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BRITISH JOURNAL OF ANAESTHESIA
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patient who had a cardiac arrest. The manufacturers inform REFERENCES 1. Miller DM. Early detection of " rebreathing " in afferent me that their packaging insert includes the instruction to and efferent reservoir breathing systems using capno- encourage oral fluid intake when Picolax is used, but I found graphy. British Journal of Anaesthesia 1990; 64: 251-255. that many nurses were not aware of this, and that individual 2. Meakin G, Coates AL. An evaluation of rebreathing with sachets of Picolax do not include this advice. It is important that patients who are given Picolax are also the Bain system during anaesthesia with spontaneous ventilation. British Journal of Anaesthesia 1983; 55: given the instruction to drink quite large quantities of fluid. In a letter from the manufacturers, they describe a study in which 487-496. 3. Miller DM. Breathing systems for use in anaesthesia. patients drank 139 ml of water every 1 h for 12 h during Evaluation using a physical lung model and classification. treatment with Picolax, and serum sodium, potassium and osmolality results suggested that this produced only mild British Journal of Anaesthesia 1988; 60: 555-564. overhydration. If oral intake is impossible, fluids should be infused i.v. M. E. DODSON Sir,—Dr Meakin's astute observations that rebreathing in the Lwerpool Bain system, detected by capnography, at a level less than two times the minute ventilation (2KE) [1] could be claimed as REFERENCES rebreathing with a magnitude which may be of clinical importance. The actual curves, using the more sensitive and 1. Barker P, Trotter T, Harming CD. Study of the effect of accurate method to discern rebreathing, showed that deviation Picolax bowel preparation on body weight, cardiovascular from the maximum effective alveolar ventilation ( VAC/ VE) line variables and haemoglobin concentration. British Journal began at 2FE. Why, then, should I have said in another earlier of Anaesthesia 1991; 66: 410P-411P. report that the recommended fresh gas flow (VF) for children 2. Campbell IT, Baxter JN, Tweedie IE, Taylor GT, Keens should be 3KE [2]? This recommendation is based upon the SJ. I.v. fluids during surgery. British Journal of Andifference in the magnitude of variability of metabolic rate aesthesia 1990; 65: 726-729. between children and adults. In the Magill or any other afferent reservoir system, the recommended VF is equal to VE and is greater than the point INTERFERENCE WITH PACEMAKER FUNCTION at which onset of rebreathing occurs (approximately 0.6-0.7 of Sir,—The recent case report by Dr Finfer [1], illustrates one the VE [1, 2]). This is to allow for changes in carbon dioxide production (Fco2) during anaesthesia. In the Bain system, the of the inherent problems of a unipolar pacing system, that of recommended VF should be greater than this point, which may inhibition by skeletal muscle myopotentials. Suxamethoniumbecome clinically significant only when VF is less than 2FE. In induced muscle fasciculations were thought to be responsible children, the potential changes in Kco, are greater than in for pacemaker failure. It has been suggested that a defascicuadults and it is therefore for practical reasons that I made the lating dose of a non-depolarizing neuromuscular blocker recommendation that VF should be 3KE for all efferent should be used or suxamethonium avoided [2]. In addition, reservoir or T systems. If one were monitoring the resting thiopentone has been documented to decrease pacemaker minute ventilation in children (and not many of us do), then I threshold [3], increasing the risk of ventricular arrhythmias must agree that VF equal to 2VE would indeed be acceptable. [4]. Permanent pacemakers with bipolar electrodes are less D. MILLER sensitive to interference [5]. This has led to their increased use Tygerberg over recent years. During the 12-month period April 1990 to March 1991, 16 unipolar and 402 (96%) bipolar pacemakers REFERENCES were inserted at our hospital. Wider adoption of this practice 1. Miller DM. Early detection of "rebreathing" in afferent will help reduce the problems encountered during anaesthesia. and efferent reservoir breathing system using capnoV. S. SIDHU graphy. British Journal of Anaesthesia 1990; 64: 251-255. London 2. Miller DM. Breathing systems for use in anaesthesia. Evaluation using a physical lung model and classification. REFERENCES British Journal of Anaesthesia 1988; 60: 555-564. 1. Finfer SR. Pacemaker failure on induction of anaesthesia. British Journal of Anaesthesia 1991; 66: 509-512. 2. Zaidan JR. Pacemakers. Ancsthcsiology 1984; 60: 319-334. PICOLAX BOWEL PREPARATION 3. Siddons H, Sowton E. Cardiac Pacemakers. Springfield, Illinois: Thomas, 1967; 110, 113. Sir,—I was interested to read the abstract of the presentation 4. Scott DL. Cardiac pacemakers as an anaesthetic problem. to the Anaesthetic Research Society on the effects of Picolax on Anaesthesia 1970; 25: 87-104. body weight and intravascular fluid [1]. The findings might 5. Werner I. Interference in pacemakers. Pace 1984; 7: account for the observation of Campbell and colleagues of the 1021-1048. increased requirement for i.v. fluids during surgery for intestinal resection [2]. My experience in anaesthetizing patients for colon resection after Picolax bowel preparation is that these patients often Sir,—Thank you for the opportunity to reply to this letter. need large volumes of i.v. fluids (up to 4 litre) to stabilize the The author quotes Zaidan in suggesting that a " defasciculating arterial pressure after induction of anaesthesia. I have also dose of non-depolarizing neuromuscular blocker should be heard anecdotal stories of collapse after bowel preparation used or suxamethonium avoided". Suxamethonium remains with Picolax before radiological examination, and of one the neuromuscular blocker of choice for rapid sequence
CORRESPONDENCE
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S. R. FINFER
