British Journal of Anaesthesia 85 (1): 166–79 (2000)
Correspondence
Placement of double lumen tubes—time to shed
light on an old problem
Editor—I read the editorial by Pennefather and Russell1 and
feel that a response is in order. Although Benumof may
advocate the routine use of fiberoptic bronchoscopy (FOB) for
double-lumen tube (DLT) placement, that is his personal opinion
and is certainly not the ‘standard of care in the USA’ as the
authors suggest.1 This statement has medico–legal implications
and is not substantiated by any objective data. Dr Benumof
and I have debated this topic for many years, and as a
controversy it remains unresolved.2 3
I agree with Pennefather and Russell that choice of an
appropriate size (large) DLT reduces the risk of misplacement.
Each patient’s airway dimensions can be measured directly
from their chest radiograph4 5 or CT scan6 7 and used as an
objective guide for selecting a DLT. If the dimensions of a
specific DLT are known and the size of the patient’s bronchus
is also known, then it is possible to choose the largest tube
that will safely fit that bronchus.
Why is this important? Even today, some anaesthetic textbooks
erroneously recommend advancing the DLT down the airway
until moderate resistance to further passage is encountered.8
Obviously, a smaller tube in a larger airway will be advanced
further if this end-point is used, increasing the chance of
malposition and hypoxaemia from upper lobe obstruction. For
adults (male or female), there is a highly significant correlation
between depth of insertion and height.9 For any patient who
is 170 cm tall, the average depth of placement is 29 cm. For
each 10 cm increase or decrease in height, the DLT is advanced
or withdrawn 1.0 cm.
Pennefather and Russell give impressive statistics to support
their contention that positioning problems occur frequently if a
FOB is not used.10–13 The studies they cite consider a tube to
be malpositioned if it is not in ideal position. Ideal position is
defined as when the proximal edge of the bronchial cuff is
immediately below the tracheal carina in the appropriate
bronchus. Most references do not report what size DLTs were
used, and in those that did inappropriately small tubes (which
presumably were advanced too far) were often chosen.10
A DLT can function perfectly well and still not be in ideal
position.13 What is clinically important is that the tube be in
satisfactory position.14 A DLT will be in satisfactory position
if it is in the appropriate bronchus, if selective lung collapse
and effective and safe isolation of the lungs are easily achieved,
and if hypoxaemia due to tube malposition does not occur.
DLT placement in a satisfactory position can usually be
achieved safely without a FOB. Pennefather and Russell quote
a 40% malposition rate in a study by Cohen and colleagues,12
but then fail to mention that there were no clinical sequeliae
from tubes Cohen considered to be in poor position and that
all patients with ‘malpositioned DLTs had similar oxygen
saturation compared to patients with well-positioned tubes’.12
It is probably safer for the proximal edge of the bronchial
cuff to be several millimetres deep in the bronchus since there
is less chance that the inflated cuff will herniate into the carina
during patient positioning or from surgical manipulation.
However, studies supporting the use of FOB would consider
such a tube as ‘malpositioned’.
Another study cited in the editorial compared traditional
blind with FOB-directed placement of DLTs.15 Those authors
© The Board of Management and Trustees of the British Journal of Anaesthesia 2000
reported equal success (and failure) rates with both techniques.
There was an 18% complication rate in over 200 patients, but
the occurrence of complications was not correlated with the
use of a FOB during intubation. When blind placement alone
was used the overall incidence of complications was 16 of 119
(13%) and when a FOB was used the incidence of problems
was actually higher (25 of 115, 21%).
Operator experience with any method increases the likelihood
of success. FOB is just one of several adjuncts (dual capnography,
spirometry, radiography) that have been used to position DLTs.
Certainly, these adjuncts can be helpful and every anaesthetist
who uses a DLT should be familiar with bronchoscopy for
confirmation of DLT position. However, no technique is fail-
safe. In my own practice and when teaching our anaesthesia
residents, I do not routinely use a FOB. I believe that all
anaesthetists must know how to place DLTs without an adjunct
since that equipment may not always be available. As one
gains more confidence and experience, there are fewer and
fewer instances when a FOB is needed. I agree with Conacher
and colleagues that ‘clinical testing for ...DLT position remains
a sound way of ensuring that placement is suitable for securing
good conditions for surgery.16
J. B. Brodsky
Department of Anesthesiology
Stanford University School of Medicine
Stanford, CA 94305, USA
1 Pennefather SH, Russell GN. Placement of double lumen tubes –
time to shed light on an old problem. Br J Anaesth 2000; 84: 308–10
2 Benumof JL. The position of a double-lumen tube should be
routinely determined by fiberoptic bronchoscopy. J Cardiothor Vasc
Anesth 1993; 7: 513–4
3 Brodsky JB. Fiberoptic bronchoscopy should not be a standard of
care when positioning double-lumen endobronchial tubes. J
Cardiothorac Vasc Anesth 1994; 8: 373–7
4 Hannallah MS, Benumof JL, Ruttimann UE. The relationship between
left mainstem bronchial diameter and patient size. J Cardiothorac
Vasc Anesth 1995; 9: 119–21
5 Brodsky JB, Macario A, Mark JBD. Tracheal diameter predicts
double-lumen tube size: A method for selecting left double-lumen
tubes. Anesth Analg 1996; 82: 861–4
6 Hannallah M, Benumof JL, Silverman PM, Kelly LC, Lea D. Evaluation
of an approach to choosing a left double-lumen tube size based
on chest computed tomographic scan measurement of left mainstem
bronchial diameter. J Cardiothorac Vasc Anesth 1997; 11: 168–71
7 Chow MYH, Liam BL, Thng CH, Chong BK. Predicting the size of
a double-lumen endobronchial tube using computed tomographic
scan measurements of the left main bronchus diameter. Anesth
Analg 1999; 88: 302–5
8 Cohen E. Anesthetic management of one-lung ventilation. In: E.
Cohen (ed.) ‘The Practice of Thoracic Anesthesia’. J.B. Lippincott Co.
Philadelphia, PA; 1995: p. 316
9 Brodsky JB, Benumof JL, Ehrenwerth J, Ozaki GT. Depth of
placement of left double-lumen endobronchial tubes. Anesth Analg
1991; 73: 570–2
10 Smith GB, Hirsch NP, Ehrenwerth J. Placement of double-lumen
endobronchial tubes. Correlation between clinical impressions and
bronchoscopic findings. Br J Anaesth 1986; 58: 1317–20
11 Alliaume B, Coddens J, Deloof T. Reliability of auscultation in
positioning of double-lumen endobronchial tubes. Can J Anaesth
1992; 39: 687–90
 Correspondence
12 Cohen E, Neustein SM, Goldofsky S, Camunas JL. Incidence of
malposition of polyvinylchloride and red rubber left-sided double-
lumen tubes and clinical sequelae. J Cardiothorac Vasc Anesth 1995;
9: 122–7
13 Klein U, Karzai W, Bloos F, Wohlfarth M, Gottschall R, et al. Role
of fiberoptic bronchoscopy in conjunction with the use of double-
lumen tubes for thoracic anesthesia. Anesthesiology 1998; 88: 346–50
14 Brodsky JB, Macario A, Cannon WB. ‘Blind’ placement of plastic
double-lumen tubes. Anaesth Intensive Care 1995; 23: 583–6
15 Hurford WE, Alfille PH. A quality improvement study of the
placement and complications of double-lumen endobronchial tubes.
J Cardiothorac Vasc Anesth 1993; 7: 517–20
16 Conacher ID, Herrema IH, Batchelor AM. Robertshaw double
lumen tubes: a reappraisal thirty years on. Anaesth Intensive Care
1994; 22: 179–83
Editor—Thank you for the opportunity to reply to Professor
Brodsky. We agree that there is a need to differentiate between
functionally significant and minor functionally insignificant (not
ideal) double-lumen endobronchial tube (DLEBT) malplacement.
We consider partial or complete occlusion of the trachea by
the bronchial cuff, partial or complete occlusion of a lobar
orifice (e.g. right upper lobe) and intubation of the wrong main
bronchus to be functionally significant. As emphasized in our
editorial Klein and colleagues1 did make this distinction. During
their initial fibreoptic bronchoscopy (FOB), malplacement was
detected in 107 patients (53%), in 25 patients this malplacement
was functionally significant (critical) despite normal findings on
auscultation and inspection. After positioning the patient for
surgery, a second bronchoscopy revealed critical malplacement
in 48 patients.
Significant DLEBT malplacement does not always impair gas
exchange. The finding by Cohen and colleagues2 that ‘patients
with malpositioned tubes had similar arterial oxygen saturation
to patients with well-positioned tubes’ was predictable and does
not weaken our argument, as implied by Brodsky. In eight of
the 21 patients studied by Cohen,2 the DLEBT was considered
to be malpositioned. In three patients, all undergoing a right
thoracotomy, the left DLEBT was not inserted deeply enough
and the bronchial cuff partially occluded the trachea. Impaired
gas exchange during one lung ventilation (OLV) would not
have been expected; to the contrary, further outward displacement
might improve gas exchange during ‘one’ lung ventilation but
impair lung collapse. In a further four patients, all undergoing
a left thoracotomy with a left DLEBT, the tube was inserted
too deeply and the bronchial carina could not be visualized.
Again impaired gas exchange during OLV would not have been
expected, although difficulty re-expanding the left upper lobe
after surgery could be anticipated. In the final patient, undergoing
a right thoracotomy with a left DLEBT blinding inserted too
deeply, impaired gas exchange during OLV could have been
anticipated. It occurred; the PaO2 during OLV was 82 mm Hg
whilst the patient was receiving a FiO2 of 1.0.
Brodsky states that Hurford and colleagues3 ‘compared
traditional with FOB-directed placement of DLTs’. They did
not. Hurford,3 audited the blind placement of DLEBTs in their
hospital; the choice of DLEBT used and lung to be intubated
were at the discretion of the anaesthetist as was the use of a
FOB to check the position of the DLEBT. When complications
occurred, a FOB was used to check the position of the DLEBT
and where possible ameliorate the underlying condition. To
benefit patients, correct tube placement needs to be maintained.
It is well recognized that tube displacement occurs during
positioning for surgery and as a result of surgical manipulation
167
and we emphasized the need for repeated bronchoscopies to
maintain optimal tube position.
