Journal of Neurosurgical Anesthesiology
Vol. 9, No. 2, p. 154-158 :
© 1997 Lippincott-Raven Publishers, Philadelphia

Case Report

Cerebral Oximetry During Circulatory Arrest for
Aneurysm Surgery

Satwant K. Samra and *William F. Chandler

Departments of Anesthesiology and *Neurosurgery, University of Michigan Medical Center,
Ann Arbor, Michigan, U.S.A.

Summary: A patient underwent surgical clipping of a complex giant intracra-
nial carotid aneurysm with the aid of extracorporeal circulation and complete
hypothermic circulatory arrest. During the entire procedure, cerebrovascular
oxygen saturation (ScO,) was spectroscopically measured. The patient expe-
rienced circulatory arrest for 34 min; for 15 of the 34 min ScO, was <34%
(minimum 32%). The patient tolerated the procedure without new neurological
deficit, thus demonstrating that the previously suggested ‘‘critical’’ level of
35% ScO, is not absolute. Key Words: Hypothermia—Hypoxia—Ischemia—
Cerebral aneurysm—Near infrared spectroscopy.

Deep hypothermia with induced circulatory ar-
rest (DHCA) is sometimes a necessary adjunct for
management of complex intracranial aneurysms
(1,2). Although significantly reduced, cerebral me-
tabolism with oxygen consumption continues even
during deep hypothermia (3), while oxygen delivery
is completely stopped during induced circulatory
arrest. This combination creates a potential for neu-
ral injury and deserves close monitoring. Near in-
frared spectroscopy (NIRS) is a technique that can
potentially monitor changes in cerebral oxygenation
and tissue oxygen utilization at the mitochondrial
level. At present, there is limited clinical experience
with this monitoring technique, and a critical value
of cerebrovascular oxygen saturation (ScO,), below
which neuronal damage takes place, is not known.
We report a case which, to the best of our knowl-

Address correspondence and reprint requests to Dr. S. K.
Samra at Department of Anesthesiology, 16323 UH, Box 0048,
1500 East Medical Center Drive, Ann Arbor, MI 48109-0048,
U.S.A.

154

edge, documents the lowest level of ScO, possible
during circulatory arrest without a new neurological
deficit.

CASE REPORT

This 43-year-old woman presented to an outside
hospital after a sudden syncopal episode that oc-
curred while she was coming out of the shower.
Found by her husband, she was unresponsive,
frothing at the mouth, and having seizure-like
movements. She had several episodes of vomiting
with possible aspiration, and a left hemiparesis.
Movement of her left arm returned within a few
hours, but weakness of her left leg persisted. A CT
scan showed subarachnoid hemorrhage, and an an-
giogram revealed a giant right carotid-ophthalmic
artery aneurysm. She was heavily sedated and
pharmacologically paralyzed. The trachea was intu-
bated and muscle paralysis maintained to facilitate
mechanical ventilation before transfer to the Uni-
versity hospital.
CEREBRAL OXIMETRY DURING CIRCULATORY ARREST 155

Examination

On admission, she was heavily sedated but her
sensorium improved over the next 48 h. She be-
came awake, alert, and oriented. A second angio-
gram again demonstrated the giant right carotid-
ophthalmic artery aneurysm that filled completely
and a left carotid-ophthalmic artery aneurysm that
was entirely thrombosed and calcified. She did not
tolerate temporary balloon occlusion of the right
carotid artery and developed ischemic EEG
changes and a pronator drift following <30 s of ca-
rotid occlusion. Based on these findings, it was
clear that carotid occlusion to trap the aneurysm
was not an option. The decision was made to use
profound hypothermia with induced circulatory ar-
rest as an adjunct for the surgical treatment of this
complex carotid-ophthalmic aneurysm.

Operation

Anesthesia was induced with Pentothal and main-
tained with isoflurane, oxygen, fentanyl, and vecu-
tonium. Depth of anesthesia was maintained to
achieve continuous burst suppression on EEG. In-
traoperative monitoring included a continuous mon-
itoring of ScO, using a tissue infrared spectrometer
(INVOS model 3100; Somanetics, Troy, MI,
U.S.A.) in addition to invasive hemodynamic mon-
itoring and peripheral pulse oximeter. The cerebral
oxygen sensor was placed on the forehead (nonop-
erated, left side) lateral to the midline and protected
from ambient light with an adhesive shield. This
sensor consists of a near infrared light transmitter
and two detectors (placed at a distance of 30 and 40
mm from it) housed within an adhesive strip. Near
infrared light at 730 and 810 nm wavelengths, se-
lected for maximum tissue penetration, is reflected
by the tissues in a parabolic curve. When placed 30
mm from the transmitter, the detector receives light
reflected predominantly through the scalp and
skull; at 40 mm, the detector receives light reflected
from the scalp, skull, and a small section of the
brain tissue. The computer in the oximeter sub-
tracts the reflected signal of superficial structures
from that of the deeper tissues, thereby calculating
the oxygen saturation of blood and brain tissue. Be-
cause 75% of the blood volume in tissue beds is in
the venous circulation, ScO, approximates venous
blood oxygen saturation.

