Unrecognised fatal anaphylactic reaction to propofol or fentanyl

Anaesthesia, 2001, 56, pages 1003±1029................................................................................................................................................................................................................................................

Correspondence

An audit of audit and continuededucational and professionaldevelopment

We conducted a postal survey of audit

and continuous educational and profes-

sional development (CEPD) arrange-

ments amongst the departments of

anaesthesia represented by consultants

attending the Twelfth South West

Thames Anaesthesia Update Confer-

ence, held in Belle Plagne this year.

One consultant in each NHS Trust

represented was sent a single question-

naire. Eighty questionnaires were dis-

tributed and 58 (73%) were completed

and returned to us. In addition to

identifying the time allocated for

CEPD and audit, by type, size and

location of hospital (Table 1), we quan-

tified attendance at CEPD and audit

meetings and qualified reasons for non-

attendance.

Of the respondents, 36 represented

district general hospitals and 22 worked

at teaching or specialist hospitals. Two

departments had seven or fewer con-

sultants, 23 had 8±15, 20 had 16±24

and 13 had in excess of 24 consultants.

Regular CEPD meetings were held by

41/58 departments (71%). An averageof 53.9 h per year were allocated fordepartmental CEPD (approximately 1 h

per week). Such meetings commonlytook place during lunch breaks (35/41).The amount of time allocated to CEPD

did not depend on the region, the typeor the size of hospital. Of the 17departments that did not have regulardepartmental CEPD sessions, the most

common excuse cited was that clinicalwork took priority (9/17).

Departmental audit meetings werearranged by 45/58 (78%) of depart-ments, commonly rostering a rolling

rota of one half-day session per month(25/45). An average of 32 h per yearwere allocated for audit meetings(approximately 2.5 h per month).

Audit invariably took place in morningor afternoon sessions (42/45 depart-ments). Similar to arrangements for

CEPD, the time allocated to audit didnot vary between the region, the type ofhospital or size of the department.

Clinical workload was once again citedas the commonest obstruction to theorganisation of regular departmental

audit meetings (9/13). Generalisedaudit sessions were organised in 9/45hospitals, such that all departments heldaudit sessions simultaneously; atten-

dance at audit in these hospitals alwaysexceeded 50%. All departments partici-pated in either audit or CEPD meet-

ings. Attendance at meetings was lessthan 30% in 5/58, 30±50% in 20/58and more than 50% in 33/58 of

departments.

The General Medical Council hasstated [1] that the doctor must both

`keep (his/her) knowledge up to date

throughout their working life. In parti-cular (s/he) should take part regularly in

educational activities which develop(his/her) competence and performance'

and `take part in regular and systematicmedical and clinical audit'. The Royal

College of Anaesthetists and Associationof Anaesthetists of Great Britain and

Ireland (AAGBI) have issued guidelinesconcerning regular audit practice and

CEPD [2] within anaesthetic depart-ments. The Audit Commission identi-

fied that a `value-for-money anaestheticdirectorate' links the personal develop-

ment needs of consultant and juniors tothose of the department and the trust

and involves trainees and non-consul-tant career grades in audit [3]. Audit

became a contractual obligation fordoctors in the early 1990s.

It is apparent from our audit that

current guidelines are not being uni-versally followed. We acknowledge that

we did not enquire after CEPD activityundertaken externally to the anaesthetic

department and that in some replies,CEPD was considered synonymous

with audit. Nevertheless, approximately30% of departments did not have formal

CEPD meetings, and general attend-ance was less than 50% in those that did.

Absence due to clinical workload wasprevalent, despite advice from the Royal

College of Anaesthetists and AAGBI [2]that `the cancellation of operating lists

may be required' and `requests forexceptions to attendance must be

resisted', in order to expedite CEPD.We suspect that CEPD is still viewed as

the monotonous pursuit of quantities ofCME credits (in order to satisfy putative

q 2001 Blackwell Science Ltd 1003

All correspondence should be addressed to Professor M. Harmer, Editor of Anaesthesia, Department of Anaesthetics, University of

Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK.

Letters (two copies) must be typewritten on one side of the paper only and double spaced with wide margins. Copy should be

prepared in the usual style and format of the Correspondence section. Authors must follow the advice about references and other

matters contained in the Notice to Contributors to Anaesthesia printed at the back of each issue. The degree and diplomas of each

author must be given in a covering letter personally signed by all the authors.

Correspondence presented in any other style or format may be the subject of considerable delay and may be returned to the author for

revision. If the letter comments on a published article in Anaesthesia, please send three copies; otherwise two copies of your letter will suffice.

Table 1 Respondents by region

London 11South East 11North West 9West Midlands 6South West 6East 5Trent 5Northern and Yorkshire 3Scotland 2

targets for professional development), an

attitude that encourages a `bums in seats'

approach to CEPD, rather than active

participation or interest. However, it issurely the quality of CEPD that is more

important than the quantity [4]. Con-

trary to popular belief, there is increas-

ing consensus on the effectiveness ofmethods of ongoing medical education

and professional development [5]. Effi-

cient, well-structured education pro-

grammes that involve self-directed

learning and reflection now exist [6],which appear to improve doctors'

performance and patient outcomes [7].

Audit forms an essential part of

CEPD. In addition to identifying

aspects of clinical practice that requirepersonal development (e.g. the attain-

ment of new skills), audit allows

anaesthetists to identify how service

provision and patient care may be

improved. Regular intradepartmentaland interdepartmental audit meetings

allow the dissemination of information

acquired by audit, constructive criticism

of clinical practice by one's peers and aforum for the development of new

theories of clinical methods.

Avoidance of statutory revalidation

can only take place if doctors are seen to

be open about, and accountable for,

maintaining excellence in practice.Clinical governance places a personal

responsibility on all doctors to maintain

clinical standards and performance. The

attainment of high standards in CEPD(of which audit is a major constituent)

should be sought by all members of the

profession.

S. M. WhiteC. Osmer

Royal Sussex County Hospital,Brighton BN2 5BE, UKE-mail: [email protected]

References

1 The General Medical Council. Good

Medical Practice, 2nd edn. The General

Medical Council, July 1988, http://

www.gmc-uk.org.

2 Royal College of Anaesthetists and

Association of Anaesthetists of Great

Britain and Ireland. Good Practice. A

Guide for Departments of Anaesthesia.

Royal College of Anaesthetists and

Association of Anaesthetists of Great

Britain and Ireland, 1998, http://

www.rcoa.ac.uk/training/

goodprac.html, http://

www.rcoa.ac.uk/CEPD/

cepdmain.htm.

3 The Audit Commission. Anaesthesia

under Examination. The Audit

Commission, 1997, http://www.audit-

commission.gov.uk/ac2/NR/Health/

anaexec.htm.

4 du Boulay C. From CME to CPD:

getting better at getting better? British

Medical Journal 2000; 320: 393±4.

5 Richards T. Continuing medical

education. British Medical Journal 1998;

316: 246.

6 Davis DA, Fox RD, eds. The Physician

as Learner: Linking Research to Practice.

Chicago: American Medical

Association 1994.

7 Toon P. Educating doctors to improve

patient care. British Medical Journal 1997;

315: 326.

Secondary transfer of intensivecare patients by helicopter

The recent letter `secondary transfer ofintensive care patients by helicopter'

(Watts. Anaesthesia 2001; 56: 589±91)demonstrates how little has beenlearned about inter-ITU helicopter

transfer in the last 14 years. As hecorrectly points out, secondary transfersare increasing in frequency yet land

ambulance transfers deplete ambulanceservices and hospitals of equipment andpersonnel.

The UK was one of the first

countries to provide a dedicated heli-copter-based interhospital ITU servicein 1987, and to demonstrate that

helicopters as a mode of transportproduce a lower mortality rate in thecritically ill than land-based transport[1]. Over the last 14 years, we have

demonstrated that it is practical andsafe. Standards have been laid down forstaff, equipment and aircraft [2]. As long

ago as 1994, the Royal College ofAnaesthetists recommended that heli-copters should be provided as part of a

total system [3] and this was supportedby recommendations of the Association

of Anaesthetists in 1996 [4]. Today,

dedicated secondary ITU transport by

helicopter is routinely available in the

Western World, Eastern Europe and

Africa, but sadly not in England and

Wales.

Dr Watts' questionnaire was illumi-

nating in so far as it reflected the lack of

enthusiasm and misconceptions that

appear unique to England and Wales.

Transporting patients in an ambulance

exempt from sections of the Road

Traffic Act is indeed dangerous and

requires additional insurance, but a

doctor transporting a patient in a

civilian helicopter is a fare paying

passenger on a commercial flight and is

exposed to far less risk than when

travelling to work in his/her own car.

Of course, training is mandatory and

secondary helicopter transfers should

only be done in dedicated aircraft with

their own medical team, which is why

the profession should view with con-

cern the fact that day after day doctors

with no training are expected to trans-

port patients in military aircraft that are

not subject to the safety standards of the

Air Navigation Order simply because

such aircraft are perceived to be free at

point of use, or alternatively travel in

primary HEMS helicopters which are

not equipped for secondary transfer.

All-weather interhospital helicopters

with dedicated medical teams can easily

be provided if each NHS Trust were

prepared to provide a budget of

£10 000 per annum, which would

only be drawn upon as needed. The

ambulance services do of course play an

integral role and are vital for control and

command but they do not have exper-

tise of intensive care management so as

to be able to make decisions as to when

a helicopter should be used, nor do they

have access and funding for such facil-

ities. The answer lies in the hands of

British intensivists who have the cap-

ability to provide high-quality interhos-

pital transport without depleting their

own staff.

A. Bristow

St Bartholomew's Hospital,London EClA 7BE, UK

Correspondence Anaesthesia, 2001, 56, pages 1003±1029................................................................................................................................................................................................................................................

1004 q 2001 Blackwell Science Ltd

References

1 Kee SS, Ramage CM, Mendel P,

Bristow AS. Interhospital transfers by

helicopter: the first 50 patients of the

Careflight project. Journal of the Royal

Society of Medicine 1992; 85: 29±31.

2 Bristow A. Medical helicopter systems

± recommended minimum standards

for patient management. Journal of the

Royal Society of Medicine 1991; 84: 242±

4.

3 The Royal College of Anaesthetists.

Guidance for purchasers. The Royal

College of Anaesthetists, July 1994.

4 The Neuroanaesthesia Society of Great

Britain and Ireland and The Association

of Anaesthetists of Great Britain and

Ireland. Recommendations for the Transfer

of Patients with Acute Head Injuries to

Neurosurgical Centres, 1996.

The unfasted elective patient

Drs Taylor and Watters report life-

threatening pulmonary oedema in a

patient undergoing elective eye surgery

under local anaesthesia (Taylor & Wat-

ters. Anaesthesia 2001; 56: 444±6). The

patient's pre-operative diuretic medica-

tion was withheld and food and drink

given 2 h before surgery in accordance

with their local policy. In keeping with

the 1993 Report of the Working Party

on Anaesthesia in Ophthalmic Surgery

[1], recommending an anaesthetist be

present during all eye lists, their patient

benefited from immediate anaesthetic

emergency management, followed by

treatment on their Intensive Care Unit.

Their patient was rescued from the twin

threats of pulmonary oedema and

aspiration, probable consequences of

drug interruption and feeding. Risk of

death for this patient was real. An

incident such as this provides an oppor-

tunity to review policies and proce-

dures, optimizing safety with efficacy.

Taylor and Watters discussion starts

by stating that this case `raises questions

about peri-operative management of

patients undergoing eye surgery under

local anaesthesia.' This is certainly true,

yet we consider that their discussion

does not develop the issues, nor answer

the important questions.

In providing an anaesthetist to service

these lists, do Drs Taylor and Watterscondone the practice of pre-operative

feeding, as well as diuretic restriction forthose patients receiving local anaesthe-

sia, when they are under anaestheticcare? Their unit permits free access tofood and drink pre-operatively. They

cite a survey of UK practice document-ing that of the 86% of ophthalmic units

with a policy on pre-operative dietarymanagement, 44% permit intake of

food and drink [2]. Their practice istherefore common, but is it correct?

This is certainly a critical incident.

Did it provoke any local review orresponse to their existing feeding or

medication policies? Is the practice ofpre-operative feeding and diuretic

restriction for these cases an optimalbalance between efficacy and safety,

convenience and complication? Asanaesthetists, do we simply respond toproblems or do we aim to prevent

them?

D. R. BallP. JeffersonDumfries and Galloway Royal

Infirmary,Dumfries DG1 4AP, UK

References

1 Anonymous. Report of the Joint Working

Party on Anaesthesia in Ophthalmic

Surgery. Royal College of Anaesthetists/

College of Ophthalmologists, 1993.

2 Morris EAJ, Mather SJ. A survey of

pre-operative fasting regimes before

regional ophthalmic anaesthesia in three

regions of the United Kingdom.

Anaesthesia 1999; 54: 1216±19.

A reply

We are grateful for the interest in ourcase report and would like to take theopportunity to respond to the points

raised.

Firstly, as stated in our discussion, thepractice of withholding diuretic therapy

on the morning of surgery is acceptedpractice in this country and as problems

seem to be exceedingly rare, it seemsreasonable to continue. Many thousands

of patients will have been subjected to

this practice without harm. When a

critical incident like the one wereported occurs, it is only right thatcurrent practice is reviewed. In addi-tion, although there is no consensus as

to the optimum time for fasting prior tolocal anaesthetic procedures, the prac-tice of non-fasting is common (both in

the UK and abroad) and again isgenerally associated with very fewproblems. We could find no similar

reports in the literature.

Second, again as stated, allowingintake of food and drink pre-operatively

is common practice. As to whether it isthe correct practice is a difficult ques-tion where many different people will

have polarised views. We can only statethat our unit has adopted this policy fora number of years and this is the first

time such an incident has caused us toquestion it. Therefore, unless similarproblems become known, we are notlikely to change.

Third, the incident did result in localdiscussion, but as this was an isolatedcase, no policy change was implemen-

ted. Should further cases like this occur,a change in policy might be appropriate.In addition, we cannot be sure that

withholding diuretic medication wasthe cause of the pulmonary oedema.An equally plausible explanation is

neurogenic pulmonary oedema result-ing from the peribulbar block itself.

Fourthly, we cannot be entirely sure

that the practice of pre-operative feed-ing and diuretic restriction is theoptimum balance, but from present

information, it would appear to be so.Despite a critical incident such as wereported, it is important not to forget

the potential problems of implementinga strict pre-operative starvation policyand the continuation of diuretic therapy,as stated in our discussion.

Finally, as anaesthetists, a significantpart of our role is risk prevention andstratification. When undertaking any

form of anaesthesia (or indeed anypractice of medicine) our prime aim isto avoid problems ± `first, do no harm'.

This is most certainly true in thisscenario. It is important not to losesight of the fact that this is a solitary case

report whereas the many thousands ofsuccessful procedures are not reported.

Anaesthesia, 2001, 56, pages 1003±1029 Correspondence................................................................................................................................................................................................................................................


I. Taylor

M. WattersPrincess Margaret Hospital,Swindon SN1 4JU, UKE-mail: [email protected]

Anaesthesia induction rooms ±sheer luxury!

