprinted with permission of Integra NeuroSciences, Plainsboro, NJ.
patients with severe head injury,
and clinicians should be vigilant
about the control of fever. Because
temperatures are measured outside
the cranium in most patients, the
information may not necessarily be
pertinent to the brain.15-17 At this
time, we have not determined what
temperature will have deleterious
effects on patients, but we have
observed a decrease in PbtO2 when
patients become febrile.
Although other monitoring sys-
tems are available for tissue oxygen
monitoring, most studies have been
done with the LICOX system (Integra
NeuroSciences/GMS, Plainsboro NJ;
Figure 1). This PbtO2 system was
developed by Wolfgang Fleckenstein
of Kiel, Germany, and has been used
in tissue oxygen monitoring since the
1980s. The LICOX system includes a
monitor with a screen for the display
of oxygen and temperature values;
cables that connect to the monitoring
probes and to the bedside monitor:
and a variety of probes for use in the
brain, cardiac muscle, and peripheral
muscles; under skin flaps; and during

CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003 19

Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
surgery. The ease of use and the pre-
calibrated “smart” card that accompa-
nies the probes make this single-step
“system calibration” appealing to bed-
side nurses. The only additional time
needed before monitoring is the tissue
“settling” time after the microtrauma
of insertion.18
Values that indicate normal levels
of tissue oxygen seem to vary between
the available monitoring systems, pos-
sibly because the technology varies,
causing some confusion among users.
However, a consensus exists that low
levels (<15 mm Hg) during the resus-
citation phase of traumatic brain
injury are predictive of poor out-
comes. Initial (first 8-12 hours after
injury) oxygen values were low in sev-
eral studies.19-21 Data from at least one
center indicated that early interven-
tion and targeted protocol-driven
management can positively affect the
outcomes of patients with severe trau-
matic brain injury.22
Debate over where to place the
PbtO2 catheter is ongoing, with
advantages and challenges in each
application. Placement in the penum-
bra of an injury (Figure 2) is useful in
assessing an increase in swelling and
regional oxygenation. The challenge
with this measurement is that the
values reflect the local area and may
not be indicative of the remainder of
the uninjured brain. Placement in
the so-called undamaged or normal
tissue allows clinicians to use the val-
ues as a representation of somewhat
normal global oxygen delivery
(Figure 3) but may not reflect the
subtleties of regional hypoxia.23-26
With the development of the
LICOX system, critical thresholds (ie,
normal and abnormal levels of PbtO2)
had to be determined. Additionally,
information on the influence of vari-
ous parameters on PbtO2, and the
impact of oxygen monitoring on
patients’ outcomes was needed.
Measurement
and Safety of Brain
Tissue Oxygen Monitoring
Numerous researchers in the
1990s sought to determine normal
and abnormal levels of brain tissue
oxygenation in both animal and
human models. The researchers dis-
covered that use of 2 different mon-
itoring systems led to different
normal and abnormal values.25,27-29
Our review of the literature on nor-
mal and abnormal PbtO2 here is
confined to the LICOX monitoring
system because the preponderance

LICOX catheter Intracranial pressure

catheter Intracranial pressure catheter LICOX catheter
Craniectomy right side
(partial removal of skull bone) Skull (bone)

Right middle cerebral Hemorrhagic area Craniectomy on right side

artery infarct inside infarcted brain
Figure 2 Computed tomographic scan shows placement of a
LICOX catheter in the penumbral area of an infarct in the
brain. Note small white LICOX catheter in the right side of the
brain. Placement of the LICOX probe in the right hemisphere
near the injury allows detection of regional oxygen status.
Skull (bone is white)
(partial removal of skull)
Figure 3 Contrast-enhanced computed tomographic scan
shows placement of a LICOX catheter in the cerebral hemi-
sphere contralateral to the injury. Placement in the left hemi-
sphere allows detection of global oxygen status.

