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The Effect of Bupivacaine Skull Block on the


Hemodynamic Response to Craniotomy
Article in Anesthesia & Analgesia January 1997
DOI: 10.1097/00000539-199612000-00022 Source: PubMed

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NEUROSURGICAL

ANESTHESIA

SECTION EDITOR

DONALD S.PROUGH

The Effect of Bupivacaine


Response to Craniotomy

Skull Block on the Hemodynamic

Mark L. Pinosky, MD*, Richard L. Fishman, MD*, Scott T. Reeves,


Sunil Patel, MDt, Yuko Palesch, PhD$, and B. Hugh Dorman, PhD,
Departments
of *Anesthesia and Perioperative
Medicine, tNeurosurgery,
Medical University of South Carolina, Charleston, South Carolina

The placement of pointed cranial pins into the periosteum is a recognized acute noxious stimulation
during
intracranial
surgery which can result in sudden increases in blood pressure and heart rate, causing increases in intracranial pressure. A skull block (blockade
of the nerves that innervate the scalp, including
the
greater and lesser occipital nerves, the supraorbital
and
supratrochlear
nerves, the auriculotemporal
nerves,
and the greater auricular
nerves) may be effective in
reducing hypertension
and tachycardia.
Twenty-one
patients were allocated in a prospective, double-blind
fashion to a control group or a bupivacaine group. After
a standardized
induction and 5 min prior to head pinning, a skull block was performed. Patients in the control group received a skull block of normal saline, while

ntracranial surgery on patients with increased intracranial pressure (ICI) poses a unique challenge
to the anesthesiologist. Although much intracranial
surgery is not particularly stimulating, certain aspects
of the operation, including laryngoscopy, insertion of
cranial pins, incision, and periosteal-dural contact, induce noxious stimulation. These noxious events can
result in sudden increases in blood pressure and heart
rate (HR), which can cause potential morbidity due to
further increases in ICI in patients with intracranial
pathology, and a greater risk for rupture in patients
with intravascular aneurysms (1). Therefore, a method
to blunt these noxious stimuli would be valuable.
Blockade of the nerves that supply the involved region
of the scalp may be effective in reducing hypertension
and tachycardia, the requirement for vasodilators, and
the requirement for an increased depth of anesthesia
early in the surgical procedure, all of which may cause
increased cerebral blood flow and an increase in ICI
(23.
Accepted for publication July 25, 1996.
Address correspondence and reprint requests to Mark L. Pinosky,
MD, Medical University of South Carolina, Department of Anesthesiology, 171 Ashley Ave., Charleston, SC 29425-2207.

1256

Analg

1996;83:1256&61

Susan C. Harvey,

MD*,

MD*

and SBiometry

and Epidemiology,

the bupivacaine group received a skull block with 0.5%


bupivacaine.
Systolic (SAP), diastolic (DAP), mean arterial pressure (MAP), heart rate (HR), and end-tidal
isoflurane were recorded at the following
times: 5 min
after the induction
of anesthesia, during performance
of the skull block, during head pinning, and 5 min after
head pinning. Significant increases in SAP of 40 +- 6 mm
Hg, DAP of 30 +- 5 mm Hg, MAP of 32 -C 6 mm Hg, and
HR of 22 + 5 bpm occurred during head pinning in the
control group, while remaining
unchanged in the bupivacaine group. These results demonstrate that a skull
block using 0.5% bupivacaine
successfully blunts the
hemodynamic
response to head pinning.
(Anesth

Analg

1996;83:1256-61)

A skull block involves regional anesthesia to the


nerves that innervate the scalp, including the greater
and lesser occipital nerves, the supraorbital and supratrochlear nerves from cranial nerve Vi, the zygomaticotemporal nerves from V,, the auriculotemporal
nerves from V,, and the greater auricular nerves. As
the practice has not been previously evaluated, we
compared the effects of skull block with 0.5% bupivacaine with that of normal saline on the autonomic
response and the anesthetic requirement associated
with head pinning in a prospective, randomized,
double-blind fashion.

