Management of physiological variables in neuroanaesthesia:
maintaining homeostasis during intracranial surgery
Tarja Randell and Minna Niskanen
Purpose of review
The recent literature on the perioperative maintenance of
cerebral homeostasis was reviewed.
Recent findings
Several studies focused on the regulation of cerebral blood
flow in patients without intracranial disease; therefore,
further studies in neurosurgical patients are needed. High
intracranial pressure and brain swelling can be controlled by
the choice of anaesthetic agents, and also by optimal
positioning of the patient. The use of positive end-expiratory
pressure may impair cerebral blood flow, but the effects
of positive end-expiratory pressure seem to depend on the
respiratory system compliance. The international
multicenter study failed to show any benefit from
intraoperative hypothermia in patients with subrachnoid
hemorrhage; similarly, the results on corticosteroid therapy
in head-injured patients are discouraging. Corticosteroid
therapy has prompted studies on the control of blood
glucose levels. While tight glycemic control has been
recommended, it can have untoward effects manifested as
cerebral metabolic stress.
Summary
From the clinical point of view, the recent research has
added only little to the knowledge on the management of
physiological parameters in neurosurgery. More adequately
powered studies focusing in specific problems, and having
a meaningful aim relative to outcome, are needed also in
neuroanaesthesia.
Keywords
autoregulation, blood glucose, cerebral blood flow,
hypothermia, intracranial pressure, ventilation
Curr Opin Anaesthesiol 19:492–497. ß 2006 Lippincott Williams & Wilkins.
Department of Anaesthesia and Intensive Care, Helsinki University Hospital,
Helsinki, Finland
Correspondence to Tarja Randell, Department of Anaesthesia and Intensive Care,
Helsinki University Hospital, Töölö Hospital, PO Box 266, 00029 HUS, Finland
Tel: +358 50 4270612; fax: +358 9 47187531; e-mail: [email protected]
Current Opinion in Anaesthesiology 2006, 19:492–497
Abbreviations
CBF
CPP
CVP
ICP
MAP
PEEP
SAH
ZFP
cerebral blood flow
cerebral perfusion pressure
central venous pressure
intracranial pressure
mean arterial pressure
positive end-expiratory pressure
subarachnoid hemorrhage
zero flow pressure
ß 2006 Lippincott Williams & Wilkins
0952-7907
Introduction
The most important aims of neuroanaesthesia are, first, to
provide adequate cerebral perfusion pressure (CPP) and
blood flow (CBF) to meet the tissue demands of oxygen
and glucose and, second, on the occasion of a decreased
supply, to protect the brain.
To achieve and maintain the homeostasis, it is essential to
understand not only the regulation of the CBF in a healthy
brain and during a number of pathological states, but also to
know the effects of the anaesthetic agents on it. After the
opening of the dura, the intracranial pressure (ICP) is
virtually zero, but the swelling of the brain can impair
the working conditions of the neurosurgeon. The effects of
various factors on the ICP must be considered during the
induction of anaesthesia and again after the dura is closed.
Fast emergence after craniotomy has been considered of
importance, because immediate neurological examination
is desirable to reveal such new deficiencies that may
need an intervention. The most commonly used anaesthetic regimens – propofol–remifentanil or sevoflurane–
fentanyl – seem to be equal in terms of emergence time
and the return of early cognitive function [1].
In this article, we have reviewed the recent publications
on the management of the essential physiological
parameters in neuroanaesthesia, and the effects of anesthetic agents are discussed.
CPP, CBF and autoregulation
In the healthy brain, the cerebral blood flow (CBF) is well
regulated to meet the demands for oxygen and glucose, but
the cerebrovascular autoregulation can be disturbed by
various pathological states and also by anaesthetic agents.
With intact autoregulation, the CBF remains constant
within a wide range of CPP and, with abrubt changes in
492
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Physiological variables in neuroanaesthesia Randell and Niskanen 493
the arterial pressure and consequently in the CPP,
dynamic autoregulation restores the CBF to the normal
level. Traditionally, CPP has been calculated as mean
arterial pressure (MAP) – ICP, but recent studies [2]
suggest that this formula is valid only if ICP is high and,
in subjects without increased ICP, the major determinant
of the effective downstream pressure is the vascular tone.
