ANESTH ANALG
2000;91:244 –51
Dr. Karkouti’s institution, “the current transfusion rate is less than
15%” fulfill the criteria required to facilitate meaningful interpreta-
tion. In contrast, in a prospective, randomized study, Olsfanger et
al. (1), administered allogeneic blood to 100% of the control patients.
Furthermore, in a similarly designed study, Hiippala et al. (3),
administered allogeneic blood to 90% of the control patients. Thus,
it is incorrect to suggest that NVHD increases the likelihood of
allogeneic blood transfusion after TKR. Finally, these transfusion
statistics support our comment that “randomizing patients into a
treatment group that would most probably be exposed to more
allogeneic blood requirements (and blood-induced complications)
was ethically unacceptable.”
Edna Zohar, MD
Brian Fredman, MB, BCh
Martin Ellis, MB, BCh
Robert Jedeikin, MBChB, FFA(SA)
Department of Anesthesiology and Critical Care
Meir Hospital
Kfar Sava, Israel
References
1. Olsfanger D, Fredman B, Goldstein B, et al. Acute normovolaemic haemodilution
decreases postoperative allogeneic blood transfusion after total knee replacement. Br J
Anaesth 1997;79:317–21.
2. Schmied H, Schiferer A, Sessler DI, Meznik C. The effect of red-cell scavenging,
hemodilution, and active warming on allogenic blood requirements in patients under-
going hip or knee arthroplasty. Anesth Analg 1998;86:387–91.
3. Hiippala S, Strid LJ, Wennerstrand MI, et al. Tranexamic acid radically decreases blood
loss and transfusions associated with total knee replacement. Anesth Analg
1997;84:839 – 44.
4. Cushner FD, Scott WN. Evolution of blood transfusion management for a busy knee
practice. Orthopedics 1999;22(suppl):s145–7.
Rattling of Unidirectional Valves as a Sign
of Secretions
To the Editor:
Respiratory management during endotracheal anesthesia involves
the following established monitors: pulse oximetry, capnography,
tidal volume, airway pressure, and a precordial or esophageal
stethoscope. In addition to these monitors, we wish to mention a
clinical caveat regarding the unidirectional valves of a circle system.
Occasionally, we have noticed the onset of “rattling” of the unidi-
rectional valves, especially the expiratory valve. This rattling is
usually first detected in the absence of changes in airway pressure,
pulse oximetry, or tidal volume. In virtually all of these cases, we
have suctioned via the endotracheal tube and found secretions. The
rattling then typically goes away. If not, this generally indicates the
continued presence of secretions and an increased risk of associated
complications.
Michael S. Stix, MD, PhD
Carl J. Borromeo, MD
Department of Anesthesiology
Lahey Clinic
Burlington, MA
Sevoflurane for Patients with Asthma
To the Editor:
In their recent article, Habre et al. (1) found that asthmatic children
tracheally intubated during sevoflurane anesthesia administration
experienced a mean 17% increase in respiratory system resistance.
They concluded that “one should be cautious when using sevoflu-
rane for endotracheal intubation in asthmatic children.” We ques-
tion whether this conclusion is warranted because 1) there is no
control group, and 2) a 17% increase in resistance is minimal and
unlikely to be of clinical consequence.
Endotracheal intubation is a significant stimulus to airway con-
striction, especially in patients with hyperreactive airways. If Habre
LETTERS TO THE EDITOR 245
et al. had studied a control group whose tracheas had been intu-
bated after thiopental, propofol, or even halothane induction of
anesthesia, they might have found a much larger increase in resis-
tance. In a group of asthmatics tracheally intubated after propofol
induction, we found a mean increase in respiratory resistance of
300%– 400% (2). Hence, an increase of only 17% after deep sevoflu-
rane anesthesia administration leads us to conclude that sevoflurane
is most likely an excellent anesthetic for the induction of an asth-
matic patient.
We also disagree with their statement that their study is at odds
with our finding that 1.1 minimum alveolar concentration sevoflu-
rane decreases resistance after intubation (3). We studied the ability
of sevoflurane to decrease resistance after intubation under thiopen-
tal anesthesia. The study of Habre et al. examined the result of
intubation under deep sevoflurane anesthesia, but did not compare
it to any other anesthetic. Had they used a control group, they might
have found that sevoflurane was an effective anesthetic in prevent-
ing a large increase in resistance—a result that would be in line with
our findings.
Michael J. Bishop, MD
G. Alec Rooke, MD, PhD
Department of Anesthesiology
University of Washington School of Medicine
Seattle, WA 98108
References
1. Habre W, Scalfaro P, Sims C, et al. Respiratory mechanics during sevoflurane anes-
thesia in children with and without asthma. Anesth Analg 1999;89:1177– 81.
2. Wu RSC, Wu KC, Wong TKM, et al. Effects of fenoterol and ipratropium on respiratory
resistance of asthmatics after tracheal intubation. Br J Anaesth 2000;84:358 – 62.
3. Rooke GA, Choi JH, Bishop MJ. The effect of isoflurane, halothane, sevoflurane, and
thiopental/nitrous oxide on respiratory system resistance after tracheal intubation.