We agree with Brodsky that every anaesthetist who uses
DLEBT should be familiar with fibreoptic bronchoscopy and
that success with most techniques, including FOB, improves
with experience. We would emphasize that for these skills to
be of practical benefit to patients, the equipment for fibreoptic
intubation not only has to be immediately available but also used.
We agree that blind placement of DLEBTs is a useful skill
to acquire and we teach our specialist registrars how to place
a variety of DLEBTs blindly. However, we require our registrars
to check and recheck the position of blindly placed DLEBTs
with a FOB; this assists in learning to blindly place DLEBTs.
Most registrars need no further convincing that a FOB should
be used in all patients.
Brodsky might argue that the use of a FOB during DLEBT
use is not a ‘standard of care’ in the USA, but he cannot, in
our opinion, reasonably argue that the case for the routine use
of a FOB is not supported by objective data. Numerous studies
have shown it is not possible to optimally place DLEBTs in
all patients without a fibreoptic bronchoscope. The section of
the recent national confidential enquiry into perioperative
deaths4 detailing the management of patients undergoing
oesophagogastrectomy provides a salutary illustration of the
potential consequences of failure to accurately place DLEBTs.
S. H. Pennefather
G. N. Russell
1 Klein U, Karzai W, Bloos F, Wohlfarth M, Gottschall R, Fritz H,
Gugel M, Seifert A. Role of fiberoptic bronchoscopy in conjunction
with the use of double-lumen tubes for thoracic anesthesia: a
prospective study. Anesthesiology 1998; 88: 346–50
2 Cohen E, Neustein SM, Goldofsky S, Camunas JL. Incidence of
malposition of polyvinylchloride and red rubber left-sided double-
lumen tubes and clinical sequelae. J Cardiothorac Vasc Anesth 1995;
9: 122–7
3 Hurford WE, Alfille PH. A quality improvement study of the
placement and complications of Double-lumen endobronchial tubes.
J Cardiothorac Vasc Anesth 1993; 7: 517–20
4 Sherry K. Management of patients undergoing oesophagectomy. In:
Gray AJG, Hoile RW, Ingram GS, Sherry KM, eds. The Report of
the National Confidential Enquiry into Perioperative Deaths 1996/1997.
London: The National Confidential Enquiry into Perioperative
Deaths, 1998; 57–61
The Haldane effect—an explanation for increasing
gastric mucosal PCO2 gradients?
Editor—We read with interest the article by Jakob and colleagues
demonstrating the possible influence of the Haldane effect on
gastric mucosal PCO2 gradients and feel that they have
highlighted an important point.1 They demonstrated that in nine
of 14 patients post cardiac surgery who had an increasing
mucosal–arterial PCO2 gradient despite an increase in total
splanchnic blood flow, that this could be attributed to the
decreased binding of carbon dioxide (CO2) to haemoglobin that
would accompany decreased splanchnic oxygen extraction.
We believe, however, that this does not negate the use of
gastric tonometry as a tool for monitoring gastric mucosal
PCO2. Figure 1 demonstrates the relationship between CO2
concentration and partial pressure as first described by
Christiansen–Douglas–Haldane in 1914.2 From this graph, it
may be seen that it requires extreme differences in haemoglobin
 Correspondence
saturation to produce clinically significant changes in PCO2
(Fig. 1).
Fig 1 The CO2 binding curves of oxyhaemoglobin (HbO2)at 100%
saturation and deoxyhaemoglobin (Hb) at 0% saturation as modified from
Christiansen–Douglas–Haldane by Mertzlufft and colleagues.5
We should also like to comment on the effect of temperature
on PCO2 measurements. The authors do not comment on the
significant rise in core temperature seen in both patient groups
during the study. It is known that temperature has an effect on
carbon dioxide production, solubility and diffusion both through
tissues and through the tonometer balloon, with production and
diffusion decreasing and solubility increasing with decreasing
temperature. Croughwell and colleagues demonstrated the effects
of warm (35.5°C) and cold (30.0°C) cardiopulmonary bypass
on the gastric mucosal PCO2 (PgCO2). PgCO2 was significantly
higher with the higher temperature 4.8 kPa vs 5.5 kPa
(P⬍0.05).2 3 In this study by Jakob and colleagues the local
gastric mucosal temperature is not known in the two groups
which, given the thermogenic properties of dobutamine via its
β1-adrenoceptor activity,4 may also contribute to the observed
mucosal–arterial PCO2 gradient.
R. Hurley
M. G. Mythen
Centre of Anaesthesia
University College London Hospitals
London, UK
1 Jakob SM, Kosonen E, Ruokonen I, Parviainen I, Takala J. The
Haldane Effect—an alternative explanation for increasing gastric
mucosal PCO2 gradients? Br J Anaesth 1999; 83: 740–6
2 Christiansen J, Douglas CG, Haldane JS. The absorption and
dissociation of carbon dioxide by human blood. J Physiol 1914; 48: 244
3 Croughwell ND, Newman MF, Lowry E, et al. Effect of temperature
during cardiopulmonary bypass on gastric mucosal perfusion. Br J
Anaesth 1997; 78: 34–8
4 Schiffelers SL, van Harmelen VJ, de Grauw HA, Saris WH, van
Baak MA. Dobutamine as selective beta(1)-adrenoceptor agonist in
in vivo studies on human thermogenesis and lipid utilization. J Appl
Physiol 1999; 87: 977–81
5 Mertzlufft FO, Brandt L, Stanton-Hicks M, Dicks W. Arterial and
mixed venous blood gas status during apnoea of intubation—proof
of the Christiansen–Douglas–Haldane effect in vivo. Anaesth Intensive
Care 1989; 17: 325–31
Editor—We read with interest the comments from Drs Hurley
and Mythen concerning our article. These authors point out
that only extreme changes in oxygen saturation will have a
clinically significant effect on the partial carbon dioxide pressure.
To demonstrate this they present the CO2 binding curves
168
of oxy- and deoxy-haemoglobin as originally published by
Christiansen–Douglas–Haldane.1
We showed that favourable changes in mucosal perfusion
(reduction of PCO2 gradient in response to increased mucosal
blood flow) may be missed because of the Haldane effect.2 In
contrast to Drs Hurley and Mythen, we did not discuss
stationary conditions in a vascular bed, but we presented data
about changes in veno–arterial and (hypothetical) mucosal–
arterial CO2 content differences. Veno–arterial CO2 content
differences are typically in the range of 10–70 ml litre–1 (Figs
3 and 4 in our publication2), whereas the CO2 content axis in
the graph that Hurley and Mythen present has a range from 0
to 900 ml litre–1. Significant changes in veno–arterial or
mucosal–arterial CO2 content differences are therefore associated
with only small changes in PCO2 gradients (Fig 4 in our
publication2). It is important to realize that, although the amount
of carbon dioxide carried in the blood by carbamino (attached
to haemoglobin) is small, the difference between the amount
carried in venous and arterial blood as carbamino compounds
is about a third of the total arterio–venous difference.3 This
accounts for the major part of the Haldane effect.
We presented the Haldane effect under different metabolic
conditions and with changes in haemoglobin and pH (Fig 5 in our
publication2). From this figure, it is evident what different effects
the same increase in blood flow may induce in the veno–arterial
(or mucosal–arterial) PCO2 gradient. Depending on the baseline
venous (or mucosal) oxygen saturation, the Haldane effect may
cause a decrease or an increase in the respective PCO2 gradient in
response to the same changes in blood flow and metabolism (Fig
5c in 2). This clearly shows that changes in oxygen extraction
have to be taken into account for the interpretation of tonometry
derived variables.
The authors also comment on the effect of temperature on PCO2
measurements. It is true that there was a small increase in blood
temperature in both study groups (0.7–0.8°C). We also reported
that the splanchnic CO2 production increased during rewarming.
The effect of temperature is of importance in the interpretation of
tonometry if it affects the relationship between the CO2 content
and the PCO2. This seems not to be the case (see below). If, as
the authors propose, changes in temperature in the range of 1°C
have significant effects on the solubility and diffusion of CO2
through tissues and the tonometer balloon, tonometry should not
be used in patients with changing body temperature due to, for
instance, sepsis. We do not believe that this is the case. Although
we do not have data on the effect of changes in temperature of
less than 1°C on the diffusion of CO2 through the tonometer
balloon, the effect of such temperature change on the solubility
of CO2 at near normal body temperature is minor.3 But if the
changes in gastric mucosal PCO2 in the reference the authors
quote4 would be explained completely by changes in temperature,
the bias in our study would be less than 0.09 kPa.
We would also like to reply to the comments from Drs De
Backer, Creteur and Vincent. As the authors correctly point out,
the splanchnic oxygen extraction decreased and the hepatic vein
oxygen saturation increased in the patients with increasing gastric
mucosal–arterial PCO2 gradients. The authors were also concerned
about the effect of temperature on the CO2 content. We believe
that it is reasonable to assume that the changes in gastric wall
temperature in these patients were comparable to the changes in
blood temperature (around 0.8°C). Mainly because dissolved CO2
content is dependent on temperature and because this content is
small (1.2–1.4 mmol litre–1 under physiological conditions3), we
find it hard to accept that an increase in temperature of less than
1°C should have a major impact on the results of our study. A
simple calculation should underline this: according to textbooks,
the arterial CO2 content in 1 litre of blood is 480 ml (21.5 mmol)
and the venous CO2 content is 520 ml (23.3 mmol)3, resulting in
 Correspondence
a veno–arterial CO2 content difference of 40 ml litre–1
(1.8 mmol litre–1). The veno–arterial difference of physically
solved CO2 is 0.17 mmol litre–1 or roughly 10% of the total CO2
content difference.3 The solubility coefficient of carbon dioxide
in plasma is 0.231 mmol litre–1 kPa at 37°C and 0.226 mmol litre–1
kPa at 38°C.3 Accordingly, the effect of increasing the blood
temperature by 1°C on the veno–arterial difference of physically
solved CO2 is in the range of 2% and on the total CO2 content
difference in the range of 0.2%, hence negligible.
