Cost of volatile anaesthetic agents.

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Journal of Anaesthesia 1995; 74: 670–673. 2. Gillman MA, Kok L, Lichtigfeld FJ. Paradoxical effect of naloxone on nitrous oxide analgesia in man. European ...
British Journal of Anaesthesia 1996;77:435–437

CORRESPONDENCE

The care of patients and transport by air Sir,—I read with great interest the recent review on pre-hospital monitoring of trauma patients1. This raised many important issues which need to be addressed further as expectations of out of hospital care increase. In Scotland there has been a fully integrated air ambulance service following a major reorganization in 1993. In addition to providing a primary patient transport service, there are also a large number of secondary inter-hospital transfers. Because of the distances involved and terrain, many of these involve air travel, using fixed-wing or rotary aircraft. In addition to adopting the Association of Anaesthetists’ guidelines on minimum standards of monitoring, it has also been suggested that the recommendations for assistance should be followed in such situations2.. Dr Morley highlighted in his review that monitoring can interfere with aircraft electrical systems. Most monitors give out a small amount of electrical activity to the surroundings; this is not true of defibrillators which, despite having been used successfully in-flight, still pose a greater hazard. It is recommended that authority is gained from the aircraft captain before defibrillators are discharged when airborne3. In addition to the function of monitors in the air environment, associated alarm systems have also come under scrutiny. The noise levels present in the back of an aircraft can render auditory alarms ineffective. It has also been demonstrated that relying on visual scanning for detection of problems leads to delays before alarm conditions are detected. Consideration is currently being given to incorporation of alarms into intercom systems to further increase safe practice4. All adverse events are more likely with prolonged journey times. With the move to centralize specialist facilities and notably paediatric intensive care units5, patient transfer requiring sophisticated monitoring is set to increase. Only by continued vigilance and debate will standards improve to keep pace with these developments.

P. J. SHIRLEY Department of Anaesthetics Aberdeen Royal Infirmary Aberdeen 1. Morley AP. Prehospital monitoring of trauma patients: experience of a helicopter emergency medical service. British Journal of Anaesthesia 1996; 76: 726–730. 2. Oakley PA. The need for standards in interhospital transfer. Anaesthesia 1994; 49: 565–566. 3. Colvin AP. The use of defibrillators in helicopters. Journal of the British Association of Immediate Care 1992; 15: 35–37. 4. Fromm RE, Campbell RN, Schlieter P. Inadequacy of visual alarms in helicopter air medical transport. Aviation, Space and Environmental Medicine 1995; 66: 784–786. 5. Dryden CM, Morton NS. A survey of interhospital transport of the critically ill child in the United Kingdom. Pediatric Anesthesia 1995; 5: 157–160. Sir,—Dr Shirley raises some interesting points which merit further comment. HEMS was certainly preceded by some air ambulance services in the UK, although it differs in several important respects. Most obvious of these is the presence of a full-time medical staff, trained specifically for the purpose of primary retrieval by helicopter of major trauma victims. It is difficult to exclude other factors when considering the specific added effect of a physician on an aeromedical prehospital team. One American study of blunt trauma patients found that patient mortality was 35 % less than predicted by trauma score and injury severity score (TRISS) methodology when the attending aeromedical team incorporated a doctor. In addition, mortality in this group was significantly lower than in a group of patients, with similar TRISS scores, attended by a flight nurse/flight paramedic team. The doctors were able to perform a wider range of practical procedures than their paramedical counterparts, including thoracostomy, cricothyroidotomy and pericardiocentesis1. On the issue of defibrillators, HEMS use the Lifepak LP10-23 (Physio-Control Corporation International, Redmond, WA, USA), which is specifically approved by the Civil Aviation Authority for the HEMS aircraft, an Aerospatiale Dauphin SA 365N. The

defibrillator monitoring unit initially caused low level interference in the 120-MHz radio frequency band and this has been resolved by special modifications. Similar problems have been encountered on testing the Lifepak LP10-59 in the Bölkow 105DBS used by Cornish First Air (personal communication, R. Dawnay, Snaefell Aviation Design). Interestingly, in-flight defibrillation can only be heard as a faint click on the aircraft headsets. Since HEMS began operations in 1989, only 18 patients have undergone defibrillation. In most instances, the defibrillator was used on scene, not in the aircraft. The three survivors had all crashed their cars after sustaining cardiac arrests while driving and their injuries were only minor. The dismal prognosis of genuine traumatic cardiac arrest has been reported elsewhere2. Auditory monitor alarms are ineffective in the HEMS Dauphin. All staff on board wear helmets. Noise levels in the aircraft are very high because of removal of the soundproofing that normally forms part of the shell of the helicopter. This modification helped to lighten the aircraft, thereby improving performance and increasing potential patient load. Staff can communicate using helmet-based headsets and microphones. To avoid unnecessary disturbance to the pilot, incorporation of any alarm system into the intercom would have to be restricted to the headsets of the doctor and paramedic.

