507 SUMMARY
’
diphtheria toxoid-antitoxin floccules with potash alum (P.D.F.) or adsorbed on aluminium phosphate (A.D.F.) form antigens that produce a satisfactory immunity in adults. The reactions produced are much fewer and less severe than those caused by alum-precipitated toxoid or by Dissolved
precipitated
Case 2.-The second patient was a small elderly man of 75 who had lost weight. The operation was a left nephrectomy for nephrolithiasis. Induction was with 0’5 g. thiopentone and 4 mg. C10, and maintenance with endotracheal cyclo-
propane.
Twenty minutes after the injection of 010 the surgeon
formol-toxoid. P.D.F. and A.D.F. are not likely to cause the Schick and Schick-control tests should reactions, be applied in all persons over the age of 6 years before immunisation is started, so as to pick out the occasional hypersensitive person who might react severely. The Schick testing, immunisations, bleedings, and recording of reactions were carried out by Dr. J. W. Henderson, Dr. 1. 0. B. Kreher, Dr. E. G. Vaughan, and Dr. E. Urdang, of the Public Health Department of the City of Johannesburg,
Though
by Dr. Bransby Welsh, of the Department of Medicine, Witwatersrand University, and by Dr. P. Agerholm Christensen and Dr. A. Zoutendyk of this Institute. It gives me great pleasure to record my indebtedness to them for their cooperation, without which this work could not havp’ been done
REFERENCES
Holt, L. B. (1947) Lancet, i, 282. Mason, J. H. (1950) J. Hyg., Camb. 48, 418. Pappenheimer, A. M. jun., Lawrence, H. S. (1948) Amer, J. Hyg. 47, 241.
Observations in case 2. The rise in the tidal volume at A may be due to the fact that these estimations were made by a different observer.
preparing to close the muscles ; it was noted that these tight and they contracted when passive ventilation was attempted. A further 3 mg. 010 was given (see figure). The tidal volume was being estimated : with a spirometer (Barry 1951). It had reached 150 c.cm. and fell to nothing after the second injection. It soon reached a level of 50 c.cm. and remained there for over two hours, when it began to increase slowly, reaching a level of 350 c.cm. five hours after the injection. During this period respiration was assisted. Pentamethonium iodide 50 ing. (C5) was given intravenously one and a quarter hours after the second injection of C10. It had no effect on the tidal volume, but caused an alarming degree of vasomotor collapse;‘ Methedrine ’ 30mg. was given intravenously, a glucose drip was started, and rapid improvement in colour and pulse followed. A tracheal tug was noted when the tidal volume reached 150 c.cm. Recovery was uneventful except for a little cough and expectoration ; the patient was discharged well eighteen days after operation. The intravenous pyelogram was good, otherwise the renal function was not investigated; was
CUMULATIVE ACTION OF DECAMETHONIUM IODIDE C. T. BARRY M.D.Paris, D.A.
J. STRATON M.B.Edin., D.A.
CONSULTANT ANÆSTHETISTS
A. R. SUTHERLAND M.B. Edin. REGISTRAR IN ANÆSTHETICS
EDINBURGH NORTHERN GROUP OF HOSPITALS
THE absence of a cumulative effect from repeated doses of decamethonium iodide (CIO) was given as one of its advantages as a muscle relaxant during anaesthesia (Hewer et al. 1949, Ellerker 1950). However, later reports (Gray 1950, Vetten and Nicholson 1950) have shown that the return of adequate respiration can be significantly delayed. We have noted 2 such cases in a series of 175 administrations carried out at the Western
General
Hospital.
Case 1.—The first patient was a man of 45 in good general condition. He had diminished air-entry and absent vocal fremitus at the left base, caused by an empyema in 1935. The operation was a partial gastrectomy for duodenal ulcer. Induction was with 0’8g. thiopentone and 4 mg. C10 ; maintenance was with endotracheal nitrous oxide and oxygen with a trace of chloroform. The incision was made nearly ten minutes after the injection of C10, and as the muscles were found to be a little tight, a further dose of 2 mg. was given with 0.2 g. thiopentone. The operation lasted for nearly two hours and the patient received two further doses of 3 mg. C10, each with 0’2 g. thiopentone. The total dosage was : 12 mg. ; thiopentone, 1.4 g. It was then noted that the intercostal muscles were paralysed and that there was a tracheal tug. No cyanosis was apparent, but ventilation was felt to be inadequate and oxygen was given. One and a half hours later the intercostal muscles began to function and there was some phonation on expiration. The tracheal tug was still present after five hours. Next day the patient still had a slight but definite tracheal tug ; he lacked facial expression and had bilateral ptosis with compensatory wrinkling of the forehead, and his limb muscles were weak. These manifestations had almost disappeared on the third day. On the sixth day signs were found at the right base suggesting a small collapse ; this cleared up without bronchoscopy, and thenceforward recovery was uneventful. A urea range test showed a satisfactory concentration, a dilution less than the expectation, and a delayed diuresis.
C10,
were
The second case confirms the view that relaxation at the end of an operation is better obtained by deepening the general anaesthesia than by, a further dose of muscle relaxant. In both cases the return of muscle tone after the first injection was not what would have been expected had there been an idiosyncrasy to the drug, and a test dose of C10 would probably not have revealed anything abnormal. It certainly seems advisable to restrict the use of this treatment to cases where a single injection will be enough. A similar case has been reported after ’Flaxedil’ (Fairley 1950) in a patient with poor renal function, but after an injection of neostigmine a good respiratory exchange was restored. Idiosyncrasy - to d-tubocurarine is known to exist (Gray and Halton 1948) but this particular type of cumulation has not been reported-perhaps because of the frequent use of
neostigmine. Thanks are due to Mr. John Bruce and to Mr. for permission to report these cases.
Selby Tulloch
REFERENCES
Barry, C. T. (1951) Lancet, Jan. 27, p. 214. Ellerker, A. R. (1950) Brit. med. J. ii, 398. Fairley, H. Barrie (1950) Ibid, p. 986. Gray, A. J. (1950) Lancet, i, 253. Gray, T. Cecil, Halton, J. (1948) Brit. med. J. i, 784. Hewer, A. J. H., Lucas, B. G. B., Prescott, F., Rowbotham, E. S. (1949) Lancet, i, 817. Vetten, K. B., Nicholson, J. C. (1950) Anœsthesia, 5, 175.