20 CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003

Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
of research has been done with this
system. It is also the system cur-
rently in use by clinicians at the
bedside in the United States.
Maas et al11 placed the oxygen sen-
sor in the white matter of the frontal
lobe and determined that baseline
PbtO2 values were 25 to 30 mm Hg.
Sarrafzadeh et al28 found that PbtO2
was between 20 and 35 mm Hg in
uninjured brain tissue.
Valadka et al25 studied 39 patients
and found that extended periods
with PbtO2 less than 15 mm Hg corre-
lated with a greater chance of death.
Any occurrence of a PbtO2 less than
6 mm Hg (no matter how long the
time below this level) was associated
with an increased risk of death.
Therefore, Valadka et al considered
a PbtO2 less than 15 mm Hg as a sig-
nificant threshold. Bardt et al29 found
that PbtO2 less than 10 mm Hg was
associated with poor outcomes (ie,
patients were severely disabled or
died). Patients who experienced a
PbtO2 of less than 10 mm Hg for
longer than 30 minutes had the
worst outcomes at discharge; 50%
died and 50% were severely disabled.
At 6-month follow-up, 22.2% of these
patients had a favorable outcome,
22.2% were severely disabled, and
55.6% had died. In the group of
patients who experienced a PbtO2
less than 10 mm Hg for less than 30
minutes, 80% were severely disabled
or in a persistent vegetative state at
discharge, yet their outcome at 6
months improved; 70% had a favor-
able outcome, 20% were severely dis-
abled, and 10% had died.
In a prospective randomized trial
by van den Brink et al,30 101 coma-
tose patients with head injury were
evaluated after placement of the brain
oxygen monitor. They were treated
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
according to the European guide-
lines for the management of severe
traumatic brain injury.31 Outcome
at 6 months was determined by the
score on the Glasgow Outcome Scale,
which is used in early prediction of
gross outcome after traumatic brain
injury. Scores range from 1 to 5,
with 1 indicating death and 5 indi-
cating a good recovery.30 Despite
aggressive management of ICP and
CPP, numerous episodes of brain
tissue hypoxia occurred. In the first
24 hours after injury, PbtO2 was
lower than 15 mm Hg for longer
than 30 minutes in 57 patients, lower
than 10 mm Hg in 42, and lower than
5 mm Hg in 22. The severity and
duration of tissue hypoxia were
directly related to poor outcome and
an increased risk of death and were an
independent predictor of outcome.
Practitioners must be cognizant
of normal PbtO2 values and appreci-
ate the effect that abnormally low
values have on patients’ outcomes.
With the LICOX monitoring system,
the normal value is thought be 20 mm
Hg or higher. Striving to maintain a
PbtO2 of 20 mm Hg or higher is an
acceptable starting point. Practition-
ers should be concerned and act
quickly when the PbtO2 decreases to
less than 15 mm Hg.30 In one study,25
4 of 5 patients with PbtO2 less than
5 mm Hg died.
Risks of Brain Tissue
Oxygen Monitoring
The risk of brain tissue oxygen
monitoring has been detailed in a
number of articles. In 9 stud-
ies,6,21,26,28,30,32-35 from 1996 through
2000, in which investigators exam-
ined safety parameters, infection,
and/or hematoma in a total of 250
patients, only 2 adverse events
CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003 21
occurred. No infections were reported,
and the adverse events were related
to small hematomas that occurred
after catheter placement.26 Dings et
al26 stated that because 3 probes
were inserted through a bolt (ICP,
temperature, and oxygen probes),
determining which of the probes
caused the bleeding was difficult.
Because ICP monitoring was done in
the reported cases26 through a bolt,
the prevalence of hematoma (4.95%)
was within the range associated with
this type of ICP monitoring (ie, via
a bolt).36
Influence of
Interventions on PbtO2
Directly monitoring PbtO2 pro-
vides vital information on the effect
of interventions in individual
patients. During the past decade,
brain tissue oxygen monitoring has
been described by numerous
authors,5,6,21,35 predominantly in
Europe, where multimodality moni-
toring has been implemented in
many intensive care units. Early
monitoring of critical parameters in
patients with traumatic brain injury
can provide useful clinical informa-
tion. Correlations of PbtO2 with
parameters such as ICP, CPP, SjvO2,
and end-tidal carbon dioxide have
been reported.5,21,37 Brain tissue oxy-
