112

Correspondence

My colleague Dr D. ApIvor has demonstrated that the insertion of a semi-rigid extension tube well up the exit duct of the plenum system prevents possible back-flow contamination. Official opposition to the use of theatre ducting for this purpose on the grounds that the vapours might damage fan motor bearings appears invalid when one asks where the vapours went prior to the anaesthetists’ leading them directly thereto. The system is already installed, there is no extra cost so why not use it? Regular and thorough servicing of the whole duct ventilating system is vital as, after smoke tests had demonstrated poor extraction, the intraduct non-return flaps have been found stuck in the nearly closed position. In anaesthetic situations where no plenum system is installed a commercial extractor fan on an outside wall can be used with the tube from an anti-pollution expiratory valve connected to a baffled segment (Fig. 1). This not only solves the pollution problem cheaply but also aids room air exchange. An outward air flow is induced in an ‘open’ tube but a true vacuum effect is negligible. Although explosive mixtures have not been used the brushless induction type electric motors and the considerable air dilution are safety factors. No fan bearings have failed despite several years’ service with halothane or trichlorethylene vapours. Consistency in the prompt connecting of venting tubes both in anaesthetic rooms and theatres is an obvious factor and a constant effort has to be made to renew awareness of the basic problem otherwise frustration with theanti-pollution impedimenta can induce slackness. Insistence on a meticulous technique may even require the anaesthetist to remind himself of the potential danger to the patient if the efficiency of key personnel is impaired’s’ and of the possibility of harm to all theatre staff. Wes? Kent General Hospital, Maidstone, Kent

C. H. BOYD

References I . BRUCE,D.L., BACH,M.J.& ARBIT,J. (1974) Trace anesthetic effects on perceptual, cognitive and motor skills. Anesthesiology, 40,453. 2. BRUCE, D.L. & BACH,M.J. (1975) Physiological studies of human performance as affected by traces of enflurane and nitrous oxide. Anesthesiology, 42,194.

Convulsions and Althesin These have been previous accounts of convulsions following the injection of Althesin.’** These have usually occurred immediately after the injection but I would like to report a case in which the epileptiform attack was delayed. A healthy 34-year-old farmer weighing 73 kg came to theatre to have a large haematoma evacuated from the right forearm. Premedication was atropine 0.6 mg and pethidine 50 mg given by slow intravenous injection. Two minutes later, when drowsiness was reported, 5.0 ml of Althesin was injected intravenously over 60-75 seconds; at the end of the injection the lash reflex was still present but this disappeared over the next 10 seconds and nitrous oxide (4 litreslmin) and oxygen (2 litreslmin) were administered with 2% halothane. After the patient had been breathing this mixture for about 60 seconds the surgeon began tentatively to prepare the intact skin with a water-based antiseptic solution. The patient moved his arm and his thighs twitched. After a further 90 seconds the surgeon tried again and the patient once more moved his arm. This time the twitching of the thighs was repeated and progressed to a mild, generalised clonicconvulsion involving all four limbsand the trunk. This lasted about 30 seconds and was not accompanied by cyanosis. When it ceased, spontaneously, the patient continued to breathe the anaesthetic mixture with 5 % halothane and 3 minutes later skin preparation followed by incision and drainage were performed without further incident. Recovery was rapid and uneventful.

Correspondence

113

In two previously reported cases’**in which the convulsions immediately followed the administration of Althesin the total dose was injected over 10 and 15 seconds respectively. The later onset of convulsions in the present case may have been due to the slower rate of injection which would give a lower peak blood level of Althesin. Induction with this drug is, in the author’s experience, quite commonly associated with twitching of the legs or arms and, less commonly, with hiccoughs. Usually the twitching is of only a few seconds’ duration and subsides as the depth of anaesthesia is increased. In the case reported here it may well be that the cerebral stimulant effect of Althesin together with that of light halothane anaesthesia3 and that of the mild stimulation summated to produce a generalised seizure. It is of interest that, like the cases reported by Rees and Uppington, the patient did not become cyanosed during the convulsion, nor was there any clinically apparent depression of respiration afterwards. Unfortunately it has not been feasible to recall the patient from his outlying farm to have electroencephalographic studies performed but he gave no medical or family history to suggest a liability toepileptiform seizures. It must beconcluded that it would be wiser to avoid Althesin in known epileptics. Harari Hospital, P.O. Box ST 14, Southerton, Salisbury, Rhodesia

RICHARD G. MCGOWN

References 1. UPPINGTON, J. (1973) Epileptiform convulsion with Althesin. Anaesthesiu, 28, 546. 2. REES, L.J. (1975) Convulsions immediately following Althesin. Anaesthesia, 30,54. 3. EVANS, D.E.N. (1975) Anaesthesia and the epilepticpatient. Anaesthesia,30,34.

Anaesthesia and hypothermia in sickle cell disease Anaesthesia for patients with sickle cell trait (HbAS) is not unduly hazardous although the dangers of sickling cannot be ruled out. Unusual techniques such as hypothermia or extracorporeal circulation in association with anaesthesia could be dangerous in persons with sickle cell trait. A Nigerian patient with an atrio-septa1 defect and who was sickle cell test positive for sickle cell trait was managed under profound hypothermia using an extracorporeal circulation incorporating a heat exchanger without any complications. The patient was cooled by Drew’s technique to a nasopharyngeal temperature of 20°C. Cardiac arrest time was 21 minutes during which the septa1 defect was repaired ; as rewarming started ventricular fibrillation returned and, on defibrillation, the heart went into sinus rhythm. Blood samples taken during cooling and warming showed no sign of sickling. The patient was artificially ventilated overnight and was extubated the following morning. The post-operative course was uneventful and she was discharged 2 weeks later. Hypoxia, circulatory stasis and cooling are factors which in this technique might be expected to contribute to sickling but at no stage was there any evidence of haemolysis, significant biochemical upset, neurological disturbance or any other changes. Department of Anaesthesia, St George’s Hospital,

Hyde Park Corner, London, S W1

S. SOMANATHAN

Letter: Convulsions and althesin.

112 Correspondence My colleague Dr D. ApIvor has demonstrated that the insertion of a semi-rigid extension tube well up the exit duct of the plenum...
146KB Sizes 0 Downloads 0 Views