Obstruction of airway equipment

Anaesthesia, 2002, 57, pages 183±208 .....................................................................................................................................................................................................................

Correspondence Outreach critical care is not the solution

I read with interest the editorial on the Acute Pain Service as a model for outreach critical care (Counsel. Anaesthesia 2001; 56: 925±6). In our hospital, the Acute Pain Service detected two cases of severe postoperative complications within the last 4 months while reviewing the patient's analgesia, prompting their return to theatre the same day. However, intensive care nursing resources are already stretched to their limits, and therefore outreach critical care is not the appropriate solution to the problem of inadequate or late initiation of appropriate intensive medical treatment at ward level. From my experience in medicine, surgery and Intensive Care, it appears to me that the problems are: doctors are not trained in caring for the critically ill; their consultants are often not familiar with critical care issues; their patients are scattered across the hospital; monitoring equipment is in short supply on the wards; and nursing staff skilled in monitoring and caring for the acutely ill patient on the ward are in very short supply. As a professional group we should address these issues ®rst. A ®rst step could be to assign doctors to work on a speci®c ward rather than with a ®rm. This would make it easier to literally ÔseeÕ the patients, hourly or more often if necessary. Second, training in Acute ¤ Intensive Care should be compulsory in all acute specialities at SHO level with an introduction to the subject for all House Of®cers. Monitoring equipment and nurses skilled in caring for patients who are unwell should not just be available in the Critical Care areas. However, most important is strong leadership from the top. Each and every Consultant should encourage his ¤ her juniors to acquire the knowledge and the skills needed to work with acutely ill patients in any acute speciality, and give the same positive feedback for Ó 2002 Blackwell Science Ltd

caring for an acutely ill patient as for a successful operation or the diagnosis of an uncommon disease. J. Kuehne St. Helier Hospital, Carshalton, UK E-mail: [email protected]

Outreach critical care

The recent editorial (Counsel. Anaesthesia 2001; 56: 925±6) rightly stated that ÔComprehensive Critical CareÕ [1] gave little guidance on how an intensive care ÔoutreachÕ service should function. The document was recognition by the Government that something needed to be done to improve the management of the critically ill hospital patient and that current critical care provision is insuf®cient to meet needs. The stated objectives of outreach, averting intensive care unit (ICU) admissions, enabling discharges and sharing critical care skills, are undoubtedly important, but are not the only goals. Early identi®cation and enabling critical care admission of appropriate patients is another aim. Clearly there is an overlap between outreach services and acute pain teams. This also applies to other services such as resuscitation and nutrition. Those of us involved in outreach know there are many hospital patients who are not receiving satisfactory care. Acute pain teams, although part of the solution, are not enough. Intensive care outreach has taken many forms from a single nurse, to 24 h, 7 days a week, multidisciplinary teams. It is unfortunate that outreach was introduced without adequate evaluation, but evidence will be forthcoming as the service is established. In the context of the National Health Service, and with the needs of the patient being paramount, it is relevant to ask several questions. These include: why has care on the wards failed, making outside support necessary?

Why should critical care units be providing this support? And, will intensive care outreach work without adequate numbers of critical care beds and staff? D. Goldhill A. McGinley The Royal London Hospital, London E1 1BB, UK

Reference

1 Department of Health. Comprehensive Critical Care: a Review of Adult Critical Care Services. London: Department of Health 2000.

Intensive care costs

I was much impressed by the hard work that went into the recent paper ( Jacobs et al. Anaesthesia 2001; 56: 643±7) on the costs of patient care in intensive care unit (ICU). It was plainly a timeconsuming and dif®cult study, which attempted to quantify, probably for the ®rst time, the cost differences between treating very ill patients and less seriously ill patients. No doubt their work will prove helpful to those who have to plan critical care services in the future and subdivide critical care beds into high dependency beds and intensive care beds. However, I have one criticism of the paper, which relates to the fact that Ônon-patient-speci®cÕ costs were excluded because they could not be related to individual patients. Whilst this argument may be technically valid, there is always an element of guesswork in calculating the costs of treatment in individual patients in a complex environment such as an ICU where bed occupancy and staf®ng levels ¯uctuate independently of each other and where nurses work ¯exibly to help each other out. We deceive ourselves if we claim 100% scienti®c accuracy in such studies. I think it would be reasonable either to divide the Ônon-patient-speci®cÕ costs equally between the patients, or to 183

Correspondence Anaesthesia, 2002, 57, pages 183±208 . ....................................................................................................................................................................................................................

devise a formula whereby these costs are calculated according to the daily cost of each patient's care, so that the patients who receive more input of care bear a larger proportion of the Ônon-patientspeci®cÕ costs. The cost of utilities, which includes such items as power, heating, water, the fabric of the building, portering, cleaning, waste disposal, medical gases and suction, is substantial and I suspect, often underestimated. On our 6-bedded ICU, in the year 1999± 2000, we paid £340 000 per annum for utilities. This represented £237 per patient day, or 20% of the mean total cost of a patient day, which was £1184 (excluding capital expenditure on replacement of equipment (Table 1). There is the danger that the true cost of critical care will be underestimated if papers of this kind exclude Ônonpatient-speci®cÕ costs and that this may lead to subsequent under funding of our specialty. W. Konarzewski Colchester General Hospital, Colchester CO4 5JL, UK A reply

We are glad to have the opportunity of replying to the letter from Dr Konarzewski. He is factually correct

in saying that the non-patient-speci®c costs were excluded from this study. We agree it may have been more appropriate to include the non-patient-speci®c costs as we are persuaded by the argument that the work may be misinterpreted as representing the total costs of patient care. The aim of the study was, however, to identify factors that could explain the variation in average daily costs between individual patients. It was for this reason, given the assumption that individual patients consume equal quantities of these non-patient-speci®c costs on a daily basis, that they were excluded. He is correct in thinking that non-patient-speci®c costs are substantial and although dif®cult to measure and assign to different clinical areas, can be as high as 50% of the total costs. Arbitrary methods of allocating these costs at a hospital level down to the intensive care unit (ICU) can also explain why one hospital would have signi®cantly higher non-patient-speci®c costs, than others. It would, however, be relatively simple to derive an average non-patient-speci®c cost per patient and accept that the variation in total nonpatient-speci®c cost between individual patients would merely be as a function of their length of stay. On the other hand, apportioning costs on the basis of Ôinput

Table 1 Annual cost of running ICU 1999±2000.

Nursing staff (regular) Utilities Drug costs Disposables Nursing staff (agency) Laboratory services Medical cover (non-consultants) Blood products Regular consultant sessions Radiology Special beds Technician (MTO3) Nutrition Physiotherapy Ward secretary

Total annual cost

Percentage annual cost

Cost patient.day)1

£624 672 £340 000 £162 689 £110 551 £89 596 £88 556 £75 700 £61 049 £39 600 £24 634 £22 038 £21 109 £15 500 £11 138 £9171

37% 20% 10% 7% 5% 5% 4% 4% 2% 1% 1% 1% 1% 1% 1%

£436 £237 £114 £77 £63 £62 £53 £43 £28 £17 £15 £15 £11 £8 £6

Number of patient days 1433. Bed occupancy 65%. Annual cost of ICU* £1 696 003. Cost per patient.day)1* £1184. *Excludes capital expenditure on replacement of equipment.

184

of careÕ, i.e. producing some kind of weighting system according to how many patient-speci®c resources are used, would be in our view, interesting but quite dif®cult. The dif®culty lies in that some of the non-patient related costs would be a function of their Ôinput of careÕ; however, others would not. We would suggest that whilst it is not ideal we will, in future, add the nonpatient speci®c costs of care. We thank him for his comments. C. Hibbert D. Edbrooke Royal Hallamshire Hospital, Shef®eld S10 2JF, UK E-mail: [email protected]

Cricoid pressure application by intensive care nurses

Dr Matthews points out that some staff who assist anaesthetists by providing cricoid pressure, including intensive care nurses, may not be adequately trained in the technique (Matthews. Anaesthesia 2001; 56: 915±17). In contrast to practice in the operating theatre, the assistant for rapid sequence induction (RSI) on the intensive care unit (ICU) is usually a nurse who has a very different training background to that of an operating department practitioner. The English National Board (ENB) regulates the curriculum for the Adult Intensive Care Course (ENB 100) for nurses. The ENB 100 syllabus does not mention RSI or cricoid pressure and there are regional inconsistencies in the teaching of skills and procedures in the ENB 100 course according to local interpretation of the syllabus [1]. As a result, a nurse on the intensive care unit may not have been taught this skill. An inadequately trained assistant may put patients at risk through failure to protect the airway adequately or by making laryngoscopy and intubation more dif®cult. Ad hoc training at the time of emergency intubation is not satisfactory and is no substitute for formal training and regular refreshment of the skill [2]. The practice of cricoid pressure and assisting with RSI should be included in the ENB 100 course so that practice of this Ó 2002 Blackwell Science Ltd

Anaesthesia, 2002, 57, pages 183±208 Correspondence . ....................................................................................................................................................................................................................

procedure in the ICU is consistent with that in the operating theatre. E. P. Segar Hospital for Sick Children, Toronto M5G 1 X8, Canada E-mail: [email protected]

References

1 Endacott R, Scholes J, Chellel A. Balancing stakeholder needs. A review of ENB 100 and 415 courses. Intensive and Critical Care Nursing 2000; 16: 3±13. 2 Segar EP, Boulanger CM, Davies AF, Allman KG. Knowledge and skill of cricoid pressure application by intensive care nurses: is formal training beneficial? Intensive Care Medicine 2001; 27: S290.

rate of this volume change is ¯ow. After the dicrotic notch (indicating aortic valve closure) the arterial pressure falls exponentially as the arterial system empties. The position of mean arterial pressure on this curve is also the position of mean arterial ¯ow leaving the arterial system. This equals mean ¯ow rate into the arterial system, which equals cardiac output. Time measurement taken as a tangent to the curve at mean arterial ¯ow determines this ¯ow rate. As this time is the time constant, it may be measured at any convenient part of the exponential curve[4], not necessarily at the mean arterial pressure level where interference around the dicrotic notch may exist. The relationship is represented by the equation: Cardiac output

Cardiac output determination using compliance

Measurement of the compliance of the arterial system may provide the key for obtaining cardiac output by using this compliance in combination with a calibrated arterial waveform. Arterial compliance has been dif®cult to measure, so that normal and pathological values are not available to the clinician, and changes occurring during most surgical operations are unrecognised. Interest in endothelial vasomotor function and the part played by nitric oxide have led to investigations of methods of measuring these changes [1]. Of particular interest is the measurement of pulse wave velocity [2], which is also a means for deriving compliance [3], as pulse wave velocity is inversely proportional to compliance and can be measured by a non-invasive method. As a calibrated arterial waveform can also be obtained by non-invasive methods, the ability now exists to combine the two systems to continuously monitor cardiac output by non-invasive means. Periodic compliance estimations will ensure that appropriate corrections are made for vasomotor changes. Compliance is a measure of volume change against unit pressure change. By multiplying the pressure scale of a calibrated arterial waveform by the compliance, the display becomes volume change plotted against time. The Ó 2002 Blackwell Science Ltd

Mean arterial pressure

Compliance Time constant

Con®rmation of this relationship is obtained by combining two accepted formulae: a Mean arterial pressure Cardiac output ´ Systemic vascular resistance [5]. b Compliance ´ Resistance Time constant [6]. So that: Systemic vascular resistance Time constant Compliance Substituting this product in formula [a] gives: Mean arterial pressure Cardiac output

Time constant Compliance

eventual display could therefore include independent values for cardiac output, stroke volume, peripheral resistance, compliance, and as well, a continuous display of the calibrated arterial waveform. This is an oversimpli®cation of a method for deriving cardiac output by non-invasive means. It has not previously been suggested but is an exciting possibility, which should be investigated. The value to anaesthetists and many other clinicians would be immense. D. I. Campbell Sydney, Australia

References

1 Doshi SN, Lewis MJ, Goodfellow J. Improving endothelial vasomotor function. British Medical Journal 2001; 323: 352±3. 2 Naka KK, Doshi SN, Ashton M, Frenneux MP, Jones CJH, Goodfellow J. Changes in pulse wave velocity in large arteries are nitric-oxide mediated. European Heart Journal 2000; 21: 357. 3 Kelman GR. Cardiovascular measurements. Applied Cardiovascular Physiology. Butterworths, Sydney 1971, 231. 4 Parbrook GD, Davis PD, Parbrook EO. Natural exponential functions. Basic Physics and Measurement in Anaesthesia, 3rd edn. Butterworth-Heinemann, Oxford 1990, 68±72. 5 Ganong WF. Dynamics of blood and lymph flow. Review of Medical Physiolog, 15th edn. Prentice Hall, Sydney 1991, 536. 6 Nunn JF. Elastic forces and lung Volumes. Applied Respiratory Physiolog, 3rd edn. Butterworths, Sydney 1987, 43.