Methods
After institutional review board approval, 21 patients
able to give voluntary written consent were randomly
allocated to a control group and a bupivacaine group.
Patients assigned to the control group received a skull
block consisting of normal saline, while the bupivaCaine group received a skull block with 0.5% bupivaCaine. The skull block was performed by the anesthesiologist in charge of the case. The neurosurgeon
and the anesthesiologist performing the block were
01996

Anesth

MD*,

by the International

Anesthesia

Research
Society
0003-2999/96/$5.00

ANESTH
ANALG
1996;83:125641

NEUROSURGICAL
BUPIVACAINE

Supratrochlear
Supra-orbital

ANESTHESIA
SKULL
BLOCK

nerve
nerve

PINOSKY
ET AL.
FOR CRANIOTOMY

1257

-A
/

upratrochlear

n.

occipital

nerve

/
w

Figure
1. Innervation
of the scalp. Note the terminal
branches
of
the ophthalmic
branch of the trigeminal
nerve, the supraorbital
and
supratrochlear
nerves. The terminal
branch
of division
two of the
trigeminal
nerve, the zygomaticotemporal
nerve, is illustrated.
The
terminal
branch of the mandibular
division
of the trigeminal
nerve,
the auriculotemporal
nerve, is also depicted.

blinded to the drug being administered.


Inclusion criteria included patients between the ages of 18 and
85 yr, ASA physical status I, II, or III, undergoing
elective craniotomy
for tumor requiring
the use of
head pinning. Patients who had a documented allergy
to bupivacaine
or who refused to participate
were
excluded from the study.
Before the induction of general anesthesia, standard
monitors (electrocardiogram,
blood pressure cuff, and
pulse oximeter probe) were placed. A standardized
induction protocol was followed for all patients which
included sodium pentothal ([STP] 4 mg/kg),
fentanyl
(2 Fg/kg),
and vecuronium
(0.1 mg/kg).
For maintenance of anesthesia, up to 1% end-tidal isoflurane
(ET-Iso) in 30% 02/70% N,O was used.
A 20-gauge catheter was placed in the radial artery
of each patient and connected to a transducer
(SummitTM pressure transducer;
Baxter, Irvine, CA) placed
at the midaxillary
level. Cranial pins in the MayfieldTM
head holder (Ohio Medical Instrument
Co., Cincinnati, OH) are placed into the periosteum,
simultaneously withconstant
pressure applied by the neurosurgeon. Systolic (SAP), diastolic (DAP), and mean
arterial pressures
(MAP) were recorded
from the
catheter-transducer
system at the following
times:
5 min after the induction of anesthesia, during performance of the skull block, at 1 min after insertion of
cranial pins, and 5 min after head pinning. Any hemodynamic
response to insertion was treated immediately with increasing concentrations
of isoflurane.
HR and ET-Is0 concentration
were recorded at the
same time as invasive blood pressure. The ET-Is0 concentration was recorded 1 min after pinning to reflect

Greater
occipital
Third
occipital

\\

nerve
nerve

Figure
2. Coronal
view of innervation
of the scalp. Note
nal branches
of the ophthalmic
branch of the trigeminal
supraorbital
and supratrochlear
nerves.
The terminal
division
two of the trigeminal
nerve, the zygomaticotemporal
is illustrated.
The terminal
branch
of the mandibular
auriculotemporal
nerve is also shown. Also depicted
are
greater,
and third branches
of the occipital
nerve.