Drs De Backer, Creteur and Vincent suggest that some of the
changes, since being within the error of the method, could have
occurred by chance. We can of course not fully exclude this, but
it is very unlikely, since for each patient the same analyser
was always used and because we have demonstrated the same
phenomenon with dopexamine in similar patients, using only the
ABL blood gas analyser.5
Accordingly, we still believe that increases in PCO2 gradient in
response to increased splanchnic blood flow do occur, and the
Haldane effect is a plausible explanation. Even in the very unlikely
situation that the observed changes in PCO2 gradient2 5 would not
be true but due to chance and methodological factors, this would
not change the main message of our paper. That is, a mean
increase in mucosal perfusion of almost 50% (which is certainly
not in the range of one error) does not result in a decrease of
gastric mucosal PCO2 gradients in more than half of the patients
studied, if similar changes in splanchnic and mucosal oxygen
consumption and CO2 production occurs. Hence, despite the
arguments of Drs De Backer, Creteur and Vincent, we are still
convinced that we have emphasized that the Haldane effect may
be involved in the dissociation between mucosal–arterial PCO2
gradients and total splanchnic blood flow.
S. M. Jakob
J. Takala
Kuopio
Finland
1 Christiansen J, Douglas CG, Haldane JS. The absorption and
dissociation of carbon dioxide by human blood. J Physiol 1914; 48: 244
2 Jakob SM, Kosonen E, Ruokonen IE, Parviainen I, Takala J. The Haldane
Effect—an alternative explanation for increasing gastric mucosal PCO2
gradients? Br J Anaesth 1999; 83: 740–6
3 Nunn JF. Nunn’s Applied Respiratory Physiology, 4th edn. Butterworth-
Heinemann, Oxford; 1993: pp. 219–46
4 Croughwell ND, Newman MF, Lowry E, et al. Effect of temperature
during cardiopulmonary bypass on gastric mucosal perfusion. Br J
Anaesth 1997; 78: 34–8
5 Uusaro A, Ruokonen E, Takala J. Gastric mucosal pH does not reflect
change in splanchnic blood flow after cardiac surgery. Br J Anaesth
1995; 74: 149–54
Editor—Jakob and colleagues suggest that the Haldane effect may
explain a paradoxical increase in gastric mucosal PCO2 (PgCO2)
secondary to an increase in mucosal blood flow. This hypothesis
is attractive, but certainly difficult to prove in critically ill patients
since it would require simultaneous measurements of gastric
mucosal blood flow, O2 saturation and PCO2. To overcome this
limitation, the authors postulated that changes in splanchnic blood
flow would reflect changes in mucosal blood flow and that changes
in hepatic vein O2 saturation (ShvO2) would reflect changes in
mucosal O2 saturation. They reported that patients with in increased
gradient between PgCO2 and PaCO2 (PCO2 gap) had a greater
increase in ShvO2, so that the Haldane effect was likely to apply.
They also reported that the hepatic venous–arterial PCO2 gradient
increased in some patients while the CO2 content differences
remained unchanged.
169
We have several concerns and comments. First, we presume that
there was an inversion between baseline and second measurement
values of splanchnic O2 saturation, since changes in oxygen
extraction and saturation should go in opposite directions. Second,
the patients in both groups experienced major changes in
temperature and temperature was not included in the simplified
formulas used to calculate CO2 contents. Third, the measurements
may be limited by technological limitations. PgCO2 was measured
using two different blood gas analysers, with one analyser
underestimating saline PCO2, so that measurements obtained with
this instrument were corrected by a correction factor calculated
from a regression analysis. However, a good correlation between
two methods does not imply a good agreement between the two
methods.2 A Bland and Altman2 analysis should have been
performed in order to check if measurements obtained by the two
methods could be interchanged before using a correction factor
for the bias. Finally, changes in PgCO2 gap were within the range
of error in the measurements. The error in PgCO2 measurements
are around 0.13 kPa. Creteur and colleagues3 recently determined
in vitro that the precision (one standard deviation) of saline
tonometry is 0.26 kPa for an equilibration time of 30–60 min.
Hence the error in PgCO2 should be around 0.52 (two standard
deviations) and the error in PCO2 gap 0.7 kPa. The changes in
PCO2 gap here were of 0.4 kPa in group 1 and 0.6 kPa in group
2. The changes in hepatic venous PCO2 gradients in patients
increasing their gradients were within the range of error of these
measurements (error ⫾0.3 kPa, changes between 0.1 and 0.3
approximately, as reported in Figure 4). Hence, the conclusions
drawn from these data that the Haldane effect may be involved
in the increase in PgCO2 observed in some patients are weak.
D. De Backer
J. Creteur
J-L Vincent
Department of Intensive Care
Erasme University Hospital
Brussels, Belgium
1 Jakob SM, Kosonen EP, Ruokonen IE, Parviainen I, Takala J. The Haldane
effect—an alternative explanation for increasing gastric mucosal PCO2
gradients? Br J Anaesth 1999; 83: 740–6
2 Bland JM, Altman DG. Statistical methods for assessing agreement
between two methods of clinical measurement. Lancet 1986; i: 307–10
3 Creteur J, De Backer D, Vincent JL. Monitoring gastric mucosal carbon
dioxide pressure using gas tonometry: in vitro and in vivo validation
studies. Anesthesiology 1997; 87: 504–10
Surgery for fractured femur and elective ICU
admission at 113 yr of age
Editor—Your case report, on Surgery for fractured femur and
elective ICU admission at 113 yr of age,1 with its accompanying
editorial,2 cannot go unremarked.
The audit reported in the editorial shows that, for their case-
mix, it was possible to reduce mortality to 1.5% for fractured
neck of femur. The case illustrates how it might be done. The nub
of the argument both present is that because such results can be
achieved, they ought to be. We thus appear to have reached the
position that all patients, whatever their age or pre-morbidity,
must be offered every available therapy, including high dependency
or intensive care, if they are to be offered surgery. This is odd,
and feels so wrong, that it needs further analysis.
First, what feels wrong about it? You have only to look to the
case report for the answer. How can be justify aggressive critical
care in a wheelchair bound, confused 113 yr old, when the best
 Correspondence
possible outcome is discharge, still confused, still wheelchair
bound? I cannot see any argument for critical care in this patient.
There are of course some very fit patients of great age who want
and merit every effort, but many elderly patients who are fully
compos mentis are actually just waiting to die, and would refuse
intensive care. Is it reasonable to offer intensive care to someone
whose best mental state is confused? When a patient is no longer
mentally competent, we are required to act in their best interests,
but this does not mean automatically prolonging life. ‘To presume
that the incompetent person must always be subjected to what
many rational and intelligent persons may decline is to downgrade
the status of the incompetent person by placing a lesser value on
his intrinsic human worth and vitality’.3 It is clear from Bland3
that we are not required to offer every available treatment when
‘acting in the patient’s best interests’. If you state that surgery
cannot be considered unless we offer full supporting care
postoperatively, then you insist on prolonging life whatever the
circumstances. That must be wrong.
The mistake is, I think, to consider all operations equal, and to
categorize them all as intended to cure. From this derives the idea
that we should not offer surgery unless we offer the back up
critical care to give the surgery a change of ‘success’. But the
assumption that we are always trying to cure the patient is wrong.
We are not. We often undertake operations where we know that
there is no chance of cure, for instance, passing an obstruction in
inoperable cancer, fixing pathological fractures, etc. We
anaesthetise for these procedures even though there is no chance
of cure; we do not offer critical care, and we regularly leave
instructions not to resuscitate. No one would criticize this.
Much surgery for fractures in the elderly is palliative. We
operate to relieve acute pain, and to allow pain-free nursing care,
care to pressure areas, use of bedpans, etc. Without the surgery,
these procedures are painful. When the fracture is fixed, they are
tolerable. We do not expect all the patients to recover, but we still
operate on them to make their last days more tolerable.
It will be argued that it is wrong to think of operations as
palliative when the patient does not have malignant disease. I
would respond that many have a potential 5-yr survival which is
less than those with malignant disease: very old patients do not
live very long, even if ‘cured’ by the operation. Further, it may
help to view the fall and fracture as the first events in the process
of dying.
How do we decide which patients’ operations are palliative,
and which curative? Sometimes the answer is obvious, in either
a very fit or a very unfit patient. Sometimes the answer is unclear,
there is some prospect of survival, though it is not high. There, I
suggest, lies the reason for operating with the patient in the best
condition possible (‘optimized’), but not offering critical care:
those for whom the operation is palliative will select themselves,
the others will survive.
I would agree with Sharrock’s contention that anaesthesia and
surgery by junior staff followed by return to the ward may be
suboptimal, and believe consultant input may be essential. I would
also agree that in some circumstances it may be inappropriate to
‘optimize’ before surgery, but not because, as he suggests, the
medical condition will not improve until the fracture is fixed (it
can often be improved, in practice), rather because when we know
in advance that an operation is palliative, it may be inappropriate
to optimize, as the target is not cure. I would also support
NCEPOD’s recommendations4 that ‘If a decision is made to
operate on an elderly patient then that must include a decision to
provide appropriate postoperative care, which may include high
dependency or intensive care support’, with the emphasis I have
added: the recommendations should not be taken to mean ‘critical
care for all’, but better and closer attention to basic care, such as
fluid balance management, in appropriate cases by appropriately
trained doctors.
170
C. P. H. Heneghan
Nevin Hall Hospital
Abergaveny, UK
1 Oliver CD, White SA, Platt MW. Surgery for fractured femur and
elective ICU admission at 113 yr of age. Br J Anaesth 2000; 84: 260–2
2 Sharrock NE. Fractured femur in the elderly. Intensive perioperative
care is warranted. Br J Anaesth 2000; 84: 139–40
3 Quoted with approval by Lord Goff of Chieveley in Airedale NHS Trust
v Bland (1993). Med Law Rep 1993; 4: 39–75
4 NCEPOD (Extremes of Age. NCEPOD 1999)
Editor—I welcome Dr Heneghan’s comments on this complex
issue. To fully reply would involve a discussion of medical ethics,
which is not my area of special interest. Nevertheless, I shall
comment on three aspects.
First, is repair of a fractured neck of femur a palliative operation?
Probably not in most cases, but if there is any doubt, I believe it
is better to consider it a curative or corrective procedure.
Secondly, should patients with confusion be treated differently?
I would prefer to treat them carefully as inadequate management
may add to the confusion state.
Finally, the quotes from NCEPOD appear to agree with the
approach I have suggested—namely, optimize intraoperative and
perioperative care. Many may benefit from a ‘Step Down’ or high
acuity care unit for several days and some will need intensive
care. My recommendation is, why not treat these patients properly
if it is helpful?
N. E. Sharrock
New York, USA
Editor—Death, it has often been said, is the old man’s friend.