gen monitoring can be used to pro-
vide information at the bedside about
responses to clinical interventions
and the success of the interventions.
In the following sections, we
address common interventions in
the management of patients with
traumatic brain injury. Measures are
usually taken to ensure adequate
perfusion, and the results are meas-
ured as the reduction in ICP and the
increase in CPP. Strong evidence
exists that hypotension and hypoxia
should be avoided and CPP-guided
therapy should be used in patients
with severe brain injury.38,39 How-
ever, these measures are often unre-
lated to the delivery and utilization
of oxygen in the brain.
Influence of Interventions to
Treat Traumatic Brain Injury
The administration of oxygen or
titration of the fraction of inspired
oxygen (FIO2) and its impact on PbtO2
Measures are usually taken to ensure
adequate perfusion, and the results are
measured as the reduction in ICP and the
increase in CPP.
has been investigated in several
studies. In 22 patients with severe
head injury, LICOX monitoring indi-
cated that increasing the FIO2 led to
an increase in PbtO2.33 Van den Brink
et al35 examined the effects of preoxy-
genation before suctioning on PbtO2
in 82 patients with head injury. In 7
patients, a decrease in PbtO2 occurred
during suctioning in 16 episodes
when preoxygenation was omitted.
In 142 episodes in which preoxygena-
tion before suctioning was used, PbtO2
levels increased.35 In 9 patients with
grade IV gliomas, increasing the FIO2
to 100% concomitantly increased the
low PbtO2 2.5- to 4-fold.40
Menzel et al41 studied the effects
of increasing PaO2 to levels higher
than the level necessary for hemoglo-
bin saturation during the early phase
after severe brain injury in a random-
ized sample of 24 patients. In the 12
patients in whom FIO2 was increased,
mean PaO2 levels increased to 359%
22 CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
(SD 39%) of the baseline in a 6-hour
enhancement session, and the dialys-
ate levels of lactate decreased by 40%.
This decrease in lactate levels may
indicate the prevention of anaerobic
metabolism in the injured brain due
to supranormal levels of oxygen.41
The proposed reason for the
increase in PbtO2 associated with an
increase in FIO2 is the enhancement
of the dissolved oxygen in plasma.
Although the dissolved oxygen in
plasma makes up only 2% to 3% of the
total arterial oxygen content, PaO2
appears to be the driving force of oxy-
gen movement from plasma to tis-
sue.30 Bedside clinicians have resisted
using oxygen therapy in patients with
severe brain injury because of per-
ceived damage due to free radicals
associated with use of the therapy,
but more aggressive management
may have a place in the treatment of
patients with severe brain injury.
Influence of Carbon Dioxide
Hyperventilation continues to
be a treatment for intracranial hyper-
tension in some institutions even
though it has deleterious effects in
patients with severe brain injury when
used injudiciously.35,42 Schneider et
al42 found that although hyperventi-
lation dramatically decreased ICP
and increased CPP, brain tissue oxy-
genation could decrease to as low as
10 mm Hg during hyperventilation.
Van den Brink35 found that in 17 of
23 patients, PbtO2 decreased during
the first 24 hours after injury because
of decreases in PaCO2 associated with
hyperventilation. It is well docu-
mented that hyperventilation in the
first 24 hours after brain injury can
cause hypoxia in the tissue at risk.37-39
Meixensberger et al7 placed an
oxygen probe in the cortex during
craniotomy and observed patients
who had no secondary swelling and
patients who had pathological
changes and swelling. Both groups
had an increase in PO2 in brain tis-
sue when they were breathing 100%
oxygen. However, although the group
with no swelling had no correlation
between tissue PO2 and arterial PO2,
the group with pathological changes
did. In addition, low tissue PO2 occur-
red in both groups after hyperventi-
lation, suggesting that some patients
are at risk for hypoxia during this
intervention. Lowering the PaCO2 pro-
duces vasoconstriction of the cerebral
blood vessels, thus reducing blood
flow and, ultimately, oxygen delivery.
Influence of CPP and ICP
Enhancing CPP by decreasing
ICP or increasing mean arterial blood
pressure can increase PbtO2. CPP
can be enhanced by using vasopres-
sors or volume expansion. Drainage
of cerebrospinal fluid, administra-
tion of mannitol, and sedation can
