INFANTILE BERI-BERI IN SINGAPORE DURING THELATTER PART OF THE JAPANESE OCCUPATION

BY

G. HARIDAS, L.M.S. (Singapore), M.RC.P.(From the Kandang Kerbau Hospital, Singapore)

The problemns presented by infantile beri-beri inSingapore during the yeas 1944 and 1945, up to thearrival of the liberating British forces on September5, 1945, were of a different character from thoseobtaining in peace-time. They were: (a) apathy ofthe authorities; (b) lack of medicines; (c) lack ofessential foods; and (d) shortage of milk or mlksubstitutes. For purpose of actual description anddiscussion, cases will be dealt with as they occurredamong children admitted to the Japanese civilianhospital caled the 'Chuo Byoin,' at KandangKerbau, Singapore. In pre-war days this was amaternity hospitaL After Japan's daration ofwar with the Allies on December 8, 1941, provisonwas made for the admision and treatment ofcasualty cases. After the fall of Singapore onFebruary 15, 1942, the Japanese converted it into avlian genral hospital and called it the 'Chuo

Byoin.' In addition to maternity beds, they pro-vided accommodation for the treatment of adultmale and female medical and surgic cases, gynae-cological cases, and sick children. There were 349beds for adults, male and female (exludingmaternity beds) and 12 beds for ick chldren.Table 1 shows the percentage mortality in childrensuffering from berin-bei, compared with the totalmortality for children and for adults.Some pre-war figues of infantile beri-beri cases

admitted into the Children's wards, GeneralHospital, Singapore, are given in table 2. TheChildren's wards accommodated 120 patients ofunder six years old. My figures during 1936 andthose of Cecily D. Williams between August, 1937,and July, 1938, are as follows:

Figure of infantile mortality and of infantileberi-beri deaths respectively for the island of Singa-pore for the years 1938 to 1944 obtained from theRegistrar-General of Births and Deaths, are given intable 3. These figues include cases treated at allGovernment and Municpal hospitals and dis-pensaries and by private practitioners Figures

TABE 1

Per-Ad- I centage

missions mortal-ity

Sick children .. 854 392 45 90Infiantile beribein 139 77 55 41Adult nix-pients 9,490 1,592 16177

TABLE 2

Ad- + Pecnage__ missions ~Deths mordtalt

1936 316 146 46 20Infantle Aug. 1937

beri- to Julyber 1938 663 328 49-47

TABLE 3

Infanle Infantilemort beri-beri

1938 5,065 251939 4,516 2591940 4,819 1511941 Not known 1311942 7,340 971943 5,052 2321944 9,039 448

between 1942 and 1945 are not very reliable, due toconditions preailing at that time.

Population figures during the Japapese regimewere unas bl; hence comparison has to bemade between the actual number of deaths of thesetwo periods, and not between the infantile deathrates

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At that time the increasing incidence of beri-beriamong the population showed that deficiency ofvitamin B1 constituted a serious menace to publichealth. Infantile beri-beri developed either:(a) in children fed on the breast milk of a womanwhose diet consisd exclusively ofhihy milled riceor who was herself suffering from latent or manifestberi-beri Cm most instances the mother appearedhealthy); or (b) in children fed either on food poorin vitamins, such as highly milled rice paste, or onlocaly made condensed or evaporated milk intro-duced as substitutes for powdered milk; or (c) inchildren fed on cow's milk with a very low vitaminB1 content.Eijkman (1897), as the result of experiments on

fowls, wrongly postulated that there exists in rice atoxin which produces polyneuritis and that this toxincould be neutralized by something present in thepericarp. Grijns (1901), thought that infection andintoxication played no part in the causation of thisdiseae and that it was the result of food deficiency.Braddon (1901, 1907), Fletcher (1907), and Fraserand Stanton (1909, 1910), from investigationscarried out in the Federated Malay States on theetiology of beri-beri, proved that beri-beri appearsin persons who almost exclusively eat highly milledrice, and that the consumption of under-milled riceor the aministration of the silvery coverings of therice was potent not only in stopping the developmentof be&-beri but also in curing it. Ito (1911),observed a case of infantile beri-beri in which themother did not have beri-beri, and called the condi-tion 'mother's-milk intoxication.' But he after-wards changed the name to ' breast-milk intoxica-tion ' because he saw cases in babies who were fed bywet nurses. In 1916, Segawa reported an interest-ing case in which nervous symptoms in a breast-fedinfant disappeared when fixed feeding was given.The mother of the infant did not have beri-beri, soSegawa thought that in addition to infantile beri-beri there was another disea of infants due tobreast feeding. This was the first case reported ofwhat is now termed ' so-alled breast-milk intoxica-

tion.' The nervous symptoms vanished quicklywhen the mother ceased to feed her baby, and re-

appeared when the milk of the mother was again

used. Segawa concluded, therefore, that the causeof the sickness must lie in breast milk and that themalady is not the same as infantile beri-beri. Inaba(1917), insisted that, although cardiac disturbancesare the most important symptoms of infantile beri-beri, the nervous manifestations of so-called breast-milk intoxication may also be seen in infantile beri-beri and are not incompatible with that diagnosis.Because of the rapidity of recovery from so-calledbreast-milk intoxication when patients are givenvitamin B1, Toyoda (1922) thought that the cause ofthe sickness was the same as that inducing infantileberi-befi.

AgeIn this series ofcases of infantile beri-beri, 123 were

breast fed, and 14 were fed on locallymade condensedor evaporated milk (see table 4). In the breast-fedgroup, the cases occurred with greatest frequencybetween the one month and four months age periods.It was also noted with less frequency in childrenbetween the seventh and eleventh months. Thelowest age on record in this series was in a locally-made condensed-milk-fed infant aged seven days(case 1). The highest age on record is in a child oftwo years. It is included here because it happenedto be breast-fed (case 2).

