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The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

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Page 1: The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

Special Article

THE DYSPEPSIAS OF SOUTHERN INDIA*

By IAN M. ORR, m.d? f.r.c.s. (Edin.) v

London Mission Hospital, Neyyoor, Travancore 1

us ?

m

* ^ ^le conditions which we a

n are called on to deal with, nothing is more

for*1111011-!? an ^ysPePsia in one of its manifold ?s- ^ew diseases are so resistant to treat-

n , so persistent in their symptoms, and

use so much chronic invalidism as do the

ZS?TlaS- dyspeptics come to our

wo su, & rooms and outpatient departments

i f

^or sif?ns of duodenal ulcer

, failing to find definite evidence of that, we

escribe an alkaline mixture, which nearly

^ ways gives some measure of temporary

com-

iinl a j sufferer, but leaves the disease

oca ted, undiagnosed, and untreated. do not wish to dwell at length on the

< imhar subject of duodenal and gastric ulcer,

:

* Ce^ , ,ln, so. ^ar as the pathology is peculiar

south India. Nor do I wish to deal with the

ause of acute abdominal pain, but rather I

ould call your attention to the interesting and

aried list of conditions that give rise to symp- oms somewhat similar, characterized mainly by

pain, indigestion and flatulence, and whose

Pathology nevertheless is so varied.

Stomach

1 *S n?^ gutters

' and all who

lave hunger pain, vomiting, and epigastric enaerness, are not necessarily suffering from

gastric or duodenal ulcer. Chronic gastritis.?This is the first and

most

common condition to which I would draw your

attention.

Pathology.?The lining of the stomach

ecomes coated with mucus which blocks the

mouth of the secreting glands. The deeper

ayer becomes infiltrated with round cells and in

an extreme degree the cells of the glands undergo

cloudy swelling and may atrophy. The ruga3 of the stomach become larger,

firmer and more tortuous; this may be demon-

strated by aj-ray, by giving a small meal of

barium and water only, and pressing the walls

?t the stomach together, so that the barium just

fills the pockets between the rugae. The body of the stomach as a whole may be affected and thus the acid-secreting glands which are-situated mainly in the body are seriously interfered with with a resulting fall in free hydrochloric acid,' or only the pyloric portion of the stomach may be affected and the hydrochloric acid in the stomach remain normal or high, i.e., we have a hypoacid gastritis and an acid gastritis. /Etiology.?This will be discussed more fully

below, but it may be said here that the taking of over-spiced and indigestible food, and irreg- ular habits about meals all tend to exaggerate it. Oral sepsis no doubt plays a part. The exhibition of certain drugs for long periods also predisposes towards it; e.g., sodium salicylate, quinine, arsenic, silver, mercury and copaiba. An atrophic form may be found in association with malignant disease; in fact it may be said that malignant disease of the stomach is always associated with atrophic gastritis and malignant disease of other organs, such as the colon breast, etc., and they usually give rise to it by the absorption of toxins from the disintegrating tumour.

Symptoms.?Discomfort and sensation of fullness which may amount to pain about one hour after food. Appetite is diminished, and there is nausea, a bad taste in the mouth, dizz- iness, regurgitation and flatulence. This is due to the lack of acid allowing decomposition and carbon dioxide formation. Hydrochloric acid is diminished and mucus is found in excess in the fasting juice. If the pyloric portion of the stomach is alone affected the hydrochloric acid may be high. Treatment.?Remove all bad teeth, septic

tonsils, and deal with sinus infection if any. Lavage with hydrogen peroxide, an ounce to the pint of water, serves to remove the mucus and allows the gastric juice to be secreted freely. This may be repeated daily for a week or until the mucus disappears. If there is hypoacidity, give hydrochloric acid in water with meals. A general tonic containing iron, arsenic and strych- nine may be given, but if not well tolerated by the stomach it may be injected in ampoule form.

Diet.?Avoid hot curries, spices, raw fruit, shell fish. Take milk, barley water, congee water, wheat, junket, chicken soup, Horlick's * Paper read to the Travancore and Tinnevelly

Medical Association on 10th March, 1935.