decrease ICP, resulting in an increase
in CPP. The overall impact of CPP
therapy on PbtO2 has been investi-
gated in several studies.
Kiening et al32 discovered that
when CPP was less than 60 mm Hg,
PbtO2 decreased. Yet, when CPP was
greater than 60 mm Hg, the effect on
PbtO2 was minimal. Bruzzone et al34
studied 7 patients with severe head
injury and noted the same correla-
tion between decreases in PbtO2 and
CPP less than 60 mm Hg. Stocchetti
et al8 refuted the 2 previous claims
that increasing CPP to more than
60 mm Hg had no effect on PbtO2.
In their study,8 when CPP was
increased from a mean of 77 mm Hg
(SD 9 mm Hg) to 96 mm Hg (SD 11
mm Hg), the PbtO2 increased from 24
mm Hg (SD 13 mm Hg) to 31 mm Hg
(SD 13 mm Hg).
Van den Brink35 found that
changing the tubing used to admin-
ister vasopressor solution caused the
CPP to decrease, with a resulting
decrease in PbtO2. Changing tubing
is common in the intensive care unit,
with an accompanying decrease in
blood pressure and CPP. Artru et al20
reported that despite increasing CPP
to normal levels and greater, patients
experienced hypoxic episodes dur-
ing measurement of brain tissue
oxygen. Using transcranial Doppler
imaging of the middle cerebral
artery, Dings et al43 found a positive
correlation between CPP and PbtO2
changes in the 7 days after evacua-
tion of a hematoma.
Kiening et al32 also reviewed the
correlation of measurements of ICP,
CPP, pulse oximetry, SjvO2, and end
tidal carbon dioxide with PbtO2 in 15
patients with traumatic brain injury.
The “time of good data quality” was
95% for PbtO2 compared with only
43% for SjvO2, supporting the use of
PbtO2 monitoring as an adjunct to
ICP and CPP monitoring. Both SjvO2
and PbtO2 correlated with CPP dur-
ing decreases in CPP, and the correla-
tion was best when the CPP decreased
to a level less than a breakpoint of
60 mm Hg, suggesting intact auto-
regulation. They concluded that tissue
oxygen monitoring is safe, reliable,
and suitable for long-term monitoring.
24 CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
In a study of 35 patients with
severe head injury, Bardt et al29
found that during elevation of ICP
and decrease in CPP, the patients
experienced cerebral hypoxia and
that the degree and prevalence of
these episodes affected the patients’
outcome. Low PbtO2 readings
occurred in 11.5% of the patients
with an ICP of 20 mm Hg or greater.
Critchley et al44 measured ICP and
CPP during craniotomy for
aneurysm clipping and found that
PbtO2 was improved when ICP was
reduced and that the effect was unre-
lated to CPP. They also found that
PbtO2 was an indicator of cerebral
ischemia in these patients.
Mannitol (an osmotic diuretic)
has been routinely used to decrease
ICP and improve CPP, but in a sam-
ple of 11 patients with severe head
injury, Hartl et al23 found that although
ICP and CPP improved, PbtO2 did
not. The investigators concluded that
ICP was not a surrogate measure of
ischemic episodes.
Barbiturates have also been used
to decrease elevated ICP. McKinley
et al45 reported the impact of barbi-
turate therapy on PbtO2 in a study of
10 patients with severe head injury.
In 3 of the patients, pentobarbital
coma was initiated, resulting in an
increase in PbtO2.
In most patients with severe head
injury, strategies to increase CPP and
decrease ICP improve PbtO2. The
studies underscore the need for indi-
vidualization of care based on each
patient’s response to therapy.
Influence of Temperature
Decreasing body temperature to
less than 37°C, that is, inducing
hypothermia, can decrease oxygen
utilization in the brain.30 In contrast
though, in a multicenter study of the
effects of hypothermia in severe trau-
matic brain injury, outcome after 6
months did not differ significantly
between patients who had hypother-
mia induced and those who did not.46
As discussed earlier, several authors13,14
reported differences between brain
and body temperatures. Anecdotally,
many clinicians have found that
increases in temperature are accom-
panied by a decrease in PbtO2.
Conclusion
Interventions that alter FIO2,
PaCO2, CPP, hemoglobin level, ICP,
and temperature and use of medica-
tions such as barbiturates can affect
oxygen delivery and/or consump-
tion in brain tissue. The key is strik-
ing a balance between all of the
parameters to ensure an adequate
PbtO2.
PbtO2 monitoring adds a dimen-
sion to care of patients with severe
traumatic brain injury. Research has
provided a basis for interventions
that can affect critical oxygen levels
in the brain. By understanding the