INFANT FEEDING

Certain problems of infant feeding presentedthemselves for solution during the Japanese occupa-tion period. Firstly there was the increasedincidence of beri-beri in pregnant woman, nursingmothers, and breast-fed children owing to the con-sumption of an exclusive diet of highly milled riceand/or tapioca or sweet potato with no vitamin B1supplement. Then we were faced with the problemof providing suitable substitutes for milk when thethen exisfing stocks of condensed milk became

exhausted. There were not enough milch cows tocater for the needs of all infants who for variousreasons could not be breast-fed. Even when cow's_

TABLE 4

Age in months 7 1 2 3 4 5 6 7 8 9 10 11 12 24 Totaland days days mth. mths. mths. mths. mths. mths. mths. mths. mths. mths. mths. mths. mths.

Breast-fed 0 27 32 16 11 7 7 2 2 6 2 0 10 1 123

Condensed milk, 1 1 1 2 3 1 0 2 1 0 1 0 1 0 14kmcalymade

Cow'smilk 0 0 0 1 1 0 0 0 0 0 0 0 0 0 2

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INFANTILE BERI-BERI IN SINGAPORE

milk was available, its purchase was not within thefinancial means of the poorer section of the popula-tion. Mothers who had too little breast milk, or

those who could not obtain milk as a substitute, usedto give the most easily obtainable food, that is,cooked highly milled rice, which was given in spoon-fuls and was stuffed into the children's mouths in theform of a thin gruel or a rice-paste without anyvitamin B1 supplements. Among the Malaysbananas were often given, both alone and mixed withhighly milled rice: and in Malay children primarydietetic disturbances and infantile ben-ben wererare, the diet of rice and bananas being quite wellborne. But much of the trouble resultd from thevery insanitary way in which the food was storedand prepared, and from the method of administringthe feeds.

Soya bean milk and sifted undermilled rice flour(or Chowbee, or bras ayam) with certain additionsto make good the deficiency in fats and in vitaminsA and C, were recommended as suitable substitutesfor milk.Medhod of preparation of soya bean milk; For one

pint of milk take 2j dessertspoonfuls of the rawbeans, wash well, and soak in water overnight.Next morning pound or grind the beans (wet). Addthe required amount of water and boil for 5 or 10minutes, stirring all the time. Then strain through athin cloth or strainer and add sugar to taste. Itcan be given in a bottle like milk. So that it willkeep till late afternoon, it is advisable not to addsugar till the food is used, and also to keep the milkin a cool place.Method of of rice gruel as a stute

for milk. Rice gruel prepared from sifted under-milled rice flour (or Chowbee, or bras ayam), withsome additions such as red palm oil and pineapplejuice to make good the deficiency in vitamins A andC, was recommended as another suitable substitutefor milk when the latter was not obtainable. Riceguel made from sifed undermilled rice flour (orchowbee or bras ayam) was analysed by Rosedale(unpublished data) and was found to work outroughly at half the value of fresh milk, with thefollowing differences: (a) gruel from sifted under-miled rice flour is rich in vitamin B1; (b) it is notablydeficient in fat and the fat is never higher than halfper cent. (good milk contains at least the percent. of fat); (c) vitamins A and C are completelyabsent in these gruels; (d) cacium is markedlydeficient; (e) carbohydrate present is starch and notlactose. (The disadvantage of starch is that ininfants under six months of age the digestion ofstarch is poor; but a choice between starvation, oran unsuitable starchy substitute such as undermilledrice gruel, must favour the latter.)Metd of p of gnrel, and dosage. Take

two full or heaped teaspoonfuls of the sifted riceflour, add to three ounces of water, and cook for a

quarter of an hour. This forms a suitable feed forbabies below four months old. From five monthsonwards the quantity of ground rie-flour is to beincreased gradually from two to three heaped tea-spoonfuls for five ounces of water. The quantity ofwater has to be greatly increased. From six monthsonwards little extras (e.g. ripe bananas, fish liver,egg, spinach, bean curd) should be added to the dietErom time to time. For additional fat, it is sug-gested that one drachm or one teaspoonful of amixture of one part of refined red palm oil and fiveparts of coconut oil be added to each of the child'sfeeds in the day for an infant up to one year, assum-ing that the infant has six or seven feeds in the day.This will greatly enhance 'thevitamin A value. Thedeficiency in vitamin C can be made up by giving theinfant the juice of ripe pineapples, commencingwith one teaspoonful once a day, gradually increas-ing this amount to one teaspoonful three times a day.

Race DkbmxouTable 5 gives the race distribution of cases of beri-

beri. The occurrence of infantile beri-beri follow-ing the consumption of milk per se, or of condensed

TABE 5

Race Chinese Indians Total

Breast-fed 120 1 2 123Locally madecondensedmilk .. 14 _ 14

Cow'smilk 1 2

or evaporated milk produced locally, may be due tothe fact that suitable fodder for cows was scarce,with the result that the vitamin B1 content of the milkmust have been low; this amount would have beenstill further reduced by the unsatisfactory methodsemployed in the manufacture of the condensed orevaporated milk.The sale of cow's milk was not controlled by the

authorities, and the following brands of cow's milkwere available: (1) undiluted cow's milk at $15.00per pau, Japanese currency (pre-war price ten centsper pau (I pau=1I0 oz.)); (2) moderately dilutedcow's milk at $10.00 per pau; (3) highly dilutedcow's milk at $5.00 per pau. Brand 3, being thecheapest, was bought by the people for feeding theirinfants, and it is not surprising that infantile beri-beri occurred in infants thus fed.