Page 2: The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

572 THE INDIAN MEDICAL GAZETTE [Oct., 1935

milk; later, go on to toasted bread and butter, boiled eggs, white fish, rice. Mention may be made of atrophic gastritis in

contradistinction to the above hypertrophic type. This is chiefly associated with the more severe anaemias and chronic venous congestion. In certain inborn errors also, hydrochloric acid may be absent. The most useful method of deter-

mining whether or not an absence of free

hydrochloric acid is merely due to mucus block- ing the ducts or to an inborn error is to inject 0.5 c.cm. of histamine*, and immediately hydro- chloric acid will be poured out in simple gas- tritis. Nervous disorders of the stomach.?The ner-

vous system and, particularly, the mental states of fear, worry, excitement, nervous exhaustion, etc., have a marked influence over the stomach. We have all experienced the pre-examination feeling of not wanting a big meal, because of a complete failure of our stomach to secrete its

daily quota of free hydrochloric acid. Or the

feeling of heaviness in the pit of our stomach when we are disappointed, ill at ease, or dis- tressed. Now let us examine these nervous

upsets of the stomach. (a) Hyperchlorhydria.?A point in physiology

is important to understand. Stimulation of the

vagus causes constriction of the sphincters and outflow of gastric juice. This stimulation of the vagus may be reflexed from gall stones or

appendix. There is a lymphatic path from the appendix to the duodenum and it has been demonstrated that chronic inflammation of the

appendix causes a spasm of the pylorus, and an increase in free hydrochloric acid, a condition favourable to the formation of gastric ulcer. A state of chronic nerve strain, such as is

common to men dealing in big business, is associated with hyperchlorhydria. Excessive in-

dulgence in pickles, spices and smoking have a

similar effect. My experience is that the normal acidity curve for the people of south India is

higher than for Europeans because of the exces- sive stimulation of the mucosa by hot curry stuffs.

Symptoms.?These are sensation of fullness and discomfort in the epigastrium and belching. There may be epigastric tenderness. The test meal reveals high acidity and yet the axray shows no positive evidence of ulcer.

Treatment consists in avoiding the anxiety state if possible. Avoid carbohydrates, espe-

cially rice, and take boiled meat, milk, albumin water, fish and green vegetables. Oily sub- stances have the effect of reducing the outflow of gastric juice and relaxing the sphincter. Hence olive oil, butter and cream should be taken.

A mixture containing magnesium and bismuth to neutralize the acidity and belladonna to

inhibit secretion and relax the sphincter is indi- cated. Sodium bicarbonate is not deserving of the popularity it enjoys, for, though it does neutralize the acid at first, it then irritates the

gastric mucous membrane, causing more acid, and the formation of carbon dioxide and belch-

ing. (b) Gastro-succorrhoea {i.e., excessive secre-

tion but not a hyperacid one). It is common in students at examination

times, in girls at puberty, etc. It is charac- terized by nausea, belching and vomiting of

large quantities, for no particular reason. In bad cases the patient may be cold with a slow pulse and sometimes headache due to stimula- tion of the vagus.

This condition has to be diffentiated from:?

acute gastritis?vomited material alkaline; migraine?headache worse and vomitus

bilious; alcoholic gastritis?occurs in early morning

after drinking bout and vomitus is mainly mucus.

Treatment.?Gastric lavage 1-2,000 silver nitrate to promote mucus formation. Bella- donna should be given internally.

(c) Hypochlorhydria.?This is found in

people suffering from nervous breakdown or

extreme nervous exhaustion; also in states of fear. It may be an inborn error, or it may be associated with one of the severe anaemias.

Symptoms.?Loss of appetite, sense of full-

ness, distaste for meat and there may be diar-

rhoea, the desire to go to stool occurring imme- diately after taking food; this is a reflex action and is a common cause of chronic diarrhoea. Treatment.?Give a diet rich in carbohydrate

and condiments, and poor in protein, the reverse of the hyperchlorhydria diet. Give an acid mixture with nux vomica and pepsin.

id) Gastric hypercesthesia.?This is found in

neurotic people who complain of unusual sensa- tions in the region of the epigastrium and belch- ing, and describe their symptoms with a wealth of detail which is apt to weary the physician. There is usually a completely normal test meal and ?-ray, but still the patient complains of

pain and tenderness and many other things, and may vomit without relief. This is a pure neurosis and must be treated by removing the patient from the environment of sympathetic friends. Sea bathing, interesting occupation, toning the body by open-air exercise, massage of the abdomen, and rubbing with spirit or

camphor. Such a patient will not be satisfied without medicine, and a general tonic containing dilute phosphoric acid, tincture of nux vomica and peppermint water will convince him that

he is being treated. One might mention here that belching which is a

symptom common to almost all gastric disorders is in most cases due to simple air swallowing and not to

* The usual dos? of histamine is 0.0005 gramme, so that the author is presumably referring to a solution containing 1 mgm. to the cubic centimetre.?Editor, I. M. G.