causes of hypoxia and low oxygen
states in the brain and planning
interventions to adjust oxygen deliv-
ery, the critical care team can maxi-
mize patients’ recovery from injury.
References
1. Centers for Disease Control (2002).
Traumatic brain injury in the United States.
Available at: http://www.cdc.gov/ncipc
/didop/tbi.htm. Accessed August 19, 2002.
2. Verma A. Neuroprotection opportunities in
traumatic brain and spinal cord injury.
Available at: www.biausa.org/Pages
/dbscip%20source/neuroprotection
.opportunities.html. Accessed August 16, 2002.
3. Hesdorffer DC, Ghajar J, Iacono L.
Predictors of compliance with the evidence-
based guidelines for traumatic brain injury
care: a survey of United Status trauma cen-
ters. J Trauma. 2002;52:1202-1209.
4. Bullock R, Chesnut RM, Clifton G, et al.
Guidelines for the Management of Severe Head
Injury. New York, NY: Brain Trauma
Foundation; 2000.
 5. Meixensberger J, Jagar A, Dings J, Baunach S,
Roosen K. Multimodality hemodynamic
neuromonitoring: quality and consequences
for therapy of severely head injured patients.
Acta Neurochir Suppl (Wien). 1998;71:260-262.
6. Meixensberger J, Jager A, Dings J, Baunach
S, Roosen K. Quality and therapeutic
advances in multimodality neuromonitor-
ing following head injury. In: Bauer BL,
Kuhn TJ, eds. Severe Head Injuries. New
York, NY: Springer Verlag; 1997:99-108.
7. Meixensberger J, Dings J, Kuhnig H, Roosen
K. Studies of tissue PO2 in normal and
pathological human brain cortex. Acta
Neurochir Suppl (Wien). 1993;59:58-63.
8. Stocchetti N, Chieregato A, De Marchi M,
Croci M, Benti R, Grimoldi N. High cerebral
perfusion pressure improves low values of
local brain tissue O2 tension in focal lesions.
Acta Neurochir Suppl (Wien). 1998;71:162-165.
9. Zauner A, Daugherty WP, Bullock R,
Warner D. Brain oxygenation and energy
metabolism, I: biological function and
pathophysiology. Neurosurgery.
2002;51:289-302.
10. Kehler U, Nowak G, Fleckenstein W, Arnold
H. Continuous measurement of PO2 in cere-
brospinal fluid. In: Ehrly AM, Fleckenstein
W, Langdraf H, eds. Clinical Oxygen Pressure
Measurement III. Oxford, UK: Blackwell
Publishing Inc; 1992:105-110.
11. Maas A, Fleckenstein W, de Jong D, van
Santbrink H. Monitoring cerebral oxygena-
tion: experimental studies and preliminary
clinical results of continuous monitoring of
cerebrospinal fluid and brain tissue oxygen
tension. Acta Neurochir Suppl (Wien).
1993;59:50-57.
12. Maas A, van Santbrink H, Kloos L, Jansen
W. Brain oxygen tension measurements in
severe head injury: possibilities for target-
ing therapy? Paper presented at: J Douglas
Miller Memorial Meeting; October 16-18,
1996; Edinburgh, Scotland.
13. Rumana Ch, Gopinath S, Uzura M,
Robertson CS. Brain temperature in head
injured patients. Paper presented at: 10th
International Symposium on Intracranial
Pressure and Neuromonitoring in Brain
Injury; May 25-29, 1997; Williamsburg, Va.
14. Henker RA, Brown SD, Marion DW.
Comparison of brain temperature with
bladder and rectal temperatures in adults
with severe head injury. Neurosurgery.
1998;42:1071-1075.
15. Ausman J, McCormick P, Stewart M, et al.
Cerebral oxygen metabolism during
hypothermic circulatory arrest in humans.
J Neurosurg. 1993;79:810-815.
16. Crowder C, Tempelhoff R, Theard M, Cheng
M, Todorov A, Dacey R. Jugular bulb tem-
perature: comparison with brain surface
and core temperatures in neurosurgical
patients during mild hypothermia.
J Neurosurg. 1996;85:98-103.
17. Mellegard P. Changes in human intracere-
bral temperature in response to different
methods of brain cooling. Neurosurgery.
1992;31:671-677.
18. LICOX [product insert]. Plainsboro, NJ:
Integra NeuroSciences/GMS; 2002.
19. Palmer S, Bader MK, Palmer J, Gross J,
Shaver T, Stalcup C. Early cerebral oxygen
desaturation in traumatic brain injury with
normal intracranial pressure. Paper pre-
sented at: CNS 2001; October 1-3, 2001; San
Diego, Calif.
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
20. Artru F, Jourdan C, Perret-Liaudet A, Charlot
M, Mottolese C. Low brain tissue oxygen
pressure: incidence and corrective therapies.
Neurol Res. 1998;20(suppl 1):S48-S51.
21. Dings J, Meixensberger J, Jager A, Roosen K.
Clinical experience with 118 brain tissue
oxygen partial pressure catheter probes.
Neurosurgery. 1998;43:1082-1095.
22. Palmer S, Bader MK, Qureshi A, et al. The
impact on outcomes in a community hospi-
tal setting of using the AANS traumatic
brain injury guidelines. American
Association of Neurologic Surgeons. J