There were two South Indian (Tamil) cases in thisseries. The comparative rarity of infantile beri-beri among the South Indian (Tamil) in spite of thediet of highly milled rice and/or tapioca is probablydue to the consumption ofother foods rich in vitaminB1, such as ragi (Eleusine Corocona) which was culti-vated to a far greater extent in Malaya than hitherto.The South Indians find ragi much more acceptable

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ARCHIVES OF DISEASE IN CHILDHOODas a food than do the Chinese. Under normal pre-war conditions, it was noted that very few cases ofinfantile ben-bei were encountered among theSouth Inians, as their staple diet consisted mainlyof parboiled rice which contained a fair amount ofvitamin B1.

Sbta s

During the period under review the economicsituation of the country was chaotic. Owing to thestranglehold exerted by the Allies on Japanesecommunkiations, there was an evergrowing shortageof essential foodstuffs. Inflation was marked andthe purchasing value of the currency very low.Black market activities were rampant. The pricesof essential foodstuffs, such as milk, eggs, meats,fish peas, and beans, increased to an extent farbeyond the reach of the average individual. Par-boiled rice was not obtainable, and there were onlylimited stocks of undermilled rice or bras ayam orchowbee, which were sold at a high price. The ricerations per month were cut down in January, 1944,to 10, 8, and 5 lb. respectively for men, women,and children under ten years of age. In order tosupplement the inadequate rice ration, sweetpotatoes and/or tapioca-foodstuffs of poor nutri-tive value-were eaten by most people. In someinstances the fathers of the infants were unemployed,in others a father with small earnings had to keepa family of five or six. Occasionally the parentswere miserly in spending money on protective foods.

Dietetic HistoryThe following is a typical economic and diet

history obtained from a mother of a child withinfantile ben-beri.The mother lives with a big family, which consists

of eleven persons including herself. The familyowns and cultivates a piece ofland, grows vegetables,rears pigs, fowls, ducks, etc. Their income is just

enough to keep the farm going and to feed andclothe the family. There is little money saved. Themother's meals are: 8 a.m., kunji (rice gruel),vegetables; 1 p.m., highly milled rice, vegetables,and fish occasionally; 6 p.m., highly milled rice,vegetables, and meat (very rarely). The motherdiffers from the rest of the family in that she has avery poor appetite, eats little, and sometimes missesmeals altogether. In some cases tapioca and/orsweet potato has to be substituted for highly milledrice. In others, kunji (rice gruel) and salt fish forone month after the birth of the child; after this rice,salted eggs, and pork (a little) comprises the diet.It is obvious that the above diets are deficient invitamin B1 and several other food nutrients. Thecircumstances leading these mothers to take thesediets are either (a) poverty or (b) a belief amongChinese mothers who are breast feeding that if theypartake of foods such as green vegetables, greenpeas, towgay, and fruits, especially during the firstmonth of the lactation period, their infants willsuffer from diarrhoea or may get wind or ' hong.'Out of eighteen mothers examined for symptoms

of beri-beri, eleven were found to be suffering fromsome form or other of the disease, such as palpita-tions, creeping sensations, numbness and tinglingin the lower extremities, weakness of legs, slightoedema of ankles, tenderness of the calves withabsence of knee- and ankle-jerks.

Types of Beri-beriJoee Albert of Manila in 1932 drew attention to

three types of infantile beri-beri: (1) the aphonic;(2) the pseudo-meningeal; and (3) the cardiac. Inmy series of cases the types recognized are: (1) theaphonic; (2) the peripheral neuritic; (3) the cardiac;and (4) the pseudo-meningeal. These four typesmay exist separately, or there may be a combinationof one or more types in an individual case. Thecommonest form was a combination of the cardiac

TABLE 6

C.: ~~C.: P.M: P.M. P.M: P.M. P.M:Types C. P.. C:A. P.N. A. P.N.: P.M. A. A: P.N C.: Total

I LA. P.N. PN

Breast- Cases 31 53 4 5 3 10 5 2 1 1 3 5 123

I)eaths 16 32 1 4 1 7 1 1 - 1 2 4 70

Local Cases 1 9 - 1 2 - 1 - - - - 14

milk Deaths - 5 - - 1 6mom i'lX4k__Deaths 1 - - - - - 6

Key to abbreviations: C.=Card[iac. P.N.==Peripberal Neuritic. A=Aphonic. P.M.-Pseudo-Menmngeal.

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INFANTILE BERI-BERI IN SINGAPOREand peripheral neuritic type, of which 62 casesoccurred in this series (see table 6). Next in orderof firquencY was the pure cardiac type, with 33cases. The pseudo-meningeal type in variouscombinations occurred in 19 cases. The cardiactype and its combinations gave rise to the severestsymptoms and climed the greatest number ofdeaths. The two deaths in the pure aphonic typewere due to enteritis and bronchopneumoniarespectively. In the periphel neuritic type, deathswere due to either enteritis of bronchopneumoma.

Mortality RateOne hundred and thirty-nine cases of infantile beri-

beri, with 77 deaths, gives a percentage mortality of55'41 per cent. This high mortality rate is due tothe fact that, owing to the low stocks of vitamin B1existing, doses extremely inadequate to cope withthe im iate acute fulminating attacks werereleased for use in each case by the Japaneseauthorities in charge. There was also a consider-able time-lag factor between seeing the patient andthe administration of the vitmin as, certain ' redtape' formalities had to be undergone beforesanction to obtain this vitamin was permitted.