I have been following the recentresurgence in correspondence regardingthe pros and cons of anaesthetic induc-

tion rooms (AR) with some interest. Iam currently a UK-trained anaesthetistcompleting a clinical/research fellow-ship in Toronto. I, too, have had to

come to terms with changing myclinical practice to in-theatre induction.

My initial reaction after arriving inCanada was very much one in supportof AR. I initially missed the `quiethaven' an AR offers away from surgical

colleagues eager to prod and poke apatient prior to and immediately afterinduction of anaesthesia. However, after

working in this system for 6 months, Inow feel there is definitely something tobe learnt from this North American

practice. I would like to take issue withsome of the points raised by Mr New-port (Newport. Anaesthesia 2001; 56:

691). He argues that ìt would take a lot

of reorganizing, and changing peoplesattitudes ¼' This is true, but it is notimpossible. It took me all of 5 days to

get used to inducing patients in theatre;it is really not difficult. With goodleadership the transition for other thea-

tre staff can be accomplished.

He further argues that `turnover timewould inevitably increase simply

because of increased induction time.' Ido not believe this to be based on soundevidence. The university hospital I am

currently working at performed 14 000elective cases in the 12-month periodApril 2000 to March 2001. Of thesecases, 4955 were in-patients and 8989

were day case patients. These figuresalso account for 2000 neuro/spinal casesdone at this tertiary referral centre for

neurosciences. There are four neurooperating rooms (OR), 10 general andorthopaedic ORs. Turn around time

between theatre cases for non-neuro-surgical cases is approximately 15 min;

it can be longer (30±45 min) for the big

neuro/spinal cases. This is better thanthe 36 min quoted on average byMazzei [1].

During the turn around period theOR is cleaned and prepared for the next

case, the anaesthetist reviews the nextpatient in the pre-op holding area, andthen when the OR is ready, he/she

escorts the patient to the operatingroom. The anaesthetist attaches mon-itoring, sites the intravenous cannulaand then induces anaesthesia (ODPs are

not allocated to each theatre andcertainly not at induction). The `turnaround time' between cases is thus more

than adequately filled and is more timeefficient. Anaesthetic induction time isnot affected. Current waiting lists at this

hospital are less than 4 months forcataract procedures or 6±12 monthsfor major orthopaedic joint surgery. A

projection of perceived time saved bythe anaesthetist between cases cannot bemade to predict long-term reduction insurgical waiting times.

Mr Newport further contests that

`people milling about' in the OR are asource of unnecessary noise and aproblem. Liu et al. [2] found that 32%of patients found noise levels at induc-

tion to be unpleasant and 16% found itdistressing. Noise prevention in the ORcan be managed. I have found that a

polite word to the other staff membersin theatre usually results in a respectfulsilence. Mr Newport continues that

patients may be more anxious by beinginduced in the OR. Soni et al. [3] foundno significant difference between

patients induced in the AR or OR.This was therefore not a major source ofanxiety.

Inducing patients in theatre is not aproblem. Canadian experience shows

that patients are not concerned, anaes-thetists (residents and staff) practice first-rate anaesthesia and nursing staff areused to the patient being induced in

theatre. I would argue that the anaes-thetic room is an expensive luxury and aliability. In the future, hospital architects

and administrators may review theexpenses incurred in building andequipping ARs. It is not a desire for

Àmericanisation' as quoted by Anderson[4], which would drive the redundancy

of ARs, but an effort to achieve more

efficiency.

R. J. SawyerToronto Western Hospital,Toronto, CanadaE-mail: [email protected]

References

1 Mazzei WJ. Operating room start times

and turnover times in a University

hospital. Journal of Clinical Anesthesia

1994; 6: 405±8.

2 Liu EH, Tan S. Patients' perception of

sound levels in the surgical suite. Journal

of Clinical Anesthesia 2000; 12: 298±

302.

3 Soni JC, Thomas DA. Comparison of

anxiety before induction of anaesthesia

in the anaesthetic room or operating

theatre. Anesthesia 1989; 44: 651±5.

4 Anderson KJ. Anaesthesia without

induction rooms. Anaesthesia 2001; 56:

589.

Anaesthetic machine checklists1

We wish to report a recent machine

failure that would have been undetected

by the manufacturer's recommended

pre-use check [1], or by the current

checklist for Anaesthetic Apparatus [2].

A DraÈger Julian anaesthetic machine

had been `self tested' by the O.D.A.

prior to the commencement of a

morning day case list. The self-test was

passed. On arrival of the anaesthetist,

the òld' anaesthetic machine check was

performed following the original guide-

lines published in July 1990 [3]. The

oxygen, air and nitrous oxide pipelines

were disconnected, as opposed to `tug

tested'. The oxygen cylinder was then

turned on. Oxygen was heard and felt

to be flowing from the disconnected

oxygen Schrader probe. The oxygen

cylinder was turned off and nitrous

oxide turned on; again gas flowed from

the disconnected nitrous oxide Schrader

probe. The machine was reconnected to

pipeline gas supply and appeared to

function normally. The machine was

replaced by another DraÈger Julian,



which underwent the same series of

tests without problem.

On full examination of the machine

by the Regional Anaesthetic Support

Service the sealing silicone washer in

the non-return valve for both oxygen

and nitrous oxide were thought to be

malfunctioning, although no obvious

damage was seen (Fig. 1). When these

were replaced the machine functioned

normally. We have been informed that a

similar valve failure has occurred within

this region in 1999. At that time only

the oxygen valve failed.

Previous failure to detect a defective

non-return valve following the current

guidelines has been reported in 1999

[4]. Our concern is that the present

recommended Checklist For Anaes-

thetic Apparatus, the manufacturer's

recommended checklist and the self-

test mechanism of the machine all failed

to detect this potentially serious failure.

Had the main oxygen supply failed and

the pipeline pressure dropped, oxygen

from the reserve oxygen cylinder would

have been diverted into the main pipe-

line rather than towards the machine

and the patient.

We suggest the pipeline disconnec-

tion test should be reintroduced into the

Checklist for Anaesthetic Apparatus.

C. Williams

C. Diaz-Navarro

Princess of Wales Hospital,Bridgend CF31 1RQ, UK

References1 Anonymous. DraÈger Julian Anaesthetic

Workstation, Instructions for Use, Software

1.n., 5th edn. DraÈger Medizintechnik

GmbH, November, 1998.

2 Anonymous. Checklist For Anaesthetic

Apparatus 2. Association of

Anaesthetists of Great Britain and

Ireland, March, 1997.

3 Anonymous. Checklist For Anaesthetic

Apparatus. Association of Anaesthetists

of Great Britain and Ireland, July, 1990.

4 Ravi Shankar S, Stacey RGW, Ravalia

A. Time to recheck the checklist?

Anaesthesia 1999; 54: 1023.

A reply

Draeger Medical is grateful for theopportunity to comment on this

reported incident.

We note the authors point regardingincreased safety by the reintroduction of

the pipeline disconnection test andwould be delighted to be involved inthis dialogue with the Association of

Anaesthetists of Great Britain and Ire-land or other appropriate bodies.

We cannot comment in detail on this

actual incident as at no time were theMedical Devices Agency (MDA) orDraeger Medical requested to investi-

gate nor were the valves returned to usfor examination. Similarly, the possiblefailure mentioned in 1999 was not

reported to the MDA or ourselves.

The Julian anaesthetic machine is

representative of many devices that are

in common use today. The pre-use

checks ask that care be taken to note

the correct pipeline pressure and that

cylinder checks are also made. In the

event of pipeline failure, with no

secondary check vales in line, the

cylinder once opened would supply

the patient with oxygen as well as

feeding backwards into the failed pipe-

line. In the worst case situation (with a

total failure of the check valve) a full

cylinder would supply oxygen for at

least 15 min. After this time, and with

total oxygen failure, the Julian would

alarm to alert the user and automatically

switch to 100% air from the medical air

supply, continuing to ventilate the

patient and supply gas in a safe way

and without interruption.

R. Sanders

Draeger Ltd,Hemel Hempstead HP2 7BW, UK

Anaesthetic machine checklists2

We read with interest the recent letters

regarding machine checks during a

recent exam OSCE (Hellewell. Anaes-

thesia 2001; 56: 487±8), recommenda-

tions for standards of monitoring during

anaesthesia and recovery (Mitchell.

Anaesthesia 2001; 56: 488), and check-

ing anaesthetic equipment (Palit & Butt.

Anaesthesia 2001; 56: 487±8).

We would like to make certain

observations. Anaesthetic machines in

different hospitals are quite variable in

terms of the integral monitoring avail-

able on them and the self-test that they

perform. At one end of spectrum is the

standard Boyle's machine for which the

original AAGBI checklist was quite

appropriate, to the other with newer

electronic machines without glass flow

meter for which the manufacturer's

checklist is most appropriate. Many

machines in use still don't have any

paramagnetic analysers built in to indi-

cate oxygen failure or even hypoxic

guard to prevent the delivery of hypoxic

mixtures. Such a device would have

prevented the disaster in Newham

where a 4-year-old child died. This

Figure 1 Non-return valves and defective washer.



becomes all the more important for

machines that use cylinders for oxygen

supply.

A number of machines still use old

style vaporisers with no lock in or

selected type of safety guard; simulta-

neous administration of anaesthetic

vapours is then possible and we are

aware of one case where a death

resulted. A vapour monitor, as belittled

by Dr Mitchell, would have prevented

this death.

In an age when patient safety and

health of healthcare workers in theatre is

paramount, all of the above measures

should be mandatory. We would like to

recommend that the AAGBI should

come out with more comprehensive

safety guidelines for machines and some

minimum mandatory safety features for

all anaesthetic machines. Machines that

do not fulfil these safety requirements

should be scrapped.

P. Bhargava

T. DexterWycombe Hospital,High Wycombe HP11 2TT, UK

A reply

Thank you for asking me to comment

on the above two letters concerning the

anaesthetic machine checklist. DraÈger

have, of course, commented on the

problem highlighted by Drs Williams

and Diaz Navarro. Drs Bhargava and

Dexter write about the disaster at

Newham. An anaesthetist was not

involved in this incident, as we under-

stand, but the AAGBI has already

responded to all Chief Executives on

this issue. All machines should only be

used with an oxygen analyser, as already

indicated in the AAGBI Standards of

Monitoring Document. Any machines

without a hypoxic guard should be

phased out at the earliest opportunity

and replaced.

Whether the AAGBI would have a

major influence on machine manufac-

ture when most machines are not UK

made is open to some debate. It could

certainly influence through its associa-

tions with the manufacturers associa-

tion, BAREMA. The AAGBI check list

is not due for review until at least next

year but the view of the Association is

that this review should probably be

brought forward a little to take into

account the problems posed by new,

sophisticated `work stations'.

R. J. S. BirksChairman, AAGBI SafetyCommittee

Checking the anaestheticmachine: a useful parallel inaviation safety

The recent correspondence related to

the anaesthetic machine checklist indi-

cates that this still seems to be a problem

area for practising anaesthetists (Palit &

Butt. Anaesthesia 2001; 56: 487, Helle-

well. Anaesthesia 2001; 56: 488). The

use of checklists built into machines by

manufacturers as reported by Palit and

Butt, whilst potentially confusing,

should not be dismissed out of hand.

Any system that has a secondary check

may be potentially useful in avoiding

errors associated with equipment faults.

We would like to report the use of a

checking device that we have seen used

whilst undertaking aeromedical retrie-

vals of critically ill patients in rural

South Australia. These fixed-wing

flights are single pilot operations and

there are requirements for procedural

checks for preflight, in-flight, landing

and post landing. A scrolling device is

fixed to the cockpit structure in the

centre of the front console, at just above

eye level (Aero products Inc, Los

Angeles, CA, USA). This is used after

each phase of checking has been

completed as verification that the cor-

rect checks have been carried out

(Figs 2 and 3). After discussing its use

with several experienced pilots, they

have indicated that it is not used as a

prompt but rather as a second check in

case anything has been overlooked with

all the other distractions that occur, such

as radio communications and monitor-

ing the instrumentation. In this respect

there are obvious parallels with the

conduct of anaesthesia and such a

device may have a place in pre-operative

machine checks and during emergen-

cies. The similarities between aviation

and medicine have been highlighted

elsewhere and in particular violation

errors (performing a checklist from

memory) are similar in both situations.

It is recognised that violations can stem

from a culture of non-compliance,

perceptions of invulnerability, or poor

procedures [1]. Inevitably a change in

culture is often resisted but in the

current environment it is imperative

that we learn from other professions in

improving our own safety standards.

Figure 2



P. J. Shirley

D. G. PogsonRoyal Adelaide Hospital,South Australia

Reference

1 Helmreich RL. On error management:

lessons from aviation. British Medical

Journal 2000; 320: 781±5.

An uncommon cause ofvaporiser failure

A case of complete failure of a vaporiser

due to overfilling is described.

A 6-month-old (7 kg) child was

scheduled to undergo repair of cleft

palate, as the first case for the day.

Routine check of the anaesthetic

machine and other equipment was

done, both in the anaesthetic room

and in the theatre. Anaesthesia was

induced with 8% sevoflurane in 100%

oxygen in the anaesthetic room. Mon-

itoring of oxygen saturation, non-inva-

sive blood pressure and ECG was

instituted. Venous access was established

through a 24G cannula in the left foot.

A 7-mg bolus of rocuronium was

administered for muscle relaxation, and

tracheal intubation was performed with

a size 4 uncuffed RAE tube. Anaesthesia

was maintained with sevoflurane in

100% oxygen while in the anaesthetic

room. Monitoring of end-tidal carbon

dioxide, Fio2 and anaesthetic gas con-

centration was added after intubation.

An infusion of remifentanil was started

at 20 mg.kg21.h21. A 12.5-mg suppo-

sitory of diclofenac and a 240-mg

suppository of paracetamol were

inserted.

The child was transferred to the

operating theatre. The inhalational

agent was changed to 1.5% isoflurane

for maintenance of anaesthesia. The

lungs were ventilated using pressure-

controlled ventilation and a circle

system with an air/oxygen mixture

providing an Fio2 of 0.5. End-tidal

carbon dioxide was maintained at

5 kPa. The child had a blood pressure

of 90/50 mmHg and a heart rate of

110 beat.min21 on transfer to the

operating theatre. Surgery commenced

5 min after transfer. The heart rate had

decreased to 90 beat.min21.

Fifteen minutes after commencement

of surgery, the heart rate started increas-

ing, reaching a maximum of 130 beat.-min21, and the blood pressure increasedto 150/100 mmHg. A 20-mg bolus ofremifentanil was administered immedi-

ately. On checking the monitor, it wasnoted that the gas analyser was notdetecting any isoflurane. The trend

display showed an exponential declineof the expired sevoflurane concentra-tion (the monitor was capable of

detecting the agent used automatically).The isoflurane vaporiser was re-checked,and was found to be full ± the level was

2 mm above the maximum fill-line,and it was locked securely on the backbar, and the dial setting was on 1.5%as set previously. The dial on the

isoflurane vaporiser was turned up to3%, but the monitor still failed todetect any isoflurane in the inspired

gas. It was then decided to revert tosevoflurane. The isoflurane vaporiserwas turned off, and sevoflurane was

turned on, which was followed by theimmediate detection of sevoflurane bythe monitor.