Trauma. 2001;50:657-664.
23. Hartl R, Bardt T, Kiening K, Sarrafzadeh A,
Schneider G, Unterberg A. Mannitol
decreases ICP but does not improve brain-
tissue PO2 in severely head-injured patients
with intracranial hypertension. Acta
Neurochir Suppl (Wien). 1997;70:40-42.
24. Hoffman WE, Charbel FT, Portillo GG,
Edelman G, Ausman JL. Regional tissue PO2,
PCO2, pH and temperature measurement.
Neurol Res. 1998;20(suppl 1):S81-S84.
25. Valadka AB, Gopinath SP, Contant CF, Uzura
M, Robertson CS. Relationship of brain tis-
sue PO2 to outcome after severe head injury.
Crit Care Med. 1998;26:1576-1581.
26. Dings J, Meixensberger J, Roosen K. Brain
tissue-PO2 monitoring: catheter stability and
complications. Neurol Res. 1997;19:241-245.
27. Doppenberg EM, Zauner A, Watson J,
Bullock R. Determination of the ischemic
threshold for brain oxygen tension. Acta
Neurochir Suppl (Wien). 1998;71:166-169.
28. Sarrafzadeh AS, Kiening KL, Bardt TF,
Schneider GH, Unterberg AW, Lanksch
WR. Cerebral oxygenation in contusioned
vs nonlesioned brain tissue: monitoring of
PtiO2 with Licox and Paratrend. Acta
Neurochir Suppl (Wien). 1998;71:186-189.
29. Bardt TF, Unterberg AW, Hartl R, Kiening
KL, Schneider GH, Lanksch WR.
Monitoring of brain tissue PO2 in traumatic
brain injury: effect of cerebral hypoxia on
outcome. Acta Neurochir Suppl (Wien).
1998;71:153-156.
30. van den Brink WA, van Santbrink H,
Steyerberg EW, et al. Brain oxygen tension
in severe head injury. Neurosurgery.
2000;46:868-878.
31. Maas AL, Dearden M, Teasdale GM, et al.
EBIC-guidelines for management of severe
head injury. European Brain Injury
Consortium. Acta Neurochir (Wien).
1997;139:286-294.
32. Kiening KL, Unterberg AW, Bardt TF,
Schneider GH, Lanksch WR. Monitoring of
cerebral oxygenation in patients with severe
head injuries: brain tissue PO2 versus jugu-
lar vein oxygen saturation. J Neurosurg.
1996;85:751-757.
33. van Santbrink H, Maas AL, Avezaat CJ.
Continuous monitoring of partial pressure
of brain tissue oxygen in patients with
severe head injury. Neurosurgery.
1996;38;21-31.
34. Bruzzone P, Dionigi R, Bellinzonna G,
Imberti R, Stocchetti N. Effects of cerebral
perfusion pressure on brain tissue PO2 in
patients with severe head injury. Acta
Neurochir Suppl (Wien). 1998;71:111-113.
35. van den Brink WA, van Santbrink H,
Avezaat CJ, et al. Monitoring brain oxygen
tension in severe head injury: the
Rotterdam experience. Acta Neurochir Suppl
(Wien). 1998;71:190-194.
CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003 25
36. Narayan RK, Kishore PRS, Becker DP, et al.
Intracranial pressure: to monitor or not to
monitor. J Neurosurg. 1982;56:650-659.
37. Kiening KL, Hartl R, Unterberg AW,
Schneider GH, Bardt T, Lanksch WR. Brain
tissue PO2-monitoring in comatose patients:
implications for therapy. Neurol Res.
1997;19:233-240.
38. Chesnut RM, Marshall LF, Klauber MR, et
al. The role of secondary brain injury in
determining outcome from severe head
injury. J Trauma. 1993;34:216-222.
39. Cruz J, Raps EC, Hoffstad OJ, Jaggi JL,
Gennarelli TA. Cerebral oxygenation moni-
toring. Crit Care Med. 1993;21:1242-1246.
40. Baunach S, Meixensberger J, Gerlach M,
Lan J, Roosen K. Intraoperative microdialy-
sis and tissue-PO2 measurement in human
glioma. Acta Neurochir Suppl (Wien).
1998;71:241-243.
41. Menzel M, Doppenberg EM, Zauner A,
Soukup J, Reinert MM, Bullock R. Increased
inspired oxygen concentration as a factor in
improved brain tissue oxygenation and tis-
sue lactate levels after severe human head
injury. J Neurosurg. 1999;91:1-10.
42. Schneider GH, Sarrafzadeh AS, Kiening KL,
Bardt TF, Unterberg AW, Lanksch WR.
Influence of hyperventilation on brain tis-
sue-PO2, PCO2, and pH in patients with
intracranial hypertension. Acta Neurochir
Suppl (Wien). 1998;71:62-65.
43. Dings J, Meixensberger J, Amschler J,
Hamelbeck B, Roosen K. Brain tissue PO2 in
relation to cerebral perfusion pressure, TCD
findings, and TCD-CO2 reactivity after
severe head injury. Acta Neurochir (Wien).
1996;138;425-431.
44. Critchley GR, O’Neill KS, Bell BA. Cerebral
blood flow and tissue oxygenation monitor-
ing during aneurysm surgery. Neurol Res.
1998;20(suppl 1):S44-S47.
45. McKinley BA, Parmley CL. Effects of injury
and therapy on brain parenchyma PO2,
PCO2, pH and ICP following severe closed
head injury. Acta Neurochir Suppl (Wien).
1998;71:177-182.
46. Clifton GL, Miller ER, Choi SC, et al. Lack of
effect of induction of hypothermia after
acute brain injury. N Engl J Med.
2001;344:739-745.
 CE Continuing Education

