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upper portion of the trachea. The introduction of theoil by means of a laryngeal syringe through theglottis may often be carried out satisfactorily, but ithas the disadvantage of uncertainty, in that somepatients cannot tolerate the procedure. Lipiodolinjection will often give invaluable assistance notonly in the diagnosis of growth in the chest but inthe more accurate determination of the extent andposition of the growth itself.

BRONCHOSCOPY, THORACOSCOPY, AND EXPLORATORYTHORACOTOMY.

Of brorxchoscopy I would say that it is a means ofexamination, the possibilities and value of which havenot received in this country the recognition which theydeserve. It is true that the results of bronchoscopicexamination may be entirely negative, but used inconjunction with other methods it should not beneglected, especially in those cases in which clinicaland radiological examination have failed to establisha diagnosis and where definite evidence of stenosisof the bronchus may be furnished by direct visionthrough the bronchoscope.

Thoracoscopy may be of the greatest value. Someof the illustrations which I have exhibited here weremade during the examination of one of my own casesat Brompton by Mr. Tudor Edwardsi2 in which thecauterisation of adhesions was considered necessary.In cases of new growth the results of endoscopicexamination may often furnish no information ofdiagnostic value ; on the other hand, they may beof the greatest assistance. Like other methods ofexamination thoracoscopy must not be regarded alone,but in conjunction with other sources of evidence. iThe final diagnosis of an intrathoracic lesion may,

as in abdominal conditions, only be determined by anexploratory operation, although invaluable help mayhave been afforded to the surgeon by the previousexamination if this has been carefully carried out.History repeats itself, and between the surgery of theabdomen and the surgery of the chest it is possible tomake an interesting comparison. While at the presenttime one is bound to admit that the possibilities inregard to the treatment of intrathoracic neoplasmshave considerable limitations, the successes of modernsurgery in the removal of some of the less malignantforms have justified an attitude of determinedexpectancy. The use of radium in the treatment ofpulmonary or mediastinal tumours, either alone orin combination with surgical measures, is to be

encouraged, since no one can yet say the last word asto its possibilities or its limitations. I would’ deprecatevery strongly the tendency to premature statementsin respect of radium therapy, for I can conceive of nogreater disservice to the public on the part of themedical profession than the broadcasting of optimisticencouragement which is not fully justified byscientific facts. The therapeutic aspect of intra-thoracic and pulmonary new growths has indeed manydisappointments, but I feel it no exaggeration to saythat the advances of the last ten years have led thoseof us who are concerned with this work to regard itwith some increase of confidence and with a vastamount of reasonable hope.

REFERENCES.1. Huguenin, R.: Cancer primitif du poumon, Paris, 1928.2. Adler, I.: Primary Malignant Growths of the Lungs and

Bronchi, New York, 1912.3. Ménétrier, P.: Progrès méd., 1886, 2s., iii., 436; Le Cancer,

Nouveau Traité de Médecine et de Therapeutique, Paris,1927.

4. Letulle, M., and Bienvenüe: Bull. et mém. Soc. méd. hôp.de Paris, 1908, 3s., xxv., 610.

5. Ewing, J.: Neoplastic Diseases, Philadelphia and London,1928, p. 851, et seq.

6. MacCallum, W. G. : A Text-book of Pathology, Philadelphiaand London, 1924, p. 1032.

7. Hanf, D. : Virchows Archiv. f. Path.-Anat., 1927, cclxiv.,367.

8. Davidson, M. : THE LANCET, 1927, i., 122; Davidson, M., andLedlie, R. C. B.: Brit. Jour. Surg., 1928, xvi., 148.

9. Golden, R. : Amer. Jour. Roentgenol, 1925, xiii., 21.10. Riviere, C.: Pneumothorax and Surgical Treatment of

Pulmonary Tuberculosis, London, 1927.11. Burrell, L. S. T., and Melville, S.: Tubercle, 1926-27,

viii., 19.12. Edwards, A. T. : Brit. Jour. Surg., 1924, xii., 69.

AN ELECTROCARDIOGRAPHIC STUDYOF THE

HUMAN HEART DURING AND AFTERNITROUS OXIDE ANÆSTHESIA.

BY G. E. S. WARD, M.D., F.R.C.P. LOND.,PHYSICIAN TO THE MIDDLESEX HOSPITAL;

AND

SAMSON WRIGHT, M.D., M.R.C.P. LOND.,LECTURER IN PHYSIOLOGY, UNIVERSITY OF LONDON,

KING’S COLLEGE.