We performed a right pterional craniotomy and

exposed the aneurysm. It became clear that direct
clipping of this thick-walled aneurysm was not fea-
sible. We cannulated the left femoral artery and
vein to initiate femoro-femoral extracorporeal cir-
culation to induce deep hypothermia to 17°C. Ven-
tricular fibrillation developed at 23°C. Circulatory
arrest was accomplished by cessation of extracor-
poreal circulation. We opened the aneurysm and
performed an endarterectomy of the thick athero-
matous wall of the aneurysm, which made feasible
the application of the clip to the now well-defined
neck. On gradual rewarming, there was spontane-
ous conversion of ventricular fibrillation to sinus
rhythm at 28°C, and the patient was weaned off the
extracorporeal circulation without problems. Ade-
quate hemostasis was achieved, and the craniotomy
wound was closed. The patient was on extracorpo-
real circulation for 172 min and experienced 34 min
of complete circulatory arrest. The total duration of
anesthesia was 10 h. There were no intraoperative
problems or complications.

Figure 1 shows the ScO, throughout the entire
surgical procedure, and Fig. 2 demonstrates details
of that same saturation during extracorporeal circu-
lation (bypass). Numerical values of ScO, were re-
corded on a floppy disc at 1-min intervals for later
analysis. Mean ScO, was 69% prebypass and 77%
postbypass. During extracorporeal circulation,
ScO, was 63% pre- and 57% postcirculatory arrest.
During circulatory arrest, mean ScO, reading over
34 min was 39%, with the range of 32 to 60%. A
gradual decrease (from 60%) in saturation was first
noticed 5 min after inducing circulatory arrest. It
reached a 35% of 35% value over the next 14 min
and remained <35% (lowest reading 32%) for the
next 15 min, at which time circulation was restored.
A second drop in saturation seen in Figs. 1 and 2
between 15:22 and 15:26 (clock time) was associ-
ated with a brief period of mechanical hypoventila-
tion during partial cardiac bypass with sinus
thythm. This drop in ScO, was accompanied by a
simultaneous decrease in peripheral oxygen satura-
tion and an increase in end tidal CO).

Postoperative Course

The patient remained on controlled ventilation
overnight. The next morning, the patient was easily
arousable, followed verbal commands appropri-
ately, and had no new neurological deficits. Over

Journal of Neurosurgical Anesthesiology, Vol. 9, No. 2, 1997
156

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S. K. SAMRA AND W. F. CHANDLER

Extracorporeal circulation \"

FIG. 1. Cerebrovascular satura-
tion during surgery.

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17:22:40

16:41:30
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15:18:39
15:34:59
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the ensuring 5 days, she developed moderately se-
vere vasospasm as indicated by increased velocities
on transcranial Doppler studies but never devel-
oped a neurological deficit. She was moved out of
intensive care on the 12th postoperative day and
discharged from the hospital 16 days after surgery.
At the time of discharge, her mental status was at
baseline according to her family.

At the follow-up 3 months after leaving the hos-
pital, she was bright, alert and oriented. Strength in
her left leg had improved enough to walk without a
cane.

DISCUSSION

The use of extracorporeal circulation to induced
deep hypothermia and circulatory arrest is well rec-
ognized as a useful adjunct in the repair of compli-
cated intracranial aneurysms. In some patients, cir-
culatory arrest is the only possible option. A ‘‘safe’’

75

FIG. 2. Cerebrovascular satura- 70
tion during extracorporeal circu-
lation. Circulatory arrest was in-
duced for 34 min. During this
time, pulse oximeter recorded he-
moglobin saturation of 100%. A
subsequent decrease in ScO, (ar-
row marks hypoventilation) was
associated with lack of mechani-
cal ventilation (during partial by-
pass) and was accompanied by
pulse oximeter reading of 80%

65
60
55
50
45 7

<¢— % Cerebrovascutar saturation —2>

duration of circulatory arrest is difficult to define
and quite variable (2,4-7). Real time, clinically use-
ful determinants of adequacy of cerebral oxygen-
ation are poorly defined and difficult to monitor.
None of the hemodynamic and neurophysiological
monitors traditionally used for intraoperative mon-
itoring provide information during circulatory ar-
rest. NIRS, first described by Jobsis (8), has subse-
quently been used by several investigators (9-13) to
monitor cerebral oxygenation.

