LATE ETHER CONVULSIONS

DR. R. F. WOOLMER &

DR. S. TAYLOR : LATE ETHER CONVULSIONS

LATE ETHER CONVULSIONS A STUDY BASED ON FOUR CASES

BY R. F. WOOLMER, B.M. Oxon. SENIOR RESIDENT ANÆSTHETIST TO ST.

HOSPITAL, LONDON ;

STEPHEN TAYLOR

THOMAS’S

AND

B.Sc., M.B. Lond.

HOUSE PHYSICIAN TO THE MEDICAL UNIT AND LATE RESIDENT ANÆSTHETIST AT THE HOSPITAL

1005

In Case 4 the day was again hot. The heart stopped, but was successfully restarted by cardiac massage, and it beat strongly as long as artificial respiration was continued. All attempts to start spontaneous respiration, however, failed and ventilation was maintained by means of the Drinker automatic respirator. This kept the patient alive for 3! hours, before the heart finally stopped. We therefore think the automatic respirator worthy of further trial. ETIOLOGY

CONVULSIONS occurring during deep ether anæsthesia were first described by Wilson, and they are now recognised as one of ether’s most serious immediate dangers. Fortunately they are rare ; the longest series seen and recorded by one man is Pinson’s 15 cases. The mortality is about 50 per cent. ; two of our four cases were fatal. Each showed the characteristic clinical picture, with minor variations, but each was treated in a different way. All occurred in the theatres of St. Thomas’s Hospital during 1935, and one or other of us was present on each occasion. TYPICAL CLINICAL PICTURE

The patient is usually due to

child or young adult with pyrexia, acute septic condition. The theatre is overheated. Atropine has been given and the dose may have been excessive. The patient is deeply anæsthetised with ether, the pupils being dilated and inactive to light. The colour is, as a rule, good, and oxygenated ether is sometimes being given. The eyelids start to twitch, then the face, and the convulsions become general. In the after fatal 5-10 of convulsions mins. cases, immediately the respiration ceases, the patient goes blue, and the heart stops ; in other cases, the convulsions stop, but the patient dies later from cardiac failure ; alternatively, recovery may follow the cessation of the convulsions. Ether convulsions have to be differentiated from ether clonus, which occurs in the early stages of anaesthesia. Clonic twitching starts in the limbs and may become very violent; it ceases as the anaesthesia deepens. True convulsions occur only after full anaesthesia has been established, and the term " late ether convulsions " is used to emphasise this difference. a

some

DESCRIPTION OF CASES

comparison, the essential features of our cases given in the Table. In Case 1 oxygenated ether was being used; the convulsions were recognised the moment they started and were easily stopped. A subsequent ether anaesthesia was given without convulsions. McDonald, Willway, and Ashworth have described For

are

similar cases. In Case 2

a second dose of atropine was given owing to delay with the previous operation. The day temperature was excessive, and the anaesthetist actually remarked upon the possibility of convulsions before starting the anaesthetic. As the surgeon needed complete relaxation however, open ether

used. So far as we know, this is the first case of ether convulsions in which the anaesthesia has been successfully continued with ether-and moreover ether from the same bottle. In Case 3, as in Case 1, a pyrexial patient had a large dose of atropine on a hot day. All the usual methods of stopping the convulsions failed, and this is, we think, the first time Evipan Sodium has been used. Its success in stopping the convulsions justifies its being tried in the future. was

’

In the past several theories as to the cause of ether convulsions have been advanced. Impurities.—Wilson found acetaldehyde and peroxides in the ether he was using when convulsions occurred, and not in other samples of ether. Walton had a similar experience. Sykes, however, records a case where acetaldehyde was absent, and peroxides amounted to only 0-05 part per million of ether. Ross Mackenzie describes sevencases where the ether was carefully analysed. The largest amount. of peroxides was 0-65 part per million, while the largest amount of acetaldehyde was 0-05 part per million ; the toxic dose of each is ! per cent., so that it is almost inconceivable that these impurities Our case (No. 2); were the cause of the convulsions. where the same ether was used after the convulsions had ceased, with no ill-effect, is strongly suggestive that ether, per se, or its impurities, is not to blame. Idiosyncrasy.—Hadfield and Kemp have thought that some patients have’an " ether convulsion diathesis." Four cases have already been mentioned where ether has been used successfully after convulsions had occurred at previous operations. Our Case 2 is even more important in discounting the suggestion of a diathesis.