Page 3: The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

Oct., 1935] THE DYSPEPSIAS OF SOUTHERN INDIA : ORR 573

iinawam gas 1U ^le stomach. The patient is

Settino- k- + swallows air, and a useful method of

act ofe\v*nn- 4

re .lze the fact and to repress it by an ^hyroirf

1 4-Si ^le a string round his neck above the

n?tico ifCa !i u ain<^. eac^ time he swallows he will

there ;? f3 c!lec. In simple stenosis, however, r'se tn e!men??.n by j'east in acid medium giving also tho ar on dioxide. In chronic venous congestion which o

^esse s ? the stomach wall fail to absorb gas ccumulates and is eventually eructated.

Muscular disorders

(1 W^n'C aiony and dilatation.?/Etiology.?

surroundin^ muscu*ar weakness and enervating living f0verloading ,?f the stomach, either by by ?.we^' or> *n the case of the very poor,

- ^ar?e quantities of food of poor

ttient ^ m 0rder *? ?btain sufficient nourish-

es) Sedentary habits. ) Auto-intoxication from chronic sepsis. hvnf^TS-These resemble gastritis and

With ? 1Jorhydria and indeed may be associated

dis? ?? Pr ?f these conditions. There is

avnJr* ?' deling of fullness, flatulence, the

0/n e w 9??d but quickly satisfied. Later

Puis ^ ,gue becomes broad and flabby, the arif) ?-S V> bands clammy, and there is headache niiiol 1?somn^a- Hydrochloric acid persists for

form* , ^er than normal, and organic acids are stnm i

ln exc.ess- ^-ray reveals a large can % ' no Peristalsis, and, while the duodenal into ??6u n?^ ^ ?*" itself, food can be squeezed sop

?

ii ^ Pa'Pation. There is no tenderness

defn T related to the duodenum, and no

uj r^nity of the duodenal cap, hence duodenal

tal?/ CaDi excluded. Also the lack of peris- te<?/S nia es. an organic stenosis unlikely. The

' meal will exclude gastric succorrhcea.

del reaimeni~Give dry diet; avoid fat, as it

ao./s emptying and decomposes into fatty inn

avoid bulky diet, like rice, which will

n rease the condition. Where the patient's

toiafSj P?rm^t> give white fish, chicken, cereals, to h? oread with jam or honey. Stimulants

Qui ? gastr^c .muscle, such as nux vomica, ^

nine and eserine salicylate, are indicated and

Kv8e?e.ra^ .tonic of iron, arsenic and strychnine q- injection if not tolerated by the mouth.

stric lavage 3 hours after meals, to prevent Vol

r?tention of decomposing foodstuff, is uable and, unless there is gastritis, magne- nn carbonate is as good a substance as any. Gastric and duodenal ulcer.?This is one of

anri fommonest diseases of this part of India

tyk- because of its frequency and the ease with

ri+l ^ resP?nds to surgical treatment we are

dv apt to treat it lightly and pass all our yspepsias over to the surgeon. It is not a

r^rnon condition, however, in other parts of

1 '? McCarrison reports that in south India

f' in every thousand of the population suffer t J duodenal or gastric ulceration, while in

0 ?ore' wb^?b is typical of north India, only <>0 per thousand are found to suffer in this

way. That is, in south India it is nearly 60 times more frequent. If the figures of central and north Travancore were examined, they would be twice or thrice that of south India in general. What is the cause of this remarkable variation ? The most suggestive possibility is the diet. A diet typical of north India contains large amounts of wheat, milk, mutton, root

vegetables, cabbage, dal and fruit. The balance

of protein, carbohydrate and fat is correct and

the vitamin elements are well represented in the

milk, wheat and vegetables. Compare that

with the diet of the poorer class Travancorean

where the staple article is tapioca and rice, both almost entirely carbohydrate and almost totally devoid of vitamin substances. The very small

amount of mutton, fish and eggs that they are able to get in no way make up the protein deficiency, and the vegetables readily available such as brinjal, ladies' finger, cucumber, etc.' are very deficient in vegetable protein and lack vitamin A. Coconut is rather better and con-

tains a fair amount of fat, but only a small

amount of vitamin A. Thus we are dealing with a population living on a high carbohydrate diet devoid of an adequate amount of vitamin

elements, vitamins A and D being particularly short (Orr, 1933).