The isoflurane vaporiser was taken tothe anaesthetic room and connected to

the anaesthetic machine. The samplingport of the anaesthetic gas analyser wasattached to the fresh gas outlet. The

vaporiser dial was turned to 1%, andoxygen was turned on at a rate of4 l.min21. The gas analyser failed todetect any isoflurane in the fresh gas.

The dial was turned up to 5% in stages,with no effect. Thereafter, the isoflur-ane vaporiser was emptied gradually.

The analyser started detecting isofluraneafter 250 ml of agent had been removedfrom the vaporiser. At this stage, the fill

level indicator showed that the vaporiserwas filled only up to the minimumlevel. However, after letting the vapori-

ser stand for approximately 10 min, thefill level was noted to rise to indicatethat it was three-quarters full.

On questioning the person who hadfilled the vaporiser at the end of the list

the previous day, it was discovered thatthe vaporiser (which had a keyed fillingport) had been tilted during the fillingprocess, in order to empty the bottle of

isoflurane into the vaporiser!

The Operation and Maintenancemanual for the Tec 5 vaporiser contains

Figure 3



a warning against attempting to fill

beyond the maximum fill level mark,and states that the vaporiser must befilled and used in an upright position

[1].

The possibility of vaporiser outputbeing reduced to zero at a critical level

of overfilling has been reported underexperimental conditions [2], but aPubMed search did not reveal any

reports of this occurring in clinicalpractice.

We concluded that the total failure ofthe vaporiser was caused by saturation of

the wicks due to over-filling, and thatalmost complete drainage of the agentwas required to make the vaporiser

function again.

P. M. FernandoD. J. PeckSt. Andrew's Centre for Burns and

Plastic Surgery,Chelmsford, Essex CM1 7ET, UK

References

1 Anon. Tec 5 Continuous Flow Vaporizer-

Operation and Maintenance Manual, Part

No. 1105±0100±000: p. 7.

2 Sinclair A, Van Bergen J. Vaporizer

overfilling. Canadian Journal of

Anaesthesia 1993; 40: 77±8.

The ProSeal Laryngeal MaskAirway

The ProSeal Laryngeal Mask Airway(PLMA, Laryngeal Mask Airway Com-pany, Henley on Thames, UK) is now

well described. The drainage tube andmodified cuff facilitate intermittentpositive pressure ventilation (IPPV)

and allow the contents of the upperoesophagus to bypass the pharynx and

be vented. It has been shown that fluidin the oesophagus will bypass thepharynx and mouth of cadavers [1] but

confirmation of this has not beendescribed in a clinical setting.

A fasted 50-year-old man (ASA 1,weight 104 kg) was admitted as a day

case to our institution for a re-excisionof a 4-mm-deep malignant melanoma.

He denied any gastro-oesophagealreflux disease. Anaesthesia was induced

intravenously and a size 5 PLMA was

inserted. Correct placement was con-

firmed as described in the instruction

manual. Anaesthesia proceeded

uneventfully for approximately 45 min

at which time particulate brownish fluid

was seen to be passing up the drain tube.

About 30±40 ml of this fluid was

suctioned out of the PLMA with

pH 3.0. There were no clinical signs

to suggest any aspiration of this material

had occurred. After removal of the

PLMA, it was seen that the contamina-

tion was confined to the inside of the

drain tube and the bowl of the mask was

clean. The patient was well postopera-

tively and discharged the same day

without performing any further inves-

tigations for the occurrence of aspira-

tion.

Regurgitation of the gastric contents

into the oesophagus and pharynx is very

common during anaesthesia [2] and

usually causes no morbidity [3]. Aspira-

tion of the contents of the oropharynx

into the upper airway occurs even during

sleep in normal adults [4]. Aspiration of a

sufficient volume of gastric contents into

the lungs may combine a particulate

injury (causing focal inflammation) with

a diffuse acidic damage. Both the volume

and the acidity of the fluid in this case

were approaching the oft-quoted values

of 0.4 ml.kg21 body weight and a

pH 2.5 [5].

Although a cuffed tracheal tube

remains the definitive airway, it will

not always remove the risk of aspiration,

since the pooled secretions above the

inflated cuff can leak into the airway via

small longitudinal folds [6]. The ProSeal

Laryngeal Mask Airway is not designed

to be a replacement for the tracheal tube

but it may offer several advantages over

the classic laryngeal mask airway.

D. J. Dalgleish

M. DolgnerUniversity of Washington Medical

Center EE201,Seattle, WA 98195, USAE-mail: [email protected]

References

1 Keller C, Brimacombe J, Kleinsasser A,

Loeckinger A. Does the ProSeal

laryngeal mask airway prevent

aspiration of regurgitated fluid?

Anesthesia and Analgesia 2000; 91:

1017±20.

2 Blitt CD, Gutman HL, Cohen D, et al.

`Silent' regurgitation and aspiration

during general anesthesia. Anesthesia

and Analgesia 1970; 49: 707±13.

3 Engelhart T, Webster NR. Pulmonary

aspiration of gastric contents in

anaesthesia. British Journal of Anaesthesia

1999; 83: 453±60.

4 Huxley EJ, Viroslav J, Gray WR, Pierce

AK. Pharyngeal aspiration in normal

adults and patients with depressed

consciousness. American Journal of

Medicine. 1978; 64: 564±8.

5 Roberts RB, Shirley MA. Reducing

the risk of acid aspiration during

cesarean section. Anesthesia and

Analgesia 1974; 53: 859±68.

6 Young PJ, Ridley SA. Ventilator-

associated pneumonia. Diagnosis,

pathogenesis and prevention.

Anaesthesia 2000; 55: 96±7.

Airway management device(AMD)

A new device has to be both safe andreliable; I would suggest the AMD is

such a new device. I refer to thecomments made in a recent letter(Mandal. Anaesthesia 2001; 56: 382).

As the registered inventor of the AMD,I have had considerable experience in itsclinical use. The original concept was to

attempt to design an airway in one adultsize. My own trial used this one size,with no more problems experienced

than in a control group of patients usingthe laryngeal mask airway. A short papersummarising this work is currentlybeing considered for publication. A

brief report of this study was used asintroductory literature on the AMD'slaunch. Following this trial, five centres

took part in a further evaluation, as aresult of which a decision to introducefurther sizes was made.

The congested tongue, inability to

secure an airway at induction, loss ofairway during anaesthesia and regurgi-tation are probably all due to failure to

size or position correctly. I believe allthese potential problems have been



addressed by developments referred to

above. Mandal's work appears to sup-

port these recent developmental

changes. I would be interested toknow in which patients and when the

regurgitation occurred? Was use made

of the suction catheter port and chan-

nel? Are the various complications

mentioned interrelated in any way?

In addition to Mandal's paper, hisrelated correspondence states: The trial

included no control group for compar-

ison, making it difficult to compare

advantages or disadvantages with other

available methods. Initial use of theAMD was much more impressive than

that of the laryngeal mask airway.

These comments change the com-

plexion of Mandal's letter and a more

detailed description regarding his var-ious complications may provide a better

understanding of their mechanism.

M. J. O'NeilHuddersfield HD3 4YS, UK

E-mail: [email protected]

A reply

Thank you for the opportunity to reply

to O'Neil's letter. It is reassuring that hehas had considerable clinical experience

in using the Airway Management

Device (AMDe) and has found no

more problems than in a control group

of patients using the laryngeal maskairway. I am sure that this is the case and

many problems could be overcome with

experience.

When we conducted our audit, we

had two different sizes of the AMDe(3±3.5 and 4±5) for clinical use. Weused them according to the recom-

mended instructions. I would be inter-

ested to know if any further sizes have

been developed with any better clinicaloutcome.

I fully agree with O'Neil that manyproblems we encountered were due to

malposition of the AMDe. However, I

am not sure whether all of these

problems, as suggested by O'Neil,could be overcome by only selecting a

proper size AMD.

In our audit, two patients had visible

signs of regurgitation through the tube.

Both of these events were noticed at the

end of the surgical procedures and

immediately after termination of gen-

eral anaesthesia. Normally, we would

not expect regurgitation in any of these

patients. We thought that these inci-

dents could be due to the lower

hypopharyngeal cuff of this device

making the upper oesophageal sphincter

incompetent and thus increasing the

risk of regurgitation.

Our experience with the AMD is

very limited, involving only 50 selective

patients. A prospective, randomised and

comparative study could provide an

answer to O'Neil's comments.

N. G. MandalPoole Hospital,

Poole BH15 2JB, UKE-mail: [email protected]

Short nasal tracheal tubes

We wish to draw attention to a problem

with Mallinckrodt uncuffed nasal tra-

cheal tubes. During an inpatient dental

list, we were unable to pass a Mal-

linckrodt size 6.0 uncuffed nasal RAE

through a patient's vocal cords because

the tube was too short, even though it

was an appropriate size, and despite an

adequate view at laryngoscopy. Figure 4

demonstrates the comparative lengths of

three size 6.0 nasal tracheal tubes. The

upper two are manufactured by Mal-

linckrodt and demonstrate the significant

difference in length between the cuffed

and uncuffed versions, 24 and 18 cm at

the nose, respectively. For comparison,

an uncuffed size 6.0 Portex nasal tracheal

tube is included, which has the length

expected if you apply the formula age/

2 1 14.5 cm. In our case the patient was

10 years old, requiring an expected nasal

tube length of 19.5 cm, which is

significantly more than the uncuffed

Mallinckrodt tube allows. Figure 5 illus-

trates the respective size 7.0 Mallinckrodt

nasal tubes with a cuffed Portex Blue

Line nasal tube for comparison, again

demonstrating the same problem.

We are unable to explain why such a

discrepancy should exist between manu-

facturers of preformed nasal tracheal

tubes. It appears that the uncuffed

Mallinckrodt tracheal tubes are consis-

tently too short. No harm came to our

patient as the problem was recognised,

and the airway secured satisfactorily

with an alternative tube; however, we

feel that this situation led to increased

morbidity as a result of incorrect tube

placement and repeat nasal intubation

P. M. Rolfe

G. L. BarkerNorfolk and Norwich UniversityHospital,

Norwich NR4 7RF, UK

Figure 4



A reply


to Drs Rolfe and Barker. The Mal-

linckrodt Nasal RAE tube was first

manufactured in Argyle in the mid

1970s, following the designs layed out

by the inventors. There have not been

any changes to the length of the tubes

since production began, and both

manufacturing plants responsible for

production of the Nasal RAE product

line adhere to the same drawings and

specifications. The difference in length

between the cuffed and uncuffed Mal-

linckrodt Nasal RAE tubes is inten-

tional. The longer cuffed tube is

generally used in the adult patient

population. The slightly shorter

uncuffed tubes are generally used in

the paediatric patient population. The

difference in length between cuffed and

uncuffed tubes is therefore dictated by

the patient population. The length of

each tube represents the distance

between the nares and vocal cords of

the average size patient within that

tube's intended patient population.

Regardless of this explanation, Mal-

linckrodt views this letter as a customer

complaint that requires further evalua-

tion. If current medical practice and

customer preference supports a change

in the length of the uncuffed nasal RAE

product line, such a change will be

implemented.

G. Bertaggia

M. VannierTyco Healthcare

Orthodontic appliances andinsertion of the laryngeal maskairway

Orthodontic appliances can complicate

airway management [1±3]. We report

here a case in which an orthodontic

appliance made insertion of the laryn-

geal mask airway with the standard

technique difficult.

A 12-year-old, 40-kg male with

Madelung deformity was scheduled for

corrective osteotomy under general

anaesthesia. Pre-operative examination

revealed a Mallampati class 1 airway. A

multibracket appliance was attached tohis upper teeth and a palatal expansion

appliance was applied across the hard

palate for treatment of malocclusion

(Fig. 6). We planned to use a laryngeal

mask airway for airway management

because he had bronchial asthma,

although some difficulty in insertionwas expected. We further planned to

intubate the trachea if laryngeal mask

insertion was impossible. We considered

removal of the orthodontic appliance,

but the patient and his mother refused

because of the cost and time involved in

replacing it. The patient had to applythis appliance for several months.

Anaesthesia was induced with propo-

fol 100 mg. Ventilation through a face

mask was easily performed. Thereafter,

insertion of the laryngeal mask was

attempted using the standard insertion

technique [4]. However, the operator

could not press the flattened maskagainst the hard palate because of the

presence of the palatal expansion appli-

ance. At the second attempt, the

operator inserted the mask towards the

base of the tongue with the jaw thrust

manoeuvre [5]. The laryngeal mask was

successfully inserted into the hypophar-ynx and the lung could be ventilated

Figure 5

Figure 6 View of the oral cavity with the orthodontic appliance.



through it. Fibreoscopy revealed that

the epiglottis was slightly down folded

into the mask. Surgery using bipolar

diathermy and removal of the laryngeal

mask were uneventful. The patient

complained of only a slight sore throat

the next day. There was no evidence of

injury to the oral cavity.

Our case illustrates that orthodontic

appliances can interfere with insertion

of the laryngeal mask airway with the

standard technique. For successful inser-

tion, the standard technique, with the

mask pressed upwards against the hard

palate, is the most reliable [4]. However,

in this case the palatal expansion

appliance impeded this procedure.

Alternative laryngeal mask insertion

technique with the jaw thrust [5] was

successful without contact with the

appliance, but it is not always effective.

Various options for airway management,

including tracheal intubation, should be

prepared prior to induction of anaes-

thesia.

It is controversial whether an ortho-

dontic appliance should be removed

before induction of anaesthesia [1±3].

In this case, as the patient's airway was

not a potential problem except for the

presence of the appliance, we expected

that mask ventilation and tracheal

intubation would be possible even if

the laryngeal mask could not be placed.

Therefore, we did not remove the

appliance in compliance with the

patient's request. However, when a

difficult airway is expected, removal of

the appliance is mandatory [2].

Other potential problems associated

with orthodontic appliances include

diathermy burns, trauma to the oral

tissues caused by manipulation of the

airway, dislodgement and aspiration, and

damage to equipment. The intubating

laryngeal mask (ILM) cannot be

inserted without contact with the

appliance because it is designed to be

pressed against the hard palate. If the

laryngeal mask or ILM is inserted

forcefully, the mask, hard palate, appli-

ance or teeth can be damaged. Careful

considerations should be paid to both

airway management and to avoiding

injury in patients with orthodontic

appliances.

K. Aoyama

E. YasunagaMoji Rosai Hospital,Kitakyushu, 801±0853, JapanE-mail:

[email protected]

I. TakenakaNippon Steel Yawata Memorial

Hospital,Kitakyushu, 805±8508, Japan

References

1 Gurkowski MA, Knape KG, Bracken

CA. Dental appliances can complicate

an otherwise normal airway. Anesthesia

and Analgesia 1993; 77: 865.

2 Webb MD. Dental considerations in

airway evaluation. Anesthesia and

Analgesia 1994; 78: 1034±5.

3 Gurkowski MA, Knape KG, Bracken

CA. Dental considerations in airway

evaluation. In response. Anesthesia and

Analgesia 1994; 78: 1035.

4 Brimacombe J, Brain AIJ, Berry AM.

The Laryngeal Mask Airway: a Review

and Practical Guide. London: W.B.

Saunders, 1997.