From the Electrocardiographic and Physiological Department,Middlesex Hospital.

THE changes which take place in the human heartduring and after nitrous oxide anaesthesia have beenstudied by means of the electrocardiograph. All theobservations were made on healthy young studentswho volunteered for the purpose. The patient wasplaced in the recumbent position and control electro-cardiographic curves were first taken from all threeleads. Anaesthesia was then induced with nitrousoxide, and curves from lead II. only were taken atshort intervals during the induction period and forseveral minutes afterwards. In most of the experi-ments pure nitrous oxide was given in the usualdental fashion, using a well-fitting face-piece con-nected to a gas-bag and cylinder. In some cases,however, air was given deliberately or inhaled acci-dentally during the induction. Deep anaesthesia wasalways obtained, and the gas was discontinued as arule just before the onset of jactitation; in someinstances slight or severe convulsions took place.Considerable cyanosis usually developed. The dura-tion of the induction period varied from 47 seconds to90 seconds, the average time being about 1 minute inthe 16 subjects studied. In addition, a small numberof observations have been made under gas andoxygen.The results with pure nitrous oxide were as follows.

Stage of Induction.1. Rate of Heart.-There is an acceleration at the com-

mencement of the induction which is emotional in origin.A further increase in rate occurs as consciousness is lost,and the maximum heart-rate is observed when the aums-thesia is at its deepest. The final rates varied from 106 to145 per minute.

2. Auricular C’oMtp!e.c.—The behaviour of the P waveshowed considerable variation in the different individuals.In most cases it was not appreciably affected. In a fewsubjects it increased markedly in height, the largest risebeing from an initial value of 3-5 mm. to 6-5 mm. (Fig. 6).In one subject the P wave decreased from 5 to 3-5 mm.during the induction, while in another subject (who hadshown at first augmentation of the wave) the’P wave dis-appeared completely at the depth of the ansesthesia.

3. P-R Interval.-The P-R interval was surprisinglystable in our experiments. In only one case was it pro-longed, and then did not exceed 0-2 seconds. In a fewsubjects there was slight shortening of the interval ; thiswas most obvious in the subject with the longest initialinterval.

4. Ventricular Complex.-The most striking and constantchanges were noted in the T wave which was affected inall subjects. In every case a decrease in height was observed.In seven cases it was abolished completely or reduced tonegligible dimensions (Fig. 1) ; in one subject the T wavewas completely inverted (Fig. 2). In several instances theS wave was followed by a long iso-electric period which endedin a small positive deflection (Fig. 5).The R wave was decreased in almost every case. The

reduction in the size of R did not necessarily run parallelwith the changes in T. Thus in Fig. 2 the T wave wasabolished after 20 seconds’ inhalation of nitrous oxide, butthe R wave was only reduced from 29-5 to 27 mm. Thelargest reductions were of the order of 25 per cent.-e.g.,from 21 to 16 mm., 25 to 20 mm., or 18 to 14 mm. In oneinstance an increase in the wave was obtained. Out ofsix subjects with a well-marked S wave, a reduction wasnoted in five-e.g., from 7 to 5-5 mm., or 6.6 to 4-5 mm.

’ Recovery Period.

’I Soon after the nitrous oxide is discontinued recoverysets in.

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After three or four minutes the rate is usually less thanit was before the administration was commenced.

2. After air was given, the P wave underwent reductionin five subjects to less than its height in the control curves.

3. The P-R interval if it had been previously modifiedsoon became normal. (Fig. 1, curve 4, however, showsslight shortening of the P-R interval after administration Iof air.)

- . - .

4. In three subjects the R wave was further definitelydecreased. Thus in subject Ro. the initial height of thewave was 21-5 mm., at the depth of anaesthesia 17-5 mm.,and after breathing air for 25 seconds it was 14-6 mm. zin nine subjects the JK. wave hadnot completely recovered at periodsof four to eight minutes after theaneesthetic was discontinued-e.g.,initial height 28 mm., at depth ofanEesthesia 18 mm., 6 minutes 25seconds later 23 mm. In two

Subject B. In this and the other figuresall records are from lead II ; the timeis shown in 1/5th sees. and the heightof waves in curves in mm. (1 millivolt =1 cm. on original records). Pure N20inhaled for 47 sees. During admini-stration, heart-rate increased from 94to 133 per min. T wave abolished after37 secs. ; R wave decreased. Afteradministration heart-rate rapidlyreturned to below its original level.Recovery in T wave noticeable afterbreathing air for 15 sees. But after2 min. (not illustrated), neither Tnor R has fully recovered.