A. P. MORLEY Department of Anaesthesia and Intensive Care Prince of Wales Hospital Hong Kong 1. Baxt WG, Moody P. The impact of a physician as part of the aeromedical prehospital team in patients with blunt trauma. Journal of the American Medical Association 1987; 257: 3246–3250. 2. Rosenmurgy AS, Norris PA, Olson SM, Hurst MD, Albrink MH. Prehospital traumatic cardiac arrest: the cost of futility. Journal of Trauma 1993; 35: 468–473.

Effect of naloxone on nitrous oxide analgesia Sir,—We would like to comment on the article by Yagi and colleagues1. These authors were unable to show naloxone inhibition of the analgesic effects of nitrous oxide when measurements of analgesia were obtained 5 min after injection of naloxone. In fact, in figure 3 they showed a non-significant increase in analgesia after administration of naloxone1. Interestingly, these authors used very low doses of naloxone. We have shown previously that with similar doses of naloxone in human volunteers, the peak effect of naloxone was measurable only within the first 2–3 min after bolus injection. This effect was not apparent after 5 min2 3. Although in a minority of subjects nitrous oxide analgesia was attenuated by naloxone2 the majority of subjects showed a transient increase in nitrous oxide analgesia2 3. These observations were confirmed later by others in animals4. From our findings we proposed the existence of two opioid systems, in dynamic equilibrium: one analgesic and the other pain producing2 3.

M. A. GILLMAN F. J. LICHTIGFELD South African Brain Research Institute Johannesburg South Africa 1. Yagi M, Mashimo T, Kawaguchi T, Yoshia I. Analgesic and hypnotic effects of subanaesthetic concentrations of xenon in human volunteers: comparison with nitrous oxide. British Journal of Anaesthesia 1995; 74: 670–673. 2. Gillman MA, Kok L, Lichtigfeld FJ. Paradoxical effect of naloxone on nitrous oxide analgesia in man. European Journal of Pharmacology 1980; 61: 175–177. 3. Gillman MA, Lichtigfeld FJ. Nitrous oxide analgesia is potentiated by low doses of naloxone: more possible evidence for a hyperalgesic opioid system. South African Journal of Science 1987; 83: 560–563. 4. Quock RM, Curtis BA, Reynolds BJ, Mueller JL. Dosedependent antagonism and potentiation of nitrous oxide antinociception by naloxone in mice. Journal of Pharmacology and Experimental Therapy 1993; 267: 117–122.

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Sir,–In a previous article1 we reported that the clinical dose of naloxone did not antagonize the analgesic action of nitrous oxide when the pain threshold test was performed 5 min after injection of naloxone in humans. As Gillman and Lichtigfeld pointed out, the dose (0.01 mg kg91) of naloxone used in the study may not have been adequate to fully antagonize the effects of the opioid2. We chose this dose according to Jaffe and Martin3 who indicated that naloxone 0.4–0.8 mg i.v. in humans can prevent or reverse the effects of mu opioid agonists. The onset of action of naloxone is fast and seen within 1 or 2 min after injection3 4. The duration of antagonistic effects is approximately 45 min after an i.v. dose of 0.4 mg5. In our previous study, measurement of pain threshold was commenced 5 min after administration of naloxone. Measurement of analgesia was obtained during the period of naloxone-induced antagonism. We also evaluated antagonism of nitrous oxide analgesia with higher doses (5 and 10 mg kg91) of naloxone by a radiant heat tail-flick test in rats (unpublished data). The results indicated that naloxone did not antagonize the analgesic action induced by nitrous oxide, even at high doses. Gillman, Kok and Lichtigfeld6 showed that the peak effect of naloxone was measurable only within the first 2–3 min after bolus injection with clinical doses of naloxone in human volunteers, but not after 5 min. The majority of subjects showed a transient increase in nitrous oxide analgesia. This interesting peak effect of naloxone might be an agonistic effect seen at high doses of naloxone. Naloxone enters the brain very rapidly. The initial brain concentration of naloxone was reported to be much higher (4.6 times) than that in serum4. Therefore, the brain concentration of naloxone may transiently reach a high level which may produce agonist effects during the short period after bolus injection of clinical doses. High doses of naloxone produce increased arterial pressure and arrhythmias which may be caused by the release of sudden intense sympathetic activity. Enhancement of sympathetic neurones by naloxone in the central nervous system may explain the transient increase in nitrous oxide analgesia 2–3 min after injection of naloxone.