Perhaps it would have best been this unfortunate lady’s friend as
well.1 Certainly in my discussions with elderly patients with life-
threatening conditions they fear more being left confused and
dependent in a home than death itself. Reaching your 114th
birthday if you cannot even tell what day it is, hardly gives cause
for celebration! I am sure few will be surprised by Dr Oliver and
colleagues’ ability to safely administer general anaesthesia to this
lady and I am unsure why this case report was accepted for
publication. I have significant reservations about the advisability
of intensive care admission and 31 days hospitalization for a
confused old lady at the end of her life, and am concerned about
the message the report may convey. Surely the issues here are
analgesia and comfort care, and dignity in death? In my opinion,
early fixation of hip fracture is almost always indicated, even in
the most demented patient, to aid provision of adequate analgesia
and nursing care. Good surgical technique and careful anaesthesia
will return the vast majority of patients to the general ward in
good condition; I agree with Dr Sharrock that these cases should
not be left to the most junior member of the anaesthetic team.2
Failure to tolerate surgery and anaesthesia, or the onset of
complications in the postoperative period, should be considered
very poor prognostic signs. The physician has special responsibility
to his patients not to officiously preserve life at all costs, and to
preserve their dignity now and in the future. The intensive care
unit has little to offer in these situations.
M. J. O’Leary
New South Wales
Australia
1 Oliver CD, White SA, Platt MW. Surgery for fractured femur and
elective ICU admission at 113 yr of age. Br J Anaesth 2000; 84: 260–2
 Correspondence
2 Sharrock NE. Fractured femur in the elderly. Intensive perioperative
care is warranted. Br J Anaesth 2000; 84: 139–40
Editor—We are grateful to those who commented about our article,
as this in itself justifies its publication. The whole purpose of the
report was to stimulate debate around the issues it raised and this
case was one vehicle to do this—a flag waving celebration of
anaesthetizing the ‘oldest old’ it was not. We fully acknowledge
that ICU admission for this lady would have been far from
appropriate given her condition on arrival in hospital. The decision
should have been made at that point for limited intervention and
‘death may well have proved to be a friend’. Unfortunately, many
decisions are made by trainee staff, outside of standard working
hours, which have major implications.
The problem and central issue is that the anaesthetists and
intensivists were not party to the original treatment decision. The
admitting team acknowledged the unsuitability for surgery, but
then proceeded to fully resuscitate the patient. The situation was
then patently different, as this lady was in pain with an unstable
fracture, with perhaps months to live. We decided to proceed to
surgery, being unable to find any other acceptable treatment option.
It was not a sudden or easy decision and even our critics are
unable to offer any better option than to commit to surgery or to
do nothing.
The next issue is the method and limits of intervention. We
agree with the comment that ‘Good surgical technique and careful
anaesthesia will return the vast majority of patients to the general
ward in good condition’, but which clinician can identify this
‘vast majority’ without error? To improve the chances of optimizing
a treatment plan for any patient we must by-pass this outdated
concept of anaesthesia and ICU being separate entities. Admission
to ICU should not be viewed as crossing a great medical chasm;
but as a continuing of treatment via operating theatres, ICU and
HDU and optimization of patients before theatre is surely the way
forward. ICU is an extension of quality anaesthetic care, or at
least it should be.
This concept should not be translated as ‘to officiously preserve
life at all costs’, but to define treatment limitation before precipitous
events force sudden moral judgements. If this patient had suffered
a cardiac arrest at any time, then like Dr Heneghen we consider
intervention to be inappropriate. However, if this patient had
suffered postoperative respiratory failure in the recovery room,
then what is the appropriate step? Extubation and death from acute
dyspnoea in a recovery environment we believe is unacceptable for
the patient, the relatives and the recovery staff and certainly does
not ‘preserve dignity’. Unplanned, emergency admission to ICU
for a pre-terminal event is likewise inappropriate.
The plan for this patient was to undergo a defined ‘period and
level of treatment’. There was agreement that there would be no
supportive measures if multi-organ failure ensued, no prolonged
ventilation and no re-admission to ICU from the general ward. If
critical deterioration did occur, then perhaps death with some
dignity could have been achieved in a controlled environment.
We do not and never will advocate ‘critical care for all’, but
believe that every case needs judgement on its individual merits
and fully support the NCEPOD recommendations in principle, but
the words ‘appropriate’ and ‘may’ do little to assist a consensus
viewpoint. Dr Heneghan also highlights the other side of the
debate. We often do anaesthetise patients who have no chance of
‘cure’ and we acknowledge that our patient overlaps into this
category. We do regularly anaesthetise for ‘palliative procedures’,
but surely not so, if we believe that they will not survive the
intra-operative period? If this is the case, then the expertise of
our palliative care physicians is either unavailable or under-utilized.
In summary, this report was designed to highlight the
implications of early decision making as soon as a patient enters
hospital and its sequelae. The treatment instigated may not be
171
everyone’s ideal, but was constructed after discussion with
relatives, nursing staff, orthopaedic surgeons, anaesthetists and
intensivists. A treatment plan was used, which was aimed at
optimizing the ‘palliative procedure’ and avoiding spur-of-the-
moment moral decisions. Limited ICU resource was incorporated
to achieve this result and paradoxically to reverse the problems
that in this case were caused by ‘attention to basic care, such as
fluid balance management’. At no time would we recommend the
preservation of life at any cost, but consider that if a job is worth
doing at all it is worth doing well.
C. D. Oliver
S. A. White
London
Increasing isoflurane concentration may cause
paradoxical increases in the EEG bispectral index
in surgical patients
Editor—We read with interest the article by Detsch and colleagues,
in which they demonstrated an increase in BIS in 39% of
patients subjected to an increase in isoflurane concentrations
during abdominal surgery.1
On closer examination of this study, it is evident that some of
these patients were ASA III, and the eldest was 70 yr old.
Inevitably, subjecting such a group of potentially physiologically
sensitive patients to double the concentration of volatile agent
necessary to maintain adequate anaesthesia, led to the frequent
requirement for a norepinephrine infusion to maintain blood
pressure.
The authors postulate that the increase in BIS is entirely
paradoxical and that the patients’ depth of anaesthesia did not
lighten. The two examples the authors gave of the raw EEG traces
tend to support this, although it would be necessary to see all the
EEG traces to confirm it. If this is so, it must be hypothesized
that intermittent EEG phenomena occurred that ‘tricked’ the BIS
into a higher number. For this to occur there must be some
increased spectral (or bispectral) power in the higher frequency
bands (⬎30 Hz for the BetaRatio, and ⬎40 Hz for the
SynchFastSlow).2 Irregular sudden step-changes in the EEG signal
could possibly have this effect on the power spectrum. The authors
comment briefly on increased alpha and beta activity and its
observed frequency and yet give no data on the difference in raw
EEG recordings between groups.
The alternative explanation is that the depth of anaesthesia
actually did lighten. The BIS increase group not only had more
patients requiring norepinephrine, but also showed a clear trend
to requiring higher infusion rates. Although this difference did
not reach significance at the P⬍0.05 level, it did at the P⬍0.1
level (using a t-test). An arousal phenomenon with inotropes has
been shown to occur during propofol infusions.3 This could be
either due to a direct analeptic effect by the inotrope, or a
pharmacokinetic effect—an increased cardiac output causing a
decrease in effective brain levels of this anaesthetic agent. Thus,
the authors’ statement, that a direct interaction between the
norepinephrine infusion and BIS is unlikely, is unfounded and it
may in fact be an important contributing factor.
The authors gave no information as to whether or not any
patients (in all three groups) actually required norepinephrine
before the increase in isoflurane concentration. For example,
it could be that the entire BIS decrease group actually had
norepinephrine prior to increasing isoflurane concentration and
none of the BIS increase group did. This information should have
been given clearly.
Finally, the authors question the validity of using BIS as a
 Correspondence
monitor of depth of anaesthesia during isoflurane anaesthesia. We
should not lose sight of the fact that BIS is only helpful as a
monitor when regarded as a single piece of the jigsaw that makes
up the picture of the anaesthetized patient. If BIS merely changes
from ‘very deep’ to ‘deep’ at these exaggerated doses of isoflurane
then it may still be regarded as a useful tool in monitoring for
awareness.
J. Andrzejowski
Sheffield, UK
J. Sleigh
Hamilton, New Zealand
1 Detsch O, Schneider G, Kochs E, Hapfelmeier G, Werner C. Increasing
isoflurane concentration may cause paradoxical increases in the EEG
bispectral index in surgical patients. Br J Anaesth 2000; 84: 33–7
2 Rampil IJ. A primer for EEG signal processing in anesthesia.
Anesthesiology 1998; 89: 980–1002
3 Andrzejowski J, Sleigh JW, Johnson I, Sikiotis L. Epinephrine has a
stimulatory effect on the bispectral index and sedation. Br J Anaesth
1999; 82: 95–6
Editor—We appreciate the comments with respect to our study1
and share several of the considerations raised. As well as the points
discussed in the original manuscript, here are some additional
comments on the criticisms raised in this letter. Our study was
prompted by the clinical observation of increases in the bispectral
index (BIS) when end-tidal isoflurane concentration was increased
during abdominal surgery in ASA physical status III as well as
elderly patients. Considering these observations as a ‘generation
of hypothesis’, the purpose of our study was to systematically
investigate BIS responses to an increased concentration of a
volatile anaesthetic rather than to investigate the mechanisms
underlying variable BIS responses. Since the computation of BIS
is based on a proprietary algorithm which has not yet been made
public in full detail, any discussion of possible contributions of
BIS sub-parameters (e.g. ‘BetaRatio’ or ‘SynchFastSlow’) to the
‘paradoxical’ BIS responses remains speculative.
In the letter it is postulated that an infusion of norepinephrine
to support systemic haemodynamics during 1.6% isoflurane may
have caused a ‘direct analeptic effect’ and thus, induced a decrease
in the patients’ anaesthetic depth. This assumption is based on a
preliminary study (n⫽8) with propofol sedation where a bolus dose
of epinephrine caused a BIS increase and an arousal phenomenon in
six patients.2 In contrast, we investigated deeply anaesthetized
patients (1.6% end-tidal isoflurane) with a continuous infusion of
norepinephrine in some patients (rather than boluses of
epinephrine). An analeptic effect of epinephrine during sedation
cannot be excluded by our study. Epinephrine may cross the blood–
brain barrier resulting in an activation of cerebral metabolism.3
Norepinephrine, in contrast, seems not to cross the intact blood–
brain barrier and thus increases in cerebral metabolism occur only
in the presence of a defective blood-brain barrier.4–6 We therefore
believe that it is very unlikely that norepinephrine can ‘antagonize’
the effects of 1.6% isoflurane.