The formula to calculate the CPP in the latter case is
MAP – ZFP, in which ZFP (zero flow pressure) represents
the MAP at which the blood flow through the cerebral
vasculature would cease. Marval and co-workers [3]
showed in 23 healthy subjects that during propofol anaesthesia, MAP and the estimated CPP decreased while
during sevoflurane anaesthesia estimated CPP was maintained close to the baseline value. Accordingly, the ZFP
increased in the propofol group and decreased in the
sevoflurane group during normocapnia. Similarly, nitrous
oxide – a cerebrovascular vasodilator – increased the
estimated CPP and decreased the ZFP in healthy volunteers [4]. These results apply only in patients with normal
ICPs; in most neurosurgical patients, however, ICP is
increased from the normal level, or the compensatory
mechanisms to maintain normal ICP can be close to
exhaustion, with the risk of sudden increases in the ICP
with only minor changes in the intracranial blood volume.
It has been reported [5] earlier that hyperventilation can
restore impaired autoregulation in patients with various
diseases and that volatile anaesthetic agents disturb autoregulation in a dose-dependent fashion. In healthy
patients anaesthetized with isoflurane first in a dose
causing electrical silence in the EEG and the dose
reduced thereafter to 0.1–0.2% less than required for
EEG silence, autoregulation was disturbed in eight of
12 subjects during normocapnia, and in none during
hypocapnia. The authors call for further studies to
confirm the effect in neurosurgical patients. With sevoflurane, 1.0–1.2% end-tidal concentration (less than
1 MAC), cerebral autoregulation was virtually intact in
normoventilated healthy patients [6]. The results
emphasize the differences between volatile anaesthetis
and the effects of different depths of anaesthesia. In the
same setting, carbon dioxide reactivity was similar in the
middle cerebral and basilar arteries. Also, cerebrovascular
autoregulation was maintained during stellate ganglion
block that increased the estimated CPP and decreased
the ZFP. The effect was considered to be due to a
decrease in the cerebral vascular tone, similar to what
is seen with the volatile anaesthetics [7].
The changes in the regional CBF have been studied [8,9]
with PET (positron emission tomography) to elucidate
the sites of action of the anaesthetic drugs. In healthy
volunteers, neither subanaesthetic nor anaesthetic doses
of sevoflurane changed the global CBF. The most significant changes were observed in areas related to pain
processing, and with 0.7 and 2.0% end-tidal concentrations, there was a decrease in the regional CBF in
the thalamus [9]. In another study [8], comparing sevoflurane at 1, 1.5 and 2 MAC or propofol at EC50 in healthy
volunteers, a reduction of global CBF was seen in both
groups, but more so in the subjects who received propofol. On the contrary, S-ketamine increases the wholebrain CBF in excess of the metabolic needs [10]. The
changes in the CBF, and consequently in the intracranial
blood volume, need to be considered in patients with
high ICP and a risk for brain swelling during surgery.
ICP and brain swelling
Controlling the high ICP, or preventing any further
increases in the ICP, are essential during the anaesthesia
induction, to avoid even short periods of insufficient
perfusion pressure followed by a secondary injury to
the brain and to improve the working conditions for
the neurosurgeon. Also, after the opening of the dura,
attempts to prevent and reduce brain swelling are often
necessary during neurosurgery. On most occasions, the
ICP is not known when anaesthesia is induced; therefore,
it is mandatory to recognize all the factors that have an
effect on it. Cold and his coworkers [9] routinely insert a
subdural cannula through the first burr hole at the beginning of craniotomy, to measure the ICP, and the changes
in it caused by any chosen variable. In a prospective study
[11] of close to 700 patients undergoing craniotomy for
supratentorial brain tumors, the independent risk factors
of intraoperative brain swelling were subdural ICP
measured at the start of surgery, the degree of midline
shift and a histopathological diagnosis of either glioblastoma or a metastasis. At an ICP of greater than 13 mmHg,
brain swelling was highly probable.
The ICP was higher and the brain swelling was more
pronounced in the prone compared with the supine
position in children with space occupying intracranial
tumors [12]. In patients with subarachnoid hemorrhage
(SAH), reverse 108 Trendelenburg position decreased
the ICP in 25 of 28 patients, regardless of the anaesthetic
agents used (propofol with either fentanyl or remifentanil), whereas the CPP remained unchanged. Also, the
dural tension, subjectively evaluated by the neurosurgeon, decreased significantly after the positioning [13].