The symptoms for which the infants were broughtto hospital were many and varied. They includedvarying degrees of dyspnoea; refusing feeds,vomiting feeds, and diarrhoea; vomiting and cough,vomiting and crying continuously; constipation;no voice, husky or weak voice; inability to passurine; inability to cry; fits; crying excessively;scanty urine; oedema of feet and legs; restlsness;flatulence; drowsiness; and convulsions. It wasonly after obtaining a careful history and examiningthe case systematically that true nature of the con-dition became evident.Fever and cough were indications of the onset of

respiratory-tract infection in the form of acutenasopharyngitis, bronchitis, or bronchopneumoniaThese acted as exciting causes for the more urgentcardiac symptoms of infantile beri-beri. Fever andcough have been recorded for periods varyingfrom thee days up to a month before the onset ofsymptoms of infantile beri-beri. Other associatedrespiratory conditions were pulmonary oedema andcongestion of the lungs.Of the gastrointestinal symptoms, refuisal of feeds,

vomiting, and diarrhoea were the commonest;occasionally there was constipation or abdominaldisension due to acute and ent gaseousdistension of the stomach and intestines. Refusalof feeds indicated anorexia, which, with vomiting,was the earliest symptom to appear. Vomitingvaried from a small amount to the mturn of the

whole feed, and was soimes followed by diar-rhoea. These dyspeptic symptoms might last froma few days to a month before the onset of cardiacsymptoms. It is possible that this dyspepsia was,like malaria in adult cardiac beri-beri, only acommon exciting cause.Aphonia varied from slight hoarseness to com-

plete loss of voice. It was noticed in 20 out of 139cases. Pure aphonia was an indication of a mildattack of beri-beri, and it was found in assocationwith the cardiac, the peripheral neuritic, and thepseudo-meningeal types. It was often Persistent,and continued after all other symptoms had cleared.Direct laryngoscopy performed on a series of caserevealed that there was oedema round about thearytenoids, and it seems possible that the aphoniawas due to this oedema. Wenckebach (1935)ascribes the aphonia to a paralysis of the recurrentlaryngeal nerve, which at first is oedematous butlater becomes permanently degenerated due topressure from below by the dilated right heart as itslips round under the arch of the aorta.The retlssness, freulness, and incessant crying

in some cases may have been due to abdominaldistension or to cough and dyspnoea.The cardiovascular symptoms of infantile beri-

beri are multiple. The first sign of circulatoryinsufficiency was persistently rapid heart rate whichfluctuated with the pulse rate. Early in the diseasethere was slight cyanosis, mostly noticeable aroundthe lips, and the breathing beme somewhatdifficult. Shortly after, dyspnoea was sometimesobserved. The second pulmonic sound wouldbecome markedly accentuated and might be heardover the sternum, denoting dilatation of the rightheart and increased pressure of the pulmonarycirculation. The dilatation might extend consider-ably beyond the right sternal border, and could bedemonstrated by percussion. In grave cases theheart sounds had a galloping rhythm. With furtherchanges in the cardiac muscle the dyspnoea becamemore marked, the accesory muscles of ritioncame into action, the alae nasi worked rapidly, andrespiratory retraction of the thorax was observed.If the child cried during this stage, cyanosis wasmore marked and the child grunted with eachrespiration. During an acute attack there wasextreme pallor and the voice became feeble andwhispering. Frequently the infant contraed hisface and mourned pitifully, as though sufferinggreat pain, became apathetic and very soon coma-tose. The extremtis became cold and the infantwas bathed in pespiration. Sometimes there weretwitchings of the extremities and the head wasretracted; occasionally there might be high fever.The skin becme congested and mottled, and theliver much enlarged. Dyspnoea became more andmore severe, and death ensued.Oedema was generally slight or moderate, and

appeared chiefly on the face and extreities. Itoften occured in association with diminution ofurine.

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ARCHIVES OF DISEASE IN CHILDHOODListlessness and limpness of the limbs were

noticed and the child 'would not play.' Pseudo-meningeal symptoms varying from mild twitchingsof limbs to violent convulsive movements. Some-times there was rigidity of the neck with tensenessof the antenor fontanelle. The infant grew eitherdrowsy or unconscious. Lumbar puncture revealeda cerebrospinal fluid that came out under increasedpressure and was clear, with practically no increasein cells or albumin. Knee-jerks and ankle-jerkswere absent if there was a peripheral neuritis. Inthe present series there were nineteen cases withten deaths, giving a mortality of 52-16 per cent.Urinary symptoms varied from diminution in theamount of urine passed to almost complete sup-pression.

Physil ExaminatioThe patients in this series can be divided into two

groups.The first group of children appeared to be well

nourished but were a little pale and flabby. Therewas sometimes slight duskiness about the lips wichcould be detected only by careful observation. Thechild was usually brought to the out-patient depart-ment because of listlessness, limpness of the limbs,huskines, breathlsness, or because it would notplay. The heart rate was usually rapid, the liverenlarged; and the knee- and ankle-jerks might ormight not be absent. This group of children appar-ently thriving on breast milk, were suffering fromthe effects of vitamin B1 deficiency (see fig. 1, p. 17).The second group of children, in addition to

suffering from the effects of a lack of vitamin B1 inbreast mil, were also not thriving on it. Theyshowed marked pallor and were undernourished.Slight puffiness of the face and slight oedema of thehands and feet were present They were restless,breathed rapidly with little or no sound, the feedswere returned, and there might be severe vomiting.There was sometimes a weak cough with no physicalsigns in the lungs. The heart beat was fast, weak,and regular, usually with no murmurs. The knee-and ankle-jerks were absent.A careful inquiiry into the health of the mother

during pregnancy, and particularly into her dietduring the last month of pregnancy and duringlactation, should be made in every case to deter-mine whether she received an adequate diet. It isnecessary to bear in mind that an infant can havehis knee- and ankle-jerks present and yet sufferfrom beri-beri. This has been proved by post-mortem examinations on cases whose knee- andankle-jerks were present and who died of an acutecardiac attack. The type of case that presentsdifficulty in diagnosis is the case with only onesymptom, like hoarseness of voice. If the knee- and

ankle-erks are present, then the presence oftachycardia, dilated heart, and enlarged liver withevidenc of crulatory failure, coupled with ahistory of breast-feeding on a vitamin B1 deficientdiet, will make the diagnosis easy. If there is nohistory of breast-feeding and the infant is fed onlocally made condensed milk or on a dilution ofcow's milk and is suffering from aphonia, diagnosisis alittle more difficult. It has to be made by aprocess ofexclusion and by a therapeutic test, that is,improvement with parenteral administration ofvitamin B1.