Curve 1 is a control curve taken beforeanaesthesia. Rate 94 per min. P 5 +.R 25. T 6 +. S 7. Induction with purenitrous oxide commenced at 0 min.0 sec.

Curve 2.-After 20 sees. Rate 120 permin. P 5 +, 6. R19, 20.84,6. T almostabolished.

Cune 3.-After 37 sees. Rate 133 permin. P 5, 5 +. R 19, 22. S 4, 6 (8). Tabolished. Anaesthetic discontinuedat 47 sees.

Cune 4.-After 1 min. 2 sees. (after15 sees. air). Rate 104 per min.P 5,5 +. R 18, 20. S 5, 6. T justreturning. P-R interval decreasedslightly.

cases the R wave finally definitely exceeded its level in thecontrol curves (Fig. 2, curve 5).

5. The T wave invariably began to return as soon as airwas given. The recovery may be obvious after 15 secondsor less. Complete recovery took place in all but two sub-jects, the shortest time taken being 67 seconds. In twocases the T wave finally exceeded its height in the controlcurves (Fig. 2, curve 5).

Discussion.These results show that striking functional changed

take place in the heart during the inhalation of purenitrous oxide. There is marked tachycardia ; theauricle shows variable changes, but conduction inthe bundle of His is but little altered. When purenitrous oxide is breathed, oxygen is washed out fromthe alveolar air and from the blood, so that anextremely severe anoxaemia is acutely produced, asis indicated by the development of cyanosis. Somedecrease in the alveolar and arterial C09 probably

direct action of the nitrous oxideor they might be secondary to theaccompanying anoxeemia.

This problem can be decidedto a considerable extent by com-paring the electrocardiographicchanges under pure gas with thoseunder gas combined with sufficientoxygen to prevent anoxaemia. Fig. 3shows that in the subject Ro. after25 seconds’ inhalation of pure gas;the T wave was abolished, theR wave reduced from 21’5 to16-5 mm., and the rate increasedfrom 90 to 124 per minute. At 53

Subject G. Pure N20 administered for90 sees. During the administrationthe heart-rate increased from 90 to124 per min. After 20 sees. the T wavewas abolished. After 45 sees. T wasdefinitely inverted ; P-R interval wasunchanged. Following administrationthe rate decreased to 77 per min. TheT wave became upright again. Finallyboth R and T exceeded their amplitudein the control curve. The string wascarefully restandardised before curve 5was taken.

Curve l.-Control curve taken beforeanaesthetic. Rate 90 per min. P 5.R 29, 30. T 4, 5. S 2, 3. Inductionwith pure nitrous oxide commenced at0 min. 0 sec.

Curve 2.-After 20 sees. Rate 108 per min.P5,6. R26,28. S2,3. T abolished ;long iso-electric period after S termina-ting in deflection which is first diphasicand then negative.

Curve 3.-After 4 sees. Rate 116 per min.P5,6. R27,29. S 3, 4. T inverted.P-R interval unaltered.

Curve 4. After 1 min. 30 sees. Anaestheticdiscontinued. Rate 124 per min.P 5, 6. R 28. T inverted. P-Rinterval unaltered.

Curve 5.-After 6 min. 40 sees. Rate 77per min. P 5t, R over 30. T 7, 8.

Subject Ro. Pure N20 inhaled for 53 sees.During administration the heart-rateincreased from 90 to 130 per min. TheT wave was abolished after 25 sees. TheR wave decreased from an average valueof 21-5 mm. to 17-5 mm. After admini-stration further reduction in the height ofthe R wave to 14-5 mm. ocf-urred. After25 sees. breathing air the rate had fallento R5 per min. and considerable recoveryof T had taken place. In this subjectafter 4 min. 15 sees. R and T had not

fully recovered.

Curve l.-Control curve before anaes-

thetic. Rate 90 per min. P 5. R 21, 22.T 6, 7. Induction with pure nitrousoxide begun at 0 min. 0 sec.

Curve 2.-After 25 Eecs. Rate 124 per minP 5, 6. R 16, 17. T trace or abolished.