CE Test Instructions
To receive CE credit for this test (ID C034), mark your answers on the form below, complete the enroll-
ment information, and submit it with the $12 processing fee (payable in US funds) to the American
Association of Critical-Care Nurses (AACN). Answer forms must be postmarked by August 1, 2005. Within
3 to 4 weeks of AACN receiving your test form, you will receive an AACN CE certificate.
This continuing education program is provided by AACN, which is accredited as a provider of continuing education in nursing by the
American Nurses Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuing edu-
cation by the State Boards of Nursing of Alabama (#ABNP0062), California (01036), Florida (#FBN2464), Iowa (#332), Louisiana
(#ABN12), and Nevada. AACN programming meets the standards for most other states requiring mandatory continuing education
credit for relicensure.

Test ID: C034

Test writer: Ruth Kleinpell-Nowell, RN, PhD, CS, CCNS
CE Test Form Form expires: August 1, 2005
Contact hours: 2.0
Passing score: 9 correct (75%)
Brain Tissue Oxygen Monitoring in Severe Brain Category: A
Test fee: $12
Injury, I: Research and Usefulness in Critical Care
Objectives:
1. Discuss the dynamics of brain injury related to oxygen
2. Identify the influence of interventions on brain tissue oxygen
3. Describe the use of brain tissue oxygen monitoring in severe brain injury