The most compelling argument against a major contribution of
norepinephrine to the paradoxical BIS responses is that 59% of
patients in the ‘BIS increase group’ and 70% of patients in the
‘BIS constant group’ did not receive norepinephrine, whereas 25%
of patients in the ‘BIS decrease group’ received norepinephrine.
Likewise, we consider it unlikely that differential BIS responses
were caused by norepinephrine-induced changes in the
pharmacokinetics of isoflurane since we studied patients with and
without norepinephrine in all groups as previously mentioned.
The suggested effect of norepinephrine on isoflurane
pharmacokinetics by an increase in cardiac output may play a role
172
with anaesthetics that are delivered at a constant infusion rate
(e.g. propofol). However, in our study the end-tidal concentration
of isoflurane was maintained constant by adjusting the inspired
isoflurane concentration. Thus, the discussion on the effects of
changes in cardiac output on brain electrical function is purely
speculative. We consider it unlikely that interactions between
norepinephrine (via ‘analeptic effects’ or via changes in isoflurane’s
pharmacokinetics) and BIS responses occur. The information that
no patient received norepinephrine during baseline or during
recovery is presented on page 35.1
According to information provided by the developer of the BIS
technology (Aspect Medical Systems Inc.), a BIS range from 40–
60 represents ‘moderate hypnotic effects’ and a BIS range between
60–70 reflects ‘light hypnotic effects’ (see www.aspectms.com
clinical user guide). The examples given in Figures 1 and 2A1
show that in these two patients the BIS increased from 39 to 62
and from 44 to 66, respectively, during the increase in end-tidal
isoflurane to 1.6%. These BIS changes would therefore relate to
a change in anaesthetic depth from ‘moderate’ to ‘light’ rather
than ‘very deep’ to ‘deep’ as suggested in this letter. Finally, we
still question the sensitivity and specificity of BIS as a monitor
of the hypnotic component of anaesthesia. It has been shown that
auditory processing and memory formation is still present at BIS
levels between 60 and 40.7 In our study, BIS at baseline shows a
hypnotic level that is just below this range and not – as stated in
the letter – very deep. Even if BIS is used just as a single piece
of the jigsaw of the anaesthetised patient’s picture, this piece
might obscure the picture.
O. Detsch
G. Schneider
E. Kochs
G. Hapfelmeier
C. Werner
Klinik für Anaesthesiologie
Technische Universität München
Munich, Germany
1 Detsch O, Schneider G, Kochs E, Hapfelmeier G, Werner C. Increasing
isoflurane concentration may cause paradoxical increases in the EEG
bispectral index (BIS) in surgical patients. Br J Anaesth 2000; 84: 33–7
2 Andrzejowski J, Sleigh JW, Johnson I, Sikiotis L. Epinephrine has a
stimulatory effect on the bispectral index and sedation. Br J Anaesth
1999; 82(Supp 1): 95–6
3 King BD, Sokoloff L, Wechsler RL. The effects of l-epinephrine and
l-norepinephrine upon cerebral circulation and metabolism in man.
J Clin Invest 1951; 31: 273–9
4 MacKenzie ET, McCulloch J, O’Keane M, Pickard JD, Harper AM.
Cerebral circulation and norepinephrine: Relevance of the blood–
brain barrier. Am J Physiol 1976; 231: 483–8
5 Berntman L, Dahlgren N, Siesjö BK. Influence of intravenously
administered catecholamines on cerebral oxygen consumption and
blood flow in the rat. Acta Physiol Scand 1978; 104: 101–8
6 Artru AA, Nugent M, Michenfelder JD. Anesthetics affect the cerebral
metabolic response to circulatory catecholamines. J Neurochem 1981;
36: 1941–6
7 Lubke GH, Kerssens C, Phaf H, Sebel PS. Dependence of explicit and
implicit memory on hypnotic state in trauma patients. Anesthesiology
1999; 90: 670–80
Flexiblade and oral trauma
Editor—Yardeni and colleagues have described the new Flexiblade
laryngoscope (Arco Medic Ltd, Omer, Israel), and suggested it
may have a role in modern day anaesthesia.1 Our department
 Correspondence

Fig 1 Sequence of x-ray radiographs of a patient with buck teeth with no damage to oral tissue.

recently tried one of these laryngoscopes and we would like to joined together. The articulations on the convex curvature of the
report a problem with its use. The flexibility of the Flexiblade posterior surface of the blade caused damage on insertion in the
relies on the fact that the surface of the blade is not smooth unlike first two patients on whom we used it. In the first patient, an
other laryngoscopes. It is made up of several pieces of metal incisor tooth was damaged and in the second, who was edentulous,

173
 Correspondence
the upper gum was made to bleed. Neither of these patients had
been predicted to be a difficult intubation and the Flexiblade was
merely being used to ascertain its ease of use. Both patients
subsequently revealed grade I views at laryngoscopy.2 Whereas a
normal Macintosh or McCoy blade would have glided over a
tooth or gum, these tissues caught in the gap between the pieces
of metal that make up the Flexiblade and caused damage. We
could envisage this being even more likely in patients with poor
mouth opening, or while manipulating the scope during a difficult
intubation. We accept that we were at the beginning of a learning
curve in the use of the Flexiblade, and that if we had persisted in
its use, the incidence of problems might have decreased. However,
there should be no learning curve as far as patient safety is
concerned. We suggest that if trials show these laryngoscopes to
be a useful addition to our difficult intubation trolley, that the
blades are used with some sort of sheath like the Larygard (Penlon,
Abingdon, England) to avoid damage to teeth or gums.
J. Andrzejowski
G. Francis
Sheffield
UK
1 Yardeni IZ, Abramowitz A, Zelman V, Katz RL. A new laryngoscope
with flexible adjustable rigid blade. Br J Anaesth 1999; 83: 537–9
2 Cormack RS, Lehane J. Difficult tracheal intubation in obstetrics.
Anaesthesia 1984; 39: 1105
Editor—Thank you for giving me the opportunity to reply to
Andrzejowski and Francis’ letter. The Flexiblade laryngoscope
was tested for nearly 2 years in the anaesthetic department of
Rabin Medical Center, Petach Tikva, Israel, and for more than
1 year in the anaesthetic department of USC School of Medicine,
Los Angeles, California, without reported oral trauma. There was
a single case of a broken incisor tooth reported from Bickur Holim
Hospital in Jerusalem, which was due to a lack of appreciation of
the versatility of the blade.
The Flexiblade is inserted with its control trigger released. This
permits the blade to be pulled back when encountering resistance
from the tongue and the mandible. As a result, the blade changes
its shape to a nearly straight one, very similar to the Miller blade.
By gentle squeezing of the trigger, flexion of the intermediate
portion of the blade is achieved, altering its curvature to unlimited
angles, ranging from 9⫾1° to 30⫾2°.1
The Flexiblade is not made up of ‘several pieces of metal joined
together’, but of one stainless steel blade, with six slots and seven
windows on the flange that is subjected to a thermal treatment
process to improve its flexibility.
The Flexiblade web width is not larger than that of other
laryngoscope webs. At 10 cm and 12 cm distance from the tip,
the web width of a size 4 standard Macintosh is 18 and 21 mm
respectively. The web width of the McCoy blade is 18 and 25 mm,
while the Flexiblade web is 14 and 15.5 mm only.
Dr Andrzejowski claimed that neither of his patients had been
predicted to be a difficult intubation meaning that, following the
Wilson classification, the mean value of the inter-incisor gap,
measured with the mouth fully open, was at least 46 mm.2 This
is sufficient space to insert a nearly straight laryngoscope blade.
Insertion of any curved, rigid laryngoscope blade in a patient
with a small mouth opening will invariably cause oral trauma
whether the flange is smooth or not. It seems that in the reported
cases the author inserted the Flexiblade while the trigger was not
released. It caused the stabilization of the blade in a fixed curved
position, which may disturb the smooth penetration of the blade
and cause oral trauma. I can imagine that in these two cases, the
mouth had not been opened as far as suggested in older and more
recent texts.3 4
174
The convex curvature of the Flexiblade is not as smooth as the
Macintosh blade but is well polished to prevent damage to oral
tissue. Insertion of the Flexiblade with the trigger released ensures
easy penetration of the blade to glide over the tongue until resting
in the vallecula. This is the time to pull the trigger, without any
additional levering manoeuvre. This might lengthen the blade,
depress the hyoepiglottic ligament, move forward the epiglottis,
depress the tongue at more than one point and reveal the tracheal
inlet. This description can be seen from the sequence of x-ray
radiographs of a patient with buck teeth, with no damage to the
oral tissue (Fig. 1).
The suggestion of the authors to use some sort of transparent
sheath to cover the blade is welcomed for both hygienic and
safety reasons. I have passed a copy of the letter with the reported
cases to the manufacturer to recommend the use of an elastic
cover on the Flexiblade.
I. Z. Yardeni
Rabin Medical Center
Petach Tikva
Israel
1 Yardeni IZ, Abramowitz A, Zelman V, Katz RL. A new laryngoscope
with flexible adjustable rigid blade. Br J Anaesth 1999; 83: 537–9
2 Wilson ME, Spegelhalter D, Robertson JA, Lesser P. Predicting difficult
intubation. Br J Anaesth 1988; 61: 211–6
3 Bannister FB, Macbeth RG. Direct laryngoscopy and tracheal
intubation. Lancet 1944; 2: 651–4
4 Fell D. The practical conduct of anaesthesia. In: Aitkenhead AR,
Smith G, eds. Textbook of Anaesthesia, 2nd edn. Churchill Livingstone
1990; 357–8
Ropivacaine 0.75% for epidural anaesthesia in a
patient with severe Takayasu’s disease
Editor—We read with interest the case report by Henderson and
Fludder which reported an epidural anaesthetic for Caesarean
section in a patient with severe Takayasu’s disease.1 The authors
used an equal mixture of lidocaine 2% and bupivacaine 0.5% for
epidural anaesthesia. The Caesarean section was uneventful despite
a decrease in systemic blood pressure from 160 to 120 mm Hg
after the first dose of local anaesthetic mixture. However,
hypotension carries a high risk of syncope or severe cerebral
ischaemia in these patients. We agree that the effect of pregnancy,
labour, and delivery are not known to alter Takayasu’s disease
activity. However, a substantial number of patients have worsening
of complications, particularly cardiac decompensation. We must
keep in mind that Takayasu’s disease is often fatal, death resulting
usually from cerebral ischaemia or heart failure.2
We would like to solicit the authors’ view on the use of
ropivacaine for epidural anaesthesia in parturients with Takayasu’s
disease. Several studies have shown that this local anaesthetic is
less cardiotoxic than bupivacaine or lidocaine.3 4 We would like
to report our experience concerning the use of ropivacaine for
epidural anaesthesia in a 23-yr-old parturient with severe
Takayasu’s disease presenting at 28 weeks gestation and scheduled
for Caesarean section for intrauterine growth retardation. The
diagnosis was made 2 yr previously after an operation for
abdominal aorta stenosis and upper mesenteric artery occlusion.