Curve 3.-After 53 sees. Anaesthetic dis-continued. Rate 130 per min. P 6.R 17, 18. T absent at first, thenrecovery commenced.

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seconds the anaesthetic was removed ; the pulse-ratewas 130, the T wave was absent at first and then showedcommencing recovery, and the R waves averaged 17-5xnm. At 68 seconds (25 seconds later) the T wave hadrecovered to 5 mm., though further decrease in the R(to 14-5 mm.) had occurred. Fig. 4 shows the effects ofgas combined with adequate amounts of oxygen.After 4 minutes 15 seconds anaesthesia was presentand the conjunctival reflex was lost; the pulse-rate,however, was only 73 per minute and the ventricularcomplex was not markedly different from that notedin the control curves.

Schneider and Truesdelll produced acute anoxaemiain normal subjects by inhalation of nitrogen for periodsof 47 to 112 seconds (average 82 seconds). None oftheir subjects completely lost consciousness, thoughin some cases twitching was noted. The pulse-ratewas found to increase from an initial level of 95 perminute to a final value of 120 per minute. When airwas again breathed the pulse-rate returned to normalor below normal in 40 seconds. It seems justifiableto conclude that the tachycardia observed under purenitrous oxide anaesthesia is wholly due to the accom-panying anoxaemia.

Greene and Gilbert 2 observed changes in theT wave (similar to those noted by us) in chronicanogaemia in man. In their experiments the oxygen-content of the inspired air was gradually lowered sothat after 20 to 30 minutes a final value of 5 to 10 per I,cent. was reached. !

Some reduction in the height of the T wave mayoccur during simple emotional tachycardia. In ourexperience the extent of such reduction for an increasein heart-rate of about 30 per minute is of the orderof 1 to 3 mm. only. The marked reduction, abolitionor inversion of the T wave which we have described

Tirn A

Same subject as Fig. 3. on another occasion. Curve 1 is acontrol curve taken before anaesthetic. Rate 57 per min.P 4, 5. R 20, 21. T 7 t, 8. Gas and oxygen were given for4 mins. 15 secs., in the proportions of about four parts N 20to one part 02 approximately: the conjunctival reflex wasabsent. At this point curve 2 was taken. Note that theheart-rate was only 72 per min. and that little decrease in theheight of R or T had occurred. (P 4. 4. R 20, 22. T 6, 7.)Compare with Fig. 3.

must be mainly due to the anoxaemia affecting the heartotherwise than through simple acceleration. This viewis confirmed by the record shown in Fig. 5, which showsthe effect of accidental inhalation of a breath of airduring the induction period. The heart-rate is124 per minute in Fig. 5 (curve 2), compared with I120 per minute in Fig. 5 (curve 3) after the air wasbreathed. Although the tachycardia persisted,immediate partial recovery of the T wave is notedin Fig. 5 (curve 3) which is presumably due to thebeneficial effects of the oxygen breathed.The cause of the changes in the R wave is not so

clear. Marked decrease in the R wave usually occursduring pure nitrous oxide anaesthesia, and is absentwith gas and oxygen. It must be pointed out, how-ever, that further decrease in the height of the R wavemay take place after air is administered.

* Compare, for example, the height of the T waves in thecontrol curves of Figs. 3 and 4, in which the pulse-rates in onesubject were 90 and 57 per minute respectively.

Lewis and Mathison 3 observed heart-block fromacute anoxaemia in the cat. In their experiments theheart-block developed after a latent period of H to41 minutes. The absence of heart-block in our

experiments may have been due to the shorterduration of the anoxaemia.

FIG. 5.

Subject S. 1 is control curve taken before anesthetic. Rate82 per min. P 3, 4. R 34, 35. S 5, 6. T 7. Pure N20 wasthen inhaled for 55 sees. After 20 sees. (curve 2) the heart-rateincreased to 124 per min. The P was 6’5 mm. comparedwith 3’5 mm. originally. T was abolished and replaced by asmall positive deflection at the end of a long iso-electric periodwhich followed S. At 37 sees. a breath of air was inhaled(curve 3). The heart-rate was scarcely altered (120 per min.)but considerable recovery in T immediate y took place.(T variable in height up to 5.) P still exaggerated, 6, 7.

Conclusion.