Illustra-ive Case ReportsCAS 1. The youngest case in the series. A

Chinese Teochew male infant, aged seven days, wasbrought to hospital on May 25, 1944. No historywas obtainable as the mother was ill at home. Theinfant #as fed on condensed milk. On admissionthe infant was poorly nourished and dyspnoeic. Hehad a temperature of 99.50 F. and the pulse and heartrates were rapid. The cord had dropped off theumbiLicus and there was no sepsis. The knee-jerkswere absent. Only I mg. of vitamin B1 was avail-able for parenteral administration. The infant diedthe next day. This was a case of infantile beri-beriof the cardiac and peripheral neuritic type.

CAs 2. The oldest case in the series. A ChineseCantonese female child, aged two years, was broughtto hospital on June 19, 1944, with a history ofdiarrhoea, vomiting, fever, and slight cough for fourdays. The child was breast-fed. On examination,the child was febrile, the extremities were cold, andshe was dehydrated and moribund. There wassome cyanosis and congestive mottling of the skin.The heart was rapid and there were few crepitationsin the lungs. The liver was little larger thannormal, and knee- and ankle-jerks were not elicited.A diagnosis of gastro-enteritis and infantile beri-beriof the cardiac and peripheral neuritic types wasestablished. The child died six hours after admis-sion. No vitamin B1 was available for treatment.

The following case report is that of a case notincluded in the series.A Chinese Hokkien female breast-fed infant, aged

five months, was admitted to hospital with a historyof loss of appetite. The mother was suffering fromherpes zoster over the right side of the chest, andshe had ceased breast-feeding four days beforeadmission. The infant was found to be pale, under-nourished, cyanosed, and dyspnoeic, with a feeblecry. There was a rise of temperature, and the heartrate was rapid. The lungs were full ofmoist sounds.The liver was larger than normal. The knee- andankle-jerks were absent A diagnosis of infantileberi-beri of the cardiac, aphonic, and peripheralneuritic types with associated lung infection wasmade. The general condition of the infant at that

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INFANTILE BERI-BERI SINGAPORE

FIG. 2. Temperature chart of a child aged five months, receiving sulphonamide-Pand injections of vitamin B1. X=sulphonamide, 0-25g. O=injections ofvitamin B1, 10 mg. intramuscularly.

time was so grave the vigorous anti-ben-ben treat-ment and treatment to control the lung infection wasinstituted immediately. Altogether, within a periodof six days, 230 mg. of vitamin B1 intramuscularly,and 3 g. of sulphonamide-P by mouth were ad-ministered (see temperature chart, fig 2). At theend of this period, there was no cyanosis and nodyspnoea. The colour of the infant had improved.Its lips and tongue were pink. The heart soundswere not so rapid, and there were only coarse rhonchiin the lungs. The liver had diminished in size. Theknee- and ankle-jerks had retumed. The infantwas quite hungry and finished all its feeds. Thefeeble voice took about six weeks to improve. Fortreatment, the infant had 230 mg. of vitamin B1intramuscularly, two injections of atropine sulphategr. 200 each, sulphonamide 3 g., and belladonnamixture.

Differential DgosisThe following diseases have to be distinguished

from infantile beri-beri: (I) idiopathic cardiachypertrophy; (2) improper feeding and indigestion;(3) congenital heart disease; (4) respiratory diseases;(5) infantile muscular atrophy of spinal origin;(6) diffuse poliomyelitis; (7) diphtheritic paralysis;(8) nephritis; (9) meningitis; (10) laryngeal diph-theria; (1 1) laryngitis of measles.

1. A patient suffering form idiopathic cardiachypertrophy, has to be distinguished from an infantwith the cardiac condition in beri-beri. There is astriking clinical similarity in the two conditions, buta history of vitamin B1 deficiency in the beri-beriinfant's mother's diet will help to differentiate theseconditions. On post-mortem examination the rightventricle of the heart is most seriously involved inberi-beri, while in idiopathic hypertrophy both sidesof the heart are attacked, the hypertrophy anddilatation of left ventricle predominating. If thereis no history of breast-feeding, then the possibility of

a clinical syndrome fitting in with the description ofinfantile beri-beri in a locally-made condensed-milk-fed baby should be considered. A therapeutic testshould be applied to settle the diagnosis. A case ofinfantile beri-beri will improve with vitamin B1injections.

2. Failure of the infant to gain weight on thebreast, with some colic, restlessness, and constantcrying, may occur in an underfed infant; and thegrosser symptoms of indigestion, such as vomiting,colic, and diarrhoea may be due to overfeeding orto infection in a breast-fed infant and yet the infantmay not be suffering from infantile beri-beri.These symptoms may exist in association withinfantile beri-beri or act as a common exciting causeof the syndrome.

3. The diagnosis of cyanosis and dyspnoea ofcongenital heart disease will be confirmed by (a) thepresence of a murmur and its location (b) thepresence of clubbing of the fingers and toes in somecases (c) a history of cyanosis from birth. A dilata-tion of the right side of the heart and an enlargedliver are present in congenital heart disease and ininfantile beri-beri. In the latter condition a historyof breast-feeding on a vitamin B1 deficient diet willbe obtained.