Anesthesiology 1997;86:1294 –9.
In Response:
We would like to point out the difficulties of including a control
group such as intubating the tracheas of asthmatic children during
thiopental administration alone as suggested. We have previously
demonstrated that sevoflurane prevented a methacholine-induced
increase in lung resistance in an animal model (1), and therefore, we
were able to proceed to the clinical investigation of sevoflurane as a
sole anesthetic for tracheal intubation in asthmatic children. Fur-
thermore, we measured total respiratory system resistance (Rrs)
during the same conditions (spontaneous ventilation and end-tidal
concentration of sevoflurane) before and after tracheal intubation,
and therefore, we can reliably compare the effect of tracheal intu-
bation on Rrs in children with and without asthma.
Rooke et al. (2) have shown that after tracheal intubation during
thiopental administration in adults without asthma, sevoflurane
decreased Rrs effectively after 10 min of exposure at 1.1 minimum
alveolar concentration. In children without asthma, tracheal intuba-
tion during sevoflurane administration did not induce an increase
in Rrs, but even a mild decrease of 4%. However, in children with
mild to moderate asthma without symptoms before the procedure,
tracheal intubation resulted in an increase in Rrs (approximately
18%), which was statistically significant but didn’t reach our defi-
nition of clinical significance as designed in the study to be 25%.
Thus, our conclusion was not to contraindicate sevoflurane in asth-
matic children, but we caution the use of the drug, especially in
children with less stable asthma in whom the increase in Rrs would
have been more intense.
W. Habre, MD
Paediatric Anaesthesia Unit
Geneva Children’s Hospital
Geneva, Switzerland
P. D. Sly, MD, FRACP
Division of Clinical Sciences
Institute for Child Health Research
Department of Paediatrics
University of Western Australia
Perth, Australia
References
1. Habre W, Wildhaber JH, Sly PD. Prevention of methacholine-induced changes in
respiratory mechanics in piglets with sevoflurane and halothane. Anesthesiology
1997;87:585–90.
246 LETTERS TO THE EDITOR
2. Rooke GA, Choi JH, Bishop MJ. The effect of isoflurane, halothane, sevoflurane, and
thiopental/nitrous oxide on respiratory system resistance after tracheal intubation.
Anesthesiology 1997;86:1294 –9.
Global Cerebral Hypoperfusion and Paco2
To the Editor:
We read with great interest Jansen et al.’s article (1), which com-
pared the effects on the jugular bulb saturation (Sjo2) of two differ-
ent kinds of anesthesia (propofol versus isoflurane/nitrous oxide),
under normoventilation and hyperventilation, in patients undergo-
ing brain tumor surgery. The authors pointed out that, within the
group of patients under normoventilation conditions who were
anesthetized with propofol, 50% of the patients presented with Sjo2
⬍50%, something which did not happen in patients who were
anesthetized with isoflurane/nitrous oxide.
In this regard, we must observe that, recently, Schaffranietz et al.
(2) published an article about patients who also underwent elective
brain tumor surgery, who were anesthetized with propofol, and in
which they tried to investigate the effect of different ventilation
regimens on Sjo2 and on other parameters of cerebral metabolism
and oxygenation. In that article, they observed that Paco2 of
31 mm Hg led to global cerebral hypoperfusion, and that the lower
limit of normoventilation should be fixed at 32 mm Hg.
Taking such a remark into consideration, we do not think that the
two groups under normoventilation in Jansen et al.’s article (1) can
be superimposed (Paco2 of 33 ⫾ 3 mm Hg in the group anesthetized
with propofol versus Paco2 of 35 ⫾ 2 mm Hg in the group anes-
thetized with isoflurane and nitrous oxide). It would be interesting
to see how many patients in the group under normoventilation and
anesthetized with propofol had Paco2 ⬍32 mm Hg, and out of
these, the number of patients who presented with low Sjo2. In
Schaffranietz et al.’s article (2), patients of all different groups were
anesthetized homogeneously, so before concluding that propofol
can lead to global cerebral hypoperfusion, and to clarify the infor-
mation given in Jansen et al.’s article (1), we should see if the Sjo2 in
patients who were anesthetized with isoflurane/nitrous oxide with
Paco2 of 31 mm Hg would remain within normal limits and more
interestingly, which Sjo2 would have patients anesthetized with
such a Paco2 and drugs without effects on cerebral blood flow.
Montserrat Olivé, MD
Montserrat Noguer, MD
Departamento de Anestesiologı́a y Reanimación
Hospital General Universitari de la Vall d’Hebron
Barcelona 08035, Spain
References
1. Jansen GFA, van Praagh BH, Kedaria MB, Odoom JA. Jugular bulb oxygen saturation
during propofol and isoflurane/nitrous oxide anesthesia in patients undergoing brain
tumor surgery. Anesth Analg 1999;89:358 – 63.
2. Schaffranietz L, Heinke W. The effect of different ventilation regimens on jugular
venous oxygen saturation in elective neurosurgical patients. Neurol Res 1998;20(Suppl
1):S66 –70.