Many of these investigators have suggested that
NIRS may have clinical application for monitoring
the brain during neurosurgical procedures and open
heart surgery. Before this monitoring technique be-
comes a clinical reality, a critical value of ScO,,
below which neuronal damage is likely to occur,
needs to be established. Ausman and co-workers (3)
attempted to establish that value in a clinical study
of seven patients undergoing intracranial aneurysm
clipping during which deep hypothermia with circu-

Hypoventilation

saturation of hemoglobin. This
graph emphasizes the response of
the cerebral oximeter to cerebral
ischemia as well as hypoxemia.

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Journal of Neurosurgical Anesthesiology, Vol. 9, No. 2, 1997
CEREBRAL OXIMETRY DURING CIRCULATORY ARREST 157

latory arrest was used as an adjuvant. Duration of
circulatory arrest in their study varied between 10
and 65 min and had a negative linear correlation
with ScOQ,. In five patients, the ScO, reading re-
mained >35%, four had excellent outcome with re-
turn to premorbid levels, and one had a good out-
come with mild new left hemiparesis. In the remain-
ing two patients with a grade IV and grade 0
hemorrhage and circulatory arrest periods of 45 and
60 min, ScO, fell to 30 and 34%, respectively. Out-
come was poor in these two patients, with changes
of diffuse cerebral ischemia confirmed postmortem.
These authors thus suggested a reading of 35% as
the critical value of ScO, below which neurological
damage may occur.

The anesthetic management and technique of hy-
pothermic circulatory arrest used for our patient
was similar to those used by Ausman and co-
workers except that continuous burst suppression
was maintained for our patient. This is not men-
tioned in their study. Our patient had ScO, <35%
for 15 min, although the duration of circulatory ar-
rest was 34 min (compared to 65 min). Our patient
responded to verbal stimuli soon after discontinua-
tion of anesthesia and left the hospital 2 weeks after
surgery without a new neurological deficit. We re-
port this case to emphasize that although ScO, has
a potential to be a useful monitoring tool, there is a
need for collection of clinical data to determine a
“‘critical’’ reading below which cerebral injury oc-
curs. In a clinical study of ScO, in patients under-
going carotid endarterectomy under regional anes-
thesia (14), it was noted that carotid occlusion re-
sulted in an ipsilateral ScO, drop between 6 and
33% from baseline without a change in clinical neu-
rological status. These findings suggest that while
ScO, changes are capable of tracking changes in
cerebral circulation, a critical value for ScO, change
that is associated with neurological dysfunction in
humans has not yet been defined. It is also possible
that a “‘critical value’’ of ScO, or a ‘‘critical change
in ScO,”’ is difficult to define because neurological
injury may be a result of multiple factors. ScO, may
be only one of these factors. A combination of de-
gree (decrease in ScO,) and duration of desaturation
may determine neurological outcome.

Deep hypothermia is used because of the brain
protection provided by hypothermia during a period
of circulatory arrest. Cerebral metabolism, how-
ever, has been shown to continue even at core tem-

perature <15°C in primate models (15). At temper-
atures of 15 to 18°C (clinical range), oxygen extrac-
tion in a primate model was 30% of the baseline. It
has been proposed that during DHCA, oxygenated
blood in cerebral microvascular circulation should
release oxygen to move along the partial pressure
gradient to mitochondria (with PO, of 3-8 mm Hg).
As partial pressure of oxygen in blood drops over
time due to metabolic consumption, desaturation
occurs. At 20°C hemoglobin saturation of 30% will
be associated with capillary PO, of 7 to 10 mm Hg,
and capillary to mitochondrial gradient will be abol-
ished, leading to cerebral hypoxia (15). This hy-
pothesis may explain why ScO, <30% may not be
seen during DHCA. A ‘‘safe’’ duration of DHCA is
difficult to define. Continuous ScO, monitoring may
help guide the duration and management of DHCA
and retrograde cerebral perfusion techniques.

Our patient with good neurological outcome had
a lower ScO, (32 vs. 35%) for a shorter duration (15
min vs. 65 min) compared to the mortality reported
by Ausman and co-workers. It could be argued that
maintenance of anesthetic depth at the level of burst
suppression in our patient might have provided
added ‘‘brain protection.”’ The greater decrease in
ScO, during the period of circulatory arrest, how-
ever, suggests that maintenance of burst suppres-
sion did not totally suppress cerebral metabolic
consumption of oxygen in our patient. This finding
of continued oxygen consumption by the brain even
during deep hypothermia (18°C) has been previ-
ously reported (2).

We conclude that ScO, monitoring has great po-
tential for patients undergoing surgical procedures
that necessitate circulatory arrest because all other
monitors of neurological integrity and oxygenation
(EEG, peripheral pulse oximetry) become nonfunc-
tional during these circumstances. ScO, has been
shown to have an excellent correlation with jugular
venous saturation and middle cerebral blood flow
velocity (13). Further clinical studies using this
monitoring technique are needed to define the crit-
ical value of ScO, that may be able to predict neu-
rological outcome either alone or in combination
with other factors.

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