4. In cyanosis and dyspnoea of respiratory originwhich may be due to laryngeal, tracheal, or bronchialobstruction, bronchitis, bronchopneumonia, oratelectasis, the history and the presence of physicalsigns in the chest will make the diagnosis clear.Differentiation may be difficult in a case wherebronchopneumonia occurs as a terminal event inberi-beri. Here again the history will be helpful insuspecting the condition.

5. Infantile muscular atrophy of spinal originwhich occurs in an infant in the first weeks ormonths of life and where the infant develops a flaccidparalysis of all the extremities will not presentmuch difficulty in diagnosis.

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ARCHIVES OF DISEASE IN CHILDHOOD6 and 7. Diffuse poliomyeitis and diphtheritic

parlysis have to be difriated from infanntlebei-ben with neuitic symptoms In diffuse poio-myelitis, the paralysis and atrophy of muscles israrely symmetrical and groups of muscles tend tobe affected. In a case of diphtheritic paralysis, inaddition to the incomplete paralysis of the limbs,the eyes and palatal and laryneal muscles areaffected and the diaphragm is weak. In infantileberi-beri, as opposed to these two conditions, thereis no definite paralysis and the neuritis of the lowerlimbs is symmetrical.

8. A case of oedema from nephritis can be dis-tingished from infantile beri-beri with oedema byte presence ofalbumin in the urine.

9. Children admitted into hospital for convul-sions due to beri-ben may have to be distinguishedfrom those with convulsions due to meningitis by theabsence of other symptoms of meingtis, such asbulging and tenseness of the anterior fontanelle,arching of the back and neck, iqtemal squint, andexaggerated reflexes. In meningtis, lumbar puncuwill reveal an abnormal cerebrospinal fluid. Theconvulsions in ben-ben have improved after treat-ment with vitamin B1 and have not been known torecur.

10 and 11. The aphonic type will have to bedifferentiated from laryngeal diphtheria and laryng-itis occurring at the onset of an attack of measles.In laryngeal diphtheria, careful examinaton of thethroat will reveal a patch ofmembrane in an exposdsituation, and from the throat swab the diphtheriabacillus will be cultured. The laryngitis occurringat the onset of an attack of measles may give rise todoubt as to diagnosis. But the presence of pyrexiaand the discovery of Koplik's spots on the buccal

mucosa will solve the problem.The importance of giving an injection of 10 mg.

of vitamin B1 when in doubt about the diagnosismust be emphasized. An improvement in thesymptoms will be noticed if it is a case of infantileberi-beri.

Post-mortem, FmdgThe following is a verbatim description given by

Tull, quoted by Wenckebach (1935): 'The interiorof the thorax was a really wonderful sight, the rightheart extending greatly to the right, the surfaceshining, the vessels under the pericardium much

engorged and the right ventricle dilated to almostbreaking point. The pulmonary artery was thesame size as the aorta. The heart was as large asthat of a normal child ten years old.' In the samecase the liver was much enlarged and the wall ofthe gall-bladder typically oedematous; there wascomplete absence of oedema of lungs.' In ihepresent seies of cases there were a number withoedema of the lungs, some with congestion of thelungs and bronchopneumonia- In the nervous

system there was marked engorgement of the cere-bral blood vessels. There was a small amount ofeffusion in the pericardial sac and in the abdominalcavity.

ProgopsiIn the aphonic type it takes about six weeks for

the voice to recover.In the pseudo-meningeal type, without complica-

tions, the prognosis is good provided adequate dosesof vitamin B1 are administered parenteraly. Ifthere is a rise of temperature, malarial infectionmust be excluded by an examination of the blood-film. During an attack of convulsions, the throatmust be clared to prevent death from suffocation.

In the cardiac type, cold, clammy hands and feetare signs of grave circulatory failure. Therefore, insuch cases, treatment for restoration of cirulationshould be energetic because it is absolutely essential

to keep the heart going until such time as vitaminB1 injections take effect. Very often cases arebrought into hospital where the circulatory failureis so severe that the infant dies before anything canbe done for its restoration.The old idea that a beri-beri heart is permanently

damaged does not hold good, provided adequatedoses of vitamin B1 are administered during theacute stage. A follow-up of cases of acute beri-benthat have recovered shows that, given the samechances as a normal infant in regard to diet and care,the former invariably grow up to be healthy andstrong.

In certain cases, an acute cardiac attack super-venes upon a subacute cardiac condition which hadbeen undiagnosed for a long period. In such casesthere is considerable oedema of the heart muscles,and thus they fail to recover even after an injectionof60 to 80 mg. of vitamin B1.

Expiratory grunt is an unmistakable sign of anacute cardiac attack. This sign can be recognizdfrom a great distance. Anxious parents often ask,' When will the infant be out of danger? ' It ispossible to say that the vitamin B1 injection will takeat least one and a half to two hours to have effect,and that, if the infant's hea2rt will respond to the drug,it should recover. It takes about one and a half toone and three-quarter hours for the grunt to cease infavourable cases. In cases that are going to endunfavourably, the grunt ceases rather early, that is,within a period of about three-quarters to one hourafter the vitamin B1 administration. The infant'srespiratory system often gets choked with secretion,the heart sounds become feeble, and it dies.Numerous fine crepitations at both bases, and

bronchial breath sounds are associated with graveprognosis. Some cases which get cured rapidly in

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INFANTILE BERI-BERI IN SINGAPOREtwenty-four hours, and are sent home, are broughtback at the end of the seoond day with signs of acutebronchitis developing rapidly into acute broncho-

pneumonia. The cause of this is probably either(a)a d avitaminosis A and D predisposing torespiratory tact infection, or (b) inhalation ofinfected mucus during the acute stage. In suchcases it is advisable to administer sulphonamide-P asa measure of prophylaxis if the temperature riseson the second day.