This confirms: Cardiac output Mean arterial pressure Compliance Time constant

Manpower requirements when implementing a partial shift system for anaesthetic juniors

A programmed lap top computer or equivalent is capable of analysing and computing information derived from a calibrated waveform together with the information from compliance measurement, averaging the results over a period of about 20 s (to smooth out variations in stroke volume and heart rate) and displaying the results. The

The New Deal for trainee doctors sets limits to the duration and intensity of work junior doctors should do. Many anaesthetic juniors' working patterns breach the New Deal [1]. In an attempt to ensure compliance, many Trusts are considering or switching to the partial shift system for anaesthetic juniors. However, signi®cant manpower increases are 185


needed for proper implementation of the partial shift system. The needed increases may be calculated. Under the partial shift system, each 24-h on-call period is split between two trainees per on-call tier. There will therefore be 24 man-hours needed per day and 7 ´ 24 168 man-hours per week just for the on-calls for each tier. With n trainees per tier, the number of hours worked per week per trainee just for on-calls, is 168 ¤ n (Handover time is not included and may need to be separately factored for lengthy handovers, e.g. ITU). In addition, Royal College training guidelines requires a minimum of three accompanied lists per week per trainee [2]. At 4 per list (including shared pre-operative visits), each trainee will need to work at least another 12 h per week in addition to the on-calls. With a maximum limit of 64 h per week, the number of hours worked per trainee is given by the equation 12 + 168 ¤ n < 64. However, it is expected that trainees will also do x number of other lists, accompanied and unaccompanied. At 4.5 h per list (including pre-operative visits), this adds up to another 4.5x man-hours per trainee. Therefore, the equation above becomes 4.5x + 12 + 168 ¤ n < 64. Rearranging, n > 168 ¤ (64 ) 12 ) 4.5x). Each trainee is also entitled to 5±6 weeks' annual leave and 6 weeks' (28 days') study leave, which makes a possible 11±12 weeks' leave per trainee. Therefore, over the entire year, an additional 11 ¤ 52±12 ¤ 52 doctors is needed per trainee for prospective cover. Therefore, the ®nal formula should be: n > 168 1 11=52=64ÿ12 ÿ4:5x: Note, however, that mixing trainees and non-trainees on each on-call tier may reduce the additional fraction of doctors needed for prospective cover, as non-trainees tend to have less study leave entitlement than trainees. The averaged leave entitlement per doctor should then be used in the formula above. The value of n may thus be calculated from the corresponding value of x (Table 2). It is evident from Table 2, that the number of lists each

186

Table 2 The relationship between x the

number of lists (over the minimum three training lists) each trainee should do, and n the minimum number of trainees per on-call tier. Since we cannot have fractions of trainees, the ÔrealÕ number of trainees needed per on-call tier is given in the rightmost column.

x

n

'Real' number of trainees needed

0 1 2 3 4 5 6 7

3.91 4.29 4.73 5.29 5.99 6.90 8.14 9.93

4 5 5 6 6 7 9 10

trainee should do, in addition to the minimum training three lists, is critically limited by the number of trainees on each on-call tier. Some generalisations have been made. Each department should therefore adjust the calculations for their particular circumstances. Nevertheless, it is apparent that many Trusts will have dif®culty implementing the partial shift system without trainee expansion. Since trainee expansion is centrally controlled, perhaps other options more amenable to local control, such as consultant or nonconsultant career grade expansion, or rationalizing anaesthetic commitments, should also be considered when planning for partial shift. The formula may be adapted for expected changes to consultant work patterns, with the imminent cominginto-force of the European Work Time Directive and increasing clinical, administrative, supervisory and teaching workloads. M. Lim Northampton General Hospital Northampton NN1 5BD, UK E-mail: [email protected]

Acknowledgements I acknowledge the help of Dr Jan Szafranski, College Tutor, Kettering General Hospital and Dr Jill White, Clinical Director, Northampton General Hospital, in writing this letter.

References

1 Department of Health Internet publication March 2001 http://www.doh.gov.uk/juniordoctors/compliance.htm 2 Royal College of Anaesthetists publication. Guidance for Trainers; Issue 5 June 2001. Probability of winning the National Lottery

I read with great interest the review article on risk perception and communication: recent developments and implications for anaesthesia (Adams & Smith. Anaesthesia 2001; 56: 745±55). The topic is indeed a confusing one and many concepts are dif®cult to grasp even for health professionals. The general public would be expected to ®nd the subject even more confusing. When it comes to the National Lottery however, their knowledge of risk seems slightly better than one would expect. Indeed a signi®cant proportion of the population are aware that the chance of winning the jackpot is somewhere in the region of 14 million to one against. This ®gure is far greater than the 2.8 million to one quoted in the aforementioned review. On closer inspection, it appears that all the ®gures quoted in Table 2 of the review are incorrect. Additionally, the authors incorrectly quote the odds of obtaining four balls plus the bonus ball. This is an irrelevance anyway, as this situation does not produce a prize any greater than obtaining four balls alone. With this in mind, I believe Table 3 should read as follows (please refer to Table 3): M. Fair®eld Leicester, UK E-mail: mfair®[email protected] A reply

We would like to thank Dr Fair®eld for his constructive comments and the Editor for offering us the opportunity to correct those errors that have been brought to our attention since the publication of our review article. On reviewing our original source [1] that provided the National Lottery proba-

Ó 2002 Blackwell Science Ltd


Table 3 Two different methods of conveying National Lottery probability data. Balls correct 3 4 5 5 6

balls balls balls balls + bonus ball balls

1 1 1 1 1

: : : : :

57 1032 55 491 2 330 636 13 983 16

bility data for Table 2, we should have reported that the probabilities quoted were for a £5 stake. Hence the probability data in our table differ by a factor of 5 from that quoted by M. Fair®eld above. We therefore agree that the probability of predicting six balls in the National lottery is 1 in 13 983 16 and this correctly represents the odds for a £1 stake. It has also been brought to our attention that the risk ladder on p. 749 quotes the risk of death from anaesthesia as given in the ÔReport on Con®dential Enquiries into Maternal Deaths for the years 1988 and 1990Õ [2] as 1 in 58 823. The correct ®gure is in fact 1 in 588 235 as implied in the text. We have therefore taken this opportunity to revise the Risk Ladder (Fig. 1), correcting the above errors as well as amending the orientation of the logarithmic graph lines that were inverted. We regret that these errors occurred, however, we feel they further emphasise the dif®culties inherent in ®nding, interpreting, and presenting risk information in a user-friendly form, even for supposedly numerate anaesthetists such as ourselves!

1754 96 1.8 0.043 0.0072

: : : : :

100 100 100 100 100

000 000 000 000 000

Anaesthesia induction rooms ± sheer luxury

Dr Sawyer's experiences in Canada easily translate to the UK (Sawyer.

Anaesthesia 2001; 56: 1006). I abandoned the use of anaesthetic rooms in 1993. Inducing anaesthesia, then disconnecting all monitoring and the breathing system, and taking the patient for an apnoeic perambulation on a sightseeing tour of the theatre suite is frankly barmy, if not downright hazardous. Objectively, if we indulge this practice, we could be accused of pandering to personal insecurity, or worse, some form of professional narcissism. What is the point of establishing minimum standards of monitoring, teaching our trainees that failure to adhere to

A. M. Adams A. F. Smith Royal Lancaster In®rmary, Lancaster, UK E-mail: Andrew.Smith@ l.baytr.nwest.nhs.uk

References

1 Barclay P, Costigan S, Davies M. Lottery can be used to show risk [Letter]. British Medical Journal 1998; 316: 124. 2 Department of Health. Report on Con®dential Enquiries into Maternal Deaths in the United Kingdom, 1988±1990. London: The Stationery Of®ce 1994. Ó 2002 Blackwell Science Ltd

Figure 1

187


these standards is a cruci®xion offence, then encouraging the baf¯ed trainee to suspend disbelief while we disregard all the rules and move the patient to the substantive anaesthetic venue? Inducing anaesthesia in theatre is in my experience safer, faster, and allows plenty of space for inserting lines without desterilizing the equipment in a cramped anaesthetic room. Moreover, after only a very short time, the surgeons were re-educated into not interfering with the patient until prepared for surgery. Indeed, many of the surgical trainees took to observing the mysterious rites of anaesthesia with a growing fascination, understanding, and dare I say it, respect? Several have since approached me for airway and ÔlinesÕ training, so I guess they must have enjoyed the anaesthetic ¯oorshow. Several interesting spin offs have bene®ted patients. One unfortunate who suffered an anaphylactic reaction at induction owes his survival (unscathed) to the ready presence of plenty of pairs of hands, best equipment, monitoring and space that in-theatre induction afforded. Moreover, I enjoy sharing my disasters with the rest of the team ± it is less stressful, not more stressful, and has led to more referrals of anaesthetic pre-assessment. The resource released by not having to equip anaesthetic rooms could be used for something of value: critical care beds, nurses to staff them and so on. Surely, in the interest of safety it is time to have a little more con®dence in our profession, and emerge from the anaesthetic room into the daylight world of the operating theatre. M. Bellamy St James's University Hospital, Leeds LS9 7TF, UK E-mail: [email protected]

Compartment syndrome

We were interested to read the recent paper (Turnbull & Mills. Anaesthesia 2001; 56: 980±7) describing three cases of compartment syndrome associated with the Lloyd Davies position. They

188

are to be congratulated on their extensive review of the literature. Although they accept that epidural analgesia may result in hypotension and may reduce perfusion in the elevated limb, they further comment that this does not mask the signs of compartment syndrome. However, this reduction in blood ¯ow in the limb may be a causative factor in compartment syndrome. The three cases they describe all had epidural analgesia, as did the patient referred to in ref. 24 [1]. A further case of bilateral compartment syndrome has been reported by Tuckey [2], which also involved epidural analgesia. We are aware also of a medico-legal case when prolonged urological surgery with epidural analgesia resulted in compartment syndrome. We have both been on the staff of St Mark's Hospital, a hospital specializing in lower abdominal surgery, for more than 25 years during which time we have performed several thousand operations in the Lloyd Davies position. No patients had epidural analgesia and we are able to report that none of these patients developed compartment syndrome. Prior to operating, the surgeon always checked the position of the patient on the table to ensure there was no compression or undue strain on the legs. Furthermore, care was taken to ensure that the second assistant with the tiresome task of pulling on the retractor for many hours while standing between the patient's legs did not compress the legs as he tired. Prior to the adoption of the Lloyd Davies position, patients having lower abdominal surgery, and in particular abdomino-perineal resection of the rectum, had the operation in three stages. Initially, the patients were supine when the abdomen was opened to assess the operability of the tumour. The patients were then turned on their side when the rectum was excised and ®nally returned to the supine position for closure of the abdomen. The adoption of the Lloyd Davies position obviated the need for these procedures and reduced morbidity. Turnbull & Mills quite correctly refer to the original paper by Mr Lloyd Davies [3] but the diagram they have produced is incorrect as is their ref. 25.

The buttocks should be in line with the end of the table; likewise the clamp holding the stirrups is shown almost midway up the table when in fact it should be held at the end of the table. The legs are not strapped but held loosely on the calf rest and secured by velcro straps. Mr Lloyd Davies replaced the sandbags under the sacrum with a beanbag. Shoulder rests were initially used but were dispensed with when the non-slip mattress was introduced. No cases of brachial plexus palsy were noted as the arms were placed by the patient's side. We both worked with Mr Lloyd Davies who was a slow but meticulous surgeon. He had been known to take up to 12 h for a complicated major surgical procedure and compartment syndrome was conspicuous by its absence. L. Kaufman P. R. Hawley London, UK E-mail: [email protected]

References

1 Goldmsith AL, McCallum DID. Compartment syndrome as a complication of prolonged use of the Lloyd Davies position. Anaesthesia 1996; 51: 1048±52. 2 Tuckey J. Bilateral compartment syndrome complicating prolonged lithotomy position. British Journal of Anaesthesia 1996; 77: 546±9. 3 Lloyd Davies OV. Lithotomy-Trendelenburg position for resection of rectum and lower pelvic colon. Lancet 1939, 74±6.

Obstruction of airway equipment

We would like to report an interesting reason for an obstructed pattern of breathing during a general anaesthetic. A laryngeal mask airway was inserted after induction of anaesthesia in an ASA II patient. Despite an easy insertion and adequate depth of anaesthesia, the respiratory pattern appeared obstructed. The capnograph trace con®rmed the clinical picture. The situation was not



Figure 2

improved by a jaw lift, so the laryngeal mask airway was removed. At no time did the patient desaturate. On removal of the laryngeal mask, a foreign body was noted. Figure 2 shows the laryngeal mask airway with a black bung within it (arrow). This was in fact the pneumatic seal of a Rusch facemask. This equipment dysfunction highlights two important principles: the need to always check the patency of airway devices and to remove an airway device if the breathing pattern appears obstructed despite simple airway manoeuvres. D. Cameron J. Onslow Royal Perth Hospital, Perth 6847, Western Australia

2 It was electrostatic and so may have ÔstuckÕ to the sucker when the cover was pulled off. 3 It curled on stretching and therefore may have wrapped itself around the sucker, rendering itself less conspicuous. The electrostasis and curling were demonstrable by testing later. There were other potential problems relating to this type of plastic: 1 The plastic is radiolucent and if inhaled would not have shown up on X-ray. 2 If it were sticking to the sidewall of a bronchus, it would be dif®cult to see. We need to package equipment so as to prevent contamination, but the packaging itself must be designed to ensure that it cannot cause problems.

piece of clear ¯exible plastic (Fig. 3). The waste bin was searched, and a piece was discovered to be missing from the inner wrapping of the Yankauer sucker matching the piece spat out (Fig. 4). This case demonstrates that a foreign body may be introduced inadvertently into the airway from ÔbenignÕ sources. On this occasion it was a piece of wrapping plastic, which had three properties that may have led to this incident: 1 It was transparent so that the sucker that it wrapped could be seen, but therefore inconspicuous and unnoticed when the patient was intubated.