The patient also had a history of left aortofemoral bypass and
postoperative acute myocardial infarction. On admission her blood
pressure was 160/110 mm Hg (usual: 130/80 mm Hg) although
she was being treated with atenolol 25 mg daily. Full neurological
examination revealed no signs or symptoms of disease. There was
 Correspondence
also no sign or symptom of cardiac or respiratory problems.
Regional anaesthesia was provided via a lumbar epidural catheter
with bolus doses of 2–3 ml of ropivacaine 0.75% every 5 min.
The blood pressure was measured every 3 min. After the first
dose of ropivacaine, the blood pressure was 145/100 mm Hg and
remained stable. Subsequent doses of ropivacaine did not alter it.
Ephedrine or i.v. fluid infusion were not required. The heart rate
remained stable. A total of 22 ml of ropivacaine 0.75% and
sufentanil 25 µg were given over 45 min to achieve a T4 level of
block. The Caesarean section was uneventful. The blood pressure
decreased after delivery to 125/79 mm Hg. The postoperative
course was uneventful and the patient was discharged 5 days later.
In most cases published previously, as in the paper from
Henderson and Fludder,1 hypotension was constantly reported and
required the use of ephedrine and rapid i.v. fluid infusion.1 2 In
our patient, there was haemodynamic stability throughout the
case. Although there are no differences between ropivacaine
and bupivacaine in terms of haemodynamic effects in healthy
parturients, we think that clinical studies comparing these two
drugs in patients with cardiovascular disease should be performed.
Ropivacaine, which is less cardiotoxic and provides better
haemodynamic stability than bupivacaine, may be of benefit for
epidural anaesthesia in parturients with severe Takayasu’s disease.
M. L. Ousmane
M. Fleyfel
Département d’Anesthésie-Réanimation
Lille
France
1 Henderson K, Fludder P. Epidural anaesthesia for Caesarean section
in a patient with severe Takayasu’s disease. Br J Anaesth 1999; 83:
956–9
2 Beilin Y, Bernstein H. Successful epidural anaesthesia for a patient
with Takayasu’s arteritis presenting for Caesarean section. Can J
Anaesth 1993; 40: 64–6
3 Morton CPJ, Bloomfield S, Magnusson A, Jozwiak H, McClure JH.
Ropivacaine 0.75% for extradural anaesthesia in elective Caesarean
section: an open clinical and pharmacokinetic study in mother and
neonate. Br J Anaesth 1997; 79: 3–8
4 Scott DB, Lee A, Fagan D, Bowler GMR, Bloomfield P, Lundh R.
Acute toxicity of ropivacaine compared with bupivacaine. Anesth Analg
1989; 69: 563–9
Editor—Many thanks for the opportunity to reply to the letter by
Ousmane and Fleyfel. There appears to be little difference in the
outcome of patients with Takayasu’s disease undergoing Caesarean
section whether ropivacaine 0.75% and sufentanil is used rather
than our mixture of bupivacaine 0.5% and lidocaine 2%. Indeed,
the volume of local anaesthetic required was identical (and within
normal limits) and the initial fall in blood pressure seen with the
first dose was comparable. Moreover, the outcome for both cases
was entirely uneventful to the mother and the fetus.
This should not be surprising. There is well-documented
evidence in the literature that ropivacaine 0.75% compares
favourably to bupivacaine 0.5% for use in epidural anaesthesia
for Caesarean section.1 It has been found to be safe and as
effective as bupivacaine with a comparable onset time, sensory
spread and motor block. However, Bjornestad and colleagues2
commented that ropivacaine 0.75% was associated with a more
profound drop in systolic blood pressure than bupivacaine during
epidural anaesthesia for Caesarean section in otherwise fit
individuals. But this has to be balanced against ropivacaine 0.75%
being less cardiotoxic than bupivacaine when given in excess or
inadvertently administered intravenously.3
Therefore the choice lies between ropivacaine with its decrease
175
in cardiotoxicity but with the potential to cause a sustained
decrease in systolic blood pressure and bupivacaine which is not
as safe in excess but seems to be better at preserving perioperative
blood pressure. Maintenance of blood pressure is paramount in
patients with Takayasu’s disease and this effect may therefore
have implications for the preferred use of ropivacaine over
bupivacaine. However, it is difficult to translate the effect epidural
local anaesthetics have on patients with normal blood vessels to
patients with one rigid and inflexible vascular tree seen with
Takayasu’s disease. There is some evidence from a number of
published case reports4 5 that blood pressure generally remains
unaffected during epidural anaesthesia for Caesarean section in
patients with Takayasu’s disease, probably as a result of the
vascular fibrosis preventing vasodilatation. However, it cannot be
assumed that this is likely to be the case with ropivacaine, it is
my opinion that it is preferable to use bupivacaine to maintain
perioperative blood pressure in patients with this disease.
K. Henderson
Brighton
UK
1 Morton CP, Bloomfield S, Magnusson A, et al. Ropivacaine 0.75% for
extradural anaesthesia in elective Caesarean section. Br J Anaesth 1997;
79: 813
2 Bjornestad E, Smedvig JP, Bjerkreim T, et al. Epidural ropivacaine
7.5 mg/ml for elective Caesarean section: a double-blind comparison
of efficacy and tolerability with bupivacaine 5 mg/ml. Acta Anesthes
Scandinavica 1999; 43: 603–8
3 Morton CP. Ropivacaine: a review. Br J Hosp Med 1997; 58: 97–8
4 McKay RSF, Dillard SR. Management of epidural anaesthesia in a
patient with Takayasu’s disease. Anesth Analg 1992; 74: 297–9
5 Beilin Y, Bernstein H. Successful epidural anaesthesia for a patient
with Takayasu’s disease presenting for Caesarean section. Can J Anaesth
1993; 40: 64–6
Midazolam premedication and thiopental induction
of anaesthesia
Editor—We read with interest the study by Wilder-Smith and
colleagues regarding the interaction between midazolam and
thiopental1. The authors concluded that midazolam premedication
potentiates thiopental induction of anaesthesia despite being unable
to demonstrate a significant difference between premedicated and
unpremedicated patients for median doses required to reach specific
pharmacodynamic end-points.
We recently concluded an institution-approved study whereby
two groups of patients were given 50 mg boluses of thiopental at
15 s intervals for induction of anaesthesia. One group (n ⫽ 20)
received no sedative premedication or narcotic pre-induction.
Another group (n ⫽ 20) received oral midazolam 3.75 mg, 30–
120 min before induction and i.v. fentanyl 100 µg, 1 min pre-
induction. The time to loss of eyelash reflex was recorded and the
effect compartment concentration (Ce) was predicted using the
pharmacokinetic–pharmacoydnamic (pk–pd) model described by
Stanski and Maitre.2
We found the median effect compartment thiopental
concentration at loss of the eyelash reflex to be 11.0 µg ml–1 in
unpremedicated patients and 8.2 µg ml–1 in patients premedicated
with midazolam. This difference was statistically significant
(Mann–Whitney U-test, P⬍0.05), and the concentration ratio
was 1.35. Despite the marked difference in methodology, the
concentration ratio we obtained was similar to the dose ratios
reported by Wilder-Smith and colleagues for loss of verbal contact
and drop flex.
 Correspondence
Using Ce to compare potency may allow direct comparison of
results derived from bolus and infusion induction methods. In
addition, while the injected dose can be calculated on a per unit
weight basis, other covariates such as age can be incorporated in
the calculation of Ce. Age has been known to influence the
pharmacokinetics of hypnotics used in anaesthesia.2 3 A lower
dose in an elderly patient may result in a Ce equal to that in a
young patient receiving a higher dose.
While it is not possible to directly measure Ce, predicted
concentrations still serve a useful purpose. The Ce-response
relationship can be used to devise dosing regimens which predict
the response in a population.4
T. A. Lim
Anaesthesiology Unit
Universiti Putra
Malaysia
K. Inbasegaran
Department of Anaesthesiology
Hospital Kuala Lumpur
Malaysia
1 Wilder-Smith OHG, Ravussin PA, Decosterd LA, Despland PA,
Bissonnette B. Midazolam premedication and thiopental induction of
anaesthesia: interactions at multiple endpoints. Br J Anaesth 1999; 83:
590–5
2 Stanski DR, Maitre PO. Population pharmacokinetics and pharmaco-
dynamics of thiopental: the effect of age revisited. Anesthesiology 1990;
63: 412–22
3 Kirkpatrick T, Cockshott ID, Douglas EJ, Nimmo WS. Pharmaco-
kinetics of propofol (Diprivan) in elderly patients. Br J Anaesth 1988;
60: 146–50
4 Wakeling HG, Zimmerman JB, Howell S, Glass PS. Targeting effect
compartment or central compartment concentration of propofol:
what predicts loss of consciousness? Anesthesiology 1999; 90: 92–7
Editor—We would like to thank Lim and Inbasegaran for their
interesting comment on our study of the interaction between
infusion induction of anaesthesia with thiopental and midazolam
premedication.1 In this study we demonstrated significant
differences in ED50 at various anaesthesia endpoints between
premedicated and unpremedicated patients. These differences were
not statistically different for median doses.
Lim and Inbasegaran suggest that the difficulties in comparing
the results of drug interaction studies using either infusion or
bolus models can be overcome by using pharmacokinetic–
pharmacodynamic (pk–pd) modeling to calculate effect
compartment concentrations, with the additional advantage that
these can take into account variations due to age. In support, they
cite the results of their own bolus induction study, showing
significant differences in effect site concentrations between
premedicated and unpremedicated patients, and resulting in a
potency ratio similar to that derived from our dosage results.