A cine phase-contrast magnetic resonance imaging (MRI)
study [14] in healthy volunteers suggests that the better
cerebrovascular and intracranial compliance in the sitting
position compared with the supine position can be a
result of reduced amount of intracranial blood and
cerebrospinal fluid.
The drugs used for the induction and the maintenance of
anaesthesia were not identified as independent risk factors for increases in ICP or dural tension or the occurrence
of brain swelling during craniotomy [11]. In patients with
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
494 Neuroanaesthesia
impaired autoregulation of the cerebral circulation, an
increase in the arterial pressure as a response to a painful
stimulus can be followed by an increase in the ICP,
as shown in patients undergoing a ventriculoperitoneal
shunt insertion [15]. When alfentanil as a bolus (10, 20 or
30 mgkg 1) followed by an infusion (10, 20 or 30
30 mgkg 1h 1, respectively) was added to fentanyl and
propofol anaesthesia, no changes in ICP or brain swelling
were noted in the study groups, or when compared with a
control group without alfentanil, although CPP decreased
in patients who received alfentanil [16]. The group sizes
were small; there were 31 patients included in the study,
but the results suggest that administration of alfentanil is
well tolerated in neurosurgical patients.
Smith and others [17 ] studied the effects of desflurane
and isoflurane, at age-corrected 1 MAC, and propofol on
the CBF velocity in children presenting for general
surgery. When propofol was changed to desflurane, the
middle cerebral artery flow velocity increased, but when
the volatile anaesthetics were interchanged, there were
no changes in the blood flow velocity. In adults, in doses
to produce similar depth of anaesthesia, the vasodilating
effect was significantly greater with desflurane than isoflurane [18]. These data suggest that due to the more
pronounced vasodilatory effect in the cerebral vasculature, desflurane is less suitable for neuroanaesthesia
than isoflurane.
Indomethacin is a known cerebral vasoconstrictor and the
feasibility of the drug has been recently discussed in a
review by Rasmussen [19]. Clinical and experimental
evidence exists of indomethacin’s vasoconstrictive effect
being mainly at the resistance vessels and indomethacin
does not affect normal autoregulation. The decrease in
CBF is not secondary to a reduction in cerebral glucose
metabolism. Furthermore, indomethacin is not likely to
cause cerebral ischaemia, and it may even be neuroprotective. In a study [20] of patients with supratentorial
tumors, after a bolus of indomethacin 0.2 mg kg 1, an
infusion 0.2 mg kg 1 h 1 was started before the anaesthesia induction with propofol, and terminated after the
opening of the dura. While indomethacin decreased the
CBF velocity before the induction of anaesthesia, indomethacin was not shown to decrease the ICP. These
results were explained by propofol-induced vasoconstriction, and that indomethacin did not cause any further
change in the blood vessel caliber. Furthermore, hyperventilation does not result in additional cerebrovascular
vasoconstriction and subsequent reduction in the ICP in
patients administered propofol and indomethacin.
Tissue oxygenation and oxygen supply (Hb)
Various physiological changes can affect brain oxygenation, as measured regionally by near infrared spectroscopy or globally by jugular bulb oxygen saturation.
In hip arthroplasty patients anaesthetized either by propofol or sevoflurane in oxygen and nitrous oxide, haemodilution to haemoglobin concentration of 80 g/L
resulted in a parallel reduction in the regional oxygen
saturation, but not in the jugular bulb oxygen saturation
[21]. The adequate Hb in neurosurgical patients during
craniotomy remains to be elucidated.
The decrease in MAP during anaesthesia induction with
propofol caused minimal changes in the regional oxygen
saturation in young and elderly patients, and the changes
were related to those in MAP [22].
Temperature
Thome et al. [23] reviewed the pathophysiological basis
of the neuroprotective effects of hypothermia in acute
and chronic phase of SAH. In the clinical setting, few
studies exist about its benefits in SAH patients, calling for
more prospective controlled studies.
