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Correspondence Declaration of Helsinki ethical review must be stringent. The medical journals have a significant role to play in this. The patient's autonomy is not threatened in some areas of clinical practice such as pain relief or local anaesthetic procedures. The patient is a free agent and can refuse the procedure and walk away. It is in such cases that the lesser principles of beneficence and non-maleficence and of justice become paramount. This is not to denigrate organised institutional ethical review which is of importance in these cases, in the case of research. Our ethics have a strong deontological basis as much as in psychiatry. Our patients have rights and we our duties. Is there any place for utilitarianism? Is there any advantage for the specialty or the companies involved in the develop ment of a new drug which outway the duty to our patients and allow the use of untried therapy? Can our specialty afford such paternalism? These are issues which need urgent and candid debate. If as a specialty we do not sort out these problems, and soon, then they will ultimately be dictated to us from our patients and by our employers. The recent legislation embodied in the Human Fertilisation and Embryology Act (HMSO 1990) now enshrines in law compulsory ethical review of clinical practice, in addition to clinical research. It is not unreasonable to assume that such compulsory ethical review of clinical anaesthetic practice may follow at some stage.

When a journal publishes articles or letters about a subject outside its own it is essential to ensure that the information published is factually correct; this is particularly the case when one enters the field of moral philosophy. A false belief is defined as a delusion. Dr Grummitt (Anaesthesia 1990; 4 5 496) is, in my opinion, incorrect in his interpretation of previous correspondence from Dr Drummond (Anaesthesia 1990; 4 5 59). Dr Drummond does not comment in his letter on approp r i d e ethical standards because his letter does not describe the information published in the article to which he refers.' Patients who attended for pain relief therapy had procedures which resulted in pain relief, that is, the aim of therapy was accomplished. Drummond states that 'treatment was ineffective' but he should justify his assertion. The correspondence has been published under the title 'Declaration of Helsinki' based upon Dr Drummond's assertion that there was some breach of this. If one reads this declaration there are contradictions between its subsections? It is perhaps time that the whole declaration is properly reviewed and modified. If one believes so sincerely in a deontological basis to moral philosophy all anaesthetic research must be prohibited since our primary duty as anaesthetists is the safe care of our patients. It is imperative, with the internal inconsistencies of the Declaration of Helsinki, that we review the entire concept of ethically acceptable standards in anaesthesia. The basic principles of moral philosophical debate are outlined elsewhere' and consist of issues of autonomy, beneficence, non-maleficence and justice. It is with the first of these that there is a significant dilemma in anaesthetic practice and research. How many patients actually understand what is the intended action of their anaesthetist in routine clinical practice? Their main concerns are, quite rightly, that they will become unconscious, that they will be safe ahd that they will recover. It is doubtful whether patients can be regarded as competent to consent to a routine anaesthetic, let alone to give consent to research during clinical anaesthesia. It is because of this that the nature and format of

P.A.J. HARDY

Gloucestershire Royal Injirmary. Gloucester GLI 3NN References

1. HARDY PM. Stellate ganglion block with bupivacaine.

Minimum effective concentration of bupivacaine and the effect of added potassium. Anaesthesia 1989; 44: 398-9. 2. DOWNIE RS, CALMAN KC. Healthy respect, Ethics in health 6 care. London: Faber and Faber, 1987. 3. BEAUCHAMP TL, CHILDRESS JF. Principles of biomedical ethics, 2nd edn. Oxford: OUP, 1983. 4. WARNOCKM, ed., MILL JS. Utilitarianism London: Collins, 1978.

Atropine during halothane anaesthesia for children

Atropine is routinely administered to prevent or to antagonise the halothane-induced bradycardia in children. Relatively large intravenous doses of atropine (0.02 mg/kg to 0.03 m a g ) are recommended.'*2 Do we need these higher dows in routine mask cases in children? Thirty-two ASA 1-2 children (3-10 years) for minor surgery were the subjects of the study. Institutional approval and parental consent were obtained. The children received no premedication, and anaesthesia was induced by

inhalation of halothane in nitrous oxide and oxygen (2 : I). When the end-expiratory halothane concentration had reached to ISYO,intravenous atropine 0.01 mg/kg (Group A, n = 17), or 0.02 mg/kg (Group B, n = 15) was administered. Halothane concentration was kept constant for 10 minutes after administration of atropine. Pulse rates were measured by Dinamap 1846 monitor (Critikon) before the induction, before atropine, and every minute for 10 minutes after atropine administration. Student's t-test was

Table 1. Mean (SD) pulse rate changes after atropine administration. Time after atropine (minutes) Halothane Group A Group B

Awake

1.5%

1

2

106 (18) 98 (12)

84 (15) 81 (11)

126 (14) 121 (14)

136 (9) 137 (9)

3

4

5

6

138 (10) 140 (10) 141 (10) 142 (10) 139 (8) 141 (6) 142 (9) 143 (8)

J

142 (9) 144 (8)

8

142 (9) 144 (9)

9

10

142 (10) 142 (10) 144 (8) 144 (8)

Correspondence utilised for statistical analysis and a p value less than 0.05 was considered significant. Age and weight were comparable in two groups. The pulse rate decreased to about 80% of pre-induction pulse rate after halothane induction, but increased to 140% of pre-induction rate after atropine administration in both groups, and there were no differences between the groups (Table I). Intravenous atropine 0.0 1 mg/kg increased the halothane-induced slowed pulse rate more than the rate in awake state. Do we need to increase the pulse rate during halothane anaesthesia more than the rate in the awake state? Since halothane-induced myocardial depression can only be at most partially improved by vag~lysis,~ the higher dose of atropine seemed unnecessary, at least when the airway is maintained by mask.