Oxford ANAESTHESIA AND BONE MARROW APLASIA Sir,—I wish to comment on the case report by Fenner and Cashman [1]. To those of us who have a long standing interest in the toxicity of anaesthetic drugs and the habits developed in recommending specific anaesthetic agents, this article is of interest. Concerning the possible toxicity of agents involved, it is of interest that avoiding nitrous oxide did not avoid the neutropenia. I have even greater interest in the recommendation "to use anaesthetic techniques based on conduction block whenever possible in patients with this type of bone marrow aplasia". Conduction anaesthesia was not "tested" in this experience. The authors have therefore recommended something different without any supporting evidence—in the presence of the fact that the patient had three uneventful recoveries from the anaesthetics actually used. W. K. HAMILTON
San Francisco REFERENCE 1. Fenner SC, Cashman JN. Anaesthesia and congenital agranulocytosis: influence of anaesthetic agent on neutrophil numbers in a patient with Kostmann's syndrome. British Journal of Anaesthesia 1991; 66: 620-624. Sir,—Thank you for the opportunity to reply to the letter from Dr Hamilton. We also were interested to note that the avoidance of nitrous oxide during the third anaesthetic did not prevent the occurrence of a further episode of profound neutropenia. It is possible that ketamine may have an effect on the bone marrow, but an effect caused by the neuroendocrine stress response, even from such a minor surgical procedure, cannot be excluded. Dr Hamilton is correct to point out that we did not use a technique based on conduction block in any of the three anaesthetics given. However, we feel that such a technique is likely to provide the best possible chance for a beneficial outcome. Regional anaesthesia is associated with a decrease in the plasma concentrations of cortisol [1] and catecholamines [2] and a reduction in postoperative granulocytosis and leucopenia [1]. The changes in glucocorticoids and sympathetic amines are known to cause short-term depression of neutrophil migration and phagocytosis [3]. Local anaesthetic agents, and in particular bupivacaine, do not have marked
inhibitory effects on leucocytic phagocytosis except in large concentrations [4]. Although we have not provided the clinical evidence to support the use of conduction anaesthesia, in a case such as this we believe that there is sufficient evidence to substantiate such a recommendation. S. G. FENNER J. N. CASHMAN
London REFERENCES 1. Rem J, Brandt MR, Kehlet H. Prevention of postoperative lymphopenia and granulocytosis by cpidural analgesia. Lancet 1980; 1: 283-285. 2. Edwards AE, Smith CJ, Gower DE, Williams CP, Ferguson BJM, Gough J, Gemmell LW. Anaesthesia, trauma, stress and leucocyte migration: influence of general anaesthesia and surgery. European Journal of Anaesthesiology 1990; 7: 185-196. 3. Boxer LA, Stossel TP. Qualitative abnormalities of neutrophils. In: Williams WJ, Beutler E, Erslcv AJ, Lichtman MA, cds. Haematology, 3rd Edn. New York: McGraw Hill, 1983; 802-815. 4. Moudgil GC. Effect of premedicants, intravenous anaesthetic agents and local anaesthetics on phagocytosis in vitro. Canadian Anaesthetic Society Journal 1981; 28: 597-601.
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induction of anaesthesia in patients at risk of aspiration of gastric contents; in such patients many anaesthetists would not wish to avoid its use. Whilst it is possible that a defasciculating dose of nondepolarizing blocking drug may reduce the incidence of pacemaker inhibition by myopotentials, I am unaware of any published research that supports this suggestion. It is still my view that the safest way to avoid myopotential inhibition is to re-programme the pacemaker to asynchronous mode in those patients in whom the use of suxamethonium is indicated. There is no doubt that bipolar pacemakers are much less sensitive to myopotential inhibition and their widespread use would reduce the incidence of this problem. However, the majority of patients with pacemakers have unipolar systems in situ and it remains essential that anaesthetists ascertain the type of pacemaker before embarking on anaesthesia.
BACTERIAL GROWTH IN PROPOFOL Sir,—Propofol infusions recently have been implicated as a medium supporting the growth of micro-organisms [1] and as a source of infection in patients following clean surgical procedures [2]. A study was performed to determine if contamination was extrinsic (contaminated during handling) or intrinsic (contaminated at the time of manufacture). Under sterile conditions, two 60-ml syringes (A and B) were prepared with propofol, attached to 1.5-m length of PVC catheter and placed on a sterile surface. At 45-min intervals over a period of 6 h, 6 ml of propofol was withdrawn from each syringe. Three millilitre was injected into an aerobic blood culture bottle and 3 ml into an anaerobic blood culture bottle. These were incubated and examined at 24, 48, 96 and 168 h. No organisms were grown from either syringe. The same procedure was repeated, but involved only washing of hands and placing the propofol on a clear surface; again two 60-ml syringes (C and D) were utilized and aerobic and anaerobic blood culture bottles inoculated every 45 min for 6 h. On this occasion Staphylococcus aureus and 5. epidermidis were identified in an aerobic blood culture bottle after 48 h. This corresponded to sampling in syringe C after 90 min. A diphtheroid organism was identified in an aerobic blood culture bottle after 168 h. This corresponded to a sample from syringe D after 180 min. The propofol syringes were left for 24 h and the remaining propofol inoculated in two blood culture bottles. Culture was negative. A nasal swab from the author grew 5. aureus. Thus organisms were not cultured from propofol syringes after preparation using a sterile technique. However, three bacterial strains were isolated using a preparation technique similar to that used in clinical practice. Thus contamination was "extrinsic". Recent surveys of anaesthetists show that aseptic technique and infection control is frequently not observed during anaesthesia [3]. Infection related to propofol infusions has