5 Aoyama K, Takenaka I, Sata T,

Shigematsu A. The triple airway

manoeuvre for insertion of the

laryngeal mask airway in paralyzed

patients. Canadian Journal of Anaesthesia

1995; 42: 1010±16.

Protective effects of acidosis

The recent paper (Story et al. Anaes-thesia 2001; 56: 530±3) provides awelcome demonstration of the utility

of the Stewart approach to the analysisof acid±base disorders in critically illpatients. The authors are to be com-

mended on their clear illustration of thepotential of this methodology to offermechanistic insights not readily attainedwith the more traditional Henderson±

Hasselbach approach. The demonstra-tion that decreases in plasma albumin, acommon finding in critically ill patients,

may have contributed to the alkalosisseen in their patients is of particularinterest. The authors suggest that an

acidifying effect of increasing plasmaalbumin concentration may play a role

in the apparent adverse effect of albu-

min therapy reported in a recent meta-

analysis [1]. This contention reveals a

common and important misconception

regarding acidosis and outcome from

illness.

While acidosis is clearly associated

with poor outcome, this does not

imply causation. Acidosis, particularly

lactic acidosis, may indicate tissue

hypoxia; however, acidosis per se is not

necessarily harmful [2]. In fact, there is

abundant evidence in the literature that

acidaemia may exert protective effects in

the context of acute organ injury.

Acidosis, metabolic and/or respiratory,

is protective in a variety of animal

models of neurologic [3], cardiac [4]

and pulmonary injury [5±7]. The

mechanisms underlying the protective

effects of acidosis are becoming increas-

ingly clear, and include attenuation of

key components of the inflammatory

process, and reduction of cellular

respiration and oxygen consumption

[2]. A recent novel hypothesis [8],

pointing out that acidosis protects

against ongoing tissue production of

further organic acids (by a negative

feedback loop), provides a mechanism

for cellular metabolic shutdown at times

of nutrient shortage, e.g. ischaemia.

This distinction between cause and

association is of particular importance in

regard to the practice of buffering,

which remains a common, if contro-

versial, practice [9, 10]. The physiolo-

gical rationale for this practice is based

on the concept that acidosis is directly

harmful and therefore must be treated.

However, there exist few if any data to

support the practice of buffering acido-

sis. In fact, there is evidence from

laboratory models of lung injury that

buffering may abolish the protective

effects of acidosis [7].

In summary, in the light of current

evidence, it may be timely to re-

evaluate our traditional concepts regard-

ing acidosis.

J. G. LaffeySt. Vincent's University Hospital,

Dublin, Ireland



References

1 Cochrane Injuries Group Albumin

Reviewers. Human albumin

administration in critically ill patients:

systematic review of randomised

controlled trials. British Medical Journal

1998; 317: 235±40.

2 Laffey JG, Kavanagh BP. Carbon dioxide

and the critically ill -too little of a good

thing? Lancet 1999; 354: 1283±6.

3 Vannucci RC, Towfighi J, Heitjan DF,

Brucklacher RM. Carbon dioxide

protects the perinatal brain from

hypoxic-ischemic damage: an

experimental study in the immature rat.

Pediatrics 1995; 95: 868±74.

4 Kitakaze M, Takashima S, Funaya H, et

al. Temporary acidosis during

reperfusion limits myocardial infarct

size in dogs. American Journal of

Physiology 1997; 272: H2071±8.

5 Moore TM, Khimenko PL, Taylor AE.

Restoration of normal pH triggers

ischemia-reperfusion injury by Na/H

exchange activation. American Journal of

Physiology 1995; 269: H1501±5.

6 Shibata K, Cregg N, Engelberts D,

Takeuchi A, Fedorko L, Kavanagh BP.

Hypercapnic acidosis may attenuate

acute lung injury by inhibition of

endogenous xanthine oxidase. American

Journal of Respiratory Critical Care

Medicine. 1998; 158: 1578±84.

7 Laffey JG, Engelberts D, Kavanagh BP.

Buffering hypercapnic acidosis worsens

acute lung injury. American Journal of

Respiratory Critical Care Medicine 2000;

161: 141±6.

8 Hood VL, Tannen RL. Protection of

acid-base balance by pH regulation of

acid production. New England Journal of

Medicine 1998; 339: 819±26.

9 Vukmir RB, Bircher N, Safar P.

Sodium bicarbonate in cardiac arrest: a

reappraisal. American Journal of

Emergency Medicine 1996; 14: 192±206.

10Levy MM. An evidence-based

evaluation of the use of sodium

bicarbonate during cardiopulmonary

resuscitation. Critical Care Clinics 1998;

14: 457±83.

A reply

We appreciate Dr Laffey's interest in ourpaper. He raises the possibility that

acidosis may be protective. We said in

our paper that the acidosis secondary to

albumin therapy might be a cause of

adverse outcome. We accept, if Dr

Laffey is correct, that this statement

would be wrong. Like the Stewart

approach to acid±base, Dr Laffey's

suggestion is contrary to much of the

mainstream thinking but has consider-

able supporting research. Further, like

the Stewart approach, the challenge for

the future is to determine the truth

through clinical studies.

D. Story

S. Poustie

R. BellomoAustin and Repatriation MedicalCentre,

Heidelberg, Victoria 3084, AustraliaE-mail: [email protected]

The use of central venouscannulae in neuroanaesthesia

The recent report on the survey of the

use of central venous (CV) cannulae in

UK neuroanaesthetic practice (Mills &

Tomlinson. Anaesthesia 2001; 56: 465±

9) made for interesting reading.

Although the indications for measuring

central venous pressure (CVP) in parti-

cular neuroanaesthetic scenarios can

always be debated, I would like to

make some comments regarding their

statement that the femoral route makes

for unreliable CVP recordings.

Access sites for CV cannulation is an

important issue in neuroneaesthesia, and

these mainly relate to the complications

associated with each. There is a real

chance of compromising the ipsilateral

cerebral circulation if accidental carotid

artery puncture during an attempted

internal jugular vein cannulation

requires manual pressure for haemosta-

sis. The subclavian approach carries

with it the usual complications alluded

to by the authors. However, I feel that

the femoral route has much to recom-

mend itself in peri-operative neuro-

anaesthetic practice.

We know from cardiac catheterisa-

tion studies that mean pressures within

the abdominal inferior vena cava are

essentially the same as mean right atrial

pressure [1]. However, it has been

shown recently [2] that excellent overallagreement was obtained in adults forsimultaneous CVP recordings from

superior vena caval and femoroiliacsites in ventilated patients. In anotherstudy, similar results were obtained with

CV cannulae placed in the superiorvena cava and the common iliac vein[3]. CV cannulae used were 15±20 cm

in length, and mean airway pressure,intra-abdominal pressure, and positive

end-expiratory pressure had no measur-able effect on the difference betweenthese pressures.

It seems that the femoral route should

be given a more prominent place forCV cannula placements in neuroanaes-thetic practice due to the obvious

advantages. If longer term CVP mon-itoring is needed later on the neuro-intensive care unit, a more traditional

approach can be employed in a con-trolled environment.

A. GuhaWalton Centre for Neurology and

Neurosurgery,Liverpool L9 7LJ, UK

References

1 Walsh JT, Hildick-Smith DJ, Newell

SA, Lowe MD, Satchithananda DK,

Shapiro LM. Comparison of central

venous and inferior vena caval

pressures. American Journal of Cardiology

2000; 85: 518±20. A11.

2 Dillon PJ, Columb MO, Hume DD.

Comparison of superior vena caval and

femoroiliac venous pressure

measurements during normal and

inverse ratio ventilation. Critical Care

Medicine 2001; 29: 37±9.

3 Ho KM, Joynt GM, Tan P. A

comparison of central venous pressure

and common iliac venous pressure in

critically ill mechanically ventilated

patients. Critical Care Medicine 1998; 26:

461±4.

A reply

We acknowledge that the pressure in theinferior vena cava (IVC) correlates wellwith that in the superior vena cava.

However, the problem remains that the



tip of a catheter inserted into the

femoral vein does not always lie in

the IVC, but has been shown to enter

the ascending lumbar vein, internal iliac

vein, superior gluteal vein, superficial

femoral vein, left renal vein and con-

tralateral iliac vein. A review article has

quoted a 25% incidence of such mis-

placements [1]. This problem was not

encountered in the three articles quoted

but there are possible reasons for this.

The article by Walsh and colleagues [2]

describes deliberate positioning of the

catheter tip using fluoroscopy. Dillon

and colleagues [3] gathered measure-

ments from a variety of catheters

including pulmonary catheter introdu-

cers and renal dialysis catheters as well as

standard triple-lumen catheters in a total

of 22 patients. A femoral dialysis

catheter or pulmonary catheter intro-

ducer, being considerably stiffer than a

standard triple-lumen catheter, might

be less likely to become misplaced

during insertion. Ho and colleagues

[4] used abdominal X-ray to confirm

position in all 20 cases; our survey

indicated only 3.5% routinely X-ray

central lines pre-operatively.

Our own experience of using stan-

dard triple-lumen catheters for femoral

central venous pressure (CVP) measure-

ment is that frequently they give a good

trace with an appropriate reading but

occasionally they do not. If accurate

measurement of CVP is thought essen-

tial, and the ante-cubital fossa approach

is unsuitable because of the need for a

multilumen catheter or for CVP meas-

urement for longer than 24 h, then we

advocate an internal jugular approach.

We acknowledge the hazards involved

in our original article and repeat that for

neurosurgical cases, the internal jugular

technique should be reserved for

experienced practitioners, ideally ultra-

sound guidance should be available

during all such cannulations and an

alternative route should be selected after

three unsuccessful attempts; a femoral

approach would be very suitable in such

case.

S. Mills

A. Tomlinson

North Staffordshire Hospital,Stoke-on-Trent ST4 6QG, UK

References

1 Malatinsk YJ, Kadlic T, Mlijek M,

Slimel M. Misplacement and Loop

Formation of Central Venous

Catheters. Acta Anaesthiologica

Scandinavica 1976; 20: 237±47.

2 Walsh JT, Hildick-Smith DJ, Newell

SA, Lowe MD, Satchithananda DK,

Shapiro LM. Comparison of central

venous and inferior vena caval

pressures. American Journal of Cardiology

2000; 85: 518±20. A11.

3 Dillon PJ, Columb MO, Hume DD.

Comparison of superior vena caval and

femoroiliac venous pressure

measurements during normal and

inverse ratio ventilation. Critical Care

Medicine 2001; 29: 37±9.

4 Ho KM, Joynt GM, Tan P. A

comparison of central venous pressure

and common iliac venous pressure in

critically ill mechanically ventilated

patients. Critical Care Medicine 1998; 26:

461±4.

The effects of diathermy onhaemodynamic stability inphaeochromocytoma

Phaeochromocytoma is a rare cause of

hypertension. It is estimated that fewer

than 0.1% of patients with hypertension

have phaeochromocytoma [1]. Clinical

and laboratory findings are based on

hormonal secretion by the tumour.

Symptoms and signs include headache,

feeling of intense malaise, sweating,

palpitations, pallor, nausea, tremor, anxi-

ety and paroxysmal or persistent hyper-

tension. The diagnosis is confirmed by

increased plasma catecholamine levels,

increased urinary vanillylmandelic acid

(VMA) and metanephrine levels [1].

Symptomatic paroxysms occur sponta-

neously, but are sometimes precipitated

by exertion, twisting, turning, straining,

bending over, micturition, coitus, physi-

cal examination of the abdomen,

imaging methods such as computed

tomography, induction of anaesthesia,

tumour palpation and the administration

of certain drugs including glucagon,

histamine, metoclopramide, tyramine,

adrenocorticotrophin, saralasin, tricyclic

antidepressants, phenothiazines, nalox-

one and imipramine [1, 2].

Our two cases of phaeochromocy-

toma had paroxysmal attacks following

the use of surgical diathermy. Both

patients had phaeochromocytoma of

the left adrenal gland. They were treated

pre-operatively with alpha and beta

blocking agents. After pre-oxygenation,

we induced anaesthesia with intrave-

nous fentanyl 5 mg.kg21 and propofol

2.5 mg.kg21 followed by atracurium

0.5 mg.kg21. Intravenous lidocaine

1.5 mg.kg21 was injected prior to

tracheal intubation. Anaesthesia was

maintained with 35% oxygen in nitrous

oxide, sevoflurane 1±2%, plus addi-

tional fentanyl (intermittent boluses of

25±50 mg every 15±30 min). During

both laryngoscopy and skin incision,

haemodynamic parameters remained

stable. However, as soon as diathermy

was used during cutting of the abdom-

inal layers, both patients developed

tachycardia, hypertension, and periph-

eral pallor. The use of diathermy was

not related to dissection or other

surgical manipulation of the adrenal

gland. As soon as the attacks occurred,

blood samples were taken to measure

plasma levels of catecholamine. During

and after both attacks, plasma levels of

catecholamine were high.

Diathermy is an electrical impulse

that may lead to the release of catecho-

lamines [3]. Patients with phaeochro-

mocytoma are very sensitive to various

external and internal stimuli. We

observed that surgical diathermy

induced paroxysmal attacks in patients

with phaeochromocytoma. Therefore,

we recommend that diathermy should

not be used during surgery in patients

with phaeochromocytoma.

G. AkcËay

M. N. AkcËay

H. A. AliciAtatuÈrk University,25171, Erzurum, Turkey


References

1 Gifford RW, Manger WM, Bravo EL.

Phaeochromocytoma. Endocrinology and



Metabolism Clinics of North America

1994; 23: 387±404.

2 Fonseca V, Bouloux PM.

Phaeochromocytoma and

paraganglioma. Baillieres Ciinical

Endocrinology and Metabolism 1993; 7:

509±44.

3 Knitza R, Olbermann M, Fischer F,

Bassler KH. Hormonal changes during

electrocoagulation of the Gasserian

ganglion under neuroleptanalgesia and

the effects of administration of a beta-

blocking agent. Anaesthesist 1978; 27:

465±8.

Pain on injection with propofol

Pain on injection with propofol is arecognised complication and can bevery distressing for the patient [1]. The

incidence of pain varies between 28%and 90% in adults during induction ofanaesthesia and may be severe [2, 3].

Various methods have been used toalleviate it [4].

We have compared the new batch of

propofol marketed by Abbott Labora-tories, containing 10 mg.ml21 propofolas an active ingredient with soyabean

oil, purified egg phosphatide as egglecithin, glycerol, sodium hydroxideand water for injection with propofol

marketed by Zeneca Limited, as Dipri-van 1% containing 10 mg.ml21 propo-fol with glycerol, purified egg

phosphatide, soyabean oil, sodiumhydroxide and water.

We used both the formulations, adding

1 ml of 1% lidocaine to 20 ml andinjected 2 ml of the mixture into a veinon the dorsum of hand by means of a

20G intravenous cannula. We then askedthe patients whether they felt any pain.We observed that the former formulationcaused less pain on injection.

It is not clear as to why oneformulation causes less pain. Klementand Arndt [5] suggested that the pain is

related to the concentration of propofolin the aqueous phase and not due to theformulation, but the propofol manufac-

tured by Abbott has egg phosphatide asegg lecithin, which is not the case withDiprivan. Whether egg lecithin reduces

the incidence of pain is not known andneeds further research.