In the nutritional research laboratories at Coonoor

an interesting experiment was carried out. Seventeen

rats were fed on a typical Travancore diet and 17 were

fed on a typical Madrasee diet which contains more

rice and no tapioca. There was a control group fed on

a well-balanced diet typical of the people of north

India. The control rats remained healthy, the tapioca- fed rats had a 94 per cent mortality and the rice-fed rats an 82 per cent mortality. Forty-seven per cent of the tapioca-fed, and thirty-five per cent of the rice-fed rats were found to have lesions of the stomach. Those

fed on tapioca diet were subject to congestion of the

stomach and gastritis and both to epithelial overgrowths and ulceration. Those of the rice diet showed a lesion

in the body of the stomach and those on the

Travancore diet on the pyloric or mucous portion (McCarrison, 1931 and 1931a). Monkeys were fed on a vitamin-deficient high carbohydrate diet and post mortems were found to show congestion and inflam-

matory changes in the mucous and submucous coats of the stomach, duodenum and lower ileum and colon

degenerative changes in the glands, loss of lymphoid elements, and invasion of the bowel wall by bacterial

organisms. In three out of ten ' monkeys thus fed,

gastric ulcer developed.

There appears to be little doubt then that

a high-carbohydrate low-vitamin diet produces a gastritis or duodenitis and renders the mucosa liable to ulcer formation. As to the cause of

the ulcer, authorities differ but the consensus of

opinion seems to be in favour of the view held

by Wilkie (1911) of Edinburgh, who has demon- strated that the first part of the duodenum is

supplied by a small branch of the pyloric artery, the supra-duodenal artery. This is an end' artery and any thrombus forming in its lumen

(which might well result from the duodenitis) would produce a loss of vascularity of that part of the gut with necrosis and ulcer formation.

Once the ulcer is formed, the gastric juice, which

Page 4: The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

574 THE INDIAN MEDICAL GAZETTE [Oct., 1935

is made more highly acid than normal by reason of the carbohydrate and the irritation of the

condiments, will prevent it healing and lead to chronic duodenal ulcer. The symptoms and treatment of duodenal

ulcer are so familiar that I need not dwell upon them here except to point out one or two im- portant facts.

(1) We have seen already that many things such as gastritis and hyperchlorhydria may cause pain, vomiting and epigastric tenderness.

(2) Hunger pain which is typical of duodenal ulcer may occur occasionally in cases of gall stones, appendicitis, dyspepsia, and excessive

smoking. (3) A feature of peptic ulcer which is not

produced by other conditions is the marked

periodicity. That is, in the early stages the

pain is only present for a few days and then completely disappears for a long period only to return again. These periods of remission become shorter and shorter, and in the late

stages when there is much associated gastritis the patient may say that he has no remission of symptoms. This periodicity corresponds to

the healing and breaking down of duodenal ulcers.

(4) The vomiting typical of a peptic ulcer occurs at the height of the pain, it relieves the

pain, and is highly acid in its reaction.

(5) The test meal and the a>ray are the final criteria by which we judge whether there is, or is not, a peptic ulcer and I would lay stress

upon the use of the fluorescent screen and pal- pation in the diagnosis. To see the stomach on the screen and mark the point of tenderness, to witness the movements of the stomach and the

way in which the duodenal cap fills is of the

greatest importance. Malignant disease of the stomach.?Here

again a few words will suffice to call your atten- tion to some important points. Moynihan (1909) propounded the view that 70 per cent of gastric ulcers became malignant and he conse- quently treated all gastric ulcers as potential cancer. Also he looked for previous ulcer

symptom in the diagnosis of cancer. Modern

surgical pathologists incline to the view that

only 5 per cent of gastric ulcers become malig- nant and that much of the material Moynihan based his statistics upon were not cancerous

ulcers at all, but merely advanced stages of

simple ulcers. The point we must note however is that the majority of cancers of the stomach we see will have a short history. Any com-

plaint of dyspepsia with loss of weight and

appetite occurring in a man over forty who has never had anything wrong with his stomach before is very suspicious of malignant disease. Cancer of the stomach will show the follow-

ing :? (1) low or absence of free hydrochloric acid; (2) a trace of blood in every specimen of

the test meal;

(3) distaste for meat; and (4) a deformity of the antrum of the stomach

in the rr-ray. Never wait to palpate a tumour before diag-

nosing cancer of the stomach. The signs and symptoms apart from the above are often indefinite and confusing, but it is far better to

operate and find no cancer than to wait until secondaries have spread to the glands and liver.