The laryngeal mask airway is a common method of securing the airway during elective and some emergency

Figure 3

Figure 4

J. A. Lack Salisbury Hospital, Salisbury SP2 8BJ, UK E-mail: [email protected]

Yet another foreign body in a laryngeal mask airway

Another airway foreign body

An ASA III, slightly overweight, 68-year-old woman presented for varicose vein surgery. She suffered from mild pulmonary insuf®ciency. She was induced with increments of propofol to 150 mg, and a laryngeal mask inserted. She did not settle, and was given a further 50 mg propofol. Since she was salivating profusely, the mask was withdrawn again, her pharynx cleared using a Yankauer sucker, and the laryngeal mask reinserted. She started coughing persistently, and eventually was given atracurium 30 mg and intubated uneventfully. At the end of surgery she was extubated. She again started coughing, and then spat out a small Ó 2002 Blackwell Science Ltd

189


An unexpected complication resulting from the use of a laryngeal mask during an operation to remove a branchial cyst

Figure 5

Figure 6

operations. I would like to report a foreign body that I came across in a sterile packed laryngeal mask airway, which could have had serious consequences. Figure 5 shows the laryngeal mask in question. The foreign body is apparently one of the cleaning rods that are used to decontaminate the laryngeal mask airway (Fig. 6). One of the cleaning rods had accidentally come loose and lodged itself in the laryngeal mask. Foreign bodies in laryngeal masks have been reported previously [1, 2]. The importance of inspection of the laryngeal mask airway visually both inside and outside cannot be overemphasised.

the branchial cyst dropped back into the operative ®eld (Fig. 8). The laryngeal mask had evidently displaced the cyst superiorly so that it lay deep to the edge of sternomastoid. The removal of the cyst proceeded uneventfully, and the patient made an uneventful recovery. The patient was fully informed of the complication postoperatively and has since been discharged back to the care of her GP. The use of laryngeal masks in head and neck surgery has become common in the last 10 years. Complications associated with the use of such airways are well recognised. However, our literature search has failed to reveal any complication similar to the one described above. Despite the fact that the operation involved a consultant anaesthetist, consultant Maxillofacial surgeon and a ®nal year specialist registrar, all of whom were cognizant of the anatomic distortion produced by laryngeal masks, this complication still occurred. The authors urge caution when using such airways when removing neck lumps.

A 42-year-old lady presented to the department of Oral and Maxillofacial surgery at Worthing hospital with a 5-year history of a painless lump in the left side of her neck. Examination revealed a mobile, ®rm, elongated, 4 ´ 3 ´ 2 cm ovoid mass in the left jugulodigastric region. Subsequent, ®ne needle aspiration and CT scanning con®rmed the presence of a branchial cyst. On admission, the position of the cyst was marked on the skin. Once anaesthetised, the patient was placed in a Ôhead upÕ position, with the head extended and turned to the right. The mass was palpated again and a skin crease incision co-inciding with the pre-operative skin marking was selected. Dissection proceeded through platysma and the anterior border of sternomastoid was de®ned. As the connective tissue over the presumed cyst was opened, whilst still in a very super®cial plane, both surgeons were disconcerted by the unmistakeable appearance of the laryngeal mask covered by strands of middle constrictor and pharyngeal mucosa (Fig. 7). At this point, on discussion with the anaesthetist, it was agreed that the laryngeal mask should be exchanged for a tracheal tube. Prior to this manoeuvre, stay sutures were placed in the edges of the pharyngeal defect to facilitate subsequent closure. The wound was then covered with damp gauze, the tubes were exchanged and the area re-draped. With the removal of the laryngeal mask,

End tidal carbon dioxide (FE¢CO2) monitoring is an essential monitor for anaesthetic safety [1]. Sudden disappear-

Figure 7

Figure 8

A. W. Wilson D. Macpherson V. Santhanam St Richards's Hospital, Chichester PO19 4SE, UK E-mail: [email protected] R. Edwards Worthing Hospital, Worthing BN11 2DH, UK A phantom capnograph trace

K. Srikanth Burnley General Hospital, Burnley BB10 2PQ, UK E-mail: [email protected]

References

1 Riley RH, Browning FS. Another foreign body in a LMA. Anaesthesia 1996; 51: 286±7. 2 Conacher ID. Foreign body in a laryngeal mask airway. Anaesthesia 1991; 46: 164. 190



ance of the capnograph waveform is one of the earliest indicators of patient disconnection from the breathing circuit. We would like to report a circumstance in which disconnection may go undetected during spontaneous breathing by capnograph alone. In our hospital, we routinely use circle systems (Bleasorb) with low ¯ow (< 2 L.min)1), to conserve anaesthetic gases. The gas sample for the side stream capnograph is drawn from the Y connector and returned to the circle system just proximal to the expiratory one-way valve through a ®lter. After a routine general anaesthetic for orthopaedic surgery with low ¯ow and spontaneous breathing, the sevo¯urane and nitrous oxide were turned off and oxygen was continued at 1 L.min)1, to allow plastering and smooth emergence from anaesthesia. When the patient was to be transferred to the trolley, the breathing system was disconnected from the laryngeal mask. To our surprise there was a continued capnograph waveform with a rate of 8.min)1 and an FE¢CO2 of 3.5 kPa. The apnoea alarm, which was set at 3 kPa, was not triggered even after 150 s. This waveform continued for more than 3 min. Careful observation of the circle system revealed rhythmic movement of the reservoir bag and the inspiratory unidirectional valve, which coincided with the inspiratory part of the phantom waveform. The phantom rate increased with increasing fresh gas ¯ow, along with a reduction in the FE¢CO2 value, and the reverse occurred with a decrease of the fresh gas ¯ow. The capnograph trace disappeared with disconnection of the sample return tube and reconnecting it distal to the expiratory unidirectional valve near the reservoir bag. The return of the capnograph sample gas to the expiratory limb of the circle system at the rate of 200 ml.min)1 resulted in reverse ¯ow of expired CO2 from the expiratory limb. This was intermittently interrupted by fresh gas ¯ow. The low fresh gas ¯ow intermittently opened the inspiratory valve when the pressure in the proximal compartment was suf®cient to lift the diaphragm. This resulted in intermittent sampling of fresh gas and previously


expired gas resulting in a square wave capnograph trace. The re-circulation of sample gas at 200 ml.min)1 prolonged the capnograph trace for more than 3 min. The phantom square wave capnograph after disconnection was reported during positive pressure ventilation with a Servo 900C ventilator by Ginosar and Baronav [2]. This was explained as due to continuous reverse ¯ow of previously expired gas from the expiratory tube, intermittently interrupted by the attempted positive pressure ventilation. Disconnection during positive pressure ventilation may be detected earlier than with the spontaneously breathing patient as a low airway pressure alarm gives additional safety. We suggest connecting the sample return tube between the expiratory valve and the absorber in the circle system and extra vigilance is required during low ¯ow anaesthesia to prevent disconnection. Girish T. M. W. Long South Warwickshire General Hospital, Warwick CV34 5BW, UK

References

1 Recommendations for Standards of Monitoring During Anaesthesia and Recovery. The Association of Anaesthetists of Great Britain and Ireland, 2000, London. 2 Ginosar Y, Baranov D. Prolonged ÔphantomÕ square wave capnograph tracing after patient disconnection or extubation. Potential hazard associated with the Siemens Servo 900c ventilator. Anesthesiology 1997; 86: 729±35.

Phantom anaesthetic vapour

We describe the unusual detection of des¯urane in the breathing circuit (circle system) by the Hewlett Packard (HP) Anaesthetic Gas Monitor (AGM) M1062A when set to automatic agent detection mode during general anaesthesia for hysterectomy in an adult female patient. All HP AGMs in this hospital were set to automatic agent detection mode by default. For the ®rst

patient on the list, the HP AGM was manually set to detect sevo¯urane during an anaesthetic that involved the patient spontaneously breathing sevo¯urane in a nitrous oxide ¤ oxygen mixture through a circle rebreathing circuit. At the conclusion of the procedure, the sevo¯urane vaporiser was turned off and the fresh gas ¯ow through the breathing circuit was stopped. The following patient was scheduled for a total hysterectomy under general anaesthesia. Intravenous induction was followed by maintenance with iso¯urane in nitrous oxide and oxygen. The HP AGM detected des¯urane in the breathing circuit instead of iso¯urane. An immediate check of the anaesthetic machine con®rmed the absence of a des¯urane vaporiser on the machine. Checking of the HP AGM revealed that it was on the automatic agent detection mode. The problem persisted for approximately 5 min before the HP AGM correctly identi®ed iso¯urane. The HP AGM identi®es anaesthetic vapour by infrared absorption [1]. In the automatic agent detection mode, it identi®es the vapour with the highest concentration and measures its concentration. It has four ®lters in the range of 10±14 lm. The ®rst, third and fourth ®lters have different absorption peaks for iso¯urane, halothane and en¯urane [1]. The second ®lter acts as the reference since the above-mentioned anaesthetic vapours have similar absorption peak at 10.6 lm [1]. However, the HP AGM has similar absorption peaks for sevo¯urane and des¯urane [1]. Because of this limitation, the HP AGM is preprogrammed to detect one agent by default in the automatic agent detection mode; this may be sevo¯urane or des¯urane. In this hospital, all the HP AGMs are programmed to detect des¯urane in the automatic agent detection mode. Hence the detection of des¯urane in the breathing circuit at the start of the second patient's anaesthetic. The reason for this decision is unknown to us. The unusual detection of des¯urane occurred because the HP AGM was set to automatic agent detection mode. At the conclusion of the ®rst case, there was residual sevo¯urane in the

191


breathing circuit. Furthermore, there may not be enough time for adequate ¯ushing of the breathing circuit prior to the start of the next anaesthetic. At the beginning of the second case, the concentration in the breathing circuit of sevo¯urane compared to iso¯urane was much higher; this lead to the wrong identi®cation of des¯urane by the HP AGM. With continued ventilation, the iso¯urane concentration in the breathing circuit subsequently built up and the HP AGM then correctly identi®ed iso¯urane as the anaesthetic agent in use. We suggest that when using the HP AGM, the selection of anaesthetic agent detection mode be set manually instead of being left on the automatic agent detection mode. We also reiterate that with the use of a circle rebreathing circuit, it should be ¯ushed through with oxygen to void the anaesthetic volatile agent prior to the start of anaesthesia for the next patient [2]. This will avoid the situation of wrongly identifying another anaesthetic agent from the one being used. D. Kang N. C. Hwang Singapore General Hospital, Singapore

References

1 HP Component Monitoring System User's Reference Manual: 2, Chapters (12±24), 8th edn. May 1995. 2 McGraw TT, Keon TP. Malignant hyperthermia and the clean machine. Canadian Journal of Anaesthesia 1989; 36: 530±2.

A reply

Thank you for allowing us to respond to this letter. Drs Kang and Hwang correctly describe the gas measurement technology and limitations of the M1026A Anaesthetic Gas Module (AGM) in a previous version that at that time was able to measure any one of the ®ve anaesthetic agents when selected manually, but could automatically identify only three of them, in this particular case halothane, iso¯urane and des¯urane or sevo¯urane. Note that the

192

reported situation would not have occurred with the current version of AGM, which is able to automatically identify all ®ve agents. Due to the described ambiguity in the absorption properties, the device cannot distinguish between des¯urane and sevo¯urane. Therefore, the user needs to con®gure the device to assume DES (if des¯urane is regularly used at this institution) or SEV (if sevo¯urane is commonly used) in AUTO identi®cation mode. If both gases are used in different cases, there is no alternative to either selecting the appropriate agent in MANUAL mode or con®guring AUTO to assume the appropriate agent by default. The phantom vapour detection results from the combination of the above effect with a second effect: one agent can be measured by the device at a given time only. If there is a transitory mix of two agents in the breathing system due to switching from one agent to another, the dominant agent with the higher concentration is identi®ed and displayed. In the reported case, the correct display would have been sevo¯urane (still dominant from the previous case), which was misinterpreted by the device as des¯urane because the user had switched the device back to AUTO identi®cation mode, but did not set sevo¯urane as the default agent in AUTO. The expected display of ISO did in fact appear as soon as iso¯urane started to become the dominant agent in the breathing system. It is important to note that the automatic agent identi®cation is a safety feature in itself because it draws the user's attention to a discrepancy between what the anaesthetist decided to deliver to the patient and what is really detected. In the reported case the wrong agent display has in fact triggered the user to take a deeper look at the problem. Also, a warning message (AGT mixture) is displayed on the monitor as long as more than one agent is detected, and a question mark is displayed next to the displayed concentration value to make the user aware of this situation. The reported problem when using the 3-agent-ID version of the AGM can

be avoided by complying with the following rules: 1 The breathing system should be ¯ushed with fresh gas when changing patients or agents. 2 The user needs to con®gure the device for being able to detect and identify des¯urane or sevo¯urane as the third possible agent: if the hospital is using sevo¯urane (and no des¯urane), the AUTO mode should be con®gured to SEV, and if des¯urane is used (and no sevo¯urane), then DES would be the correct default con®guration. In case both des¯urane and sevo¯urane are used on the same machine in different cases, the correct agent to be measured should be selected manually. W. Huehn Phillips Medical Systems E-mail: [email protected]

Anaesthetic machine safety ± the story continues

I read with interest the recent correspondence regarding the anaesthetic machine checklist (Bhargava & Dexter. Anaesthesia 2001; 56: 1007±8, Shirley & Pogson. Anaesthesia 2001; 56: 1008±9) and would like to raise further points for discussion. Drs Bhargava and Dexter state that Ômany machines do not have paramagnetic oxygen analysers built in to indicate oxygen failure ¼Õ. I agree that many machines, especially older ones, do not have paramagnetic oxygen analysers built-in, but battery driven fuel cell oxygen analysers can easily be utilised thereby overcoming this problem. Furthermore, the Association of Anaesthetists of Great Britain and Ireland (AAGBI) Checklist for Anaesthetic Apparatus 1997 [1] clearly states during the introduction that: ÔAs before, the working party bases this checklist on the obligatory use of an oxygen analyser on every anaesthetic machine. This approach will ensure that hypoxic mixtures are not delivered to patients and also detect mis®lling of oxygen cylinders, contamination of liquid oxygen reservoirs and incorrect connections within the machine.