S. Gupta

A. RavaliaH. R. JonnadaKingston Hospital,Kingston upon Thames KT2 7QB,

UK

References1 Lomax D. Propofol injection pain.

Anaesthesia and Intensive Care 1994; 22:

500±1.

2 Stark RD, Binks SM, Dutka VN,

O'Connor KM, Amstein MJA, Glen

JB. A review of safety and tolerance of

propofol (Diprivan). Postgraduate

Medical Journal 1985; 61 (Suppl. 3):

152±6.

3 Mangan D, Holak EJ. Tourniquet at 50

mm Hg followed by intravenous

lidocaine diminishes hand pain

associated with propofol injection.

Anesthesia and Analgesia 1992; 74: 250±

2.

4 Tan CH, Onsiong MK. Pain on

injection of propofol. Anaesthesia 1998;

53: 468±76.

5 Klement W, Arndt JO. Pain on

injection of propofol. effects of

concentration and diluent. British

Journal of Anaesthesia 1991; 67: 281±4.

Persistent cough followingtarget-controlled infusion (TCI)with propofol

I would like to report an unusual side-effect following propofol TCI for seda-

tion. A 60-year-old, non-smokingwoman presented for elective revisionof her right hip prosthesis. The first

operation was performed in 1994 underepidural anaesthesia; no sedation wasgiven at that time. Apart from being

overweight (104.7 kg), there was nosignificant past medical history, noallergies and she was not on anymedication. Spinal subarachnoid anaes-

thesia was established using 2.8 ml ofplain bupivacaine and 10 mg of fentanylinjected at the L223 level. Twenty

minutes after establishing the block,TCI propofol was started with a0.8 mg.ml21 target concentration. Five

minutes later, the patient started coughing.As the patient was still communicating,

she was asked if she had suffered a recent

cough or chest infection, which she

denied. The saturation was satisfactory

(99% on 4 l.min21 oxygen via a

Hutchinson face mask), so oxygen was

discontinued as I suspected the dry

oxygen was the cause of her cough. As

the cough persisted and the surgeon

complained of the patient's movements,

I increased the target concentration to

1.5, then 2.0 mg.ml21 over 10 min, but

this made the cough worse. Oxygen

saturation was still over 94% on air. The

propofol infusion was stopped, and

within 10 min the patient stopped

coughing. The patient was in the

supine position and there was no

evidence of aspiration at any stage.

The incident has been reported to the

Committee on Safety of Medicines as

well as AstraZeneca, the manufacturing

company.

As I could not find any similar

reported side-effect with propofol, I

wonder if anyone else has experienced a

similar problem. I would appreciate any

comments.

E. E. Aly

Queen's Hospital,Burton upon Trent DE13 0RB, UKE-mail: [email protected]

Unrecognised fatal anaphylacticreaction to propofol or fentanyl

I read with interest the recent letter

describing a fatal anaphylactic reaction

(Konarzewski & De'Ath. Anaesthesia

2001; 56: 497±8). However, there are

a few related issues that I feel need to be

addressed.

Although it is possible for anaphylaxis

to manifest in the first instance by

cardiovascular collapse [1, 2], I believe

that the reported anaesthetic induction

doses were rather generous, particularly

on the second occasion. This could have

been the cause of the unsuccessful

resuscitation. On the first occasion,

assuming that neither the combination

of a beta-blocker with moderate cardiac

pathology nor the hypothyroidism con-

tributed to the described scenario, it is

still not unusual for significant brady-

cardia and hypotension to occur in an



unstimulated patient following induc-

tion of anaesthesia with the described

dose. In view of this incident, care

should have been exercised on the

second occasion in titrating the induc-

tion dose. I note, however, that even

though premedication was omitted, the

expected central and cardiovascular

depressant effects of the given dose

clearly exceed those of the induction

dose given on the first occasion.

Although the elevation in the post-

mortem tryptase is the most important

supporting finding in the diagnosis of

fatal anaphylaxis, serum tryptase was

reported to be elevated in a series of 31

out of 49 autopsy cases where there was

no evidence of fatal anaphylaxis [3, 4].

Therefore, the rise in serum tryptase

cannot be considered as a conclusive

indicator of anaphylaxis. Histamine

release is non-specific for severe ana-

phylactic reactions or mast cell degra-

nulation as most drugs and procedures

(e.g. cardiopulmonary resuscitation) can

induce low levels of histamine release in

the majority of patients. The urinary

level of the histamine metabolite,

methyl histamine, is raised even follow-

ing minor anaphylactoid reactions [5,

6].

I would also question the statement:

`A post-mortem specimen contained

methyl histamine 51.6 ng.mmol21'. I

assume this refers to the aforementioned

urine sample (although urinary methyl

histamine measurement units are usually

expressed in relation to urinary creati-

nine). Urine analysis would only be

relevant if taken from a patient who

survived the suspected reaction, and had

time to excrete the metabolites of

histamine.

May I also point out what could have

been a minor error: M. C. Laxenaire

reported the life-threatening reactions

to propofol in 1992.

On balance, the lack of allergic

history, clinical skin and lung manifesta-

tions, and drug-specific IgE antibody

testing in this case enforces the impres-

sion that resuscitation failure could have

been caused by the cardiovascular

depressive effect of anaesthetic induc-

tion in a vulnerable patient, and not

necessarily the result of an unrecognised

anaphylactic reaction. Nevertheless, the

later cannot be excluded.

Y. Girgis

The Royal Orthopaedic Hospital,Birmingham, UKE-mail: [email protected]

References

1 Fisher MM, Baldo BA. The incidence

and clinical features of anaphylactic

reactions during anesthesia in Australia.

Annales Francaises d'Anesthesea et de

Reanimation 1993; 12: 97±104.

2 Vuitton D, Neidhardt-Audion M,

Girardin P et al. Epidemiologic

characteristics of 21 peranesthetic

anaphylactoid accidents observed in a

population of 12,855 surgically treated

patients. Annales Francaises D Anesthesie

et de Reanimation 1985; 4: 167±72.

3 Randall B, Butts J, Halsey JF. Elevated

post-mortem tryptase in the absence of

anaphylaxis. Journal of Forensic Science

1995; 40: 208±11.

4 Edson E, Van Hage-Hamsten M. beta-

Tryptase measurements post-mortem in

anaphylactic deaths and in controls.

Forensic Science International 1998; 93:

135±42.

5 Cottineau C, Drouet M, Costerousse F,

Dussaussoy C, Sabbah A. Importance of

plasma (histamine and tryptase) and

urinary (methylhistamine) in

perianaesthetic anaphylactic and/or

anaphylactoid reactions. Allergie et

Immunologie 1996; 28: 270±6.

6 Doenicke A. Is atracurium

contraindicated in patients with a

known allergy to drugs? Anesthesiology

1993; 78: 607±9.

A reply

Many thanks for giving us a chance toreply to Dr Girgis who makes severalinteresting observations on our recent

letter.

Dr Girgis' main concern is that thepatient might have died purely becausethe anaesthetist had administered an

unduly generous dose of inductionagents on the second occasion, ratherthan from an anaphylactic reaction. We

disagree for three reasons. Firstly, whenthe patient's death was discussed at an

audit session, it was felt by our con-

sultant colleagues that the induction

with propofol 150 mg, fentanyl

0.25 mg and midazolam 5 mg, whilst,

perhaps generous, was certainly not

large enough to kill a robust 63-year-

old woman of 89 kg by its direct

cardiovascular depressant effect.

Second, we received expert advice

from the National Adverse Drug Reac-

tions Advisory Service at the Depart-

ment of Immunology, Northern

General Hospital, Sheffield, both in

writing and by telephone, to the effect

that our patient had died from an

anaphylactic reaction. It was felt that

the substantial increase in tryptase levels

from 5.3 to 185 mg.l21 was absolutely

confirmatory of this. Third, we have

evidence of the patient being `primed'

for IgE-mediated anaphylaxis by expo-

sure to propofol and fentanyl at the

previous anaesthetic and having an

adverse reaction at that time.

With regard to the observation on

methyl histamine, our statement should

indeed have read: `A post-mortem urine

specimen contained methyl histamine

51.6 ng.mmol21'. We apologise for the

absence of the word urine and accept

Dr Girgis' comments about urinary

methyl histamine.

Finally, we agree that M. C. Lax-

enaire reported life-threatening reac-

tions to propofol in 1992 and the

fourth reference in our original letter

acknowledges his contribution to the

literature.

To conclude, we remain convinced

that our patient died from a true

anaphylactic reaction and are anxious

to alert our colleagues to the fact that

severe anaphylactic reactions can present

with cardiovascular collapse without any

pulmonary or cutaneous manifestations.

W. Konarzewski

S. De'AthColchester General Hospital,

Colchester CO4 5JL, UK

Can propofol cause keratitis?

There have been many reports of

propofol causing complications in

patients, but I would like to report a



possible complication of propofol in the

anaesthetist.

Recently, I was inducing anaesthesia

in a patient and while injecting propofol

into the intravenous cannula injection

port, it splashed into my face and some

went into my eyes. As I was a solo

anaesthetist I continued with the induc-

tion, gave a muscle relaxant and intu-

bated the patient. After that, I washed

my eyes with tap water. My eyes were

painful for only a few minutes.

That evening I went swimming, but

when I returned home, both my eyeswere red. The next morning, they were

very red and slightly painful. Fortu-

nately, I was anaesthetising for an

ophthalmology list and the surgeon

noticed my eyes. She advised me to go

immediately to the eye clinic where I

was examined by a Consultant Ophthal-

mologist. When my eyes were exam-

ined under a slit lamp, he found

marginal keratitis in both eyes and

keratoconjunctivitis in one eye, which

he believed was due to an immunolo-gical (allergic) reaction. Maxitrol eye

drops (dexamethasone 0.1%) were pre-

scribed six times daily for 2 days and the

inflammation subsided after 48 h, with

no further treatment required.

After listening to the history, the

ophthalmologist excluded the water

from the swimming pool as a cause for

the keratitis. The question remains

could it have been the propofol? Alter-

natively, could it have been a coinci-

dence? I would be interested to hear

from other colleagues who have had asimilar problem.

H. Ameen

Princess of Wales Hospital,Bridgend CF31 IRQ, UK

Systemic spread of vecuroniumfollowing use in peribulbarregional anaesthesia

With reference to G. Reah et al. [1], I

would like to report an unfortunate if

not entirely unpredictable side-effect of

employing vecuronium to augment

peribulbar anaesthesia.

In common with Reah et al., I have

experienced some unpredictable levels

of akinesia when performing peribulbar

blocks and was intrigued to read theirgroundbreaking study. Being mostinterested to employ their techniqueand using their paper as a reference, I

started my own series. Eventually, Iperformed 30 peribulbar blocksemploying vecuronium to improve the

akinesia through its neuromuscularblocking action.

All patients had intravenous access

established pre-anaesthesia and weremonitored with pulse oximetry andECG. Neuromuscular monitoring was

not felt to be necessary as (apart frombeing painful) the patients, being con-scious, would be able to report any

decrease in muscle power. Starting witha solution of 9.5 ml of plain lidocaine2% with 300 units hyalase and 0.25 ml

(0.5 mg) vecuronium, I used 1 ml ofamethocaine 1% topically to the corneafollowed by a single median injectionwith a 25-mm 25 G needle. A Honans

balloon was inflated to 30 cm waterpressure and was applied for 5 min.After 15 patients, my results were

subjectively no better than normal.This perhaps is not surprising as Reahet al. also found that in their vecur-

onium group they still described 11/30blocks as poor.

Because of this and also believing

incorrectly that significant systemicspread via intravenous injection wouldbe heralded by the predominant effects

of the local anaesthetic (a view shared byReah et al.), I increased my dose ofvecuronium to 0.5 ml (1 mg) for thefollowing 10 cases. No adverse effects

were detected but, unfortunately,neither was any noticeable improve-ment in akinesia. In the last five cases,

2 mg of vecuronium was used and inthe last of these a problem arose.

A 72-year-old woman presented for

cataract surgery and received the sameanaesthetic as I have described. Fiveminutes after the block, the Honans

balloon was removed and adequateakinesia was demonstrated. The patientwas then transferred to the operating

room and prepared for surgery.

Exactly 9 min postinjection thepatient complained, in a whisper, that

she was having some difficulty inspeaking and 1 min later she reported

some respiratory distress. At this point,

surgical preparation was discontinued

and the patient was sat up in order to

assist her breathing. A rapid neurologi-

cal examination showed that she had

reduced power but normal sensation in

all four limbs. Her blood pressure was

210/70 mmHg, indicating that inad-

vertent intrathecal injection was unli-

kely to be the cause.

Suspecting systemic spread of the

vecuronium, the patient was immedi-

ately given neostigmine 0.75 mg and

glycopyrrolate 0.15 mg. In less than

1 min she had made a complete recov-

ery. Surgery was postponed, however,

and the patient was observed in recov-

ery for 1 h before returning to the

ward. That evening the patient was

discharged home.

In the Reah study, the vecuronium

dose was one-quarter of that which I

used and this is most likely to explain

why I observed an episode of clinically

significant systemic spread, whereas they

did not. On top of this, their solution

contained 1 : 440 000 epinephrine,

which may also have been a contribu-

tory factor in reducing systemic spread.

The Reah study, however, was, as they

attest, relatively small and inferences as

to the safety of the technique should be

made with caution. With only 30 in

their treatment group, the upper limit of

the 95% confidence interval for the

occurrence of such complications may

still be as high as 10% [2]. Given this,

and the fact that Reah still observed a

high proportion of poor blocks (an

observation with which I concur), it

may be that the margin of safety

between minimum effective and max-

imum safe dose is very small. The use of

vecuronium in this way cannot there-

fore be recommended unless larger

more powerful studies can confirm its

safety in the future. Ironically, in their

discussion, Reah et al. propose that with

the current trend towards topical anaes-

thesia for certain ophthalmic work, any

benefit from the use of vecuronium

might soon be rendered obsolete. For

my own part, I think I will avoid using

it henceforth.

As for my 72-year-old patient, she

was re-admitted 1 month later and had



an uneventful procedure under regional

anaesthesia without vecuronium.

T. W. B. AllanCity General Hospital,Stoke-on-Trent, UK

References

1 Reah G, Bodenham AR, Braithwaite P,

Esmond J, Menage MJ. Peribulbar

anaesthesia using a mixture of local

anaesthetic and vecuronium. Anaesthesia

1998; 53: 551±4.

2 Hanley JA, Lippman-Hand A. Journal of

the American Medical Association 1983;

249: 1743±5.

Huntington's chorea: use ofrocuronium

We would like to report a case of

Huntington's chorea where rocuroniumwas successfully used as a muscle

relaxant. A 33-year-old female, weigh-ing 45 kg, with recently diagnosed

Huntington's disease presented for elec-

tive dental clearance. Her medicalhistory included increases in muscle

spasms, tremors in the upper limbs,choreaform movements and impair-

ment of memory over the last6 months. She also suffered from

asthma and depression. Her regular

medications were salbutamol and becla-zone inhalers, diazepam and fluoxetine

20 mg b.d. She was recently com-menced on tetrabenazine 12.5 mg

twice daily to control chorea afterconfirming the diagnosis by genetic

testing. The patient was needle phobicand emotionally labile.