the terminerve, the


branch
of
nerve
nerve,
the
the lesser,

the time necessary for isoflurane end-tidal concentration to change. Isoflurane


was monitored
continuously after induction of anesthesia via Raman spectroscopy (Ohmeda Rascal II, Madison, WI>.
After induction
of anesthesia,
baseline hemodynamic variables were recorded and the skull block was
performed
5 min before head pinning. The supraorbital and supratrochlear
nerves were blocked with
2 mL of solution as they emerged from the orbit with
a 23-gauge needle introduced
above the eyebrow perpendicular
to the skin. The auriculotemporal
nerves
were blocked bilaterally with 5 mL of solution injected
1.5 cm anterior to the ear at the level of the tragus; the
needle was introduced
perpendicular
to the skin and
infiltration
was made deep to the fascia and superficially as the needle was withdrawn.
The postauricular
branches of the greater auricular nerves were blocked
with 2 mL of solution between skin and bone, 1.5 cm
posterior to the ear at the level of the tragus (Figure 1).
The greater, lesser, and third occipital nerves were
blocked with 5 mL of solution using a 22-gauge spinal
needle, with infiltration along the superior nuchal line,
approximately
halfway
between the occipital protuberance and the mastoid process (Figure 2).
A MayfieldTM head holder was used for all of the
craniotomies
in the study.
The MayfieldTM
head
holder uses pointed pins that are inserted simultaneously through the dermis engaging in the periosteum to secure the head in a stable position
for
surgery.

1258

NEUROSURGICAL
BUPIVACAINE

ANESTHESIA
SKULL
BLOCK

PINOSKY
ET AL.
FOR CRANIOTOMY

At the time of head pinning, if the HR or MAP


increased by more than 20% over baseline, the following rescue maneuvers
were performed.
The anesthesiologist would first attempt to control the blood pressure and/or HR with an increase in concentration
of
isoflurane to a maximum concentration
of 1 minimum
alveolar anesthetic concentration
(MAC) (1.15% endtidal concentration).
If the MAP or HR remained
greater than 20% over baseline values, the patient was
given a single dose of STP (2 g/kg).
An esmolol
bolus of 0.5 mg/kg
was then administered
if prior
maneuvers were not successful.
The difference in mean age between the two drug
groups was tested for statistical significance
by the
Students t-test. The Fishers exact test was used to
determine the significance of the distribution
of men
and women in the two drug groups.
Repeated-measured
analysis of variance was applied to the baseline-adjusted
measurements
of SAP,
DAP, MAP, HR, and ET-Is0 obtained during skull
block, head pinning, and at 5 min after pinning.
An (Y level of 0.01 was used to determine the significance of each test result to account for the fact that
five related measurements
were examined using the
same data. However,
for the readers benefit, the exact
P values yielded by the statistical tests are provided in
the following
section.
All statistical
analysis were performed
using the
software (SAS/STAT@ software; SAS, Inc., Cary, NC).
Results are presented as mean - SEM.

Results
The mean ages for the 11 patients in the bupivacaine
group and the 10 patients in the control group were
57 + 4.1 yr and 45 ? 4.7 yr, respectively
(P = not
significant).
Thirty-six
percent (4 of 11) of the bupivacaine group and 20% (2 of 10) of the control group
were men (P = not significant).
However,
the small
size of the group provided
low power for detecting
differences in age or gender. Past medical history was
significant for hypertension
in 3 of 11 patients in the
bupivacaine group and 1 of 10 patients in the control
group. All patients underwent
elective craniotomy for
tumor removal.
Table 1 presents the mean & SEM values for the five
measurements
for each drug group at baseline. The
results of the univariate analyses of the difference in
the means are also presented. Although
at baseline,
the mean difference between the two groups was significant (P = 0.01) for DAP, the two groups had similar mean values of SAP, MAP, HR, and ET-Iso. The
HR for both bupivacaine
and control groups after
anesthetic induction averaged 71 2 3 bpm. Moreover,
the percent concentration
of ET-Is0 for the bupivaCaine and control groups at baseline were similar
(0.58% + 0.06% vs 0.72% +- 0.06%, respectively).