There are certain other conditions that we must consider to make our review complete.

Gall stones and cholecystitis.?'The special interest of this condition lies in the fact that it is so very uncommon in this part of the world. In Neyyoor we always examine the

gallbladder in our abdominal operations, so

that few if any gross pathological changes in this organ have not been seen and dealt with; yet in a series of 2,300 upper abdominal opera- tions, only in 38 has gallbladder pathology been noted, a ratio much smaller than that found in western countries or even in central India. It is well recognized that the formation of gall stones depends on three factors:?-

(1) increased cholesterin in blood, (2) some

impediment to the flow of bile, and (3) some

chronic inflammation in the wall of the gall- bladder.

Increase in cholesterin is found mainly in

pregnancy, hence gallbladder disease is more

common in women. It is said to be increased in typhoid fever. It is definitely increased in certain diets and may be reduced by a choles- terin-free diet.

Biliary stasis is probably more associated with people living sedentary lives, and, as the

average Indian woman is more a domestic

drudge than her European sister and wears

clothes which are freer and do not compress the lower thorax, she probably suffers less from

biliary stasis.

Infection of the gallbladder is said to occur in typhoid fever. Cushing (1898) found 30 per cent of these gallbladder cases had suffered from typhoid. Another observer, Chiari, found Bact,. typhosus in the gallbladder of 19 out of 22 persons who had suffered from typhoid. Now surely in a land like this, where typhoid is extremely common, we would expect to find a

higher ratio of gallbladder disease. I have no experimental evidence to give you and can

only throw out a suggestion which perhaps someone may be able to substantiate or refute.

Though the gallbladder mucosa is frequently infected by typhoid, the other two factors

necessary for stone formation are absent, namely, (a) increased cholesterin, as the poorer people at any rate live on a cholesterin-free diet and (b) lack of biliary stasis due to the costume and activity of the poorer women. So it is an ill wind that blows nobody any good; the diet that brings us peptic ulcer and gastritis safeguards us from gall stones.

Page 5: The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

Oct., 19351 THE DYSPEPSIAS OF SOUTHERN INDIA : ORR 575

in h i ^ occasionally occur, particularly

di , le better classes who can afford a richer

svn' fn ^ behoves us to be familiar with the Jptonis and differential diagnosis,

to' y\nPt?ms-?Periodicity is absent in contrast

tlier1 ^01 ^iere may have been attacks but

tlm G

11 a ,ways a continuous discomfort between iaunr? u8' T^ere usually a history of

thf> +?'CC' jaundice may not be present at

a sf "I10 examination. The patient, usually Da in0" Aye^-uourished individual, complains of full

H1 ? r^bt hypochondrium, a feeling of

lv- nes<: relieved by belching, not relieved by ee?

^ rp}v.n an<^ made worse by taking fat or

this peculiar to gallbladder infection, an'rl Uf staste t?r meat is typical of malignancy ?

? , ."ypochlorhydria. The free hydrochloric

eont 1S+ ?

anc* ^?e to^a^ acidity low, which cjr- ra;Ls w*th peptic ulcer and hvperchlorhy- 0f u' tenderness is most marked over the tip on +?

costal cartilage and is more marked taking a deep inspiration.

('?il ^ Pigment stones and those on which

.rlv.01!11]11 ^las .

been deposited are seen by the

bl'/n an ^c'ea as to fbe function of the gall- rv-1 can be obtained by cholecystography,

be lse<\ses 01 ^6 'pancreas.?Reference will only chr

11 ?

e ,^? two conditions that give rise to ?nic abdominal pain and indigestion.

iiiof, '^'eulic calculi. This is not common but we have

the ,

IJlree ^ses recently in Neyyoor. In one,

detailed below typ*ca* and pronounced; they are

subip?,J.'>aif,ent S'as ;,1 ^un man, not like a gallbladder coIioKr' Sl'ffered from repeated attacks of acute