We have calculated effect compartment concentrations from the
results of our study using the same pk–pd model described by
Stanski and Maitre.2 For our patients, the median calculated
thiopental effect site concentration at loss of verbal contact was
15.5 µg ml–1 (interquartile range: 9.9–18.5) for unpremedicated
patients, and 12.7 µg ml–1 (8.9–15.9) for premedicated patients,
resulting in a median effect site concentration ratio of 1.22 – close
to the median dose ratio of 1.26.1 The difference between the two
median effect site concentrations is not statistically significant
(Mann–Whitney U-test, P⫽0.4).
While the effect site concentration ratio in both studies is
similar, median effect site concentrations in our study are 40–
50% higher than those obtained by Lim and Inbasegaran. The
176
difference in concentrations may in part be explained by the
addition of i.v. fentanyl to midazolam premedication by Lim and
Inbasegaran. It may also be due to methodological differences
either in endpoint determination, i.e. loss of eye-lash reflex vs loss
of verbal contact, or in study design, i.e. waiting for the endpoint
to occur after giving a bolus vs determining it during continuous
infusion. These differences will continue to need to be taken into
account in comparing drug interaction studies. The technique of
using predicted effect site concentrations to make the results of
different drug interaction models comparable warrants further
investigation and deserves to be included in future studies.
O. H. G. Wilder-Smith
Nociception Research Group
Bern University
Switzerland
1 Wilder-Smith OHG, Ravussin PA, Decosterd LA, Despland PA,
Bissonnette B. Midazolam premedication and thiopental induction of
anaesthesia: interactions at multiple endpoints. Br J Anaesth 1999; 83:
590–5
2 Stanski DR, Maitre PO. Population pharmacokinetics and pharmaco-
dynamics of thiopental: the effect of age revisited. Anesthesiology 1990;
63: 412–22
Patient-controlled analgesia in labour
Editor—The article by Thurlow and Waterhouse on the use of
remifentanil patient-controlled analgesia (PCA) in parturients with
contraindications to the use of epidural analgesia in labour, was
interesting.1 Remifentanil is being used extensively in general
anaesthetics, and this opens up a new application for its use as an
effective analgesic modality during labour. I would like to add
some further information pertaining to this rapidly developing
area of clinical practice.
The use of an arbitrary figure (platelet count ⬍100 000 mm–3)
as a contraindication to epidural analgesia in labour is questionable.
Belin and co-workers report the largest series of parturients who
had an epidural anaesthetic placed without complications when
the platelet count was ⬍100 000 mm–3.2 None of their patients
had any clinical evidence of bleeding or decreasing platelet count
at the time of epidural catheter placement. They recommend that
a patient’s entire clinical presentation be taken into account when
deciding on the appropriate anaesthetic technique.
Based on a recent survey, most anaesthetists (66% of those in
academic practice and 55% of those in private practice) will place
an epidural anaesthetic when the platelet count is between 80 000
and 100 000 mm–3.3
While the authors mention the use of pethidine and fentanyl
PCA techniques during labour, butorphanol tartrate, an analgesic
possessing mixed agonist-antagonist activity at opiate receptors,
also has a use in intravenous PCA in parturients prone to drug-
seeking behaviour (lacks euphoric activity).4 The use of PCA with
tramadol, a synthetic analogue of codeine that binds to mu opiate
receptors and inhibits norepinephrine and serotonin uptake, for
the control of pain associated with labour has been described.5 A
potent analgesic efficacy, equivalent to meperidine or morphine
for moderate pain, along with negligible respiratory depressant
activity and minimal side-effects makes it suitable for this
technique.
Frank and co-workers compared the use of nalbuphine (3 mg)
and pethidine (15 mg) PCA techniques in a double blind
randomized trial on 60 patients during the first stage of labour.6
Group mean values of pain scores of nalbuphine-medicated
primiparous women were statistically lower than those of
 Correspondence

pethidine-medicated patients (P⬍0.01). No differences were noted
in sedation, uterine contractions, maternal cardioventilatory
variables, fetal heart rates or Apgar scores. Another group in a
recent study report the use of patient-controlled meperidine (10–
15 mg every 10 min) analgesia in 259 women of mixed parity in
spontaneous labour at full term.7
Finally, Burrows and colleague studied 513 (7.6%) cases of
thrombocytopenia occurring in 6715 consecutive deliveries. Of
these cases, 65.1% consisted of healthy women in whom
thrombocytopenia was incidentally discovered, 13.1% were
healthy women with an obstetric or medical condition such as
diabetes or premature labour and 21% were hypertensive patients
and patients with immune thrombocytopenia.
This information, in association with that offered by the authors,
helps us to understand better the way to deal with the labour
analgesic requirements of the parturient with associated
thrombocytopenia.
A. Anand
Department of Pain Management/Anesthesiology
Medical College of Wisconsin
Milwaukee
WI, USA
1 Thurlow JA, Waterhouse P. Patient-controlled analgesia in labour
using remifentanil in two parturients with platelet abnormalities. Br J
Anaesth 2000; 84: 411–3
2 Beilin Y, Zahn J, Comerfold M. Safe epidural analgesia in thirty
parturients with platelet counts between 69 000 and 98 000 mm–3.
Anesth Analg 1997; 85: 385–8
3 Beilin Y, Bodian CA, Haddad EM, Leibowitz AB. Practice pattern of
anesthesiologists regarding situations in obstetric anesthesia where
clinical management is controversial. Anesth Analg 1996; 83: 735–41
4 Vogelsang J, Hayes SR. Butorphanol tartrate (stadol): a review. J Post
Anesthsia Nurs 1991; 6: 129–35
5 Lewis KS, Han NH. Tramadol: a new centrally acting analgesic. Am J
Health-System Pharm 1997; 54: 643–5
6 Frank M, McAteer EJ, Cattermole R, Loughnan B, Stafford LB,
Hitchcock AM. Nalbuphine for obstetric analgesia. A comparison of
nalbuphine with pethidine for pain relief in labour when administered
by patient-controlled analgesia (PCA). Anaesthesia 1987; 42: 697–703
7 Sharma SK, Sidawi JE, Ramin SM, Lucas MJ, Leveno KJ, Cunningham
FG. Cesarian delivery: a randomized trial of epidural versus patient-
controlled meperidine analgesia during labor. Anesthesiology 1997; 87:
487–94
8 Burrows RF, Kelton JG. Thrombocytopenia at delivery: a prospective
survey of 6715 deliveries. Am J Obstet Gynecol 1990; 162: 731–4
Editor—We thank Dr Anand for his interest in our case report.1
We would like to reply to some of the points he raised. In our
discussion, we stated that epidural analgesia for labour is not
recommended if the platelet count is less than 100 ⫻ 103 ml–1
(normal ⬎150 ⫻ 103 ml–1).2 We accept that Beilin and colleagues
reported no complications when the platelet count was less than
100 ⫻ 103 ml–1 in their series of 30 parturients.3 Epidural
haematoma, although infrequent, is a true emergency and must be
decompressed within a few hours to prevent permanent
neurological damage. Parturients who present with a low platelet
count at time of delivery and in whom pregnancy is uneventful
differ from those parturients with thrombocytopenia due to
increased platelet destruction. An epidural for labour may be
considered safe in a patient with a platelet count of less than
100 ⫻ 103 ml–1 if there is no risk that the platelet count has
decreased further and that there is no associated platelet dysfunction
or other coagulation abnormality.2 We agree with Dr Anand that
the whole clinical presentation should be taken into account when
deciding on specific analgesic techniques.
Patient-controlled analgesia techniques are not new to obstetrics.
We accept that various opioids have been used with a PCA device
in labour,4–7 but remifentanil may have advantages compared to
other opioids due to its rapid onset time and rate of hydrolysis.
J. A. Thurlow
P. Waterhouse
Bristol, UK
1 Thurlow JA, Waterhouse P. Patient-controlled analgesia in labour
using remifentanil in two parturients with platelet abnormalities. Br J
Anaesth 2000; 84: 411–3
2 Rolbin SH, Abott D, Musclow E, Papsin F, Lie LM, Freedman J. Epidural
anesthesia in pregnant patients with low platelet counts. Obstet Gynecol
1988; 71: 918–20
3 Beilin Y, Zahn J, Comerfold M. Safe epidural analgesia in thirty
parturients with platelet counts between 69 000 and 89 000 mm–3.
Anesth Analg 1997; 85: 385–8
4 Vogelsang J, Hayes SR. Butorphanol tartrate (stadol): a review. J Post
Anesth Nurs 1991; 6: 129–35
5 Lewis KS, Han NH. Tramadol: a new centrally acting analgesic. Am
Health-System Pharm 1997; 54: 643–5
6 Frank M, McAteer EJ, Cattermole R, Loughnan B, Stafford LB,
Hitchcock AM. Nalbuphine for obstetric analgesia. A comparison of
nalbuphine with pethidine for pain relief in labour when administered
by patient-controlled analgesia (PCA). Anaesthesia 1987; 42: 697–703
7 Sharma SK, Sidawi JE, Ramin SM, Lucas MJ, Leveno KJ, Cunningham
FG. Cesarian delivery: a randomized trial of epidural versus patient-
controlled meperidine analgesia during labor. Anesthesiology 1997; 87:
487–94
Difference in pre-intervention and post-inter-
vention thromboelastography times
Editor—In the report by Gorton, Lyons and Manraj,1 the difference
in pre-intervention and post-intervention thromboelastography
times is probably an artefact of sampling technique. The first
sample was withdrawn through a 16-gauge cannula, whereas the
second sample was taken through a 22-gauge cannula. There was
thus a difference in the sampling technique. It is recognized that
sampling blood through small bore needles can induce pre-
activation of coagulation in the sample, resulting in artificially
shortened clotting times. This could account for the difference in
thromboelastography measurements found. To eliminate this error,
the study should be repeated with both samples taken from the
same place.