Congestion of the Rolandic area from jugular obstruction is suggested by Hewer, who advises raising the chin to relieve it. In Case 2 the manoeuvre of lowering the chin was tried and the convulsions immediately became worse. Rolandic congestion may therefore be of some significance. 002 accumulation is believed by Pinson to be the cause. Actually COis a most effective agent in treatment. Atropine overdosage.—Hornabrook suggested this. It occurred in two of our four cases, and is a factor frequently but by no means always present. Sepsis.-This too is often but not invariably present. Enormous numbers of septic cases have ether an2esthesia without convulsions. Over-oxygenation.—Mennell thought this might be the primary factor. It was present in one of our cases, but another was definitely cyanosed. Cyanosis has several times been described as a precursor of ether convulsions. It is obvious that none of these views is at all satisfactory. We suggest that ether anaesthesia upsets the normal heat-regulating mechanism of the body and we wish to support Dickson Wright’s hypothesis that heat-stroke may playa big part in the aetiology of ether convulsions. Our evidence is as follows : (1) In three of our four cases the day temperature was excessively high. Hadfield’s cases at St. Bartholomew’s Hospital, London, all occurred during the summer. (2) The association of ether convulsions with pyrexia is well known. All our cases were pyrexial, and the post-operative temperatures were high. Temperatures during the convulsions were unfortunately not taken. Mackenzie :records a case where, during the convulsions, the

1006

DR. R. F. WOOLMER &

DR. S. TAYLOR : LATE ETHER CONVULSIONS

temperature was 108° F. Cold sponging lowered the the use of the ether bomb, the principle of which temperature and stopped the convulsions. When was to deliver superheated ether vapour into the the patient was back in bed the temperature rose patient. (6) Bull describes the case of an Arab to 106-8° F., and convulsions started again. Once woman who had convulsions under chloroform. The heat at the time was too great for the use of more cold sponging proved successful, though the ether. died later. an (3) By stopping sweating, (7) Convulsions are one of the manifestations patient of heat-stroke. Willcox describes the heat hyperoverdose of atropine tends to reduce heat loss. Its association with ether convulsions has already pyrexia form of heat-stroke as follows : " The onset been mentioned. (4) The hyperpncea which CO2 may be sudden, with rapid rise of temperature, produces, not only removes ether but also heat from coma and convulsions ... the skin is hot and dry, the body. It has already been shown that ether and the face flushed and cyanosed... the pupils are itself is probably not the cause of the convulsions. dilated ... fibrillary twitchings of the muscles and convulsions usually occur ... and pulmonary oedema The beneficial effect of C02in relieving convulsions is a terminal event." This description would do may well be due to its action in accelerating heat loss. (5) In 11of Pinson’s 15 cases the convulsions followed very well for an ether convulsion. FOUR CASES OF ETHER CONVULSIONS

1007

CLINICAL AND LABORATORY NOTES

the trachea should be intubated.

PROPHYLAXIS AND TREATMENT

In the belief that the heat-stroke hypothesis provides the best explanation which has so far been offered for the aetiology of ether convulsions, we advise appropriate means of prophylaxis and treatment. The anaesthetist should limit pre-operative atropine to gr. 1/150 in children and young people with acute septic diseases and a temperature of over 100° F., especially in hot weather, and he should avoid excessive coverings, above all mackintoshes, for such patients in the theatre. He must be constantly on the watch for the first twitch of the eyelids or mouth in these patients, and, if it occurs, he must treatment immediately. To treat the convulsions, COand oxygen should be given at once. If they do not cease within a minute, evipan sodium should be injected intravenously. While preparing the evipan, cold sponges and ice should be applied to the body and face. If necessary,

apply

To combat cardiac

failure, adrenaline and Coramine should be given, and for respiratory failure, artificial respirationmanually, or mechanically by means of the McKesson machine and the Drinker respirator or Bragg-Paul pulsator ; the latter is probably preferable, as the Drinker apparatus tends to conserve heat. REFERENCES

Ashworth, H. K.: Brit. Med. Jour., 1935, i., 851. Bull, L. J. F.: Ibid., 1927, ii., 471. Hadfield, C. F. : Proc. Roy. Soc. Med., 1928, xxi., 1699.

Hewer, C. L. : Recent Advances in Anæsthesia and Analgesia,

London, 1932. Hornabrook, R. W.: Brit. Med. Jour., 1927, ii., 471.