The patient was premedicated withranitidine 150 mg orally. We performed

a modified rapid sequence inductionusing 8% sevoflurane in oxygen and

rocuronium 25 mg with a view tominimising the risk of aspiration. The

trachea was intubated 1 min after the

administration of rocuronium. Anaes-thesia was maintained with sevoflurane,

nitrous oxide and fentanyl 0.1 mg.Ondansetron 4 mg was administered as

an anti-emetic. The surgeon infiltratedinto the operating site 6 ml lidocaine

2% with 1 : 80 000 epinephrine.

Surgery was completed in 20 min.

Using a peripheral nerve stimulator,the patient had two twitches of the

train of four stimulation at 30 min, wasreversed with neostigmine 2.5 mg and

glycopyrrolate 0.5 mg and sevofluranewas discontinued. After 5 min, the

patient regained consciousness and wasextubated. The postoperative period

was uneventful and the patient wasdischarged home the next day.

Huntington's chorea is a rare heredi-

tary disorder of the nervous system. It isinherited as an autosomal dominant

disorder and is characterised by pro-

gressive chorea and dementia. Involve-ment of pharyngeal muscles makes these

patients susceptible to pulmonaryaspiration [1]. Decreased plasma choli-

nesterase activity and prolongedresponse to succinylcholine has been

reported [2].

In a recent report, thiopental, succi-nylcholine and mivacurium have been

used safely [3]. Sevoflurane and rocur-onium can be used for modified rapid

sequence induction [4]. Since ourpatient expressed a clear phobia to

needles, we selected inhalational induc-tion with sevoflurane as a method of

choice. In our patient, rocuroniumproduced predictable duration of

muscle relaxation without any evidenceof altered pharmacodynamics. Rocur-

onium may provide a suitable alterna-tive for rapid sequence induction in

these patients.

G. KulemekaC. MendoncaWalsgrave Hospital,

Coventry CV2 2DX, UKE-mail: [email protected]

References

1 Stoelting RK, Dierdorf SF,

McCammon RL. Anaesthesia and Co-

Existing Disease, 2nd edn. New York:

Churchill Livingstone, 1998: 307.

2 Propert DN. Psuedocholinesterase

activity and phenotypes in mentally ill

patients. British Journal of Psychiatry

1979; 134: 477±81.

3 Nagele P, Hammerle AF. Sevoflurane

and mivacurium in a patient with

Huntington's chorea. British Journal of

Anaesthesia 2000; 85: 320±1.

4 Lowry DW, Carroll MT, Mirakhur RK,

Hayes A, Hughes D, O'Hare R.

Comparison of sevoflurane and propofol

with rocuronium for modified rapid-

sequence induction of anaesthesia.

Anaesthesia 1999; 54: 247±52.

Sevoflurane in acuteintermittent porphyria

Evans and colleagues describe two cases

in which sevoflurane was used on

patients with a documented history of

acute intermittent porphyria (Evans et al.

Anaesthesia 2001; 56: 388±9). We are

concerned that there is no mention of

local research ethics committee approval

or informed consent as outlined in the

journal's instructions to authors. Whilst

the Bolam [1] principle may apply, the

issue of failure to disclose a significant

risk as outlined in Pearce [2] must be

paramount. The declaration of Helsinki

states that `concern for the interests of

the subject must always prevail over the

interests of science and society' [3]. This

does not seem to have been considered,

especially in case 2 where the patient

had suffered years of severe symptoms

secondary to porphyria.

Evans et al. quote from a recent

review article [4] that the safe use of

sevoflurane has never been described in

acute intermittent porphyria. The same

review article states that there is more

than an adequate range of pharmacolo-

gical agents available for use in the

porphyric patient.

They end their report by suggesting

that `caution be advised'. Although many

drugs are labelled as safe or unsafe on the

basis of anecdotal reports [4] such as this,

we have to ask why the appropriate

ethical standards were not considered and

these patients exposed to a drug of

unknown porphyrinogenicity when safe

alternatives were available?

V. Perkins

D. R. Ball

P. Jefferson

Dumfries and Galloway Hospital,Dumfries DG1 4AP, UK



References

1 Anon. Bolam v Friern Hospital

Management Committee [1957]

IWLR 582.

2 Anon. Pearce v United Bristol

Healthcare NHS Trust, [1998]. EWJ

no. 617.

3 Anonymous. World Medical

Association declaration of Helsinki.

Recommendations guiding physicians

in biomedical research involving human

subjects. Journal of the American Medical

Association. 1997; 277: 925±6.

4 James MFM, Hift RJ. Porphyrias.

British Journal of Anaesthesia 2000; 85:

143±5.

A reply


to the issues raised by Perkins et al. We

entirely share their ethical concerns for

our patients. Indeed, the authors include

someone with a personal interest in

anaesthesia for porphyria and a former

Chairman of a local research ethics

committee (LREC). The involvement

of such an ethics committee was not

appropriate in this instance; the choice of

anaesthetic was that of the anaesthetists

concerned, after consideration of the

evidence. Had the anaesthetic been

chosen purely to establish the safety of

sevoflurane without LREC review, we

would have been among the first to

protest. Further, in the context of the

report, any discussion that was held with

the patients was therefore irrelevant and

omitted from the report in the interests

of clarity. The suggestion that publica-

tion would be of value arrived out of a

post hoc discussion among the authors

provoked by the recent review by James

and Hift [1]. Prior to this, the best

available data on choice of inhalational

agent was derived from an earlier review

of the subject from the same institution

[2]. In this review article, halothane was

considered to be the safest inhalational

anaesthetic option, with enflurane con-

sidered unsafe and no data available for

isoflurane or other agents. There were

also concerns raised regarding the safety

of propofol especially by infusion. Given

that the level of recent and current

experience with halothane was rapidly

declining, for a considerable period there

was in fact a lack of agents with a suitable

proven safety profile, and good reason tobelieve that the newer volatile anaes-

thetic agents ought to be safe. This view

was later supported by James' recentreview. That anaesthetists are already

using sevoflurane to anaesthetise such

patients is undeniable, as since the reportwas published, we have been informed

of one further case in which sevoflurane

was used without incident in a porphyricpatient. We therefore felt that to report

these patients was important, especially

with the relative paucity of drug safetydata available for acute intermittent

porphyria. In this area it is unlikely thata formal trial would ever be conducted,

and as Evans has suggested, the future

decisions about the safety of any drugwill be based on anecdotal reports. We

recognise that three patients are insuffi-

cient to provide confidence in the safetyof any drug, and hope that this report

will provoke those already using sevo-

flurane to report their experiences, goodor bad, in order that useful denominator

data may be obtained.

P. R. EvansS. Graham

C. M. KumarSouth Cleveland Hospital,

Middlesbrough TS4 3BW, UK

References

1 James MFM, Hift RJ. Porphyrias.

British Journal of Anaesthesia 2000; 85:

143±53.

2 Harrison GG, Meissner PN, Hift RJ.

Anaesthesia for the porphyric patient.

Anaesthesia 1993; 48: 417±21.

A sensitive anaesthetist?

I am writing for some advice regarding aphysician friend who has malignant

hyperthermia. This was diagnosed by a

caffeine and halothane contracture testfollowing muscle biopsy. This was insti-

tuted after his brother suffered malignant

hyperthermia under anaesthesia. Theproblem is that he is considering a

career in anaesthetics. I understand the

current recommendations for theatre

levels of inhalational agents averaged

over an 8-h period are 100 ppm fornitrous oxide, 50 ppm for isoflurane andenflurane, and 10 ppm for halothane.There are more stringent regulations in

North America where the values are25 ppm for nitrous oxide and 2 ppm forthe halogenated agents. Does anyone

know of doctors who have been in asimilar situation, or of any research toindicate that there may be a dose±

response nature to MH so that peoplein his predicament, however rare, maypursue an anaesthetic career without

ending up on the intensive care unitthemselves? I appreciate this is a veryunusual case, but none the less, aninteresting one.

A. TillyardChelsea and Westminster Hospital,London, UKE-mail: [email protected]

Anaesthesia in an unusuallocation

We read with interest the letter (Meek.Anaesthesia 2001; 56: 608) concerning abottle of trilene, which was found in the

possession of a non-medical person. Wewould like to make a comment regard-ing the legal classifications of this agentin the United Kingdom. Trilene was

classified as a `Pharmacy medicine (P)'and not `Prescription Only Medicine(PoM)' as suggested in the letter. This

means that it was available to the publicto buy without a prescription, but onlythrough a registered pharmacy and under

the direct supervision of a pharmacist.We have further noticed that sevofluraneis the only inhalational agent in currentUK clinical practice classified as a

`Prescription Only Medicine (PoM)'while all the other inhalation agents areclassified as `Pharmacy medicine (P)',

and this has raised the question of whywe have such a different legal classifica-tion for agents having similar clinical

effects and toxicity.

W. AliJ. PatemanPrincess Royal Hospital,

Haywards Heath RH16 4EX, UKE-mail: [email protected]



A national survey of epiduralpractice

We recently attempted to compare ouruse of epidural solutions for postopera-tive pain with those being used in other

centres nationally. The previous com-parative surveys, found on performing aMedline search, focused mainly on

obstetric practice, and those that didconcentrate on postoperative pain wefound to be inconclusive, so we decided

to perform a postal survey [1, 2]. Weenclosed a questionnaire in the PainNetwork Journal, a quarterly journal ofthe Pain Network (a network of

approximately 700 pain nurses).

We received replies from 74 centres ±these offered a total of 103 solutions(Table 2), with the maximum number

of solutions offered by any one centrebeing seven. Ninety-seven of the 103solutions used bupivacaine in combina-tion with an opioid ± the other six

comprised plain bupivacaine or ropiva-caine. Fentanyl was the opioid used in64 solutions (59.8%); diamorphine was

used in the other 33 solutions (30.8%).

Thirty-four centres offered patient-

controlled epidural anaesthesia. Back-ground infusions ranged from 2 to15 ml.h21 (minimum mean

5.06 ml.h21, maximum mean9.7 ml.h21). Bolus dosage range was2±10 ml (mean 5.24 ml). Lockout

range was 15±60 min (mean 27.2 min).

During 2000 we used bupivacaine

0.15% and diamorphine 100 mg.ml21

and had four episodes of respiratorydepression requiring naloxone (an inci-

dence of 1.3%). Based on this national

survey and our unacceptably high rate

of respiratory depression, we changedour dose of diamorphine to50 mg.ml21. Since changing to thisconcentration, we have managed 150

epidurals on the wards and have not, asyet, needed to use naloxone.

A standard, nationally agreed, solu-

tion for epidurals for postoperative painwould help to facilitate multicentreresearch and audit data collection.

Perhaps a first step would be for thosehospitals using up to seven solutions torationalise their practise. This is notbeyond the scope of most Acute Pain

Services.

Epidurals fail to produce optimalanalgesia for a variety of reasons. It

seems almost certain that placing thecatheter at the wrong dermatome levelis the commonest reason. The other

reasons for failure include the catheternot being in the epidural space, fallingout of the epidural space, having aninsufficient infusion rate or when there

is a large visceral component to thepain.

The majority of solutions in the

centres who replied were based onbupivacaine 0.1% or 0.125%. A fewcentres, we included, are using strongersolutions as first line. It is likely that if

good analgesia occurs with an opioidmixed with bupivacaine 0.15%, thenthe same result is probable with one

based around 0.1%.

What is more contentious is thechoice and quantity of the opioid;

perhaps this is where multicentreresearch should concentrate. We foundthat when we halved the concentrationof diamorphine, we rid ourselves of a

worryingly high incidence of sedationand respiratory depression. One of theauthors (M.A-W.) experienced a similar

problem at a centre using 10 mg.ml21

of fentanyl, which resolved when thisconcentration was halved. From this we

can conclude that there is a safe upperlimit of opioid concentration, but whatis not known is the lower effectiveconcentration for either drug, or which

is safer and more effective.

We decided not to change our opioidto fentanyl as we felt diamorphine to be

preferable. This was based on a combi-nation of clinical experience and a

literature review. Our clinical experi-

ence has made us passionate advocatesfor epidural diamorphine, as we believeit has fewer systemic effects than

fentanyl, as well as working across awider range of dermatomes. Fentanylhas far greater systemic absorption than

diamorphine [2, 3]. This means acontinuous infusion containing fentanylhas the potential for accumulation and

respiratory depression, but it appears thesafe limit of diamorphine may well be

50 mg.ml21. A multicentre study com-paring the two opioids may be the onlyway to resolve this debate.

We continue to audit our activities

and look forward to seeing a morecomplete audit of National activity.

L. BannonM. Alexander-WilliamsD. Lutman

Broomfield Hospital,Chelmsford CM1 7ES, UK

References

1 Liu SS, Allen HW, Olsson GL. Patient

controlled epidural analgesia with

bupivacaine and fentanyl on hospital

wards: Prospective experience with

1030 surgical patients. Anesthesiology

1998; 88: 688±95.

2 Scott DA, Beilby DS, McClymont C.

Postoperative analgesia using infusions

of fentanyl and bupivacaine.

Anesthesiology 1995; 83: 727±37.

3 Williams B, Wheatley R. Epidural

analgesia for postoperative pain relief.

Royal College of Anaesthetists Bulletin

2000; 2: 68±71.

Combinations of opioids forepidural analgesia

With reference to the letter describing

simultaneous infusions of epiduralopioids with epidural local anaesthetics(Cohen. Anaesthesia 2001; 56: 398),

epidural local anaesthetic infusions pro-vide excellent analgesia but only in thedermatomes covered by the band block.

Short-acting opioids such as fentanyl areoften added to decrease the dose of thelocal anaesthetic drug required so as to

decrease motor block and improve

Table 2

Bupivacaine concentration0.1% 38 solutions (37.3%)0.125% 40 solutions (39.2%)0.15% 13 solutions (12.7%)0.25% 11 solutions (10.3%)

Fentanyl concentration, 2 mg.ml21 2 solutions (3.1%)2 mg.ml21 27 solutions (42.2%). 2 mg.ml21 35 solutions (54.6%)

Diamorphine concentration, 50 mg.ml21 14 solutions (42.4%)50 mg.ml21 8 solutions (24.2%). 50 mg.ml21 11 solutions (33.3%)



haemodynamics [1, 2]. Unfortunately,

as mentioned by Dr Cohen, and I am

sure an observation made by manypractising anaesthetists, visceral pain

control is better achieved using opioids.

Consequently, we routinely use inter-mittent epidural boluses of 3±4 mg of

morphine at 12-hourly intervals, in

addition to the usual epidural infusionof a mixture of ropivacaine 0.2% with

fentanyl 2 mg.ml21 for thoracic and

major abdominal surgery. This hasdecreased the requests for management

of breakthrough pain and alleviated the

demands on our overworked doctorsmanaging patients on the acute pain

service.

P. LeeSingapore General Hospital,Singapore 169608

References

1 Buggy DJ, Hall NA, Shah J, Brown J,

Williams J. Motor block during

patient-controlled epidural analgesia

with ropivacaine or ropivacaine/

fentanyl after intrathecal bupivacaine

for caesarean section. British Journal of

Anaesthesia 2000; 85: 468±70.