The effect of induced hypothermia on outcome of 1001
SAH patients undergoing neurovascular surgery was studied in a large international multicenter study – IHAST
(the Intraoperative Hypothermia for Aneurysm Surgery
Trial) [24]. In the normothermia group, body temperature was kept between 36 and 378C and, in the hypothermia group, the target temperature was between 32.5 and
33.58C. Rewarming was started after the last clip had
been secured. The study could not show any benefical
effects associated with intraoperative hypothermia. At
the follow-up, 90 days after surgery, 66% of patients in
the hypothermia group and 63% of patients in the normothermia group were classified as having good outcome
(Glasgow outcome scale 1). There were no differences
between the groups with respect to postoperative adverse
events, with the exception of bacteremia, which occurred
more often in the hypothermia group. The limitations of
this study were the relatively short time for cooling, the
uncontrolled postoperative care and the ‘crude’ tool used
for outcome assessment. Until so far, there is no evidence
that induced intraoperative hypothermia improves the
outcome of SAH patients.
Ventilation strategy and cerebro–pulmonary
interactions
Patients with acute head injury or SAH often suffer from
respiratory failure caused by neurogenic pulmonary
edema and acute lung injury. This pathological process
may even result in the development of cardiogenic shock
[25]. Acute lung injury has recently been reported [26] to
occur in 27% of SAH patients and is associated with
increased hospital mortality. The treatment of respiratory
failure should be aggressive and mechanical ventilation
should be started early enough, because hypoxia and
hypercarbia may worsen the secondary brain injury.
Positive end-expiratory pressure (PEEP) ventilation is
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Physiological variables in neuroanaesthesia Randell and Niskanen 495
generally used to maintain adequate oxygenation. This
treatment may have deleterious effects on CBF and ICP
by causing hypotension and thus decreasing CPP and
resulting in a decrease in brain oxygen delivery and in
cerebral ischemia. As patients with simultaneous intracerebral and lung injury undergo surgical interventions, it
is also important to know the potential adverse effects of
anesthetic agents on vascular permeability in lung.
Muench and co-workers [27] studied the effects of various
PEEP levels on ICP, brain tissue oxygen tension, regional
CBF and haemodynamic variables. In the experimental
part, in healthy pigs, elevation of PEEP up to 25 cmH2O
did not have adverse effects in ICP, brain tissue oxygen
tension or regional CBF, although the central venous
pressure (CVP) increased. Arterial oxygenation improved
and carbon dioxide values increased. In the clinical part of
the study, elevation of PEEP up to 20 cmH2O did not
affect arterial oxygenation, carbon dioxide or cardiac index
but increased CVP in patients with SAH. Changes in ICP,
however, were only moderate. The elevation of PEEP
resulted in significant decrease of MAP and regional CBF,
indicating disturbed cerebral autoregulation. Normalization of MAP restored regional CBF. The study suggests
that maintenance of MAP is the most important factor
to ensure sufficient cerebral oxygenation. A limitation of
the study was that the study patients did not have
lung injury, and required mechanical ventilation due to
neurological deficits.
Caricato and co-workers [28] investigated the intracranial
effects of PEEP in 21 comatose patients, eight of whom
had low respiratory system compliance. In patients with
normal respiratory system compliance, incremental
PEEP increased CVP and decreased MAP and CPP
and in patients with low respiratory system compliance,
elevation of PEEP up to 12 mmHg did not influence
MAP or CPP. On average, ICP did not change in either
group. The variations in ICP were unpredictable, however, as ICP increased in 38% of all study patients. The
respiratory system compliance may be one of the main
factors affecting the transmission of PEEP to the intracranial system. Therefore, the authors recommend
measurement of respiratory system compliance to
identify patients with a risk for harmful effects of PEEP
on the intracranial system.
PEEP, however, may also affect cerebral circulation by
CO2-mediated mechanisms. Twelve patients with brain
injury and severe acute lung injury were divided into
recruiters and nonrecruiters according to the effects of
PEEP on volume–pressure curves of the respiratory
system. In recruiters, elastance of the respiratory system decreased and PaCO2, ICP, mean Vmca and
cerebral venous hemoglobin oxygen saturation (SjO2)
remained stable after application of PEEP, while in
nonrecruiters, elastance increased as did also PaCO2,
ICP, mean Vmca and SjO2. The authors concluded that
effects of PEEP on cerebral hemodynamics depend on
the recruitment of alveolar units and PaCO2 variations
[29]. Thus, it seems that the effects of PEEP on ICP in
head injury or SAH patients with concomitant lung
depend on various factors, and monitoring both cerebral
perfusion and ICP and lung mechanics in patients with
simultaneous central nervous and respiratory system
damage is advisable. As the studies so far show somewhat conflicting results, more clinical studies to clarify
this issue are needed.