Mark your answers clearly in the appropriate box. There is only 1 correct answer. 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
❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b
❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c
❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d

Program evaluation Name

Agree Neutral Disagree
Objective 1 was met ❑ ❑ ❑ Address
Objective 2 was met ❑ ❑ ❑
Objective 3 was met ❑ ❑ ❑ City State ZIP
The content was appropriate ❑ ❑ ❑
My expectations were met ❑ ❑ ❑ Phone ( )
This method of CE is effective ❑ ❑ ❑
for this content E-mail address

The level of difficulty of this test was: AACN member number

❑ easy ❑ medium ❑ difficult
To complete this program, it took me ❑ I would like to receive my certificate via e-mail (check box)
hours / minutes.

Mail this entire page to AACN, 101 Columbia, Aliso Viejo, CA 92656, (800) 899-2226

26 CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003

Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
CE Test Questions
Brain Tissue Oxygen Monitoring in Severe Brain Injury, I: Research and Usefulness in Critical Care

1. How many cases of traumatic brain injury are 7. What is the level of PbtO2 in an uninjured brain?
reported each year in the United States? a. 20 mm Hg to 35 mm Hg
a. 80 000 b. 15 mm Hg to 20 mm Hg
b. 500 000 c. 10 mm Hg to 20 mm Hg
c. 100 000 000 d. 5 mm Hg to 10 mm Hg
d. 1 500 000
8. What level of PbtO2 is associated with an
2. Which one of the following is not associated with increased risk of death?
secondary brain injury? a. Greater than 15 mm Hg
a. Cerebral edema b. Less than 15 mm Hg
b. Cerebral ischemia c. There is no association
c. Chemical changes associated with direct trauma d. None of the above
d. Disruption of axons with primary injury
9. Which one of the following is not a strategy to
3. What is the correct percentages of brain-to-fluid increase PbtO2?
ratio within the brain? a. Increase cerebral perfusion pressure (CPP)
a. 60% brain tissue, 20% blood, 20% cerebrospinal b. Decrease intracranial pressure
fluid c. Increase mean arterial blood pressure
b. 70% brain tissue, 20% blood, 10% cerebrospinal d. Decrease body temperature to less than 37°C
fluid
c. 80% brain tissue, 10% blood, 10% cerebrospinal 10. What level of CPP causes a decrease in PbtO2?
fluid a. Greater than 60 mm Hg
d. 90% brain tissue, 5% blood, 5% cerebrospinal b. Less than 60 mm Hg
fluid c. CPP has no effect on PbtO2
d. None of the above
4. What is the location of probe placement for brain
tissue oxygen monitoring? 11. Which one of the following measures does not
a. Grey matter result in a decrease in intracranial pressure or an
b. Posterior ventricle increase in CPP?
c. Deep white matter a. Drainage of cerebrospinal fluid
d. Central culcus b. Administration of mannitol
c. Sedation
5. After brain injury, what is the relationship of d. Decreasing mean arterial blood pressure
brain temperature to core body temperature?
a. Brain temperature is higher than core body 12. With brain injury, placement of a brain oxygen
temperature monitor in which cerebral hemisphere allows for
b. Core body temperature is higher than brain the detection of global oxygen status?
temperature a. Contralateral
c. Temperatures are similar b. Superior
d. Temperatures are identical c. Inferior
d. Ipsilateral
6. What is the response in the partial pressure of
brain tissue oxygen (PbtO2) to a fever?
a. Pressure increases
b. Pressure decreases
c. No change
d. Pressure initially increases, then decreases

CRITICALCARENURSE Vol 23, No. 4, AUGUST 2003 27

Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014
Downloaded from http://ccn.aacnjournals.org/ by guest on May 13, 2014