ANESTH
ANALG
1996;83:1256-61

Table 1. Baseline Hemodynamic


Profile and Isoflurane
Concentration
of Bupivacaine
and Control Groups
Group
Baseline
SAP
DAP
MAP
HR
ET-Is0

Bupivacaine
(rl = 11)
122
71
87
72
0.58

t?
+
+
2

5.8
2.8
3.5
3.1
0.06

Control
(n = 10)
112
60
79
71
0.72

+
t
+
2
-c

2.9
2.6
2.9
2.9
0.06

P value*
0.13
0.01
0.11
0.94
0.14

Values
are mean 2 SEM.
SAP = systolic
blood
pressure;
DAP = diastolic
blood pressure;
MAP =
mean arterial
pressure;
HR = heart rate; ET-Is0 = end-tidal
isoflurane.
* P value is the result of the Students
t-test on the difference
between
the
two groups.

The results of the repeated-measured analyses of


variance on the baseline-subtracted measurements on
each of the five variables are provided in Table 2. The
positive values in the table indicate increases over the
corresponding baseline values for the variable. During
placement of the skull block there was no significant
change from baseline in either the bupivacaine or
control group with respect to HR, or SAP, DAP, and
MAP (Table 2). Moreover no additional isoflurane was
required relative to baseline for either treatment group
during the placement of the skull block. There was
also no difference between the two treatment groups
in any of the blood pressure values during placement
of the skull block. For the bupivacaine and control
groups, respectively, HR (73 + 3.8 bpm vs 79 +
3.5 bpm) and ET-Is0 concentration (0.60% + 0.06% vs
0.72% ? 0.07%) were also similar.
Significant increases in hemodynamic variables occurred during head pinning in the control group relative to baseline values (Table 2). SAP increased by
40 -t 6 mm Hg and DAP by 30 + 5 mm Hg from
baseline during pinning in patients in the control
group (Table 2). There were also significant increases
in MAP (32 t 6 mm Hg) and HR (22 ? 3 bpm) during
pinning in the control group. An increase in the requirement for isoflurane at pinning over baseline values was also observed in the control group (ET-Is0
pinning 1.05% 2 0.12% vs ET-Is0 baseline 0.72% t
0.06%). Thus, despite a significant increase in anesthetic concentration in the control group, there was a
significant change in hemodynamic variables. ET-Is0
was also unchanged during pinning, indicating no
requirement for additional anesthesia in the bupivaCaine group.
Significant overall drug effect as well as time effect
were observed in all variables except ET-Iso. The control group had substantially higher values of baselineadjusted hemodynamic variables at all three time
points compared to the bupivacaine group.
Rescue maneuvers during pinning were not required in any patient in the bupivacaine group. Nine

ANESTH
ANALG
1996;83:1256-61

Table

NEUROSURGICAL
BUPIVACAINE

ANESTHESIA
SKULL
BLOCK

PINOSKY
ET AL.
FOR CRANIOTOMY

1259

2. Differences Between Baselineand SubsequentIntervals in the Control and Bupivacaine Groups

At skull block
Variable
SAP
DAP
MAP
HR
ET-Is0

Control

Bupivacaine

13 + 5.4

2 2 3.9

9 + 3.9

1 5 3.5
0 k 3.5
1 + 2.6

11 + 4.6
8 + 3.3
0.00 2 0.1

0.02 + 0.02

At pinning
Control
39
30
33
23
0.3

k 6.2
-+ 5.2
k 6.1
2 5.3

+ 0.1

Postpinning

Bupivacaine
4 k 4.4
2 2 2.9
6 + 2.7

-1 + 2.2
0.1 + 0.1

Values
are mean ?SEM.
SAP = svstolic
blood
oressure:
DAl = diastolic
blood oressure:
MAP
I
* P value associated
w&h Wilks lambda
statistic
for thetime
effect.
t P value associated
with F statistic
for the drug effect.

= mean

of the 10 patients in the control group required rescue


with STP. Two of the nine patients also required intervention with esmolol.