There is still considerable difference of opinionabout the significance of the normal T wave of theelectrocardiogram (for discussion see Katz 4). It iswidely held that the T wave represents the " stageof retreat "-i.e., the disappearance of the excitationprocess at the apex and its persistence at the base ofthe heart. There is a general consensus of opinionthat abolition or inversion of T in lead II. indicatesserious functional or structural cardiac derangement.It seems justifiable to conclude that the acuteanoxaemia produced during anaesthesia with purenitrous oxide seriously depresses the ventricularmyocardium. The change is of a temporary nature,and is rapidly recovered from ; but even in ourhealthy subjects recovery was sometimes not com-plete after several minutes. It is possible that inpatients with heart disease the immediate changesmight be of a more serious nature, and it is con-ceivable, too, that they might be of a more lastingcharacter. It suggests that pains should be taken insuch patients to avoid any anoxaemia developingby giving adequate amounts of air or oxygen incombina-tion with nitrous oxide.

Summary.The changes in the human heart during pure

nitrous oxide anaesthesia have been studied electro-cardiographically in 16 subjects. The principalresults obtained were (1) tachycardia ; (2) reduction,abolition, or inversion of the T wave in lead II. ;(3) reduction in the R wave ; (4) variable changes inthe P wave; (5) little change in the P-R interval.The tachycardia and modifications in the T wave areattributed to the accompanying anoxaemia. Thepractical implications of these findings are discussed.

We are indebted to Drs. Anderson, Gray, Rose, andSlaughter for help with the administration of the

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anaesthetics, and to the students of the hospital who Ikindly offered themselves as subjects for this work. IReferences.

1. Schneider, E. C., and Truesdell D. : Amer. Jour. Physiol.,1923, lxv., 379.

2. Greene, C. W., and Gilbert, N. C.: Arch. Int. Med., 1921,xxvii., 517.

3. Lewis, T., and Mathison, G. C.: Heart, 1910-11, ii., 47.4. Katz, L. N.: Physiol. Rev., 1928, viii., 447.

ASTHMA IN CHILDREN.

THE VALUE OF SUGAR IN ITS PREVENTIONAND TREATMENT.

WITH A NOTE ON THE TREATMENT OF INFANTILE

ECZEMA.

BY A. ARNOLD OSMAN, D.S.C., M.R.C.P. LOND.,PHYSICIAN, QUEEN MARY’S HOSPITAL, STRATFORD, E. ;

MEDICAL ASSISTANT, GUY’S HOSPITAL.

(From the Department for Medical Investigations,Queen Mary’s Hospital).

IN a previous paper 1 attention was drawn to theimportance of ensuring an adequate supply of sugar,in any form, in’the diet of children, and it was shownhow readily many of the minor symptoms of dis-ordered health in children can be cured and pre-vented by this simple measure. It was pointed out,too, that amongst the disorders which apparentlyyielded quite readily to this treatment were somecases of asthma. The object of the present paperis to record four cases of typical bronchial asthma inchildren who have been rendered entirely free fromattacks over periods of one to two and a half yearsby the simple addition of sugar to the diet andwithout any other form of treatment. During thepast six years other cases have been treated in thesame manner, with success varying chiefly with thecare and persistency with which the treatment hasbeen supervised by the parents, though it is not tobe expected that all cases will respond so favourablyas the four described below.Rackemann 2 has shown that asthma in children

is often completely controlled by careful attentionto the hygienic conditions under which the childlives, but in the cases considered here an increasedallowance of sugar in the diet was the only alterationmade in the daily life of the child. All the patientswere treated at, home by the parents, and were seenregularly in the out-patients’ department at fort-nightly intervals. The treatment simply consisted ingiving three drachms of powdered glucose in lemonadethree times a day, in between meals, with extra sugarand " sweets " as recommended in the paper referredto above for debilitated children. In each casethis treatment resulted in a marked improvement inthe general health and spirits, in addition to the com-plete disappearance of the asthma. No evidence hasbeen obtained as to the mode of action of sugar inthese cases, but I am inclined to attribute its bene-ficial effects to the improvement in the generalhealth. Barber and Oriel,3 however, consider thatin these cases there is some hepatic dysfunction, andthat sugar exerts its beneficial action on the liver.CASE l.-A boy, aged 8 years, had suffered from bronchial