I agree that the presence of a hypoxic guard may have prevented the unnecessary death of the young child at Newham General Hospital, but herein lies a further issue. It could be argued that it was not the lack of a hypoxic guard or the apparent lack of an oxygen analyser on the machine that led to disaster, but that it was caused by the Ôhuman factorÕ; namely, a piece of specialised anaesthetic equipment being used by someone unfamiliar with the safety features, pre-use checklist or its proper usage. In simple terms, it was not the machine but the man behind the machine. Training, I believe, is the cornerstone of good clinical practice and safety. Therefore, we as anaesthetists have a duty of care to help train non-anaesthetic personnel in the correct procedures if they are to use these pieces of anaesthetic equipment in areas such as Accident and Emergency. Continuing on a similar theme, one must welcome any potential advance in anaesthesia that may improve the quality of care that we can deliver. It was therefore interesting to read the letter from Drs Shirley and Pogson regarding the possibility of improved safety using computerised aide-memoires. The use of computer technology in anaesthesia is becoming prevalent but I would like to introduce two issues. The AAGBI guidelines state clearly that ÔIt is strongly recommended that a record of the check performed should be kept; this is best done by the use of a speci®c logbook attached to each anaesthetic machineÕ. I have recently completed a 6-month post as a resident in paediatric intensive care at Guy's Hospital, London. A large number of patients on the unit either present with upper airways obstruction or have the potential to develop it, for example, post extubation. The use of an inhalational induction was therefore a common procedure. For this purpose we had an old Boyles machine, which utilised both cylinder and pipeline supply, with a fuel cell oxygen analyser attached. The machine was checked every day and also prior to use, and this was recorded by the ticking of boxes against each of the criteria laid down in the AAGBI 1997 checklist. This


acted as not only and aide-memoire but as a visual record that the check had been performed and by whom. Of course this system could lend itself to being computerised to facilitate the process. I believe that not only the performance of pre-operative checks but also the recording of these checks is important, especially in this litigious age. The maxim ÔIf you did not record it then it did not happenÕ could quite easily slip from a lawyers lips. Finally, I fully welcome the comments from Dr Birks and feel that it is appropriate that the checklist is updated to incorporate new technology, and that this be done sooner rather than later. S. A. Hellewell Southampton General Hospital, Southampton, SO16 6YD, UK E-mail: [email protected]

Reference

1 Checklist for Anaesthetic Apparatus, 2. London: Association of Anaesthetists Great Britain and Ireland 1997.

Halothane vs. sevo¯urane in the dif®cult airway

We read with interest the recent study (Girgis et al. Anaesthesia 2001; 56: 613±15). The authors suggest that sevo¯urane may be superior during gas induction of patients with dif®cult airways although they only suggest that sevo¯urane is the better agent Ôin terms of speed of awakeningÕ. While more rapid awakening would seem to be desirable, we believe that this would make airway management more dif®cult. Following an inhalational induction, there is a period of airway manipulation both to examine the airway and to achieve de®nitive airway access (usually by intubation). If the depth of anaesthesia lightens too quickly, then the patient may develop an acute airway obstruction due to laryngospasm which, in a patient with an already compromised airway, may prove to be life threatening. This study demonstrates well that the concentration of sevo¯u-

rane may fall from 2 MAC to 0.23 MAC in only 3 min. We would argue that this would not provide ideal conditions for managing a dif®cult intubation. In light of the above, whilst we agree with the authors that sevo¯urane is superior in terms of speed of awakening, we believe that halothane remains the most appropriate volatile to use for the Ôdif®cultÕ airway, as changes in depth of anaesthesia are more gradual. S. J. Mills E. P. McKiernan Royal Preston Hospital, Preston PR2 9HT, UK E-mail: [email protected]

A reply

Thank you for the opportunity to reply to Dr Mills and Dr McKiernan's letter, referring to our recent article. Although it is our opinion that sevo¯urane is an overall better agent for induction of anaesthesia in patients with dif®cult airways, we were careful not to make such a statement in our article. Instead, we limited ourselves to suggesting that patients may wake up more rapidly if the airway obstructs completely during inhalation induction of anaesthesia. Our attitude was obviously based on our recognition that various factors may in¯uence the preference of individual anaesthetists. However, we are happy to continue the debate of halothane vs. sevo¯urane in dif®cult airway management. We would therefore like to ask the readers to consider three possible scenarios, which could occur while dealing with anticipated dif®cult airways. Scenario 1: Inhalation induction is complicated by complete airway obstruction. Our paper suggests that sevo¯urane may be the better agent in this situation, as patients would wake up more rapidly. Scenario 2: Inhalation induction is uncomplicated and when adequate depth of anaesthesia is reached, direct laryngoscopy and tracheal intubation are carried out in a swift and straightforward fashion. We would then suggest that sevo¯urane is as good as

193


halothane as the change in depth of anaesthesia during the short period of airway manipulation with either agent would be insigni®cant. Scenario 3: Inhalation induction is uncomplicated and when adequate depth of anaesthesia is reached, attempted laryngoscopy fails to reveal the larynx or attempted intubation of a visualised larynx cannot be achieved. If using sevo¯urane, one would then re-apply the facemask, maintain anaesthesia and consider the available options. These could include waking the patient up, using the ®breoptic laryngoscope, performing tracheostomy or even switching to halothane (if it is anticipated that further attempts at direct laryngoscopy and intubation do carry a reasonable chance of success). In the latest event, nothing would have been lost and had halothane been used from the start, the options would have remained the same. Therefore, in scenarios 2 and 3, both halothane and sevo¯urane are equally safe, if used appropriately. However, one can never know which patient may present as the ®rst scenario. Accordingly, we contend that sevo¯urane may indeed be the best option when starting an inhalation induction. Y. Girgis The Royal Orthopaedic Hospital, Birmingham, UK E-mail: [email protected]

imately 24 h previously when his shirt had caught ®re. Although he had no symptoms or signs of burns to his airway, the mechanism of injury gave a high index of suspicion. In addition, he had a severe ®xed kyphosis secondary to long standing ankylosing spondylitis, with mouth opening of only two ®ngerbreadths due to apposition of his chin to his sternum. From previous anaesthetic records he had been increasingly dif®cult to intubate, requiring an awake ®breoptic intubation for his last anaesthetic 2 years previously. The awake ®breoptic intubation was performed by two consultants experienced in the technique. Standard monitoring was attached, and 2 L.min)1 oxygen administered via a nasal prong. A 1-mg bolus of midazolam was given, and a remifentanil infusion commenced at 0.1 lg.kg)1.min)1. Having anaesthetised the nasopharynx with topical cocaine and 4% lidocaine, the bronchoscope (Olympus LF-2), loaded with a 6.5-mm armoured tracheal tube, was advanced through the right nostril into the pharynx. The larynx was dif®cult to visualise due to its anterior position, and was also red and oedematous. After 10 min of attempted intubation, the scope was apparently manoeuvred through the cords into the trachea.

C.M. Frerk Northampton General Hospital, Northampton, UK

194

However, since the mucosa was grossly oedematous, no tracheal rings could be identi®ed and a satisfactory view of the carina could not be obtained. It was then decided to connect the sample tubing of the capnograph to the suction port of the bronchoscope (Fig. 9). When the suction port was opened, a satisfactory end tidal carbon dioxide trace was displayed, con®rming that the scope was indeed located in the trachea (Fig. 10). A 6.5-mm armoured tube was railroaded over the scope, and anaesthesia induced using propofol. Although capnography should always be used once the tracheal tube has been positioned [1], it is rarely necessary prior to this in an awake patient. Its use has been described as a respiratory rate monitor during ®breoptic intubation [2], but this case illustrates that when extreme anatomical changes are encountered, all the techniques in an anaesthetist's armoury may need to be called upon in order to achieve a secure airway. D. S. Earl S. Shinde K. E. Bullen J. A. Carter Frenchay Hospital, Bristol BS16 1LE, UK E-mail: [email protected]

Novel use of capnography during an awake ®breoptic intubation

Normally during a ®breoptic intubation, visual identi®cation of airway anatomy ensures correct placement of a tracheal tube. We would like to report a case in which capnography was utilised to con®rm correct scope placement during a particularly dif®cult intubation. A 54-year-old gentleman presented for debridement and split-skin grafting of 45% truncal burns, sustained approx-

Figure 10

References

Figure 9

1 Recommendations for Standards of Monitoring During Anaesthesia and Recovery, 3rd edn. The Association of Anaesthetists of Great Britain and Ireland December 2000. 2 Neidhart G, Kovac AK, Bremerich DH, Kessler P. Remifentanil-propofol for bronchoscopic fiber optic intubation



under capnographic control. Anaesthetist 2000; 49: 523±6. Arterial line insertion

If the trans®xion technique of nonseldinger arterial cannulation is used, when the metal needle stylet is removed, an epidural loss of resistance syringe with plunger pulled back is attached to the plastic cannula. The plastic cannula is slowly withdrawn; when in the lumen of the artery, the syringe will slowly ®ll with blood and the cannula can be advanced with the knowledge that it remains in the artery. Because the splinting effect of the metal stylet is lost, we rotate the cannula using the syringe, screwing the cannula into the artery, which reduces skin and arterial wall resistance to advance and prevents buckling of the cannula. For direct nontrans®xion cannulation, the ¯ashback chamber on the metal stylet can be changed for a loss of resistance syringe, giving more time for manoeuvres. M. Dollman W. F. S. Sellers Kettering General Hospital, Kettering NN16 8UZ, UK

Flush volume for a vascular access device

I would like to report a study looking at the volume of ¯ush required after using a Port-a-cathÒ II vascular access device. Several indwelling vascular access devices are available for administration of long-term parenteral therapy. When present, such a catheter may also be used for intravenous induction of general anaesthesia. Following its use, ¯ushing of the system is crucial to remove residual drugs. Failure to carry this out adequately could be catastrophic should even a small volume of drug be ¯ushed intravenously when the line is next used. This is particularly pertinent to paediatric anaesthetic use. The effectiveness of ¯ushing will depend on various factors including the volume of ¯ush. A commonly used device is the Port-a-cathÒ II single lumen Polysulphone ¤ Titanium Venous Access Ó 2002 Blackwell Science Ltd

System with 1.0 mm internal diameter ¤ 78 cm length polyurethane catheter (SIMS Deltec, Inc.). The system consists of a portal with self-sealing silicone septum, accessible by percutaneous needle puncture, and a single-lumen catheter. Priming volumes, as given by the manufacturer, are 0.5 ml for the portal and approximately 0.7 ml for the nonshortened catheter. The manufacturers suggest that, after drug administration, the system be ¯ushed with 5 ml of normal saline followed by 5 ml of heparin solution. This recommendation is not based on speci®c study data. There is a paucity of research into minimum ¯ush volumes, although one study addressed the issue in giving set extension tubing [1]. It was shown that rapid ¯ushing, producing non-laminar ¯ow, was more ef®cient at removing residual drug than slower ¯ow. I proceeded to determine the in vitro minimum safe ¯ush volume required for the Port-a-cathÒ. An 18G needle was used to access the device. The line was primed with 0.4% trypan blue solution. A variable ¯ush volume, between 1 and 10 ml, of sodium chloride 0.9% was then injected rapidly using a 10-ml syringe. Following the ¯ush, in order to determine the amount of trypan blue remaining in the vascular access system, 10 ml of sodium chloride 09% was injected slowly using a 10-ml syringe, and the ¯uid emerging from the catheter tip collected. The concentration of dye in the collected ¯uid was determined by measuring its optical density (at 240 nm wavelength) using spectrophotometry (Pye Unicam,

SP6-550 UV ¤ VIS). The Port-a-cathÒ was thoroughly purged before repeating the process with a different ¯ush volume. The data collected are shown in Fig. 11. The curve levels out at a ¯ush volume of 5 ml implying that greater ¯ush volumes were no more effective. This is the minimum safe ¯ush volume in vitro when injected rapidly. Other factors are relevant in vivo including the hydrostatic pressure at the line tip, i.e. the central venous pressure. In conclusion, the manufacturer's instruction for a 5-ml ¯ush (followed by 5 ml of heparin solution) is adequate when injected rapidly. This study will be reassuring to users of this Port-acathÒ and could easily be repeated for other vascular access devices. A. Brennan The Calderdale Royal Hospital, Halifax HX3 0PW, UK

Reference

1 Hutton P, Thornberry EA. Factors affecting delivery of drug through extension tubing. British Journal of Anaesthesia 1986; 58: 1141±8.