Ibaraki Children’s Hospital, 3-3-1, Futaba-dui, Mito, 311-41, Japan

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M. YAMASHITA M. TSUJI

References 1. STEWARD DJ. Anesthesia for outpatient surgery. In: STEWARD DJ. Manual of pediatric anesthesia, 3rd edn. New York: Churchill Livingstone, 1990: 106-10. 2. MOTOYAMA EK. Induction of anesthesia. In: MOTOYAMA EK, DABISPJ, eds. Smith> anesthesia for infants and children, 5th edn. St Louis: C.V. Mosby, 1990: 257-68. 3. YAMASHITA M, HORIGOME H. Echocardiographic evaluation of vagolytic effects of hyoscine butylbromide in paediatric halothane anaesthesia. Agressologie 1989; 30: 489-91.

Hyoscine derivatives in children A 14-month-old boy who weighed 8.4 kg presented for endoscopic retrosrade cholangiopancreatography to be carried out in the, X ray department under general anaesthesia. He was alert and fit apart from unexplained jaundice of hepatobiliary origin. Investigations were all within normal limits apart from these liver function tests: bilirubin 100 pmol/litre, alkaline phosphatase 1732 units/litre, aspartate transaminase 1496 units/litre, alanine transaminase 1210 units/litre and albumin 33 g/litre. Anaesthesia was induced with Entonox and isoflurane. Atracurium 0.6 mg/kg was injected through an indwelling 22-gauge cannula and a plain 4.0-mm tracheal tube inserted. Maintenance of anaesthesia was with Entonox, isoflurane 0.5-1.0%; atracurium 2 mg was given as required. Ventilation of the lungs was by hand through a Jackson-Rees T-piece. Difficulty with cannulation of the common bile duct was experienced during the operation and, without knowledge of the writer 10 mg of hyoscine n butyl bromide (Buscopan) was administered intravenously by the endoscopist to relax the sphincter of Oddi. The procedure was abandoned after approximately one hour and percutaneous transhepatic cholangiography was performed without difficulty. Subsequently the patient’s lungs were ventilated with oxygen and residual neuromuscular paralysis was reversed with neostigmine 80 pg/kg and atropine 20 pg/kg. Spontaneous ventilation was promptly restored. The child remained extremely sleepy, disorientated, had a flushed appearance, dilated pupils, dry mouth and Cheyne Stokes type breathing. Seventy minutes

elapsed before he was awake and able to make active efforts to remove the orotracheal tube. The delayed recovery was thought to be due to hyoscine for two reasons. The clinical signs were compatible with hyoscine overdosage and the anaesthetic agents employed are short acting. The endoscopist confirmed that Buscopan was given only if cannulation of the common bile duct proved difficult; the dosage was approximately 1 mg/kg. The case has several important implications. Ten milligrams (approximately 1.25 mg/kg) of hyoscine hydrobromide is an excessive dose compared with the (adult) recommended dosage of 10 mg initially, repeated in 30 minutes time (if necessary) to a maximum of 20 mg (up to 0.25 mg/kg) as indicated by the manufacturers, Boehringer Ingelheim Ltd. Anaesthetists must have knowledge of the nature and dosage of drugs which are given by other doctors during operative procedures and should be informed personally before their administration since such drugs may have a profound effect upon the anaesthetic. Hyoscine is best avoided in persons under one year or over 65 years of age and alternative methods of relaxation of the sphincter of Oddi should be considered in these age groups. Anaesthetists need to be vigilant at all times and particularly when other drugs are administered. Queen Elizabeth Hospital, Birmingham BIS 2TH

J.L. DANKS

Transient blindness We read with interest the recent case report about loss of vision after transurethral resection of the prostate (TURP).’ A similar case of glycine absorption has recently occurred in our hospital. Our case had some features that do not appear to have received much attention. A previously healthy 72-year-old man was undergoing transurethral resection of a large prostate under spinal anaesthesia. Towards the end of the operation he became restless with a bradycardia and hypotension. He responded somewhat to blood transfusion and ephedrine; however, after an hour in the recovery room, he became progressively more drowsy. He was admitted to the ICU where his cardiovascular system was stable but started spontaneous twitching movements, and showed a positive Chvostek’s sign. Hypertonic saline was started but he had a generalised convulsion and his trachea was intubated and his lungs ventilated. His fluid management and biochemical results are shown in Table 1. His pupils were fixed and dilated for

12 hours, but he had a gag reflex and no other signs of brainstem dysfunction. He started to wake up and his trachea was extubated 40 hours after operation and he made an uneventful recovery. Firstly, the biochemical results suggested the presence of 10-20 mmol/litre of an anion that caused a metabolic acidosis and severe disproportionate hypocalcaemia. The major metabolites of glycine are serine and glyoxylic acid, which are in turn metabolised to pyruvate and oxalic or formic acid. Hyperoxaluria is reported to occur after TURP and it seems likely that this patient suffered some degree of hyperoxalaemia. We suggest that in the treatment of a cardiovascular emergency in a TURP, the possibility of hypocalcaemia be remembered. The presence of unreactive pupils supports the contention that high levels of glycine have direct inhibitory effect on the retina as occurred in the case reported by Russell. It is interesting to speculate on the reason for the ‘lucid interval’ between the absorption of the glycine and the