T. MASHIMO M. YAGI Department of Anaesthesiology Osaka University Medical School Osaka, Japan 1. Yagi M, Mashimo T, Kawaguchi T, Yoshiya I. Analgesic and hypnotic effects of subanaesthetic concentrations of xenon in human volunteers: comparison with nitrous oxide. British Journal of Anaesthesia 1995; 74: 670–673. 2. Yaksh TL, Howe JR. Opiate receptors and their definition by antagonists. Anesthesiology 1982; 56: 246–249. 3. Jaffe JH, Martin WR. Opioid analgesics and antagonists. In: Gilman AG, Rall TW, Nies AS, Taylor P, eds. The Pharmacological Basis of Therapeutics, 8th Edn. Oxford: Pergamon Press, 1990; 485–521. 4. Ngai SH, Berkowitz BA, Yang JC, Hempstead J, Spector S. Pharmacokinetics of naloxone in rats and in man: Basis for its potency and short duration of action. Anesthesiology 1976; 44: 398–401. 5. Evans JM, Hogg MIJ, Lunn JN. Degree and duration of reversal by naloxone of effects of morphine in conscious subjects. British Medical Journal 1974; 1: 589–591. 6. Gillman MA, Kok L, Lichtigfeld FJ. Nitrous oxide analgesia is potentiated by low doses of naloxone: more possible evidence for a hyperalgesic opioid system. European Journal of Pharmacology 1980; 61: 175–177.

Difficult tracheal intubation Sir,—Difficult tracheal intubation is a major cause of anaestheticrelated morbidity and mortality, and any change which may lead to a reduction is to be welcomed. However, we were interested that when West and colleagues studied a tracheal tube designed specifically for this reason, they used a size 8 tube for females and size 9 for males1. While we know of no firm evidence that decreasing the size of the tracheal tube facilitates intubation in cases of difficulty, it does seem to be true in both our experience and that of others2. Furthermore, it has been known for many years that small tracheal tubes can be used safely and without complication during positive pressure ventilation2. It has become routine practice at this institution to use 6-mm tubes in females and 6.5-mm in males. We believe that West and colleagues would have found an increased success rate and shortened learning time had they used smaller tracheal tubes in their simulation of a difficult intubation.

The authors’ incidence of 33 % for sore throat is similar to that quoted in other studies3, but 1–3 % of patients may still have hoarseness up to 6 months after intubation4. This value may be expected to be even higher in cases of difficult intubation where greater degrees of laryngeal trauma are likely to occur3. We believe that decreasing the size of the tracheal tube makes intubation easier and reduces the incidence of laryngeal damage. Stout and coworkers5 have shown that the incidence of hoarseness and sore throat may be reduced substantially by using tracheal tubes of size 7 or less. We believe that small tracheal tubes can be used routinely, and should be used when laryngoscopy is difficult.

C. J. BROOMHEAD D. VAUGHAN Department of Anaesthesia National Hospital for Neurology and Neurosurgery London 1. West MRJ, Jonas MM, Adams AP, Carli F. A new tracheal tube for difficult intubation. British Journal of Anaesthesia 1996; 76: 673–679. 2. Stenqvist O, Sonander H, Nilsson K. Small endotracheal tubes. Ventilator and intratracheal pressures during controlled ventilation. British Journal of Anaesthesia 1979; 51: 375–380. 3. Jones MW, Calting S, Green DH, Green JR. Hoarseness after tracheal intubation. Anaesthesia 1992; 47: 213–216. 4. Kambic V, Radsel Z. Intubation lesions of the larynx. British Journal of Anaesthesia 1978; 50: 587–589. 5. Stout DM, Bishop MJ, Dwersteg JF, Cullen FC. Correlation of endotracheal tube size with sore throat and hoarseness after general anesthesia. Anesthesiology 1987; 67: 419–421.

Sir,—Our thanks to Drs Broomhead and Vaughan for their comments. The crucial step is to get the introducer into the right hole; when that is achieved, intubation with our tube is easy; that is its main advantage. It seems unlikely that smaller tubes would have altered the intubation time. With a Magill tube, when the introducer is in place, there is still the problem of preventing the bevel snagging on the cords and a smaller tube is often helpful, but with the new method a smaller tube is needed only if the larynx is abnormally small. The problem is simplified because instead of two possible causes of resistance, there is only one. Occasionally, some resistance is felt and a smaller tube is needed. Recent data1 suggest that over the past decade the incidence of failed intubation in obstetrics has increased. The authors imply that part of the explanation is that junior staff have less experience of obstetric general anaesthesia than in the past. If that is correct then it underlines our conclusions. On the other hand, routine use of a small tube implies that there is never any need to change tubes, which is perhaps an advantage. The authors also refer to Stout and colleagues2 who found that with size 7 tubes the incidence of sore throat was 22% compared with 33% in our study. But this could be fortuitous (P:0.1); a larger sample might show a real difference. Thus the case for smaller tubes is not proved but we agree that it merits further study. May we add that the most serious cause of trauma is the novice who attempts to handle difficult intubations with no clear picture of the problem or its solution. This is perhaps the strongest argument in favour of our training drill.