The effects of anesthetic agents on vascular permeability
in lung in the presence of head injury or intracranial
hemorrhage are poorly documented. The effects of isoflurane and sevoflurane on the development of neurogenic pulmonary edema were studied in a rat model by
exposing the animals to room air, 1.5% isoflurane or 2.5%
sevoflurane. Fifty-eight per cent of rats in the control
group, 100% of those exposed to isoflurane and 5% of
those exposed to sevoflurane developed neurogenic
pulmonary edema after the injection of fibrinogen and
thrombin into the cisterna magna. In the lungs exposed
to isoflurane, immunohistochemical staining of bronchial
epithelial cells for vascular endothelial growth factor
demonstrated an increased expression. Sevoflurane
exposition lacked such harmful effects [30]. The
clinical implications of these findings remain to
be established.
Corticosteroid therapy and intraoperative
hyperglycemia
In a recent large international multicenter study –
CRASH (corticosteroid randomization after significant
head injury) [31,32] – the benefit of corticosteroid
therapy has been questioned in head injury patients.
Indeed, the risk of death from all causes within 2 weeks
was higher in the group receiving corticosteroid treatment (21.1%) than in the placebo group (17.9%) [31]. The
risk of death remained elevated also at 6 months [32].
The reasons for increased mortality in this study constituting 10 008 randomized patients, however, remained
unclear. It has been speculated, that one factor modifying
the findings of the CRASH trial may be hyperglycemia
caused by corticosteroid therapy [33].
Lukins and Manninen [34] conducted a prospective
nonrandomized study about the association of dexamethasone therapy and blood glucose levels among nondiabetic patients undergoing craniotomy. The study
showed that patients who received dexamethasone
before, during and after surgery had significantly
higher peak glucose concentrations (11.0 2.0 mmol/l)
than those receiving it during and after surgery
(8.5 1.2 mmol/l) or those who did not receive
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
496 Neuroanaesthesia
dexamethasone (7.8 2.1 mmol/l). The increase was, on
average, 5.5 mmol/L and the peak occurred 8–10 h after
the induction of anesthesia. Patients in three study
groups, however, had different underlying disease and
had undergone different types of surgery. The decision
about dexamethasone treatment was made by the surgeon. Also, the dexamethasone dosage and the duration
of therapy were variable.
Even a single dose of 10 mg dexamethasone seems to
significantly increase blood glucose concentration. In a
study [35] in 20 nondiabetic patients scheduled to
undergo craniotomy, 10 patients received 10 mg dexamethasone and 10 received placebo. Blood glucose concentrations increased over time compared with baseline
values in both groups, but the magnitude of the increase
was significantly greater in the dexamethasone group.
Patients belonging to the dexamethasone group, however, were older, and older patients are more likely to
suffer from impaired glucose tolerance. Perioperative
blood glucose concentration monitoring should continue
for at least 12 h postoperatively if intraoperative dexamethasone is used [34].
Convincing evidence that tight glycemic control has
beneficial effects in critically ill and in cardiac surgical
patients exists [36] and early hyperglycemia was associated with poor outcomes in patients with head injury [37],
and insulin treatment appeared well tolerated and feasible in SAH patients [38]. In a retrospective analysis of
data [39] from 47 traumatic brain injury (TBI) patients,
however, intensive insulin therapy was associated with
signs of cellular distress, as indicated by changes in
microdialysis markers. Whether tight glycemic control
improves outcome in patients undergoing neurosurgical
operations remains to be found out in further randomized
and controlled studies.
Conclusions
Several studies on the effects of various factors on
cerebral circulation in healthy subjects exist, but the
results are to be interpreted cautiously in the neuroanaesthesia context. The untoward increases in ICP and
intraoperative brain swelling can be controlled with careful positioning but also by pharmacological means. Two
multicenter studies showed discouraging results: intraoperative hypothermia does not benefit the SAH patients,
and the value of corticosteroid therapy in head injury
patients has been questioned.
From the clinical point of view, the recent research has
added only little to the knowledge on the management of
physiological parameters in neurosurgical patients. More
adequately powered studies focusing in specific problems, and having a meaningful aim relative to outcome,
are needed also in neuroanaesthesia.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (pp. 579–580).
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Physiological variables in neuroanaesthesia Randell and Niskanen 497
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