Experience of complications of percutaneous dilatational tracheostomy

Percutaneous dilatational tracheostomy (PDT) is performed with ever increasing frequency on intensive care units in the UK. As well as evidence of a reduction in incidence of long-term complications from this method com-

Figure 11 Optical density of collected ¯uid with variable ¯ush volume. 195


pared to open surgical tracheostomy [1±3], it is time- and cost-effective, and convenient as a procedure that can be done outside of theatre without the need of either a surgeon or theatre space. Furthermore, this negates the potential hazards of transferring critically ill patients away from the intensive care unit. The development of user-friendly apparatus for PDT has further increased its popularity and many consider it a safe technique [4]. However, a concerning aspect of PDT is the potential for severe acute complications. Whilst those in the postoperative period may be lower, evidence suggests a higher incidence of perioperative complications, including death, with PDT than with surgical techniques [3]. Acute severe haemorrhage, loss of airway including tracheostomy misplacement, oesophageal rupture, tracheal dissection, pneumothorax and haemothorax have all been described. A discussion with colleagues in the anaesthetic coffee room usually reveals that many of those who have performed PDT can recount tales of horror of one or more such events. Fortunately, most patients seem to survive their ÔnearmissesÕ and suffer no further morbidity, but a few do not. Unless the acute events are recorded as a critical incident or as part of an ongoing audit, it is possible that under reporting of acute complications occurs as patient followup focuses on long-term outcomes. To examine the experience of acute complications of practitioners who perform PDT, 60 anonymous surveys were distributed to consultant and trainee anaesthetists of a local teaching hospital department. Questions were asked regarding the grade of anaesthetist, how many PDTs each individual had performed and their experience of acute complications, including haemorrhage, pneumothorax, haemothorax, oesophageal rupture, and tracheal dissection. Free comments were invited for other complications not speci®ed by the survey. They were also asked which type of PDT equipment they most commonly used and whether they routinely used a bronchoscope to assist tracheostomy placement.

196

In total, 47 questionnaires were returned, giving a response rate of 78%. Of the respondents, 18 were consultant anaesthetists (38%), 22 were SpRs (47%) and 7 were SHOs (15%). The number of PDT performed by each individual is shown in Table 4. Of the 42 respondents that had performed PDT, 23 (55%) reported experience of acute severe complications. The most common of these reported was that of haemorrhage, with 10 (24%) reporting it as a sole complication, and a further 9 (21%) reporting it alongside others. Eight (19%) of the respondents had voluntarily described either a loss of airway or misplacement of the tracheostomy during the procedure. Three (7%) of the respondents reported causing pneumothoraces to patients undergoing PDT and two (5%) had seen surgical emphysema as a direct complication. One individual reported having caused a haemothorax during PDT and none of the respondents had experienced oesophageal rupture or tracheal dissection. Of those anaesthetists who had performed PDT, the most popular kit used was the Ciaglia TM dilator kit, with 16 (38%) respondents using it; 6 (14%) used the Blue Rhino TM, whilst 8 (19%) reported using a combination of both. Ten (24%) used Portex TM and the remaining 5% used other kits including Rusch TM and Mallinkrodt TM . Of those who had performed PDT, 37 (88%) reported using a bronchoscope routinely in assisting placement. This survey con®rms the popularity of PDT, with 89% of respondents having performed it at least once. It also demonstrates that acute and often severe, potentially life-threatening complications are not uncommon during this procedure, with over 50% of respondents experiencing one or more.

Table 4 No. of PDT performed

No. of anaesthetists

0 1±20 > 20

5 27 15

Several modi®cations in practice to PDT have been suggested to reduce the incidence of such complications. One modi®cation that has been widely adopted is the use of a ®breoptic bronchoscope, which has been suggested for use in assisting correct placement and to reduce the risk of airway loss [5]. The majority of respondents in this survey routinely used a bronchoscope to assist placement of PDT and this is arguably recognised as good practice. However, of the eight who reported loss of airway or misplacement of the tracheostomy, six reported routinely using a bronchoscope. Also, there is little evidence to suggest that bronchoscopy reduces the incidence of haemorrhagic events from a PDT. Some studies have suggested that the risk of haemorrhage could be minimised by the use of ultrasound techniques to identify the position of major vessels in the neck before performing the PDT [6, 7]. Operator experience may also play a part in the incidence of acute complications. One study demonstrated a signi®cant learning curve for performing PDT, particularly in the ®rst 20 patients, with most complications occurring during acquisition of early experience in the technique [8]. In this survey, 27 people fell within this early learning curve episode. Over half (55%) of these, however, reported having never experienced a complication. Paradoxically, of the 15 who had performed greater than 20 PDTs, twothirds had. This survey is too small to deduce any statistical signi®cance from such ®ndings, and it may well be that those in the ÔexperiencedÕ group had seen their complications within their ®rst 20, or perhaps it justi®es the old adage Ôif you havenÕt seen a complication, you haven't done enough'. Another important issue of PDT that may enhance safety is appropriate patient selection and surgical referral of patients with potentially dif®cult or unusual anatomy. Other suggestions include making an adequate incision to enhance identi®cation of the tracheal rings [5] and the use of capnography to con®rm correct placement [5, 9]. Thus, whilst the increasingly popular PDT has undoubtedly proven its worth



on the intensive care unit, it would seem wise to heed the tales of the many who seem to have experienced neardisasters and to continue to regard it as a signi®cantly invasive procedure that is not without complications, the safety of which can be enhanced by adopting sensible precautions and appropriate technique modi®cations. H. Wise Poole Hospital Poole, BH15 2JB, UK

5

6

7

References

1 Freeman BD, Isabella K, Lin N, Buchman TG. A meta-analysis of prospective trials comparing percutaneous and surgical tracheostomy in critically ill patients. Chest 2000; 118: 1412±18. 2 Cheng E, Fee WE Jr. Dilatational vs Standard tracheostomy: a meta-analysis. Annals of Otology, Rhinology and Laryngology 2000; 109: 803±7. 3 Dulguerov P, Gysin C, Perneger TV, Chevrolet JC. Surgical or Percutaneous Tracheostomy: a meta-analysis. Critical Care Medicine 1999; 27: 1617±25. 4 Cooper RM. Use and safety of percutaneous tracheostomies in intensive

8

9

care-report of a postal survey of UK practice. Anaesthesia 1998; 53: 1209±27. Marx WH, Ciaglia P, Graniero KD. Some important details in the technique of percutaneous dilatational tracheostomy via the modified Seldinger technique. Chest 1996; 110: 762±6. Hatfield A, Bodenham A. Portable ultrasonic scanning of the anterior neck before percutaneous dilatational tracheostomy. Anaesthesia 1999; 54: 660±3. Muhammad JK, Major E, Wood A, Patton DW. Percutaneous dilatational trachesotomy: haemorrhagic complications and the vascular anatomy of the anterior neck. A review based on 497 cases. International Journal of Oral and Maxillofacial Surgery 2000; 29: 217±22. Massick DD, Powell DM, Price PD, Chang SL, Squires G, Forrest LA, Young DC. Qualification of the learning curve for percutaneous dilatational tracheostomy. Laryngoscope 2000; 110: 222±8. Coleman NA, Power BM, van Heerden PV. The use of end-tidal carbon dioxide monitoring to confirm intratracheal cannula placement prior to percutaneous dilatational tracheostomy. Anaesthesia and Intensive Care 2000; 28: 191±2.

Figure 12 Double lumen tracheal tube in situ. The patient is in the right lateral position.


Single-lung ventilation via a double lumen tube in a patient with a tracheostomy

A recent letter in this journal described the use of a ®breoptically directed ÔsteerableÕ endobronchial blocker in association with a tracheostomy tube to provide single-lung ventilation in a patient with a permanent tracheostomy (Matthews et al. Anaesthesia 2001; 56: 492±3). Other techniques available include double lumen tracheostomy tubes and endobronchial intubation with a single lumen tube. We would like to describe the use of a conventional double lumen tube in this situation. A 44-year-old man presented for left pneumonectomy for an upper lobe squamous cell carcinoma, just 2 months following a total laryngectomy for a squamous cell laryngeal carcinoma. The patient was anaesthetised with midazolam 1 mg, morphine 5 mg, thiopental 325 mg and vecuronium 10 mg, and was easily ventilated using a paediatric face mask positioned over the tracheostomy. A right-sided 37G Mallinckrodt double lumen tube was passed through the stoma and into his trachea. The correct position of the tube was checked clinically and con®rmed with a ®breoptic bronchoscope. Once the patient was in position for a left thoracotomy, the tube lay easily on the side of his face as shown in Fig. 12. We feel there are a number of advantages to this technique. Firstly, double lumen tubes are usually more readily available than double lumen tracheostomy tubes or bronchial blockers. Second, anaesthetists have more experience positioning double lumen tubes than bronchial blockers, and ®nally, once the patient is positioned and prepared for surgery, the extra length and ¯exibility of the double lumen tube allows easier access to the airway, facilitating such manoeuvres as suctioning and checking tube position intra-operatively with a ®breoptic bronchoscope. We would recommend this technique as a simple solution to what can be an awkward problem.

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M. C. Renton I. D. Conacher Freeman Hospital, Newcastle upon Tyne NE4 6BE, UK E-mail: [email protected]

Acid-base disorders in the critically ill

The recent paper (Story et al. Anaesthesia 2001; 56: 530±3] provides a welcome demonstration of the utility of the Stewart approach to the analysis of acidbase disorders in critically ill patients. The authors are to be commended on their clear illustration of the potential of this methodology to offer mechanistic insights not readily attained with the more traditional Henderson-Hasselbach approach. The demonstration that decreases in plasma albumin, a common ®nding in critically ill patients, may have contributed to the alkalosis seen in their patients is of particular interest. The authors suggest that an acidifying effect of increasing plasma albumin concentration may play a role in the apparent adverse effect of albumin therapy reported in a recent metaanalysis [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 dysoxia; 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 hypercapnic, 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 increasingly clear, and include attenuation of key components of the in¯ammatory 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 shut198

down at times of nutrient shortage, e.g. 7 Laffey JG, Engelberts D, Kavanagh BP. Buffering hypercapnic acidosis worsens ischaemia. acute lung injury. American Journal of This distinction between cause and Respiratory Critical Care Medicine 2000; association is of particular importance in 161: 141±6. regard to the practice of buffering. Buffering of acidosis remains a com- 8 Hood VL, Tannen RL. Protection of acid-base balance by pH regulation of mon, if controversial practice [9, 10]. acid production. New England Journal of The physiologic rationale for this pracMedicine 1998; 339: 819±26. tice is based on the concept that acidosis is directly harmful and therefore must 9 Vukmir RB, Bircher N, Safar P. Sodium bicarbonate in cardiac arrest: a be treated. However, there exists little if reappraisal. American Journal of Emergency any data to support the practice of Medicine 1996; 14: 192±206. buffering acidosis. In fact, there is evidence from laboratory models of 10 Levy MM. An evidence-based evaluation of the use of sodium bicarbonate lung injury that buffering may abolish during cardiopulmonary resuscitation. the protective effects of acidosis [7]. Critical Care Clinics 1998; 14: 457±83. In summary, in the light of current evidence, it may be timely to re-evaluate our traditional concepts regarding acidosis. J. G. Laffey St. 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±4. 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.

A reply

We appreciate Dr Laffey's interest in our paper. Dr Laffey 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 were 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 considerable 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. Bellomo Austin and Repatriation Medical Centre,Victoria 3084, Australia E-mail: [email protected]

Inadvertent catheterisation of a partial anomalous pulmonary venous channel during central venous cannulation

A 71-year-old Chinese woman with a history of ischaemic heart disease, atrial ®brillation and non-insulin-dependent diabetes mellitus was admitted with necrotizing fasciitis of her right leg. On admission, she was septic with signs of diabetic ketoacidosis. A central venous catheter was inserted via the Ó 2002 Blackwell Science Ltd


Brachiocephalic vein RIJ central venous catheter Superior vena cava

Anomalous venous channel Tip of LIJ catheter

Figure 13 Digital subtraction venography with the injection of contrast medium through the LIJ catheter showing the anomalous venous connection at the point where the internal jugular vein continues into the left brachiocephalic vein.

right subclavian vein to aid ¯uid resuscitation. A chest radiograph showed that the catheter tip was in the ipsilateral internal jugular vein, and was therefore removed. After induction of general anaesthesia, another central venous catheter was inserted via the left internal jugular (LIJ) vein. As the pressure waveform and readings were consistent with that of a central vein, and there was good blood ¯ow on aspiration of the ports, this catheter was used for monitoring and infusion purposes during surgery. Following surgery, she was transferred to the surgical intensive care unit where the admission chest radiograph revealed that the central venous catheter was projected along the left lateral border of the heart. As the location of this catheter was unclear, another catheter was inserted via the right internal jugular (RIJ) vein with no complications. On closer inspection, the pressure waveforms from the two catheters were morphologically different with the pressure recorded via the LIJ catheter 5 mmHg higher than that from the RIJ catheter. Blood aspirated from the LIJ catheter showed a PaO2 of 212 mmHg, whilst that from the radial arterial cannula was 196 mmHg. Blood aspirated from the RIJ catheter had a PaO2 of 52 mmHg. These blood samples were taken simultaneously while the patient's lungs were being ventilated with an inspired oxygen concentration of 40%.