C. J. Richard
Department of Anaesthetics
Edinburgh Royal Infirmary
Edinburgh
UK
1 Gorton H, Lyons G, Manraj P. Preparation for regional anaesthesia
induces changes in thromboelastography. Br J Anaesth 2000; 84: 403–4
Editor—We are not aware of any evidence to suggest that
coagulation as measured by thromboelastography (TEG) is
influenced by the size of cannula used for venepuncture. To test
this hypothesis, we performed TEG on five volunteers using a 16-
gauge and a 22-gauge Venflon placed in opposite forearm veins,
using a standardized technique with intradermal lidocaine. Blood
taken from the larger cannula showed greater coagulability in all
four TEG variables than that taken from the smaller cannula. For
the difference to become statistically significant, we would have

177
 Correspondence
needed to study 150 to 200 subjects. We speculate that the larger
cannula produces more endothelial damage, releasing coagulation
activators.
It is likely that there is a cannula-induced artefact, although the
differences are too small to be clinically significant. However, the
changes seen are in the wrong direction to explain our original
findings. The point we wished to make in our Short Communication
was that TEG changes attributed to colloid infusions in vivo might
have an alternative explanation. We hope that Dr Richard would
approve if we acknowledge that a different cannula sequence
would have supplied an unrelated explanation. We have sought to
demonstrate that fine differences in technique can generate changes
in vivo that might be erroneously attributed. We hope that in this
respect, we share a common aim.
H. Gorton
Leeds
UK
Separating the treatment effect of atropine from
its prophylactic benefits during inhalational
induction of anaesthesia in young children
Editor—The interesting study by Shaw and colleagues1 highlights
the difficulties in separating the treatment effect of atropine
from its prophylactic benefits during inhalational induction of
anaesthesia in young children. Atropine does exactly what it
says on the label, as shown by the reduction in excessive
secretions and increased heart rate in those infants premedicated
with 40 µg kg–1 orally. If the need to give succinylcholine
during an inhalational induction is a proxy measure of airway
difficulty, their finding that 15–16% of patients needed this
intervention, regardless of whether they received atropine
premedication, is interesting. Why give succinylcholine in this
situation at all unless there is actual or impending airway
difficulty? It is also noteworthy that similar proportions of
patients experienced arterial desaturation below 94%. If these
outcome measures are clinically relevant, then atropine
premedication appears to offer no protection.
This study is a demonstration of the experienced anaesthetist’s
sixth sense, normally difficult to quantify but usefully summarized
as the ability to anticipate and avoid trouble. It should not give
comfort to the less experienced, however, because the authors
have not shown that atropine premedication avoids the need to
intervene with ‘...swift, appropriate airway management’ to prevent
clinically significant arterial desaturation.
Inhalational induction in infants remains a challenge even to
the experienced anaesthetist and judicious premedication, whether
sedative or anticholinergic, plays an important part. Just how the
margin of safety can be increased, by which treatments and in
which patients, needs further clarification.
P. Wolstencroft
M. A Stokes
Department of Anaesthesia
Birmingham Children’s Hospital
Birmingham
UK
1 Shaw CA, Kelleher AA, Gill CP, Murdoch LJ, Stables RH, Black AE.
Comparison of the incidence of complications at induction and
emergence in infants receiving oral atropine vs no premedication. Br
J Anaesth 2000; 84: 174–8
178
Editor—Thank you for the opportunity to reply to Drs Wolstencroft
and Stokes. We agree that the debate on appropriate premedication
will continue but feel that our study has contributed to current
knowledge. We have shown that the incidence of airway
complications is significantly reduced in infants receiving 40 µg kg–1
oral atropine preoperatively. We have also shown that our patient
population did not have an increased incidence of adverse effects
attributable to atropine administration. It is difficult to comment
on succinylcholine administration as this was left to individual
anaesthetic discretion. We agree that there was no statistically
significant difference between the two groups for arterial
desaturation below 94% but argue that reduction in airway
complications may afford a greater ‘margin of safety’. We feel
that atropine premedication continues to have an important role
in providing safe anaesthesia in infants.
C. Shaw
London
UK
Side-effects of alcoholic iodine solution (10%)
Editor—We read with interest the article by Raedler and
colleagues1 and subsequent correspondence regarding contamina-
tion of needles used during central neural blockade. Much of the
correspondence related to the ideal solution for skin disinfection
prior to needle placement. The ideal solutions suggested were
chlorhexidine in alcohol or 10% iodine in alcohol.
We should like to report three cases of local inflammatory
reactions following elective Caesarean section, which are thought
to be related to the use of alcoholic iodine solution. Three healthy
patients presented for elective Caesarean section, none gave any
history of allergy to iodine. The operations were carried out under
spinal anaesthesia by two different anaesthetists. The usual skin
preparation in our unit is aqueous iodine solution, but these
patients were all prepared with alcoholic iodine solution (10%).
All three patients subsequently developed superficial painful
inflammatory reactions (including in one patient, blisters) on their
buttocks where the iodine solution had run down their backs. To
the best of our knowledge, the diathermy plates were correctly
applied to their thighs. We have no explanation for the occurrence
of these injuries other than a local concentration effect of pooled
alcoholic iodine, perhaps exacerbated by heat and the occlusive
effects of drapes and the rubber mattress of the operating table.
Following these events, we discovered that similar problems had
occurred in the unit some years earlier which had led to the
introduction of aqueous iodine for skin preparation.
We would therefore urge caution in the widespread adoption of
alcoholic iodine in skin preparation for regional techniques prior
to Caesarean section. We recommend careful drying of patients’
backs and buttocks before positioning on the operating table.
R. J. Chilvers
M. T. Weisz
Department of Anaesthesia
Peterborough Hospitals NHS Trust
Peterborough
UK
1 Raedler C, Lass Fliörl C, Pühringer F, et al. Bacterial contamination of
needles used for spinal and epidural anaesthesia. Br J Anaesth 1999;
83: 657–8
 Correspondence
Paediatric Intensive Care
Editor—Bennett’s1 review of Paediatric Intensive Care was
interesting to read. The article provides an overview of the
pathophysiology of meningococcal disease (MD) and its clinical
manifestations. We would like to emphasize some aspects of the
early management of this disease, which are likely to involve
anaesthetist trainees. Trainees may not have encountered this
patient group before and may not be familiar with publications on
their management, as they are predominantly in paediatric journals.
At St Mary’s Hospital, London, 425 critically ill children with
MD were referred to the paediatric intensive care unit from 72
hospitals in the south east of England between June 1992 and
September 1998. An algorithm has been developed for the early
management of these patients from personal experience and
practice.2
MD has a wide spectrum and may present either as meningitis,
septicaemia or both. Early management of these cases is often
carried out in district general hospitals, where anaesthetists are
called upon for resuscitation, especially airway control, artificial
ventilation and vascular access. Trainee anaesthetists faced with
this challenging emergency need to be aware of the nature of the
disease and the key resuscitation issues. Depending on whether
septicaemia or meningitis predominates, the major clinical
management problem will be either shock or raised intracranial
pressure respectively; or in some cases both.
Few other diseases are as rapidly progressing as meningococcal
septicaemia (MS), which has mortality of nearly 50%. Early
recognition, aggressive resuscitation, specialist advice and transfer
to a tertiary centre with paediatric intensive care have been shown
to significantly reduce mortality in the paediatric population. There
has not been such a decrease in mortality in the adult population.
Recognizing early features of compensated shock (tachycardia,
cool peripheries, tachypnoea, confusion, poor urine output and
increased capillary refill time) is the factor which determines
outcome in this group of patients. Hypotension is a late and
usually pre-morbid sign of shock in children. Treatment of shock
involves careful attention to the ABC of resuscitation and early
administration of oxygen. Intra-osseous access may be required
in some infants with difficult peripheral cannulation. Fluid
resuscitation with colloids, (we use 4.5% HAS), in 20 ml kg–1
boluses, should be promptly instituted in the face of early,
compensated shock. Generalized capillary leak in MS may
necessitate large amounts of fluid and if signs of shock persist,
inotropic support may also be required. Dopamine and dobutamine
infusions can be prepared as dilute solutions of 3 mg kg–1 in
50 ml crystalloid, and safely started via peripheral vascular access.
If signs of shock persist after 40 ml kg–1 fluid resuscitation,
risk of pulmonary oedema is increased and we advocate early,
elective intubation, using a rapid sequence induction (RSI)
179
consisting of atropine, thiopental and succinylcholine. A cuffed
endotracheal tube, where possible, facilitates the management of
pulmonary oedema and is preferred. Volume resuscitation and
inotropic support, where indicated, should be continued before,
during and after intubation. Boluses of colloid and inotropes must
be drawn up for use if necessary during induction. Morphine or
fentanyl and midazolam boluses may be used for adequate sedation
and analgesia. In severe shock, epinephrine and norepinephrine
may be required centrally. During volume resuscitation, regular
review to assess adequacy of fluid replacement is mandatory and
hourly urinary output monitoring serves as a sensitive marker for
end-organ perfusion. A variety of metabolic, biochemical and
haematological derangements may also occur which can contribute
to myocardial depression and worsen shock. Hypoglycaemia,
hypocalcaemia, hypokalaemia, metabolic acidosis, coagulopathy
and anaemia must be anticipated, monitored (hourly) and corrected.
If arterial pH is less than 7.2, bicarbonate should be infused.
Death in meningococcal meningitis (MM) is mainly due to
raised intracranial pressure and children should be monitored for
this complication. Coexistent shock, which may be seen in 40%
of cases, must be treated as a priority. Management of raised
intracranial pressure involves the principles of neurointensive care.
Elevation of the head-end of the bed to 30° with the head
midline; early, elective and controlled intubation following RSI;
normocapnoea; minimal handling; and adequate sedation are the
key principles. Seizures must be treated according to the APLS
guidelines. An acute rise in intracranial pressure should be treated
with mannitol 0.25 g kg–1 followed by frusemide 1 mg kg–1 and
repeated if necessary. Internal jugular venous cannulation must be
avoided. Lumbar puncture is strictly contraindicated in these
patients.
Until the arrival of the retrieval team and transfer to a tertiary
centre, anaesthetists play a significant role in influencing the early
management and the outcome of these children. In our experience,
a proportion of patients are suffering significant critical events
secondary to inappropriate management. Protocols such as the
one we outline provide uniform management guidelines for the
multidisciplinary team caring for children with such complex and
rapidly progressive disease, and aim to reduce regional variations
in early morbidity.
A. Cooney
N. Mehta
Departments of Paediatrics and Anaesthesia
St Mary’s Hospital
Paddington
London, UK
1 Bennett NR. Paediatric intensive care. Br J Anaesth 1999; 83: 139–56
2 Pollard AJ, Britto J, et al. Emergency management of meningococcal
disease. Arch Dis Child 1999; 90: 290–6