TreatentThe tatment of infantile ben-ben can be divided

into: (1) treatment of the mother; (2) treatment ofthe infant.Treatment of the mother consists in attention to

her health and diet during pregnancy and during thelactation period. As parboiled or undermilled ricewas not obtainable, overnilled rice and/or tapiocaor sweet potato had to be taken. Tapioca, sweetpotato, and overmilled rice contain small amounts ofvitamin Bl. In the process of milling the rice, thevitamin B, ~vhich is found in the husk and outerlayers of the grain is removed. The very valuablemineral salts are also removed with the husk. As,through ignorance, the public do not supplment thediet with vitamin B1, hypovitaminosis B1 results.The consumption of an exclusive diet of overmilWrice is harmful, because the high carbohydrate dietwill require a correspondingly high ingestion ofvitamin-B,-containing foods. Good sources ofvitamin B1 are soya bean, green dhall, peanut, ncepolishings, husked rice, hen egg, duck egg, and saltedduck egg.The data in table 7 have been obtained from

Leong (1940), who did a fairly complete assay

of the B1 content of foods obltinable in Malaya.of the pecuiar beief that green dhall,

gren vegetable, and bean sprouts will give rise towind or ' hong ' in the mother and green diarrhoeain the infant, it is difficlt to make the mothers taethese foods. Ibe mothers w waned of thedangrs of abstention from these valuable foods.If the mothe refused to take them in spite ofadvice,weekly or fortnightly intamusular injections ofvitamin B1 or tablets of this vitamin were given.The mother should be examined for signs andsymptoms of vitamin B1 deficiency, such as creepingsensations, numbness and tingling in the lowerextremities, weakness of legs and slight oedema ofthe ankles, tenderness of calves with absence ofknee- and ankle-jerks.The most dangerous feature of infantle beri-beri

is that the mother does not realize the gravity of thediseae in her infant until alarming symptomsdevelop. We always advocate that all infantsfrom poor families should be brought to the out-patient department for attention and advice. Themedical officer could detect the symptoms of beri-ber in its early stages and give suitable advice andtreatment.Before the introduction of vitamin B1 for paren-

teral administration, treament of the baby conistedof (1) weaning the infant from the breast andadministering condensed milk feeds; (2) givingbrewer's yeast powder or Marmite; (3) aministe-

ing cardiac stimulants in cardiac failure, and oxygenfor the cyanosis. This line of treatment provedunsatisfactory. Since the introduction of potentitamin B1 preparations, we have been able to intro-duce systematic treatment. If the case belongs tothe group which has been described previously as

TABLE 7VITAMIN B1 CONTENT OF FOODS

English name | Scentific name Local name Units pei 100go

Soya bean Glycine hispida Kachang Soya 240Soya bean curd 9.. Tauhu 11Soya bean curd (hardened) ,, ,, Towkua 43Soya bean milk .... ,, _- 8Green dhall Phaseolus radiatus Kachang hijau 270Peanut Arachis hypogea Kachang goreng 235 (baked)Rice polisbings - Dedak 600-0Husked nrce Oryza sativa Bras ayam 140Bean sprouts Phaseolus radiatus Taugeh 13 (fried)Sweet potato .. .. Ipomoea batatas Keledek 28 (boied)Tapioca .. .. .. Manihotulissima Ubi kayu 19 (boiled)Milk, fresh cow's.. - Susu lembu 3Hen egg, yolk .. .. Telor ayam 110-270 (boied)Duck egg, yolk .. .. Telor itek 2)0-375 (boiled)Salted duck egg, yolk .. Telok as 210-40 (boied)

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ARCHIVES OF DISEASE IN CHILDHOODthriving on breast milk but which is only manifest-ing symptoms of vitamin B1 deficiency, the tret-ment is as follows: (1) breast-feeding is continued;(2) the mother is put on an anti-bei-ben diet con-sisting of husked rice or 'bras ayam' four ounces,soya bean curd or 'tauhu' four ounces; greenvegetables four ounces; bean sprouts or ' taugeh 'four ounces; green dhall two ounces; (3) she isgiven 10 mg. vitamin B1 daily for six days, and thistreatment is discontinued when once the symptomsin the child have improved; (4) the infant is givenintramuscular or intravenous injections of vitaminB1, the amount depending upon the severity of thecase; (5) after discharge, the mother is instructed tofollow a dietetic regimen similar to the one she hadbeen taking in the ward, and to attend the out-patient department weekly.Vitamin B1 preparations have been put out for use

in two forms, tablets for oral administration andsolutions for parenteral administration, expressedin igrammes (1 mg.=333 international units).For rapid effect, vitamin B1 should be administeredin large doses either intravenously or intracardiac-ally. It is excreted rapidly, and no toxic effects hadbeen noted in my series of cases.For intravenous administration, the supenor

longitudinal sinus through the anterior fontanelle ischosen. About 7 c.cm. of blood is withdrawn as ameasure of venesection, and through the sameneedle 10 mg. of vitamin B1 is injected. If there isno improvement within an hour, the injection isrepeated. In addition, intramuscular injections ofvtamin B1 should be administered in 10 mg. doses.It is never safe to give ess than 10 mg. as an initialdose. If, as occasionally happens, intravenousadministration is unsuccessful, intracardiac injec-tions must be given as a final resort. The dis-advantage of this method is that the needle may notreach the heat, and if it does reach the heart thereis considerable bruising of the myocardium, as hasbeen demonstrated at autopsy on a few cases thathave died.The total dosage depends upon the severity of the

case. In the milder cases about 20 to 25 mg., and inthe more severe cases 60 to 70 mg. may be necessarybefore improvement in the condition is noted. Theresults of vitamin B1 injection in cases that are im-proving are: (1) cyanosis kssens and disappearseventually; (2) dyspnoea improves; (3) the infant'scolour improves; from the dusky colour of cyanosis,he becomes pink; (4) if he has been restls before,henowliesquietlyinbed; (5) therateoftheheartslowsdown; (6) vomiting disappears; (7) the knee- andankle-jerks return in some cases where they havebeen absent before.Symptomatic treatment consists of: (1) for per-

sistent abdominal distnsion, flatus tube, rectalwash-out, and pituitrin i c.cm.; (2) injection ofatropine sulphate, gr. h, for moist sounds in thelungs; (3) bromide and chloral for convulsions;