Doppler ultrasound studies con®rmed that the LIJ catheter was lying within a vein in the neck. Venograms were then performed with the injection of contrast medium through both catheters. The tip of the LIJ catheter was located within a vessel inferior to the con¯uence of the left internal jugular and subclavian veins (Fig. 13). As blood was ¯owing towards the catheter from this anomalous channel, manual injection of the contrast medium could not reveal the origin of this anomaly. Contrast medium injected through the RIJ catheter was seen to enter the right side of the heart and the pulmonary circulation, followed rapidly by the anomalous channel. The LIJ catheter was removed, though on another occasion it was used for central venous access, when the catheter tip went into the brachiocephalic vein. Anomalous pulmonary venous connections occur when at least one pulmonary vein is connected to the right atrium either directly or indirectly via a venous tributary. A partial anomalous pulmonary venous connection (PAPVC) occurs when one or more, but not all, the pulmonary veins connect to the right atrium. These may be found in association with atrial septal defects. There are a number of potential variants, but the variants with anomalous right pulmonary veins are said to be twice as common as those involving the left side. PAPVCs are usually asymptomatic, remain undiagnosed during life and are

incidental post mortem ®ndings [1]. The incidence ranges from 0.4 to 0.7% in different series. Although they are associated with cardiopulmonary malformations, there are no known risk factors for the development of this abnormality. The haemodynamic consequence is a left-to-right shunt and the consequent volume overload to the right heart with dilatation of the right atrium, right ventricle and pulmonary artery. The left heart chambers tend to be unaffected and the cardiac output remains normal. Pulmonary hypertension is not a recognised complication. Surgical correction is not required in the absence of other cardio-pulmonary malformations. The slightly different pressure waveform morphology that we observed is in contrast to previous reports [2, 3] of PAPVC catheterisation, in which an early sign was a markedly abnormal waveform with pulsatile ¯ow of bright red blood. The explanation for these was wedging of the catheter in the pulmonary vein, resulting in the transmission of the pulmonary arterial pressure waveform. Such waveform anomalies, if recognised early, may indicate misplacement of the central venous catheter. This case illustrates the value of check chest radiographs in the correct identi®cation of central venous catheter position. Congenital vascular abnormalities are rarely diagnosed in this way unless catheterisation of either a left superior vena cava or a partial anomalous pulmonary venous channel occurs. If the left superior vena cava is catheterised, the catheter will be seen to travel in a left paramediastinal path initially, then cross the mediastinum deeper within the thorax. In such a situation, the pressure waveforms would conform to that of a normal central vein. Digital subtraction angiography has been used to de®ne PAPVCs without subjecting patients to the risks of conventional angiography [4]. Non-radiological methods of diagnosing the presence of partial anomalous pulmonary venous channels include transthoracic [5] or trans-oesophageal [6] echo cardiography. Transthoracic echocardiography done on this patient a few years previously had merely revealed bi-atrial

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enlargement and did not suggest the presence of an atrial septal defect. We felt it was unnecessary to subject her to trans-oesophageal echocardiography when there was little doubt about the diagnosis after the radiological studies. C. J. C. Cheng B. L. Lim B. S. Tan Singapore General Hospital, Singapore 169608 E-mail: [email protected]

References

1 Ward KE, Mullins CE. Anomalous pulmonary venous connections; pulmonary venous stenosis; atresia of the common pulmonary vein. In: Garson A Jr, Bricker JT, McNamara DG, eds. The Science and Practice of Pediatric Cardiology. Lea & Febiger Philadelphia ¤ London 1990, 1145±72. 2 Orme R, Harper L, Olliff JFC. Case of the month. In what's my line? British Journal of Radiology 1998; 71: 457±8. 3 Wylam ME, Schmidt GA. Serendipitous discovery during jugular catheterisation. Partial anomalous pulmonary venous connection. Chest 1996; 98: 493±5. 4 Sider L, Fisher MR, Minzer RA. The evaluation of partial anomalous pulmonary venous return with the use of digital subtraction angiography. Chest 1984; 86: 97±9. 5 Higgs AG, Paris S, Potter F. Discovery of left-sided superior vena cava during central venous catheterization. British Journal of Anaesthesia 1998; 81: 260±1. 6 Garduno C, Chew S, Forbess J, Smith PK, Grocott HP. Persistent left superior vena cava and partial anomalous pulmonary venous connection: incidental diagnosis by transesophageal echocardiography during coronary artery bypass surgery. Journal of the American Society of Echocardiography 1999; 12: 682±5.

Correct nomenclature for stereo isomers

Recently, there has been a move to produce enantiopure agents, thereby reducing unwanted or potentially toxic

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effects associated with certain anaesthetic agents. It therefore seemed appropriate for a review on levobupivacaine (McLeod & Burke. Anaesthesia 2001; 56: 331±41) to appear with a short reÂsumeÂ of optical isomerism. However, I was disappointed on two counts, one to ®nd the information given concerning the naming of chiral molecules to be inaccurate, and secondly with the inadequate description of symmetry. When considering stereoisomerism in general and optical stereoisomerism in particular, there is a need for accuracy, which I felt was lacking in the general introduction to this review. As an example, there was no attempt to make clear the distinction between geometric stereoisomers and optical stereoisomers ± a point often missed by trainees preparing for examinations. The S and R con®gurations are, as correctly pointed out, based on the absolute con®guration of the four asymmetrical groups around the chiral centre, usually a carbon atom but often a quaternary nitrogen. Unfortunately, the three-dimensional nature of this arrangement does not lend itself to being represented unambiguously on a ¯at plane such as a piece of paper. Thus, it is inaccurate to suggest Ôof the four atoms surrounding the stereogenic centre, the order of size from highest to lowest is notedÕ. A more accurate description is: ®rstly, identify the atom with the lowest atomic number, then imagine you are looking through the base of the tetrahedron formed by the four atoms toward the atom previously identi®ed. The three remaining atoms now lie in a single plane and if the order of their atomic number count, starting with the highest and moving round to the lowest, follows a clockwise sequence then it is the R form, if anticlockwise the S form. Thus, the entries made in Table 1 are actually wrong since one always starts with the highest atomic number and moves around to the lowest, but if you do start with the lowest, then moving from lowest to highest anticlockwise gives the R form and clockwise the S form. Those who are interested should refer to The Penguin Dictionary of Chemistry [1], starting with the entry for Ôoptical activityÕ. For an

explanation of what to do when, for example, two or more of the atoms attached to the chiral centre are carbon atoms, but with different substitutions, look under Ôsequence ruleÕ. I also found the section ÔSymmetryÕ to be unnecessarily brief. The description of symmetry given is for re¯ectional symmetry only. There are other forms of symmetry, namely translational (of importance in tessellations) and rotational symmetry. This latter is of importance when considering complex molecules like atracurium that have several chiral centres and are rotationally symmetrical as this reduces the total number of possible three dimensional spatial conformations (from 16 to 10 in the case of atracurium). I do understand that article length is limited, but clarity must not be sacri®ced at the expense of accuracy. S. A. Hill Southampton General Hospital, Southampton SO16 6YD, UK

Reference

1 Sharp DWA, eds. The Penguin Dictionary of Chemistry 1990, 5th edn. 287, 356.

Hypo-osmolar Hartmann's

The recent paper (Gray et al. Anaesthesia 2001; 56: 461±5) con®rms the association between bladder pressure during surgery for trans-urethral prostatectomy and absorption of irrigating ¯uid. In describing movement of ¯uid between body compartments during this procedure they state explicitly that they assume iso-osmolarity. However, their anaesthetic technique militates against this because they administer intravenous Ringer's Lactate (Hartmann's solution). This is a hypo-osmolar ¯uid (between 273 and 278 mosmol.l±l, depending on formulation) compared with plasma (between 285 and 290 in mosmol.l±l). Its use therefore interferes with their assumption that infusion of this ¯uid can exacerbate peri-operative osmotic complications especially hyponatraemia [1]. There are other problems with using this ¯uid. It is incompatible with transfused blood (the calcium binding the



citrate anticoagulant of blood) and the vasopressor metaraminol. This drug may become more popular because methoxamine is to be withdrawn. Finally, peri-operative infusion of Hartmann's solution can worsen glycaemic control of diabetics, a relatively common group of patients presenting for prostatectomy [2]. Whilst our comments do not detract from the author's results, we write to mention that other types of ¯uid therapy may be more reasonable. D. R. Ball V. Perkins Dumfries and Galloway Royal In®rmary, Dumfries DG1 4AP, UK

References

1 Gill G, Leese G. Hyponatraemia: biochemical and clinical perspectives. Post Graduate Medical Journal 1998; 74: 516±23. 2 Thomas DJB, Alberti KG. Hyperglycaemic effects of Hartmann's solution during patients with maturity onset diabetes. British Journal of Surgery 1978; 50: 185.

Effective labelling is dif®cult, but safety really does matter

The recent letter discussing the Poggendorf effect (Nott. Anaesthesia 2001; 56: 917) is helpful in understanding some of the complex psychological aspects of labelling and safety. His suggestion that a second person must also read the label before the administration of any drug is certainly of value, but raises a number of issues. The ®rst concerns resource ± a survey of New Zealand anaesthetists found that in only 1.5% of circumstances was a second person routinely available throughout the anaesthetic to check drugs before their administration [1]. The second, more important issue, however, relates to human fallibility. We have received a number of routine audit reports documenting errors made by nursing staff who have used a two-person check, but still got it wrong. Part of the problem seems to be the suggestibility of human


beings. If the second person is shown a label and asked if it is indeed drug X, then there is a chance that he or she will read the label as drug X, even if it is in fact a similarly named but different drug. We have developed a new system designed to reduce the propensity for error during drug administration in anaesthesia [2]. One feature of this system is the use of large legible labels that include bar codes. When a syringe with such a label is scanned by the barcode reader just before administration, a computer speaks the name of the drug as a ®nal check of the syringe's contents. The computer is of course not open to suggestion and our system has already demonstrated its ability to facilitate anaesthetists' efforts to avoid drug error. In this way, we have embodied the principle of the two-person check, in a manner that utilises a less expensive resource than a trained health professional, and that capitalises on the strength of machines in an area in which humans are prone to error. The approach also makes possible the inclusion of various alarms for expired drugs and allergy alerts. No safety system can be expected to eliminate errors and accidents entirely [2, 3]. We therefore agree with Dr Nott's statement that colour coding by class of drug will not eliminate error on its own. Neither will the use of the bar-coded Ôtwo-person checkÕ described above. However, we believe that each would be a signi®cant improvement on the status quo, and both should be incorporated into a wide-ranging approach to error reduction, which includes (so far as possible) all aspects of the drug administration environment in theatre and indeed beyond [2, 4, 5]. The use of colour-coded (and barcoded) user-applied syringe labels does nothing to address the problem of ampoule labelling. We have previously suggested that manufacturers should supply injectable drugs in appropriately labelled pre®lled syringes to remove one error-prone step from the process of drug administration [4]. In reality, this will be a long time coming, and the current state of labelling on most ampoules can only be described as

appalling. Figure 14 shows two ampoules from a drug trolley at our hospital, which were recently involved in a substitution near miss. These ampoules are compliant with the current NHS speci®cation for ampoule labelling [6]. Yet, despite the fact that the ®gure shows the drug brand names facing forward (in the largest text on the ampoule), the ampoules remain very dif®cult to read and distinguish from one another. The black writing on clear glass is hard to read because the writing on the other side of the ampoule shows through and obscures critical information. The NHS speci®cation suggests the use of a yellow background for the lettering on ampoules to increase legibility ± but obviously it is simpler and allowable for manufacturers not to bother. The bands at the base of these ampoules may look like an identi®cation aid such as the rings sometimes used to indicate the length of action of a drug [7], but they are in fact specialised barcodes (without expiry dates) used by the manufacturer (personal communication, Abbott Laboratories). We use custom-made pre®lled syringes where practical in our new system [2, 4]. In addition we have designed a Ô¯agÕ or supplementary label attached to the ampoule by a licensed

Figure 14

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pharmaceutical manufacturer with a loop of clear plastic [2]. The ¯ag label adds the drug name, drug class, its classspeci®c colour cue and a barcode, all in a highly legible manner, without obscuring any of the ampoule's original details (Fig. 15). When the contents of the ampoule are drawn up, the selfadhesive ¯ag label can be removed and attached to the syringe as part of the drawing-up process. Consistent colour standards for userapplied syringe labels in anaesthesia already exist in Australia, New Zealand, Canada and the United States (discussed in [2]). In addition, ampoule standards also exist in Canada and the US, which allow the use of a colour-coded border, consistent with the aforementioned syringe label standards, around the Ôcritical information panelÕ ± thus permitting the use of consistent ampoule and syringe label colour cues [8, 9]. Ampoule colour coding by class of drug was suggested 19 years ago, but remains undeveloped [7]. While it may be convenient from an administrative, bureaucratic or manufacturing perspective to have different standards for ampoules and syringes, this makes no sense in terms of the ergonomics and safety of a clinician administering a drug to a

Figure 15 202

patient. There is no doubt that getting the detail of effective labelling standards right is dif®cult, but if safety really does matter [10], then these dif®culties must be overcome. Resolution of these problems is long overdue.