2 Sia AT, Ruban P, Chong JL, Wong K.

Motor blockade is reduced with

ropivacaine 0.125% for parturient-

controlled epidural analgesia during

labour. Canadian Journal of Anaesthesia

1999; 46: 1019±23.

Misconnection misadventure

We would like to respond to recentcorrespondence calling for a mechanical

safeguard to reduce the risk of mis-

connection (Lanigan. Anaesthesia 2001;56: 586). We have recently had a case

where a 50-ml syringe containing

bupivacaine was partly dispensed intra-venously via a patient-controlled

analgesia (PCA) device. The patient

had undergone a palliative bypass pro-cedure to relieve bowel obstruction due

to disseminated bowel carcinoma. Initi-

ally, she received analgesia via anepidural infusion of bupivacaine

0.167% and diamorphine 50 mg.ml21

with good effect until day 2 post-

operatively when the epidural was

found to be ex situ. An intravenousPCA device was commenced to delivermorphine with reasonable effect. Onthe morning of day 5 postoperatively,

her morphine PCA syringe was erro-neously exchanged for a prefilled syr-inge containing bupivacaine and

diamorphine. Fortunately, shortly afterthe syringe change, she was reviewed bya member of the acute pain service, the

incorrect syringe was identified andreplaced with one containing mor-phine. By this stage she had received

only 5 ml of the bupivacaine solutionand, as might be anticipated, hadsuffered no ill effects. The patientreceived a full and frank explanation of

the event.

It is our normal practice to manageepidural infusions and PCA morphine

on the wards. Patients on these devicesare visited daily by the Acute PainService (APS). However, syringe

changes and patient observations areundertaken by the ward staff. Over theyears the following system has devel-oped in an attempt to allow these high

tech devices to be utilised safely outsideof a high care area:

1 Acute Pain Service: the nurse led

APS sees all patients receiving epiduralanalgesia or PCA daily until the deviceis removed. The APS is available duringnormal working hours for further help

and advice. After hours and on week-ends the anaesthetic on call team takesover.

2 Ward nurse education: the APS runsa programme of continuing educationto ensure the nursing staff remain

familiar with these techniques. Arecord is kept of trained nurses oneach ward. Only these nurses areallowed to change the syringes on

these devices.

3 Prescriptions: for clarity we havepreprinted stickers for epidural and

PCA prescriptions. These are colourcoded.

4 Drug presentation: for epidurals, asthe concentration of bupivacaine

(0.167%) is not straightforward, wehave our 50-ml syringes prepared bythe pharmacy. The label on the syringe

clearly states `for epidural use only'. Wedo not make use of commercially

available large prefilled bags of local

anaesthetic as we feel that if there was tobe a misconnection, the potential forpatient morbidity is greater. In contrast,for the PCA solution, the pharmacy

prepares a 50-ml bottle containingmorphine 1 mg.ml21. For administra-tion, the nurses are required to draw up

the contents of the bottle into a 50-mlsyringe.

5 Storage: epidural prefilled syringesare stored in the ward refrigerator in

sealed bags. PCA morphine bottles arestored in the controlled drugs cupboard.

6 Syringe drivers: for epidurals weutilise the IVAC Medical SystemsP2000 syringe pump, each of which is

clearly marked `for epidural use only'.They have also been modified to delivera maximum rate of 9.9 ml.h21. For

PCAs we utilise the Graseby 3300 PCApump, which has a locked, clear plasticcover. Only members of the APS arepermitted to change the PCA settings.

7 Connection: as with all devices

currently in use in the UK, the syringeis connected to the patient via anextension line with a luer lock con-

nector.8 Management protocols: the ward

nursing staff are required to performfrequent observations on these patients.The observation charts contain clear

protocols on how to manage patientsthat breach certain predefined limits,e.g. blood pressure, respiratory rate,

sedation, pain score, etc.Although we recognise that there

may be advantages to patient-controlledepidural or regional analgesia, we havedecided not to introduce these techni-

ques to our hospital as there is thepotential for confusion by ward staff.We have also discouraged the simulta-

neous use of PCA morphine andopioid-free epidural infusions. We haveattempted to make the two systems asdistinct as possible. So in this case what

went wrong? There were a couple ofcontributory factors:

1 The epidural sticker prescription hadnot been cancelled when this technique

was stopped.2 The PCA prescription was prescribed

by hand by a non-anaesthetist, i.e. nocoloured sticker was used.

These stickers are designed to be



obvious and it is conceivable that the

handwritten prescription was over-

looked. However, this does not explain

the insertion of a syringe containingbupivacaine into a driver that is only

ever used for intravenous use. This final

error has been described as a slip lapse

error and is perhaps the most difficult toguard against [1].

This is the fourth case of misconnec-

tion that we have had over the last

5 years; two of these have involved

intravenous administration of bupiva-

caine. Fortunately, both cases wererecognised early and neither patient

came to harm. Staff inexperience was

not a factor in either of the errors. It

does seem that, while we have thesituation of universal connectors, mis-

connection errors are bound to con-

tinue. The time is right for a mechanical

safeguard. This may take the form ofnon-interchangeable connectors, or of

intelligent syringe drivers that are able

to recognise the contents of the syringes

inserted into them and are programmedto respond appropriately.

A. Hutton

I. ChristieDerriford Hospital,

Plymouth PL6 8DH, UK

Reference

1 Merry AF, Webster CS. Labelling and

drug administration error. Anaesthesia

1996; 51: 987±8.

Luer-lock epidural connections

We were interested in the recent

correspondence (Lanigan et al. Anaes-

thesia 2001; 56: 585). We agree that thesimplest modification is to reverse the

luer-lock connections and as such have

been working with a major manufac-

turer. The syringe (Fig. 7) is nowavailable, and is undergoing bench

testing. To produce a safe system for

epidural infusions it is also necessary to

manufacture an epidural filter with a

male connector, and a method fordrawing up epidural solutions. We

expect to be able to present for pub-

lication the details of a complete safe

system for epidural infusions in the near

future. There are no plans at present to

produce intrathecal needles with male

connectors, but this will be required in

future.

A. Moriarty

A. Liley

N. Llewellyn

Birmingham Children's Hospital,Birmingham B4 6NH, UK

Hip flexion for lumbar puncture± not easy in obstetric practice

We read with interest the article (Fisher

et al. Anaesthesia 2001; 56: 266±71)

demonstrating radiographically that

increasing the degree of hip flexion

increases the width of the lumbar

interspinous spaces. They describe

how greater hip flexion can be achieved

in the sitting position by asking the

patient to `hug' their knees towards the

chest. As obstetric anaesthetists, we are

very keen to maximise ease of insertion

of our neuraxial blocks but we have

found it virtually impossible to achieve,

let alone maintain this position in the

majority of our parturients, since the

heavily gravid abdomen precludes it.

We would like to describe an alter-

native sitting position that does allow a

greater degree of hip flexion than the

usual arrangement, whereby the par-

turient sits on the edge of the bed with

her feet supported on a stool or chair.

The patient is asked to adopt the

crossed-leg or `lotus' position whilst

sitting on the bed. Perhaps surprisingly,

this is not uncomfortable for the

majority of labouring mothers, provides

a stable base when sitting, and enables

the patient to be brought closer to the

anaesthetist's side of the bed, an advan-

tage with the trend towards the use of

wider beds. This position obviates the

need for stools and pillows and may go

some way towards widening the lumbar

interspaces, since the hips are indeed

flexed, but are also externally rotated.

Further radiological studies would be

necessary to show this is indeed the case.

To our knowledge this position has not

been previously described for insertion

of neuraxial blocks in obstetric patients.

However, we believe that, patient

comfort permitting, the lateral decubi-

tus position should remain the position

of choice. Not only does it allow

significant hip flexion but it causes less

maternal hypotension [1], and that

anaesthetists who use it routinely are

less likely to have difficulty with inser-

tion when required to use this position

in an emergency [2±4].

Figure 7



F. Plaat

L. McCready-HallQueen Charlotte's & ChelseaHospital,London W12 0HS, UK


References1 Yun EM, Marx GF, Santos AC. The

effects of maternal position during

induction of combined spinal-epidural

anesthesia for cesarean delivery.

Anesthesia and Analgesia 1998; 87: 614±

18.

2 Stone PA, Kilpatrick AWA, Thorburn

J. Posture and epidural catheter

insertion. Anaesthesia 1990; 45: 920±3.

3 Russell IF. Spinal anaesthesia ± sitting

or lateral positions? Anaesthesia 1996;

51: 198±9.

4 Kinsella SM. Lateral positioning for

regional analgesia during labour. British


Paraesthesia during spinalneedle placement

We read with interest the paper on

nerve trauma with atraumatic spinalneedles in obstetric practice (Reynolds.Anaesthesia 2001; 56: 238±47). We

would like to add the following com-ments.

Prospective study has shown that theoccurrence of paraesthesia during spinalneedle insertion is a worrying sign.There is an increased risk of prolonged

or permanent paraesthesia in suchcircumstances [1]. An incidence ofparaesthesia of 10±15% has been

reported with atraumatic needles [2];we would therefore suggest that theinsertion technique of atraumatic or

pencil point needles be reconsidered todecrease or eliminate the occurrence ofparaesthesia. As previously reported [3],atraumatic needles are blunt and con-

siderable pressure may be required toovercome ligament resistance. In asituation where unrestrained, or uncon-

trolled pressure is applied, there is alikelihood of the needle overshootingthe dura and therefore the risk of nerve

root trauma. In the author's experienceof supervising anaesthetic trainees,

paraesthesia or worse, painful paraesthe-

sia occurs when there has been an

unrestrained push.

Ideally, a dural click should be felt in

all cases and the advance of the needle

stopped. However, atraumatic needles

differ both in vivo and in vitro [4]. In the

author's experience, with the Polymedic

25G atraumatic needle, a dural click is

present in the majority of cases using a

controlled push technique [4]. How-

ever, with Beckton and Dickinson 25G

or 27G Whitacre needles, a dural click

is not present in most cases. It is

therefore possible that overshooting

and therefore paraesthesia may be

more common with some makes of

needles than others. With such needles,

we would suggest the withdrawal of the

stylet to check for CSF at the presumed

spinal needle CSF placement.

Given the anatomical variation of the

spinal cord termination, and the under-

estimate of lumbar interspace, we would

add that the spinal insertion technique is

paramount to avoid the risk of nerve

trauma.

G. Samsoon

K. GrewalKingston Hospital,

Kingston upon Thames KT2 7QB,UK

References

1 Auroy Y, Nachi P, Messiah A, Uti L,

Rouvier B, Samii K. Serious

complications related to regional

anaesthesia. Anesthesiology 1997; 87:

479±86.

2 Hopkinson JM, Samaan AK, Russell IF,

Birks RJS, Patrick MR. A comparative

multicentre trial of spinal needles for

Caesarean section. Anaesthesia 1997; 52:

1005±11.

3 Ali SM; Samsoon G. Are pencil point

needles safe for subarachnoid block?

Anaesthesia 1998; 53: 1132±3.

4 Cesarini M, Torrielli R, Lahaye F,

Mene JM, Cabiro C. Sprotte needle for

intrathecal anaesthesia for Caesarean

section: incidence of post dural

puncture headache. Anaesthesia 1990;

45: 656±8.

Abdominal field block: a newapproach via the lumbartriangle

I wish to describe what I believe to be anovel approach to abdominal field

block. The technique, as originallydescribed, entails multiple injectionsand administration of potentially toxic

doses of local anaesthetic agent [1]. Thisnew approach involves identifying theneurovascular plane of the abdominal

musculature and injecting a local anaes-thetic agent therein. The only area ofthe abdominal wall where the internaloblique muscle can be localised directly

is the `lumbar triangle of Petit' where itforms the floor of this triangle. In mostpeople, the lumbar triangle is situated

just behind the highest point of the iliaccrest. Local anaesthetic agent depositedin the area of the lumbar triangle will

block the lower intercostal nerves, theiliohypogastric and the ilioinguinalnerves as they traverse between sub-

costal margin and the iliac crest.

The iliac crest [2] has ventral and

dorsal segments. The ventral segmenthas external and internal lips and arough intermediate zone. The crest's

summit is level with the L324 inter-vertebral space. The lower fibres of theexternal oblique and the latissimus dorsimuscles are attached to the external lip.

A variable interval exists between themost posterior attachment of externaloblique and the most anterior attach-

ment of latissimus dorsi. Here, the crestforms the base of the `lumbar triangle ofPetit'. The floor of the triangle is the

internal oblique muscle, which isattached to the crest's intermediatearea. The transversus abdominis muscleis attached to the anterior two-thirds of

the crest's inner lip. The lumbar triangleis bounded anteriorly by the freeposterior border of external oblique,

posteriorly by the lower, lateral marginof latissimus dorsi and inferiorly by theiliac crest. The seventh to eleventh

intercostals nerves, subcostal nerve,iliohypogastric and ilioinguinal nerves,all run a variable part of their courses

between internal oblique and transver-sus abdominis muscles.

With the patient in the supineposition, a finger is walked posteriorly



from the anterior superior iliac spine

along the top of the iliac crest until it

dips slightly inward. On further poster-

ior movement, the finger-tip is felt to

slip over the edge of a muscle. At this

point, the finger is assumed to be

abutting on the lateral border of latissi-

mus dorsi where it is attached to the

external lip of the iliac crest (Fig. 8).

Without moving the hand, the skin is

pierced anterior to the finger-tip with

an 18G cutting needle at the level of the

external lip. A 24G, blunt-tipped, 2-

inch needle (1Plexufixw, Ref:

0489 1562, B. Braun.) is inserted per-

pendicular to the skin until it touches

bone of the external lip (Fig. 9). There-

after, the needle is slowly advanced over

the intermediate zone of the iliac crest

until a definite `pop' or `sensation of

giving way' is felt. At this juncture, the

needle has reached the plane betweenthe internal oblique and the transversusabdominis muscles. After negativeaspiration, 20 ml of a local anaesthetic

agent is injected. Only one injection isrequired for a unilateral incision, e.g. inappendicectomy, while bilateral injec-

tions are administered for midline ortransverse abdominal incisions. For asuccessful block, the injectate must

disappear between the muscle layerswithout any apparent swelling of theabdominal wall.

I have used this technique for morethan 2 years and performed the abdom-

inal field block via the lumbar triangleon more than 200 patients without anyuntoward sequelae. For bilateral injec-

tions, the maximum dose limit of thelocal anaesthetic agent is carefullyobserved. If the needle is advanced too

far, a second `pop' is felt. This indicatesthat the needle has passed through thetransversus abdominis muscle attachedto the internal lip of the iliac crest and

must be withdrawn and re-inserted.Even after the second `pop', theneedle would have to pass through the

transversalis fascia and parietal perito-neum before reaching the peritonealcavity. The use of a fine-gauged, blunt-

tipped needle helps to minimise thepossibility of visceral damage if theneedle is advanced too far inadvertently.