Kemp, W. N.: Brit. Jour. Anæsth.,1932, xi., 169. McDonald, N.: Proc. Roy. Soc. Med., 1928, xxi., 1706. Mackenzie, J. R. : Brit. Med. Jour., 1931, i., 440. Mennell, Z. : Proc. Roy. Soc. Med., 1928, xxi., 1705. Paul, R. W. : Ibid., 1934, xxviii., 436. Pinson, K. B. : Brit. Med. Jour., 1927, i., 956. Sykes, W. S. : Ibid., 1930, i., 1123. Walton, A. C. R. : Ibid., 1928, ii., 8. Willcox, Sir W. : Price’s Text-book of the Practice of Medicine, London, 1933, p. 382. Willway, F. W. : Brit. Med. Jour., 1935, i., 764. Wilson, S. R.: THE LANCET, 1927, i., 1117. Wright, A. D. : Brit. Med. Jour., 1935, i., 949.

CLINICAL AND LABORATORY NOTES ANEURYSM OF THE SPLENIC ARTERY SIMULATING CHOLECYSTITIS

gastrohepatic omentum above the stomach and midway along the lesser curvature of the stomach. The tumour was firm, fluctuant, and about the size of a tangerine

The walls were calcareous and crackled when No pulsation was seen or felt, and the tumour was thought to be a pancreatic cyst, and was incised. Blood escaped with considerable force and the stream was The diagnosis of an aneurysm was at seen to pulsate. once obvious. By firm pressure on the aorta with the fingers it was possible to control the haemorrhage. The position of the aneurysm was such that removal was impossible, and an attempt to sew up the incision in the aneurysm failed because the walls were so calcareous orange.

BY S. E. RESIDENT SURGICAL

ANEURYSMS

pressed.

OSBORNE, L.M.S.S.A.

OFFICER, WORTHING HOSPITAL, SUSSEX

the

of

splenic artery,

although

would at first sight be and and Anderson expected, Gray in 1929 were able to collect 58 recorded examples.1 The present case has certain unusual features. uncommon,

are

not

as rare as

Miss A, aged 43, a cook, was sent to the Worthing Hospital as a case of acute cholecystitis. She gave a history that apart from pneumonia and influenza, her only illness was in 1909, 27 years previously, when an operation was performed for suspected disease of the gallbladder. The operation scar is a paramedian supraumbilical one : evidently the gall-bladder was inspected and found to be normal and the appendix removed through this high incision.

The present symptoms began six years ago, when the

first complained of abdominal pain coming on in attacks at infrequent intervals, colicky in nature, beneath the right costal margin, radiating through to the right shoulder and aggravated by stooping. A feeling of fullness was noticed in the epigastrium, discomfort after meals, and very troublesome flatulence. There was continuous nausea but only occasional vomiting. Fatty foods were not tolerated and brought on pain. Occasionally after the attacks there was slight jaundice, but the urine was not noticed to be deeply coloured and clay-coloured stools were not a feature.

patient

Examination.-The patient and

apprehensive.

stout, very nervous, Temperature, 98’4° F. pulse-rate, was

96 ; respirations, 20. There was some tenderness over the gall-bladder on palpation, and slight tenderness in the

epigastric region, which persisted for some time afterwards.

The heart and chest were normal.

No other abnormalities the diagnosis of gall-stones with cholecystitis was made. An opaque cholecystogram showed that the gall-bladder filled and emptied normally and no stones were demonstrated. Operation.-Under ethyl chloride and ether anæsthesia the abdomen was opened through a midline incision and the gall-bladder inspected. Many adhesions were present, but no gall-stones were felt either in the gallbladder or in the common bile-duct. A large whitishgrey round tumour then came into view, lying in the were

to be

found, and

1Anderson, W., and Gray, J. : Brit. Jour. Surg., 1929, xvii., 267 ; see also Brockman, R. St. L.: Ibid., 1930, xvii., 692.

A photograph of the spleen (s), aneurysm

kidney (K) dissected post mortem.

(A),

and

that the stitches cut out as soon as they were inserted. The patient had by this time lost a considerable amount of blood, and as her condition was giving rise to some anxiety, the wound in the aneurysmal sac was closed by two pairs of curved artery forceps, which were left in situ. The abdominal wound was closed and the patient returned to bed. Post-operative treatment.-The patient was given the usual restoratives and a blood transfusion of 26 oz., and on the following day her general condition had improved. On the third day the clamps were removed. On the ninth day after the operation she was taking food well and did not complain of pain or feeling unwell. There At 12.20 A.M. was some serous discharge from the wound. a sudden severe secondary haemorrhage took place, and in spite of blood transfusions, morphia, and hasmoplastic ’ serum the patient collapsed and died at 10.15 A.M. Pathology.—Post-mortem examination revealed a large and flabby heart with excess of fat. The aortic valves were normal and free of vegetations. There was no