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2

3

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5 Webster CS, Anderson D, Murtagh S. Safety and peri-operative medical care. Anaesthesia 2001; 56: 496±7. 6 Anonymous. Ampoule Labelling ± NHS Specification 1994 Revision. National Pharmaceutical Supply Group, 18 March. C. S. Webster 7 Smellie GD, Lees NW, Smith EM. D. J. Mathew Drug recognition by nurses and A. F. Merry anaesthetists. Anaesthesia 1982; 37: Green Lane Hospital, 206±8. Auckland, New Zealand 8 Anonymous. Labelling of Drug E-mail: [email protected] Ampoules, Vials, and Prefilled Syringes (Z264.2±99). Etobicoke: Canadian. References Standards Association 1999. Merry AF, Peck DJ. Anaesthetists, 9 Anonymous. Standard Specification errors in drug administration and the for Labels for Small-Volume law. New Zealand Medical Journal 1995; (100 Ml or Less) Parenteral Drug 108: 185±7. Containers (D4267±95). Philadelphia: Merry AF, Webster CS, Mathew DJ. American. Society for Testing and Materials A new, safety-oriented, integrated drug 1995. administration and automated anesthe- 10 Birks RJS. Safety matters. Anaesthesia sia record system. Anesthesia and 2001; 56: 823±4. Analgesia 2001; 93: 385±90. Webster CS, Merry AF, Larsson L, McGrath KA, Weller J. The frequency and nature of drug administration error Persistent cough following during anaesthesia. Anaesthesia and target-controlled infusion (TCI) Intensive Care 2001; 29: 494±500. with propofol Webster CS, Merry AF, Ducat CM. Safety, cost and predrawn emergency I was interested to read the description drugs. Anaesthesia 2001; 56: 818±20.

of a persistent cough during sedation with propofol given by TCI (Aly. Anaesthesia 2001; 56: 1016). I have seen similar coughing in patients anaesthetised for lower limb or gynaecological surgery with a combination of central neural block and propofol sedation given by TCI. Patients were in the supine or lateral position and received supplementary oxygen via a simple variable performance mask. In my experience, the coughing often responds to raising the target propofol concentration to hypnotic levels, in which case a Guedel airway may be required. However, on occasion I too have resorted to waking the patient up. Of 28 cases anaesthetised in this way, about 15% have coughed in the manner described by Dr Aly. Neither regurgitation nor aspiration occurred in any patient. C. J. D. Maile Ronkswood Hospital, Worcester WR51HN, UK E-mail: [email protected] Ó 2002 Blackwell Science Ltd


Use of herbal medicines in ambulatory surgical patients

We conducted a study to examine the frequency and pattern of herbal medicine usage in patients admitted for day care surgery. As they waited in the holding area of the operating department, 387 consecutive patients attending the hospital for day case surgery were asked to complete a questionnaire. No patient refused to participate. All unpremedicated, ASA physical status I and II patients were included. The questionnaire included questions about use of herbal medicines in the pre-operative period, source of information ¤ referral about herbal preparations, knowledge of side-effects and coincident administration of prescription medications. We also asked whether the patient's general practitioner or surgical team had been informed that the patient was taking a herbal medicine. There were 387 completed questionnaires from 186 males and 201 females. The mean age of subjects was 39 years (range 13±82 years). Forty-seven patients (12.1%) were currently taking a herbal remedy. The mean age of positive respondents was 38 years (range 18±70 years). Sixty-eight percent of those taking herbs were female. Of the 47 patients taking a herbal preparation, 27.7% were taking more than one preparation, and 34% were taking a prescribed medication in addition to the herbal product. There was a wide variety of preparations in use, with garlic, ginseng, echinacea and arnica being the most frequently reported. Twenty-seven percent of those taking a herbal preparation were doing so on the advice of an alternative practitioner. Thirty-two percent had learned of the herbal medicine from the media, and 31% had learned of the preparation by Ôword of mouthÕ. One patient had obtained the information from the Internet. In response to the question regarding side-effects of the herbal medicine they were taking, 42 (89.4%) of patients replied that they did not know of any potential side-effects.


In general, the patient had not informed their family practitioner that they were taking a herbal product, with only 29.8% stating that their doctor was aware, and 83% said that the surgical team was also unaware, many patients commenting that they had not been asked about alternative medicines. Case reports in the current literature have questioned the safety of many herbal remedies [1]. In particular, several have been implicated in serious drug interactions with prescribed medications [2, 3]. Recent studies carried out in the United States have shown that signi®cant numbers of patients are taking herbal medicines in the preoperative period [4, 5]. Data from these studies suggest that up to 22% of patients are using herbal preparations. It is clear from the results of this study that a substantial proportion of patients presenting for day-case surgery are taking herbal medicines. The prevalence of 12.14% in our study is lower than North American ®gures, but still represents over 1 in 10 patients. In 1998, Eisenberg et al. estimated that one in ®ve US adults taking prescription medications were also using herbal medicines and risked developing adverse interactions between herbal medicines and prescription drugs [4]. Our study suggests that 34% of preoperative patients are using concomitant medications. In the present study, less than one ®fth of those taking herbal preparations had informed medical staff of this fact. This may be due to the commonly held belief that herbal products are natural and are therefore safe. This is a matter for concern, as many of these products are potent and potentially harmful. Many patients commented that they had not been asked speci®cally about herbal remedies, vitamins or minerals. We would suggest that questions relating to the use of alternative therapies should now become a standard part of the patient's admission history and pre-operative assessment. At present the particular risks associated with herbal medicines in relation to anaesthesia are unclear. However,

awareness of some of the known effects of some of these preparations should help us, at least in theory, to predict possible problems. The most important side-effects and interactions to be aware of are cardiovascular instability, bleeding and prolongation of anaesthesia. Much of the information available on herbal medicines is at present anecdotal and awaits further study. However, given that these preparations do not require a product license, it is unlikely that they will ever be subjected to the same rigorous study as conventional pharmaceutical preparations. Indeed, concerns over safety have precipitated calls for licensing legislation to be extended to herbal medicines [6]. Recently, the Irish Medicines Board has recommended that the herbal medicine St. John's Wort be made subject to prescription control [7]. In conclusion, patients are taking herbal medicines on a regular basis, frequently in conjunction with prescribed medication. In general, they are not aware of any possible sideeffects, and therefore regard these preparations as innocuous. There is certainly a potential for signi®cant interactions and side-effects to occur, and we should take this into account in our pre-operative assessment [8]. Further research into this area will be necessary before ®rm recommendations can be made regarding herbal medicines and their effects on anaesthesia and surgery. S. Crowe G. Fitzpatrick M. F. Jamaluddin Adelaide, Meath and National Children's Hospital, Dublin 24, Ireland E-mail: [email protected]

References

1 Windrum P, Hull DR, Morris TC. Herb±drug interactions. Lancet 2000; 355: 1019±20. 2 Piscitelli SC, Burstein AH, Chaitt D, Alfaro RM, Falloon J. Indinavir concentrations and St. John's wort. Lancet 2000; 355: 547±8. 3 Ruschitzka F, Meier PJ, Turina M, Luscer TF, Noll G. Acute heart

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4

5

6

7 8

transplant rejection due to St. John's wort. Lancet 2000; 355: 548±9. Tsen LC, Segal S, Pothier M, Bader AM. Alternative medicine use in presurgical patients. Anesthesiology 2000; 93: 148±51. Eisenberg DM, Davis RB, Ettner SL et al. Trends in alternative medicine use in the United States, 1990±97. Journal of the American Medical Association 1998; 280: 1569±75. De Smet PAGM. Should herbal medicine-like products be licensed as medicines. British Medical Journal 1995; 310: 1023±4. Irish Medicines Board. 9th edn. Drug Safety Newsletter February 2000. Ang-Lee MK, Moss J, Yuan CS. Herbal medicines and perioperative care. Journal of the American Medical Association 2001; 286: 208±16.

Overcoming dif®culties with percutaneous tracheostomy

We read with interest the recently published investigation of the Blue RhinoTM percutaneous tracheostomy set (Bewsher et al. Anaesthesia 2001; 56: 859±64). We note that one of the problems cited was the fact that the tracheostomy created by the dilator was not big enough to easily accommodate a size 8 Mallinckrodt ShileyTM tracheostomy tube. As we have been working on the same intensive care unit from which the paper originated, we feel it necessary to communicate how this problem has been overcome. On examination of the aforementioned tracheostomy tube, it is found to have an external diameter of 12.2 mm. If this is substituted for a size 8 Portex Blueline UltraTM, the passing of the tube is more easily achieved. Not only does the Portex tube have a smaller external diameter (11.9 mm), but it also has a softer and more malleable tip. It is also similar to the ShileyTM tube in that it retains the advantage of a detachable inner tube. A. MacKillop D. Acharya Victoria Hospital, Blackpool FY3 8NR, UK

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Cheese, drug labels and anaesthetic room error

A recent editorial and correspondence over several years draw attention to drug labelling and its importance in the avoidance of drug error in the anaesthetic room [1±4]. Labelling of the packaging, ampoule and syringe are important but not unique factors in anaesthetic room drug error. It is of concern that whilst other areas of error in medicine undergo vigorous systems analysis, we seem to be looking no further than the issue of labelling ± if we could only get the label right, we would never make a drug error. The mechanisms of cognition and of cognitive error are well described elsewhere [5, 6]. Should we not take a more analytical approach to this problem rather than the simplistic one that discussions about drug labelling seem to invite? Giving drugs in the anaesthetic room is a classic example of latent error. We have been set up. What other group of health professionals prescribe, dispense and administer potentially lethal drugs to patients we may have met only minutes before without any system of checking? Errors are going to happen no matter how careful we are. In the past we may have been slow to implement change, as one single change was not going to make the system perfect. Now, with understanding of the ÔSwiss CheeseÕ phenomena, it is apparent that we must take every step possible, no matter how small, to make the system as good as we possibly can whilst accepting that perfection is unlikely in a system that relies to any extent upon individuals reading drug labels. The drawing up of drugs is an example of a skill-based action, which as such is governed by patterns of preprogrammed instructions (schemata) that is largely subconscious. Skill based errors are known as slips ± they are unintended actions. There are several factors, both endogenous and exogenous, that make slips more likely and could be avoided [5]. Fatigue, sleep loss, alcohol, drugs and illness are examples of endogenous factors that are thought to make slips

more likely and are under the control of the individual. Exogenous factors are more dif®cult for the individual to control. Overwork and stress are all emotions we are familiar with, but should we really be rushing to get an over-optimistic list ®nished? The environment in the anaesthetic room is important. The temperature should be appropriate for both you and the patient. Noise should be kept to a minimum and interruptions not allowed. Fear and anxiety are good for you in moderation, but excess results in under-performance. They normally arise when undertaking occasional practice or working in an unfamiliar environment. Departments should not allow this to happen. It is important that we, as individuals, realise that when we are angry we are more likely to make a mistake. Boredom should be avoided, and breaks during long cases facilitated. Many of us have developed patterns of work that we consider to be safe practice. Some are common sense, others more controversial. We should share this information, encourage debate and re-examine our own practice. For example, what practical steps can be taken to avoid drug error in the anaesthetic room? The standardisation of anaesthetic room drug cupboards is a ®rst step, removing those drugs that are not often used and keeping drug stock centrally to avoid crowded cupboards. Only the drugs in use speci®cally for that list should be removed from that cupboard by the anaesthetist and placed on the work surface. Drugs would be kept alphabetically, with no labels on the shelf. No individual ampoule should ever be put back into a box, and they should not be removed from the packaging and kept elsewhere. Ampoules should be for single use only and not left open on the bench. When a supplier for a particular drug is changed, each individual anaesthetist should be informed and warning labels attached to the drug boxes. It has been assumed that best practice is that the anaesthetist who is going to administer the drugs should draw them up. Perhaps the Operating Department Assistant should draw them



up and we check them? The diluting of drugs is a potential source of error. The commonest slip is giving a wrong drug but in the right sized syringe [7]. Should we draw all induction agents up into a 20-ml syringe, all neuromuscular blocking drugs into a 5-ml syringe and all analgesics into a 2-ml syringe? If local anaesthetic is to be used, it should be drawn up and used before the induction agent is drawn up. Conversely, if the block is to be performed after induction, draw the local anaesthetic up only once the patient is asleep. These suggestions ignore the issues that surround labelling, and individually will not prevent drug error. However, taken together, they may work synergistically to make error much less likely. Anaesthetic department practice, pharmacy policy, theatre management, the physical environment we work in and our own well being all play a role in anaesthetic room drug error. Until we accept the multifactorial causes of these errors, they will continue to happen Table 5 The A±Q Anaesthetic Assess-

ment Algorithm.

with alarming frequency and potential for disaster. C. P. Leng Northampton General Hospital, Northampton NN1 5BD, UK

References

1 Birks RJS. Safety Matters. Anaesthesia 2001; 56: 823±4. 2 Nott MR. Misidentification, in-filling and confirmation bias. Anaesthesia 2001; 56: 917. 3 Dill-Russell P, Dhileepan S. Sodium citrate bottles. Anaesthesia 2001; 56: 401±2. 4 Heneghan CP. Drug labelling ± a place for colour coding? Anaesthesia 1996; 51: 600±1. 5 Leape LL. Error in Medicine. Journal of the American Medical Association 1994; 272: 1851±7. 6 MerryAF, Webster CS. Labelling and drug administration error. Anaesthesia 1996; 51: 987±8. 7 Fasting S, Gisvold SE. Adverse drug error in anaesthesia, and the

A±Q alphabetic anaesthetic assessment algorithm

As a SHO, I tend to forget to ask certain questions or do certain assessments. I therefore developed an alphabetic anaesthetic assessment algorithm to help me do a complete assessment (Table 5). With experience, the algorithm takes about 3 min to complete for an ASA I patient. Using the algorithm also helped in the Primary OSCE exams. As a more senior anaesthetist, I am less likely to forget the important points of an anaesthetic assessment. However, all too often, missing notes or anaesthetic charts mean that I have to annotate my anaesthetic assessment on my theatre list. An abbreviated alphabetic anaesthetic assessment algorithm helps me maximise the limited

Classi®cation

A±Q algorithm

Comments (e.g. or esp)

Biodata

Age Body weight Current problem and procedure Time of damage Exposure to previous anaesthetics Family history Gastric problems

Time between food and trauma

Surgical issues Anaesthetic history Medical problems

Anaesthetic assessment

Interactions Obs Discussion


impact of coloured syringe labels. Canadian Journal of Anaesthesia 2000; 47: 1060±7.