(4) 02 for the cyanosis; (5) treatment for rapidrestoration of ciulation as follows: (a) brandy tobe rubbed on the lips; (b) brandyUvin atspoon-ful of water to be given by mouth four-hourly;(c) one tablet of vitamin B1 (1-2 mg.) with onedrachm of carminative mixture for infants to begiven half-hourly til improvement is notied;(6) hot water bottles to be applied to limbs and sidesof trunk; (7) do not push fluids too rapidly becausethe stomach will become distended and the infantwill vomit with regurgitation offluid into the lungs.

In dealing with the type that is not thriving onbreast milk or where the mother is suffering fromberi-beri, the infant is weaned and is given a suitablesubstitute feed to make good the vitamin deficiencies.The rest of the treatment is the same as that outlinedfor the type that is apparently thriving on breastmilk.

If a breast-fed infant is brought to hospital fortreatment of a complaint other then beri-beri, it isalways advisable to administer a prophylatic dose ofvitamin B, intramuscularly, say 5 mg., because anumber of such children have collapsed suddenlyand have died. Autopsy revealed the cause of deathto be infantile beri-beri.

Smy1. Infantile beri-beri is B1 avitaminosis.2. In Singapore during the latter part of the Jap-

anese occupation it occurred in breast-fed, locallymade condensed-nilk-fed and very-occasionally incow's-milk-fed infants.

3. It occurred in four forms: (a) aphonic;(b) peripheral neuritic; (c) acute cardiac; (d) pseudo-meningeal.

4. The clinical signs indicating a cardiac attackare dyspnoea, cyanosis, tachycardia, dilatation ofthe right side of the heart, accentuation of the pul-monary second sound, and enlarged liver, and inextreme cases Ercongestive mottling of the skin.

5. It is not common in infants who are breast-fedby mothers who are poor and who eat unmilled rice.

6. It is common in the poor who eat highlymiLled rice.

7. An absence of knee- and ankle-jerks is notessential for the diagnosis. It may be purely acardiac affection.

8. Vitamin B1 solutions administered parenter-ally have proved satisfactory in the treatment of thiscondition.

9. It is never safe to give less than 10 mg. as aninitial dose.

10. The diet of the nursing mother determines thecondition of her milk.

11. The symptoms of vitamin B1 deficiency in themother are palpitations, creeping sensations, numb-ness and tingling in the lower extremities, weakness

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INFANTILE BERI-BERI IN SINGAPORE 33of legs, slight oedema of ankles, and tenderness ofcalves with absence of knee- and ankle-jerks.

Summary of Difficulties and New Features seen inInfantile Beribei duing the Japanese OccupationPeriod.

1. Difficulty in getting vitamin B1 in adequateamounts to save a case.

2. The prohibitive price, 10 mg. of locally pre-pared vitamin B1 costing $250.00 Japanese currency,and 10 mg. of foreign-prepared vitamin B1 costingbetween $600.00 to $700.00 Japanese currency.

3. Secondary infections: frequency of lung com-plications, especially bronchopneumonia, afterapparently efficient treatment. This was not seenin pre-war days.

4. Associated avitaminosis A, B, and D: morecommon in locally made condensed-milk-fed babiesand probably also accounting for the secondaryinfection. Such children are pale and thin with sub-rickety manifestations.

5. Cardiac collapse is more severe.

I have to thank Colonel W. J. Wickers, DeputyDirector of Civil Affairs (Medical), British MilitaryAdministration, Singapore, for permission to

publish this paper, and Dr. C. J. Oliveiro, biocbemistduring the Japanese occupation period, for manyuseful suggestions in its compilation.

REFERENSAbt, Isaac A. (1935). Amer. J. Dis. Child., 50, 456.Albert, J. (1932). Mschr. Kinderheilk., 54, 80.Braddon, W. L. (1901). Fed. Malay St. Mfed. Arch.

(1907). The Cause and Prevention of Beri-beri,London.

Eijkman, C. (1897). Virchows. Arch., 148,523; 149, 187.Fletcher, W. (1907). Lancet, 1, 1,776.Fraser, H. and Stanton, A. T. (1909). Lancet, 1, 451.

(1909-1911). Studies from Inst. for Med.Res. Fed. Malay Str., Nos. 11 and 12,Singapore.

- , (1910). Lancet, 2,1,755.Grijns, G. (1901). Geneesk. Tijdschr. Ned.-Ind., 41, 3.Haridas, G. (1937). J. Malaya Branch Brit. med. Ass.,

1, 26.Inaba, I. (1917). Zika-Zasshi, No. 210.Ito, S. (1911). Ibid., No. 137.Leong, P. C. (1940). J. MalaYa Branch Brit. med. Ass.,

4, 66.Segawa, M. (1916). Zika-Zasshi, No. 189.Toyoda, T. (1922). Zikken-lho, 8, 88.Wenckebach, K. F. (1935). The Beri-beri Heart (a

summary in English by Tull, J. C.) Govt.Printing Office, Singapore.

Williams, C. D. (1938). J. Malaya Branch Brit. med.Ass., 2, 113.

(For Photographic illustration of this Article see page 17)

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