In Response:
We appreciate Olivé and Noquer’s comments regarding our article
(1). From the data of our study, one may observe that of the three
patients in the propofol group who had Paco2 values ⬍31 mm Hg,
all had a jugular bulb saturation Sjo2 ⬍40%. Of the seven patients
with Pco2 values ⬎31 mm Hg, three had Sjo2 of 50% and lower,
whereas two of these three patients had Paco2 values of 36 and
37 mm Hg. A broad range of Paco2 values that are clinically accept-
able during neurosurgery, thus may be responsible for low Sjo2
values. The study by Schaffranietz and Heinke (2), quoted by Olivé
and Noquer, shows that patients who underwent brain tumor sur-
gery under propofol anesthesia and ventilated with oxygen in air at
Paco2 levels of ⬍31 mm Hg, had Sjo2 values ⬍50%. From these
results, the authors stated that the lower Paco2 limit from ventila-
tion should be fixed at 32 mm Hg, tacidly implicating that low Sjo2
values, indicating global cerebral hypoperfusion, would not occur at
Paco2 levels ⬎32 mm Hg. However, in Schaffranietz and Heinke’s
(2) study of 60 brain tumor patients, a certain number of patients
ANESTH ANALG
2000;91:244 –51
were excluded from further study because of primary low jugular
venous oxygen saturation of ⬍50%, probably at relative normoven-
tilation. These excluded patients might have been exactly those
patients in our study who showed Sjo2 ⬍50% at the higher Paco2
levels of 35 mm Hg and above. Of the isoflurane/nitrous oxide
group in our study, all patients had Paco2 ⬎31 mm Hg. No patients
showed Sjo2 ⬍50%. This is also confirmed by a study of Matta et al.
(3) in 12 brain tumor patients anesthesized with isoflurane (0.5%–
1.0%) in an O2-air mixture. At Paco2 values of 30 mm Hg and Pao2
values of 100 mm Hg, none of those patients had Sjo2 ⬍50%.
Thus, not only the results of our study, but also those of others,
show data that suggest that during isoflurane/nitrous oxide anes-
thesia at Paco2 values ⬎31 mm Hg, Sjo2 remains higher than 50%,
although during propofol anesthesia, a certain number of patients
consistently show Sjo2 values less than 50%. Whether these Sjo2
values under 50% will have any clinical consequences needs to be
further investigated.
Gerard F. A. Jansen, MD
Mohan B. Kedaria, PhD, MD
Joseph A. Odoom, PhD, MD
Department of Anesthesiology
Academic Medical Centre
University of Amsterdam
Amsterdam, The Netherlands
Bas H. van Praagh, MD
Ziekenhuiscentrum Apeldoorn
Apeldoorn, The Netherlands
References
1. Jansen GFA, van Praagh BH, Kedaria MB, Odoom JA. Jugular bulb oxygen saturation
during propofol and isoflurane/nitrous oxide anesthesia in patients undergoing brain
tumor surgery. Anesth Analg 1999;89:358 – 63.
2. Schaffranietz L, Heinke W. The effect of different ventilation regimes on jugular
venous oxygen saturation in elective neurosurgical patients. Neurol Res 1998;20(Suppl
1):S66 –70.
3. Matta BF, Lam AM, Mayberg TS. The influence of arterial oxygenation on cerebral
venous oxygen saturation during hyperventilation. Can J Anaesth 1994;41:1041– 6.
Is Awake Intubation Necessary When the
Laryngeal Mask Airway Is Feasible?
To the Editor:
The American Society of Anesthesiologists’ difficult airway algo-
rithm begins with preoperative evaluation of the difficult airway
and stresses awake intubation if difficulty in airway is predicted (1).
Excellent preoperative airway evaluation tests have been described
(2,3). However, as these tests cannot completely predict airway
difficulty (4), there are many patients in whom some difficulty in
airway, although not extreme, is predicted. In these patients, indi-
cation of awake intubation is controversial.
Prospective study has clarified the role of the laryngeal mask
airway (LMA) as an important means to rescue patients whose
lungs cannot be ventilated and whose trachea cannot be intubated
(5). There are a number of reports that have described the successful
use of the LMA as a ventilatory device and/or an effective conduit
for tracheal intubation in patients with strongly suspected difficult
airway (6,7). Thus, in addition to routine airway evaluation tests,
whether the LMA is correctly placed and can provide adequate
ventilation when the cannot-ventilate-cannot-intubate situation
arises should be evaluated if general anesthesia is induced in pa-
tients with possible difficult airway.
Limited mouth opening and restricted atlanto-occipital joint ex-
tension are important factors that make the LMA placement difficult
(6 – 8). The former impedes the LMA placement by varying degrees
depending on severity (6,7). With respect to the latter, we have
demonstrated that the LMA placement becomes impossible when
the angle between the oral and pharyngeal axes is less than 90° at
maximal head extension (8). A neck lateral radiograph is useful in
measuring mouth opening and the angle between the oral and
pharyngeal axes. In addition, use of the LMA is contraindicated in
patients with oropharyngeal pathology or an increased risk of as-
piration (6,7). Thus, the angle between the oral and pharyngeal axes