History Asthma BP Cardiac Diabetes Epilepsy Fags per day Glasses of alcohol Hospitalisations Infections Joint problems Kitchenware Last meal and drink Medications Noxious Obs and labs Plan postpone for optimisation? premedication pre-operative peri-operative postoperative Questions?

Re¯ux, hiatus hernia, gastritis ¤ ulcer

URTI, sepsis Neck, back, arti®cial joints Dentition, Mallampati and Wilson scoring

Allergies

e.g. invasive monitoring Ask patient for questions

205


space on the theatre list. For example, for an ASA I patient, I may write E 4 GHI0 JKL 4 M0 N0 P NSAID PR, in any available space. The annotation has the bene®t of reminding me of the questions I asked or did not ask, when the anaesthetic chart ®nally turns up for documentation. In fact, the annotation may be used as a standard form of documentation on anaesthetic charts, if there is general agreement within the reader's department to do so. I therefore submit the A-Q anaesthetic assessment algorithm for fellow anaesthetists to use and adapt. M. Lim Northampton General Hospital, Northampton NN1 5BD, UK E-mail: [email protected]

An unusual complication of fasting

We would like to describe an unusual complication of fasting in children: An 18-month-old child was admitted to our day case unit for a gastroscopy. In accordance with our usual practice EMLA cream was applied to the back of the hand of the child and covered with a non-occlusive dressing. The parents had adhered to our guidelines of fasting the child pre-operatively. During the endoscopy procedure performed under general anaesthesia, the gastric fundus was visualised and it was noted that the fundus was covered with a large piece of the non-occlusive dressing. This was then removed with no ill after effects. It is a usual practice to apply EMLA cream to children's hands in preparation for theatre. The non-occlusive dressing is applied to improve the effectiveness of the cream and to hold the cream in place. In young children, the EMLA cream and the non-occlusive dressing are then covered by a bandage in order to prevent the child removing the cream and the dressing altogether. In this case, as was later revealed, the patient Ôslipped through the netÕ and a bandage had not been applied. Children of this age have a tendency to place things in their mouth, and in 206

this case the dressing was torn and swallowed. This action could have potentially disastrous consequences if the dressing was inhaled as a foreign body causing upper airway obstruction, which is a real possibility in children with small airways. Extra care should be taken to ensure that the occlusive dressing is safely covered with an additional bandage in young children if Emla cream is considered necessary, especially in hungry children! J. Easby B. McLain S. JuÈrgens University Hospital of North Tees, Stockton TS19 8PE, UK

Can propofol cause keratitis?

I read with interest the recent letter (Ameen et al. Anaesthesia 2001; 56: 1017±18) describing a possible complication of propofol in an anaesthetist. I would like to report a similar incident, which I experienced a few months ago when I was anaesthetising an elective surgical patient for herniorrhaphy. In common with Dr Ameen, whilst I was injecting propofol into the injection port of an intravenous cannula, most of the propofol splashed into my eyes. Immediately I experienced an intense burning sensation and was blinded for a few minutes. I was the sole anaesthetist and unfortunately could not proceed with the anaesthetic. Therefore, help was summoned and another anaesthetist had to complete the anaesthetic. As regards to my eyes, I immediately washed them with tap water and later rinsed them with sterile water. The burning gradually subsided over a period of a few minutes and I did not suffer any ill effects from the propofol. The above incident fortunately occurred in the daytime when help was immediately to hand. Furthermore, we had a trainee ODA, who went to call for assistance, while the Senior ODA maintained the patient's airway while waiting for another anaesthetist. A critical incident form was completed, and later discussed in the local Morbid-

ity and Mortality meeting. The major concern expressed was had such an incident occurred in the night, it might have resulted in a more serious incident with a partially anaesthetised patient and an incapacitated anaesthetist. M. B. Reddy Northampton General Hospital, Northampton NN15BD, UK

The incidence of pulmonary oedema in ®t patients of African origin

I would like to report three cases of pulmonary oedema in ASA 1 patients of African origin. I believe that it is easier to cause pulmonary oedema in medically ®t patients of African origin than patients of other races. The ®rst case was a 46-year-old, 92 kg male who developed pulmonary oedema following a short episode of laryngospasm on emergence from anaesthesia. He had had elective hand surgery and had received 1 L intravenous ¯uid during 2 h of surgery. The second case was a 28-year-old, 63 kg female who had an elective Caesarean section under general anaesthesia. She received 2.5 L intravenous ¯uid during 1 h of surgery during which there was 1.5 L blood loss. She developed pulmonary oedema postoperatively. The third case was a 34-year-old, 61 kg male who had emergency surgery to drain a scrotal haematoma following an inguinal hernia repair. Pre-operatively, he was dehydrated, and he received 2 L intravenous ¯uid during 1 h of surgery. Postoperatively he also developed pulmonary oedema. In each case the diagnosis was con®rmed on X-ray, treatment was with furosemide and oxygen, and resolution occurred within 24 h. Each patient was looked after by myself and was recorded in a log of unusual cases, which I have kept for 10 years. During that time, I have anaesthetised approximately 5000 ASA 1 patients. I estimate that 500 of these have been of African origin including the three cases reported above. I have had no unexpected cases Ó 2002 Blackwell Science Ltd


of pulmonary oedema in the remaining 4500 patients, who have been mainly of European, Asian, or Oriental origin. Although in each of the three cases reported above there were some provoking factors to cause pulmonary oedema, it seems surprising that each patient was of the same racial group. By applying the Fisher exact test to the frequency table (Table 6), the level of statistical signi®cance is given as p < 0.001. I have found no evidence in the literature to support my contention that it is easier to cause pulmonary oedema in ASA 1 patients of African origin than other patients, although some colleagues have provided anecdotal evidence to support my hypothesis. I would be interested if readers have any comments. B. Norman Chelsea and Westminster Hospital, London SW10 9NH, UK

cannulaÕ should be used. Such a cannula is manufactured by Becton-Dickinson and Co. The vial access cannula is attached to the drawing up syringe and its cover removed. The coloured plastic spike of the cannula is inserted through the centre of the vial bung until the cannula shoulder reaches the vial bung. The drug is then withdrawn into the syringe. The arrow tipped spike does not form a rubber core and prevents any debris being withdrawn with the drug. The cannula is removed leaving the coloured spike lodged in the bung for dispersal. This avoids the problems of stopper coring, the subsequent discarding of the drug and of needle stick injury, protecting both patient and anaesthetist. G. Nicol Western Hospital, Footscray, Victoria 3011, Australia

Reference

Preventing rubber stopper coring

I read the recent letter about the accidental injection of rubber bung pieces into patients (Chikungwa. Anaesthesia 2001; 55: 828) and can offer a solution. The problem is becoming more common as many drugs now come in a bunged vial. Although most of these bungs are not made of latex, stopper coring can occur with any rubber-topped vial. Manufacturers recommend discarding any product where coring is thought to have occurred [1]. The problem usually occurs when a large bore blunt drawing up needle is used. Instead of using a sharp needle, which increases the risk of needle-stick injury to draw up drugs, a Ôvial access

Table 6 Race

Pulmonary oedema

No pulmonary oedema

African Non-African

3 0

497 4,500


1 Camegie C. Are we causing latex sensitisation unknowingly? Anaesthesia 2001; 55: 828.

Non-English information on ampoules and drug packageinserts

I was surprised on returning to my base hospital in London that some of the everyday drugs used by anaesthetists had foreign (non-English) labels on the ampoules. Firstly, I noticed that glycopyrronium 0.2 mg, 1 ml ampoules were labelled in German and bupivacaine 0.5%, 10 ml ampoules were labelled in Italian. Essential information such as drug name, concentration, volume and expiry date were fairly obvious. I then found that the drug packageinserts (for both doctors and patients) were in German for the glycopyrronium and Italian for the bupivacaine. There was no English translation immediately to hand, although they were apparently available from the hospital pharmacy. I ®nd the drug package-inserts a valuable source of information for users as well as medical students and other staff in training, especially during theatre sessions.

I was wondering whether others had had similar experiences with ÔforeignÕ ampoules and if this was a subtle attempt by the powers-that-be to force NHS staff to become more multilingual and pro-European! G. Wearne King's College Hospital, London SE5 9RS, UK E-mail: [email protected]

Anaesthetic history of a patient: 250 anaesthetics in 30 years

We wish to present a unique case who has experienced nearly 250 anaesthetics during 30 years and has had an exceptional opportunity to observe the development of anaesthesia from a patient's perspective. We interviewed her following her 80th birthday and 240th anaesthetic. At the age of 3 years, our patient accidentally ingested alkaline caustics, which caused stricture of the upper oesophagus. The community doctor started dilations, and this procedure was repeated frequently for 50 years without any analgesia or anaesthesia. ÔThe dilations were sometimes painful and I was afraid of them, yet I don't remember anything especially negative about them. Perhaps, even as a small child, I understood that they helped me and afterwards I could eat again. Later, however, the stricture progressed and dilations were more dif®cult and painfulÕ. The dilations were ®rst performed under general anaesthesia in 1970. Concomitant diseases appeared along with advancing age. Our patient has general arteriosclerosis, coronary heart disease with seven myocardial infarctions (MI), arterial hypertension, diabetes and dietary anaemia. Recently, the procedures have often been postponed because of chest pain and fatigue. The anaesthetic history of the patient is a good overview of the development of general anaesthesia practice. The ®rst anaesthetics consisted of thiopental, pethidine, succinylcholine infusion and halothane. From 1975 to 1982, there was a period of Ôneurolept anaesthesiaÕ (fentanyl and droperidol). Through the 207


use of several inhalation anaesthetics (en¯urane, iso¯urane and des¯urane), opioids (fentanyl and alfentanil) and muscle relaxants (alkuronium, vecuronium and atracurium), the recent method has been propofol and remifentanil infusions, sevo¯urane inhalation and mivacurium. From the patient's point of view, the major improvement has been in the quality of recovery. ÔFalling asleep has always been easy and it has remained similar. Waking up and the recovery period have changed a lot during the years. Even though I am much older now, it is easier to recover. Earlier it took a week and I used to be very tired and kept forgetting things. Now it only takes 2 or 3 days, even though my health is a lot worse. At best, I have recovered in a day. Only lately, as my health has deteriorated, have I been afraid of the procedures. I have learned to trust in you and I know you do your best. I am over 80years-old now and have done quite well to get this far.Õ The modern anaesthetic methods allow safe anaesthesia to elderly patients with multiple concomitant diseases. The ASA class of our patient has progressed from I to IV because of old age, multiple MIs and other diseases. In spite of this, according to the anaesthetic records, the peri-operative haemodynamic responses have remained similar and a MI during an emergency laparotomy has been the only major complication. Even though not actively examined, there has been no clinical indication of

organ toxicity, such as liver or renal failure or bone marrow depression, following numerous exposures to, e.g. nitrous oxide or halothane [1, 2]. During the ®rst years, cognitive failure lasted for up to a week. The patient herself considered diazepam to be responsible and later refused to have it. Halothane metabolites may also have delayed recovery [3]. From the patient's point of view, falling asleep following the intravenous administration of an anaesthetic has been similar but the recovery period has improved markedly during three decades. We do not know what might be the world record in the number of anaesthetics experienced by one person. The experiences of our patient are certainly unique, and we are grateful for her comments. L. Kotiniemi S. Autio K. Hyrynkangas Oulu University Hospital, FIN-90029 OYS, Finland E-mail: leena.kotiniemi@ppshp.®

References

1 Baden JM, Rice SA, Metabolism and Toxicity. In: Miller RD, eds. Anesthesia, 4th edn. Churchill Livingstone, New York 1994, 157±84. 2 Kharash ED. Volatile Anesthetics: Organ Toxicity. In: Atlee JL, ed. Complications in Anesthesia. Philadelphia: W.B. Saunders Co 1999, 57±9. 3 Harkin CP. Delayed Emergence. In: Atlee JL, ed. Complications in Anesthesia.

Philadelphia: W.B. Saunders Co 1999, 189±91. Just who do they think we are?

National Anaesthesia Day has been and gone, hopefully leaving the general public with an improved awareness of the role of the anaesthetist. Whilst all this is highly commendable, I can't help feeling more concerned about the astonishing degree of ignorance existing much closer to home. Sadly, it appears that many of our colleagues also have very little idea of our practice or even of our quali®cations. As an illustration, I present three recent incidents. A ward nurse accompanying a patient to theatre remarked that she too would like to become an anaesthetist and asked if she would need to have A-levels. After a successful cardioversion carried out in the anaesthetic room, the medical houseman had second thoughts about leaving and asked the anaesthetist if she would like a doctor to remain with her while the patient woke up. An anaesthetist from the intensive care unit whilst reviewing a patient on the ward was told by nurses that he could not write on the drug chart as Ôonly doctors are allowed to do thatÕ. I am sure that many readers will have similar examples. Perhaps next year we need to hold National Anaesthesia day inside the hospital! R. Spencer Gloucestershire Royal Hospital, Glouceter GL1 3NR, UK

Erratum Adenotonsillectomy in children: a comparison of morphine and fentanyl for peri-operative analgesia. Anaesthesia 2001; 56: 1193±7. We wish to apologise for an error which was printed in this paper. Drs Streets and Johnson were identi®ed as Specialist Registrar and Senior House Of®cer in Anaesthesia respectively. Dr Streets is in fact the Senior House Of®cer and Dr Johnson the Consultant Paediatric Anaesthetist at Derriford Hospital, Plymouth PL6 8DH, UK. 208