Discussion
Acute increases in HR and arterial blood pressure can
be deleterious in the neurosurgical patient with increased ICI or with cerebral aneurysms (4). Acute
arterial hypertension can further increase ICI with a
risk for herniation, and may also result in pulmonary
edema and ruptured cerebral aneurysms (5). Therefore, prevention of acute hypertension in the neurosurgical patient due to noxious stimuli such as head
pinning would be desirable. The present study demonstrates that a skull block with 0.5% bupivacaine
attenuates hypertension and tachycardia seen during
head pinning. The most significant findings of the
present study were that a skull block can attenuate the
hemodynamic response associated with head pinning,
and that a skull block removes the requirement for
additional anesthesia or vasoactive drugs during the
period of head pinning. Therefore, this study demonstrates for the first time that addition of a skull block
to the anesthetic plan for patients undergoing craniotomy will successfully prevent the hyperdynamic response to head pinning without increasing the requirement for volatile anesthetics or antihypertensive
drugs.
The use of local anesthetics as an adjunct in the
anesthetic management of the patient presenting for
craniotomy has been previously reported. Hillman et
al. (2) reported successful hemodynamic attenuation
with 0.5% bupivacaine without vasoconstrictor. In this
study, the surgeon infiltrated the local anesthetic
along the incision line and along the proposed scalp
flap line. There was notable cardiovascular stability in
the bupivacaine group. However, the study did not
include placement of head holding pins as a time
point. Hartley et al. (13) had similar finding in a pediatric patient presenting for craniotomy. This study
again used skin infiltration by the neurosurgeon but

Control
24
17
17
9
0.3

arterial

+
+
+
+

4.9
5.1
7.2
3.8

t 0.1
pressure;

P value

Bupivacaine Time effect*


-4 + 4.8
-3 + 3.0

0.004
0.005
0.004
0.002
0.054

1 + 3.4
-5 + 2.6

0.1 2 0.04
HR

= heart

rate;

ET-Is0

= end-tidal

Drug effectt
0.0001
0.0004
0.002

0.001
0.130
isoflurane.

there was no reference to the use of head holding pins.


Rubial et al. (3) performed regional blockade of the
occipital and frontal nerves and found it to be a useful
method for maintaining hemodynamic stability during head pin placement. This study included a group
of patients that had infiltration of local anesthetic at
the pin site. There was also hemodynamic attenuation
to pin placement in this group when compared to the
baseline.
Isoflurane is a volatile anesthetic that has the potential to increase cerebral blood flow, cerebral blood
volume, and ICI (7). Despite these undesirable properties, isoflurane is a safe inhalational anesthetic for
neuroanesthesia. It caused no change in cerebral blood
flow in a study of patients receiving approximately
1.5 MAC of total inhaled anesthesia (isoflurane added
to N20) with concomitant hyperventilation
(7). This
coupled with the observed 50% reduction in cerebral
metabolic rate would suggest the safety of the use of
isoflurane for neuroanesthesia (8). However, other
studies have shown that small-dose isoflurane may
cause an increase in ICI in patients with malignant
brain tumors, despite prior, modest hyperventilation
(9). Thus, although isoflurane may be an appropriate
volatile anesthetic for neuroanesthesia, its safety cannot be assured under all conditions. Therefore, the
present study chose to limit the concentration of
isoflurane to 1 MAC for maintenance anesthesia for
patient care considerations.
STP has been used to control the hyperdynamic
effects of noxious stimuli for neurosurgical procedures. However, its use is not without deleterious
sequelae. One major disadvantage of barbiturates is
dose-dependent cardiovascular depression. Myocardial contractility is decreased owing to a lack of available calcium, and peripheral vasodilation occurs secondary to lowered sympathetic tone, both of which
will result in a reduction in blood pressure (8). In the
hemodynamically compromised or hypovolemic patient, the decrease in blood pressure can be dramatic.
Moreover, when large or repeated doses of STP are
used, zero-order kinetics are followed with a t,;,s