M. JONAS John Radcliffe Hospital Oxford R. J. WEST Derriford Hospital Plymouth A. P. ADAMS Guy’s Hospital London F. CARLI McGill University Montreal, Canada R. S. CORMACK Northwick Park Harrow 1. Hawthorne L, Wilson R, Lyons G, Dresner R. Failed intubation revisited: 17 yr-experience in a teaching maternity unit. British Journal of Anaesthesia 1996; 76: 680–684.

Correspondence 2. Stout DM, Bishop MJ, Dwersteg JF, Cullen FC. Correlation of endotracheal tube size with sore throat and hoarseness after general anesthesia. Anesthesiology 1987; 67: 419–421.

437 Table 1 Cost of volatile agent required to maintain an alveolar concentration of 1 MAC, of the chosen volatile agent, at various fresh gas flow rates, for periods of 30 or 60 min Fresh gas flow rate (litre min91)

Cost of volatile anaesthetic agents Sir,—I read with interest Dr Barker’s letter on the cost of volatile anaesthetic agents1. When the costs of various agents are listed, one is tempted to make comparisons, and economic concerns are of increasing importance in our practice. However, for fair comparison of the available agents, we need to consider the amount of anaesthetic required to provide a similar depth of anaesthesia and this extends beyond making comparisons of similar potencies at set fresh gas flow rates. Differences in solubility of various agents in the blood and tissues become important. The amount of anaesthetic agent required may be divided into that required to provide adequate anaesthesia at the start (to load up the circuit and the patient’s lungs), to that required to replace anaesthetic taken up into the blood and then into the tissues of the body, and also make account of that supplied in excess of uptake and therefore lost from the circuit and wasted. The relative cost of the available agent varies with the fresh gas flow chosen. Estimates have been made of the volume of liquid anaesthetic required based on uptake kinetics and circuit performance at various fresh gas flow rates to sustain an alveolar concentration of 1 MAC for four of the volatile agents listed by Dr Barker2. I have included the price per millilitre of liquid anaesthetic, from the British National Formulary3, to calculate the cost of the volatile agent required (table 1). There are limitations to the calculations: at low fresh gas flows, conventional vaporizers may be unable to supply sufficient agent, for example at 0.2 litre min91 at 1 MAC, isoflurane vaporizers cannot supply a sufficient amount of isoflurane for the first hour, whereas desflurane vaporizers are unable to do so for the first 10 min. The increased fresh gas flow required to compensate for the limitations of the vaporizers would increase the estimated cost noted in table 1, but this would be greatest for the more soluble volatile agents. In addition, there is some concern on the use of sevoflurane at low fresh gas flows4. Table 1 shows, as would be expected, that for any given volatile agent, cost increases with increased fresh gas flow, but also that the relative cost of the less soluble (and newer) volatile agents is reduced at lower fresh gas

Halothane 30 min 60 min Isoflurane 30 min 60 min Sevoflurane 30 min 60 min Desflurane 30 min 60 min

0.2

1

2

4

6

£0.13 £0.20

£0.17 £0.28

£0.23 £0.38

£0.34 £0.59

£0.45 £0.80

£1.56 £2.46

£2.26 £3.74

£3.12 £5.42

£4.80 £8.70

£6.51 £11.97

£1.62 £2.41

£3.10 £5.36

£4.97 £8.95

£8.66 £16.24

£12.40 £23.52

£1.30 £1.96

£2.87 £5.06

£4.84 £8.91

£8.76 £16.62

£12.67 £24.35

flows. This illustrates that when comparing the costs of volatile anaesthetic agents, consideration must also be given to uptake kinetics and fresh gas flows used.

M. DANIEL Department of Anaesthesia Glasgow Royal Infirmary Glasgow 1. Barker I. Cost of volatile agents. British Journal of Anaesthesia 1996; 76: 749. 2. Eger EI II. Uptake and distribution. In: Miller RD, ed. Anesthesia, 4th Edn. New York: Churchill Livingston, 1994; 101–123. 3. British National Formulary. London: British Medical Association and Royal Pharmaceutical Society of Great Britain, 1996; 518–519. 4. Eger EI II, Martin JL, Tinker JH. The safety of sevoflurane has not been adequately established. Anesthesia and Analgesia 1996; 82: 431–432.

ERRATUM British Journal of Anaesthesia 1996; 76 (Suppl. 2): A.45 In the methods section of this abstract, the dose of morphine was reported incorrectly: morphine 0.9 mg/kg should read morphine 0.09 mg/kg. We apologize to the authors for this confusion.