The block may not be easy in obesepatients because of difficulty in identify-ing landmarks. In these subjects, thepoint of needle insertion is chosen

2.5 cm behind the highest point of theiliac crest, a landmark easily palpable inmost people. In elderly patients, the

whole thickness of the iliac crest can begrasped between two fingers due to theloss of muscle mass and tone. It makes

block easier to perform, bearing inmind that the needle tip must not beadvanced beyond the inner lip of thecrest. In small children, the lumbar

triangle is felt like a tiny hole in theabdominal wall just behind the highestpoint of the iliac crest. I recommended

a 24G 1-inch needle (1Plexufixw, Ref:0489 152, B. Braun) for use in children.If extraordinary resistance is felt during

injection, the needle may have lifted theperiosteum in which case it should be

Figure 8

Figure 9



withdrawn and re-sited. Finally, I would

emphasise that this new approach ofabdominal field block via the lumbar

triangle should be avoided in patients

with a lumbar hernia in which thehernial sac protrudes through the

lumbar triangle.

A. N. Rafi

Mid-Western Regional Hospital,Limerick, Republic of IrelandE-mail: [email protected]

References

1 Atkinson RS, Rushman GB, Lee JA. A

Synopsis of Anaesthesia, 10th edn.

Bristol: Wright, 1987: 637±40.

2 Williams PL, Warwick R, Dyson M,

Bannister LH. Gray's Anatomy, 37th

edn. Edinburgh: Churchill Livingstone,

1989: 422±6.

EMLA or Ametop, and for howlong?

How long do topical anaesthetics taketo work? We agree with your corre-

spondents (Morgan-Hughes & Kirton.

Anaesthesia 2001; 56: 495±6) thatchildren need more than 1 h for

EMLA to be effective. It has beencompared with Ametop with results

that suggest there might be a differencein their rate of onset [1]. Full anaesthesia

can be achieved with either agent but

analgesia and alleviation of pinprickpain may occur first.

We studied the incidence of pain-free

injection as reported by patients under-going routine venepuncture for induc-

tion of general anaesthesia. Wecompared EMLA cream, a eutectic

mixture that facilitates penetration of

the stratum corneum (Astra, KingsLangley, UK) and Ametop gel (Smith

& Nephew, Hull, UK) in 225 men and251 women aged between 16 and

94 years. Four patients were includedmore than once. There were 20 patients

in each group, 11 groups with each

agent and two groups as controls. Allwere unpremedicated. The cream or gel

was applied in a thin layer to the cubitalfossa with no dressing, wiped off after

an arbitrarily chosen but precise time

from zero to 10 min and venepuncture

performed in this area by one operator

(M.N.) using a single manufacturer 21

gauge needle and identical technique.

The time was measured by stopwatch.

Immediately, and before giving any

injections, the patient was asked neu-

trally `would you say that actually hurt?'

An unequivocal `no' was taken as a

positive response, and `hardly' or `felt,

but did not hurt' are examples of

responses also accepted as positive.

However, mention of `sharp', `needle

prick' and qualified replies especially if

ambiguous such as `just a little', `not a

lot' or `no, not really' were recorded as

negative. If interrupted or inadvertently

encouraged for instance, the answer was

not counted.

Our findings are shown in Fig. 10.

Bias cannot be excluded but we found

that a placebo effect was demonstrated.

In the control groups, the incidence of

pain-free injection was 30 or 40% rising

to 50% if either treatment was applied

briefly. After EMLA, there was an

increasing proportion of patients with

time who reported no pain. In contrast,

with Ametop, the placebo effect

appeared to continue for 2 or 3 min

and then the proportion who were

pain-free fell before rising again later.

Approximately 7% of responses were

considered equivocal, most occurring at

about 4 min. At 10 min, 19 out of 20

patients after EMLA responded `no' to

the question but only five out of 20 after

Ametop. The overall difference

between the agents was significant

(Chi squared p , 0.001). EMLA and

Ametop compared similarly when the

groups were separated into men and

women.

The results are biased against a

positive outcome as all equivocal

answers were taken to be negative.

Question and tone of voice were

critical. Whilst the placebo effect is

clearly therapeutic, it was possible to

identify additional analgesia after a

topical agent was used and that the

onset of this action was faster with

EMLA.

So, for how long? Both EMLA and

Ametop provide effective anaesthesia for

cannulation after 1 h in adults [2, 3] but

a shorter application time to remove the

pin-prick sensation may be perfectly

satisfactory. Does it matter? It depends

on whether anaesthesia is really neces-

sary or if analgesia would be sufficient.

Most patients dislike pain; additionally,

vasovagal reactions have been described

in association with anxiety and painful

venepuncture [4]. Ametop may be

preferable in children because it is less

vasoconstrictive than EMLA. Never-

theless, we believe EMLA to be quicker

Figure 10



to effective relief of pinprick pain in

adults. For the future, a micropyrotech-nic device may provide very rapidpainless injection and replace theneedle [5]; and it is better business not

to hurt your customers!

M. R. NottRoyal West Sussex Hospital,Chichester PO19 4SE, UK

References

1 Lawson RA, Smart NG, Gudgeon AC,

Morton NS. Evaluation of an

amethocaine gel preparation for

percutaneous analgesia before venous

cannulation in children. British Journal of

Anaesthesia 1995; 75: 282±5.

2 McCafferty DF, Woolfson AD, Boston

V. In vivo assessment of percutaneous

local anaesthetic preparations. British


3 Browne J, Awad I, Plant R, McAdoo J,

Shorten G. Topical amethocaine

(Ametop) is superior to EMLA for

intravenous cannulation. Canadian

Journal of Anesthesia 1999; 46: 1014±18.

4 Kinsella SM, Tuckey JP. Perioperative

bradycardia and asystole: relationship to

vasovagal syncope and the Bezold-

Jarisch reflex. British Journal of

Anaesthesia 2001; 86: 859±68.

5 Stix G. Little bangs: making thrusters

for micromachines. Scientific American

1998; 279/5: 28.

EMLA ± 1 h is not enough forvenous cannulation

It is ironic but fortuitous that an audit of1±5 year olds should question theminimum duration of application of

eutectic mixture of local anaesthetics(EMLA) prior to venous cannulation(Morton-Hughes & Kirton. Anaesthesia2001; 56: 495±6). It is ironic because

this age group may have the fastest onsetof action (or minimum effective appli-cation time) of any age group above a

year. It is fortuitous because, if theminimum application time is consideredtoo short, then the conclusion should

apply to all ages above a year.

The minimum effective applicationtime in adults is at least 45 min [1, 2],

with a similar 50±60 min in children

aged 4±17 years [3]. Whether 1±5 yearolds have a faster onset of action is amoot point. Only one study (quoted byMorton-Hughes and Kirton) is con-

fined to this age group [4] with effectiveanalgesia for intravenous cannulationestablished at 30 min. In one other

study [5], the youngest age group (4±6 year olds) had a significantly betteranalgesic response to EMLA than older

age groups, although it is uncertain ifapplications were of a similar durationbetween the groups. Unfortunately, all

other paediatric EMLA studies have ageranges that extend into their teens,which frustrate any attempt at confir-mation.

Is the concept of a minimum effec-tive application time important? In the

emergency/urgent situation it mostdefinitely is. However, in the electivesituation it is not how soon analgesia ispresent, but rather how successful is the

local anaesthesia.

Morton-Hughes and Kirton's audithighlights the well-documented fact

that with an increasing duration ofEMLA application (up to 2 h), increas-ing anaesthetic success is achieved [6, 7].

This is a function of nerve fibre size,with analgesia (to pinprick) precedingloss of sensory (touch and pressure)

perception [6]. In adults, analgesicsuccess, measured by a statistical increasein the depth of needle insertion into the

skin, is present after 60 min of EMLAapplication, while the sensory depth isonly significantly increased 30 min later[6]. This time lag between analgesia and

anaesthesia is the reason why someresearchers specify a minimum applica-tion time of 90 min [7]. In patients old

enough to recognise a needle as anoxious stimulus, the presence oftouch or pressure sensation despite

analgesia may be perceived as inade-quate analgesia.

Chang and colleagues, who studied

178 children aged 3±10 years, found animpressive 94 and 95% success withEMLA cream and patch, respectively,

after application times between 60 and180 min [8]. This supports the principleof increased anaesthetic efficacy withincreased duration of application.

In the elective situation, where best

practice demands that 100% of local

anaesthetic cream applications are at anappropriate time before a plannedintravenous induction, we shoulddemand a duration of application con-

sistent with 95% anaesthetic successduring venous cannulation, as opposedto the minimum effective (analgesic)

application time. To achieve this end,one hour is not long enough.

B. M. BiccardUniversity of Natal,Congella, 4013, South Africa

References

1 Ehrenstrom-Reiz G, Reiz S, Stockman

O. Topical anaesthesia with EMLA, a

new lidocaine-prilocaine cream and the

Cusum technique for detection of

minimal application time. Acta

Anaesthesiologica Scandinavica 1983; 27:

510±12.

2 Maddi R, Horrow JC, Mark JB,

Concepcion M, Murray E. Evaluation

of a new cutaneous topical anesthesia

preparation. Regional Anesthesia 1990;

15: 109±12.

3 Hallen B, Olsson GL, Uppfeldt A.

Pain-free venepuncture. Effect of

timing of application of local

anaesthetic cream. Anaesthesia 1984; 39:

969±72.

4 Hopkins CS, Buckley CJ, Bush GH.

Pain-free injection in infants. Use of a

lignocaine-prilocaine cream to prevent

pain at intravenous induction of general

anaesthesia in 1±5 year old children.

Anaesthesia 1988; 43: 198±201.

5 Arts SE, Abu-Saad HH, Champion

GD, et al. Age-related response to

lidocaine-prilocaine (EMLA) emulsion

and effect of music distraction on the

pain of intravenous cannulation.

Pediatrics 1994; 93: 797±801.

6 Bjerring P, Arendt-Nielsen L. Depth

and duration of skin analgesia to needle

insertion after topical application of

EMLA cream. British Journal of

Anaesthesia 1990; 64: 173±7.

7 Lander J, Hodgins M, Nazarali S,

McTavish J, Ouellette J, Friesen E.

Determinants of success and failure of

EMLA. Pain 1996; 64: 89±97.

8 Chang PC, Goresky GV, O'Connor

GO, et al. A multicentre randomized



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https://www.researchgate.net/publication/20511179_In_vivo_assessment_of_percutaneous_anaesthetic_preparations?el=1_x_8&enrichId=rgreq-8301d8ef57ac783c3dc7168e6f6ad4e5-XXX&enrichSource=Y292ZXJQYWdlOzI0NjQ2Njk1NjtBUzoxNTIxNDU2MDUxNzMyNDhAMTQxMzI4NTc0Nzg1Nw==




https://www.researchgate.net/publication/16699218_Pain-free_venepuncture_Effect_of_timing_of_application_of_local_anaesthetic_cream?el=1_x_8&enrichId=rgreq-8301d8ef57ac783c3dc7168e6f6ad4e5-XXX&enrichSource=Y292ZXJQYWdlOzI0NjQ2Njk1NjtBUzoxNTIxNDU2MDUxNzMyNDhAMTQxMzI4NTc0Nzg1Nw==





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study of single-unit dose package of

EMLA patch vs EMLA 5% cream for

venepuncture in children. Canadian


Unexpected benefit from`recovery' positioning

A 22-year-old otherwise fit woman of

Afro-Caribbean origin with suspected

ruptured ectopic pregnancy was taken

to the operating theatre for laparoscopy.

Rapid sequence induction was carried

out using etomidate and succinylcho-

line. Nitrous oxide, isoflurane and

mivacurium were used to maintain

anaesthesia and neuromuscular paralysis,

respectively. Since the laparoscopy

revealed a ruptured tubal ectopic preg-

nancy and 1200 ml of free blood in the

peritoneal cavity, laparotomy was car-

ried out using a low transverse incision.

Left salpingectomy was performed and

the abdomen closed after ensuring

adequate haemostasis. Fluids were

replaced as appropriate and the patient

remained haemodynamically stable

throughout the procedure. The patient

was then transferred onto the bed and

placed in the `recovery' position.

Although the patient was breathing

spontaneously through the tracheal

tube, she was still sedated and hence

she was not extubated. After a couple of

minutes, it was noticed that the sheets

underneath were soaked with blood.

The patient was transferred to the

operating table and re-anaesthetised.

Re-exploration revealed about 400 ml

of blood clots, and the bleeding to

originate from the area of ectopic

pregnancy. Left oophorectomy was

carried out which controlled the bleed-

ing. Laboratory tests ruled out any

coagulopathy. Subsequent anaesthetic

and clinical course was uneventful.

It is likely that if this patient had been

lying supine, the rebleeding would have

been suspected at a later time when the

patient would have shown clinical or

laboratory signs of continuing blood

loss. The `recovery' position placed the

abdominal wound in a dependant posi-

tion and allowed the blood to gravitate

onto the sheets fairly quickly.

S. Kannan

S. PatelCity Hospital,Birmingham B18 7QH, UK

A risk associated with theshared airway in reconstructivepalate surgery

Surgery of the head and neck often

involves the sharing of the airway

between surgeon and anaesthetist with

all the inherent risks. We would like to

share an unusual experience of such a

case involving cleft palate repair in an

18-month-old child.

The patient, undergoing a staged

repair of the hard and soft palate, was

anaesthetised in a standard fashion using

an inhalational induction and muscle

relaxation. The trachea was intubated

with an appropriately sized south facing

RAE tube. Once transferred to theatre,

the surgeon began to take a 3D palatal

impression with STD Firmer Set Vinyl

Polysiloxane Impression Material Putty.

The putty is workable in less than 60 s

and sets hard after 5 min. After allowing

the setting time, the surgeon attempted

to remove the mould but the putty had

inadvertently been wrapped around the

tube and had set hard (Fig. 11). The

putty was removed along with the

tracheal tube. A second tracheal tube

was obtained and re-sited. The patient

came to no harm. Risks of airway

dislodgement or obstruction are some-

times encountered with the use of the

Dott mouth gag but we have never

before been faced with a putty-related

extubation.

M. X. Clark

D. T. Knights

M. Henley

Nottingham City Hospital,Nottingham NG5 1PB, UK

Pre-oxygenation: silence theflush

Patients who refuse to have their faces

covered for pre-oxygenation may accept

oxygen blown at them through an

anaesthetic circuit. We are studying the

use of the Bain circuit and have found

that the addition of two breathing filters

eliminates the fierce draft and noise of

the emergency oxygen (Fig. 12), a

problem noted by others during pre-

oxygenation using a Hudson mask and

oxygen flush.

S. Robinson

W. F. S. Sellers

Kettering General Hospital,Kettering NN16 8UZ, UK

Figure 11



Paternal pulse oximetry

Recent correspondence concerning

`paternal complications' in the delivery

suite (Ghinigie et al. Anaesthesia 2001;

56: 603±4) reminded me of an incident

I observed several years ago during a

Caesarean section under spinal

anaesthesia. All had gone smoothly

and the mother had been delivered ofa healthy baby. As I was recording myobservations on the anaesthetic chart, Ichecked the position of the pulse

oximeter. Rather to my surprise, Inoted that the probe was now posi-tioned on the proud father's finger.

The attending midwife had removed itfrom the mother to allow an unim-peded hug with baby and placed it on

the father's finger to prevent alarming.Vigilance!

V. PerkinsDumfries and Galloway Royal

Infirmary,Dumfries DG1 4AP, UK

Figure 12



Unrecognised fatal anaphylactic reaction to propofol or fentanyl

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