1260

NEUROSURGICAL
BUPIVACAINE

ANESTHESIA
SKULL
BLOCK

PINOSKY
ET AL.
FOR CRANIOTOMY

of 60 hours. Therefore, in the most extreme cases,


patients may take up to 80 hours after the STP is
discontinued
before neurologic evaluation can be performed (10). It is noteworthy
that none of the patients
who underwent
bupivacaine skull block required STP,
whereas nine of the ten patients in the control group
required additional STP during pinning. In addition, if
the skull block reduces the requirement
for maintenance isoflurane
in the bupivacaine
group, then an
earlier postoperative
neurologic
assessment
may be
possible. Additional
studies examining recovery from
anesthesia
in patients with a skull block may be
valuable.
Local anesthetics
in combination
with a vasoconstrictor have long been injected into the scalp prior to
craniotomy
to promote hemostasis
without
adverse
sequelae (10-12). A bupivacaine
solution containing
1:400,000 epinephrine
has been used in scalp infiltrations with no observed increase in MAP or HR (6). The
present study used bupivacaine 0.5% as the local anesthetic because of its long duration of action and
safety when used in the vascular tissue of the scalp
(2,131. In agreement with prior studies, we observed
no alteration in any hemodynamic
variable or adverse
effect associated with the performance
of the skull
block. A vasoconstrictor
was not included with the
bupivacaine
in the present study, as an inadvertent
intravascular
injection or systemic absorption
could
cause hypertension
(11).
The fact that no patient in the bupivacaine
group
required additional maneuvers
to control the hyperdynamic response to pinning suggests that the block
was successfully
performed.
This, coupled with the
fact that several
anesthesiologists
performed
the
block, suggests that the block is easy to learn, is reproducible, and the success rate is excellent. The skull
block places the administration
of the local anesthetic
in the hands of the anesthesiologist.
This allows better
use of personnel, in that the anesthesiologist
can attend to the anesthetic management
of the patient
while the neurosurgeon
can position and prepare the
patient for surgery. There is also an advantage over
local infiltration
in that the neurosurgeon
may have
the opportunity
to reposition
the pins without
the
requirement
for further maneuvers
to blunt the sympathetic response to pinning.
The results of this study suggest that two types of
neurosurgical
patients may benefit from the addition
of a skull block in the anesthetic plan; patients with
increased ICI and those presenting for aneurysm clipping. One of the primary
anesthetic management
goals of patients with cerebral aneurysms
is to avoid
rupture of the aneurysm
by maintaining
a stable or
low aneurysmal-to-intracranial
space transmural
pressure gradient. This is accomplished
by avoiding precipitous arterial pressure increases associated
with
noxious stimuli, such as head pinning. Thus, a skull

ANESTH
ANALG
1996;83:1256-61

block may decrease morbidity


by preventing
acute
hypertension
during certain aspects of these neurosurgical cases. Similarly, the patient with increased ICI
secondary to the presence of an intracranial tumor will
also benefit from the a skull block. The stimulation
from pinning can lead to marked increases in ICI.
Acute intraoperative
arterial hypertension
has been
associated with intracranial
hypertension
in patients
with intracranial tumors with peritumoral
edema (14).
In summary, the present study demonstrates
that a
skull block using 0.5% bupivacaine successfully
blunts
the stress response to head pinning. Moreover,
no
patient who received a bupivacaine
skull block required additional maneuvers
to control the sympathetic response to head pinning, whereas nine of the
ten patients without bupivacaine
skull block required
additional medications
to control the hyperdynamic
response. Further studies are needed to determine the
effectiveness
of this technique in other neurosurgical
procedures
such as aneurysm clipping.
The authors
gratefully
acknowledge
Frye, BS, and manuscript
preparation

statistical
by Amy

analysis
by Louise
Fesperman.

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BUPIVACAINE

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1996:83:1256-61

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of bupivacaine
epinephrine.

after injecAnesthesiol-

ANESTHESIA
SKULL
BLOCK

PINOSKY
ET AL.
FOR CRANIOTOMY

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