asthma since he was 3 years of age. Up till then he hadbeen in normal health. The attacks apparently dated fromwhooping-cough contracted at the age of 3. The attacksgenerally occurred at monthly intervals throughout theyear, and lasted for two or three days. He was an onlychild, small, pale, thin, and delicate-looking, but brightand intelligent, sometimes, but not habitually, consti-pated. His tonsils and adenoids had been removed at4t years of age. There was no family history of asthma oreczema. At the age of 6 he began to have typical attacksof cyclical vomiting with the usual pyrexia. These attacksoccurred at about monthly intervals but did not coincidewith the attacks of asthma or bear any apparent relationto the latter, though on two occasions the history of thesymptoms suggests that the asthma was preceded by

symptoms of cyclical vomiting-viz., pyrexia, headache,and vomiting.Treatment was commenced in August, 1926, and he was

given three drachms of glucose thrice daily, with extrasugar at meals, and sweets. Until December, 1928, he hadno further attacks of asthma. For the previous 12 monthshe had ceased to attend hospital, and he admitted that hehad recently not been having his usual allowance of sugar ;as a result, he had a single attack of asthma. The treat-ment was resumed and since then, until he was last seen inAugust, 1929, he had had no more asthma or cyclicalvomiting. This boy has therefore had only one attack ofasthma during the past three years.CASE 2.-A boy of 8, the elder of two children, was

thin, small for his age (weighing 40 lb. 4 oz.), and verynervous. He looked a good colour and was not consti-pated. The family history as regards asthma was unreliable.He had never suffered from cyclical vomiting. At the ageof four months he had had " eczema," and at two and a haliyears pneumonia. The attacks of asthma had begun atthe age of 5, and had occurred at intervals of 14 to 21 days.They began with a cough which was succeeded by difficultyin breathing, and generally started at about 2 A.M., andlasted for 48 hours.

Treatment was commenced on August 16th, 1928, andwas followed by a most remarkable improvement in appear-ance and physique, and he has since (up to June, 1929) hadno further attacks of asthma.

CASE 3.-A boy, aged 4 years, was an only child, with apale face and a flabby and watery body. He was first seenon March 9th, 1927, when he was 2l years old. There wasno family history of asthma or eczema. He had hadbronchitis and pneumonia in the previous winter. He wasalways constipated. When seen he was in a typical attackof bronchial asthma; there was marked prolongation ofthe expiratory phase and the chest was full of sibilantrales and rhonchi. For the previous nine months he hadbeen having similar attacks at intervals of three weeks.Treatment was commenced as in the previous cases. A

week later he was much better and was able to go out of’doors. He has attended hospital since at fortnightlyintervals and had had no further attacks of asthma byJune 6th, 1929 - that is, for a period of two years and three-months.CASE 4.-A boy, aged 4t years, whose maternal grand-

mother had suffered from asthma, was an only child, wellbuilt, and healthy looking. For the past three years he-had suffered from attacks of cough and shortness of breath,mostly commencing during the night, and occurring everytwo or three weeks, both winter and summer. In some ofthe attacks he had headaches and vomited, and was saidto be feverish. His weight was 2 st. 12 lb. 4 oz.

Treatment with sugar was begun on Feb. 18th, 1928.No further attacks occurred until Dec. 1st, when he had amild attack. Examination of the urine showed excess ofacetone bodies, suggesting that he was for some reason nothaving sufficient sugar. Renewed instructions as to theimportance of treatment were given, and no further attackshave been experienced.From a consideration of these cases it seems that

an increased allowance of sugar, as such (i.e., not as.starchy foods), in the diet alone was sufficient toprevent recurrence of asthma in these four childrenover a considerable period of time. The result justifiesthe hope that a simple and effective cure and pre-ventive measure has been found for this distressingdisorder, at least in some cases. Unfortunately, so.far as my experience goes, sugar is without value inthe treatment of asthma in adults.

It is not possible to lay down more precise rulesfor the exact amount of sugar required in a givencase. In general it may be said that that amount--ascertained by trial-must be given which willensure that the urine does not contain an excess ofacetone bodies (positive Rothera reaction) under anyconditions of stress-i.e., worry, excitement, or

infection. In practice, this would generally seem. tobe met by the doses given in the cases here recorded.The administration of alkalis in these cases does notappear to enhance the action of the sugar in any way.

Sugar in the Treatment of Infantile Eczema.In view of the supposed connexion between eczema.

and asthma in children, it is of interest to note that,quite contrary to the usual teaching, sugar alsoappears to be of some value i-ri the treatment ofinfantile eczema. This is so subject to spontaneousrecovery and remissions that little would be gained