'?ft sfir, 'lj'11 c radiated to the left and to the

had n ? i rIi was tender in the epigastrium and iaunrl.'o

a u- im raP1(* Pi'lse. There was no history of

an qff.0]^ 1ch ?ught to have given us the clue, for

JaunHi. ot biliary colic without at least a trace of

i'a(iia(n(?f l ""common. Also the pain did not

Usual ; ?-i- anc' right scapular region as is '

!? fj]Q Jeff y co '' but across the epigastrium and

dii0nG f?a^lire ?t pancreatic calculi which is of

Hilar va^ue that they contain large

forp m ca^c^um carbonate and are there-

rpin ca.,y scen by the x-ray; they can be . 'emoved by operation. Van !?mc. pancreatitis? This is of two

ann GS' ^n^r^?bular and interacinar. They are

effJw ^ s*milar in aetiology but differ in the CoUc b ley cause. The first affects only the

tho^ +i ex^ernai secretion, the interacinar on

and ? *iaiK* *-s a Seneral fibrosis of the gland affects the islets of Langerhans, giving rise u glycosuria.

-'Etiology.?Infection plays the primary part; ttlay reach the gland by

aoi^- ^le Pancreatic duct, and is more often ?-?~o ciated with acute pancreatitis,

iim blood stream in intestinal stasis, and

follow typhoid, or con -e ^mpbatics; there is an intimate

(In 11]<?C^10n between the lymphatics of the ?denum and gallbladder, and the pancreas,

and it is undoubtedly by this route that the chronic pancreatitis we see commonly arises.

Symptoms.?It affects middle-aged men and women; there is often a previous history of

typhoid. There is a general bodily wasting indigestion and attacks related to food but which may last over one or two meals. The

appetite is poor and vomiting gives no relief. There is tenderness in the epigastrium radiating to the left and into left shoulder.

Stools.?Large and bulky and more oily than normal. Microscopically they show an increase in fat, but they can be distinguished from the fatty stools of gall-stone obstruction in that there is a great increase in unsplit fats. The

unsplit fats can be distinguished from the split fats by staining with Nile blue which shows the globules of unsplit fat as bright red spots in a deep blue field. Unaltered meat fibres will be seen also, but there will not be much change in carbohydrate metabolism.

Special tests depend on the power of the pan- creatic secretion to digest gelatin. A drug such as iodoform is given in a gelatin-coated capsule. If the pancreatic secretions are working actively the capsule will be digested and iodine will

appear in the saliva in four hours. In pancrea- tic disease however the gelatin-coated capsule will pass unaltered by the pancreatic ferments. The diastase reaction is a very uncertain test

and only positive in extreme degrees. At opera- tion the gland is often found to be enlarged and hard.

Treatment.?Depends firstly on dealing with any duodenal or biliary sepsis by surgical measures, but, if no lesion in either of these

organs is found, justifying a cholecystectomy or gastroenterostomy, the correct procedure is to drain the gallbladder. This acts by draining away a possible source of sepsis and also as the pancreatic and common bile duct, in the

majority of people, open into the ampulla of \ ater it is a means of draining the pancreatic duct (figure 1). I have carried out this in four cases recently with good results.

i Showing the common bile duct and pancreatic duct opening into ampulla of Vater. Hence drainage of the gallbladder will also indirectly drain the

pancreatic duct.

pj,r i Showing the common bile duct and pancreatic duct opening into ampulla of Vater. Hence drainage of the gallbladder will also indirectly drain the

pancreatic duct.

Page 6: The Dyspepsias of Southern India - Semantic ScholarSpecial Article THE DYSPEPSIAS OF SOUTHERN INDIA* By IAN M. ORR, m.d?f.r.c.s. (Edin.) v London Mission Hospital, Neyyoor, Travancore

576 THE INDIAN MEDICAL GAZETTE [Oct., 1935

Appendix dyspepsia

This much-maligned organ carries far more than its share of responsibility for surgical intervention, largely because it is so easy to

remove a healthy appendix and the mortality is practically nil, while the removal of a gall- bladder is a more formidable procedure. So

many unfortunate patients have an innocent

appendix skilfully removed and are left to

suffer from chronic cholecystitis, salpingitis, or

visceroptosis. Nevertheless apart from acute appendicitis

there is a condition known as chronic appendix dyspepsia, and owing to the lymphatic drainage of the appendix and its connection with the duodenum an unhealthy appendix may upset the gastric function to a considerable degree. A few points on the diagnosis of chronic appen- dix dyspepsia will therefore be in keeping here :?

(1) There will nearly always be a history of one, two or three acute attacks, rarely more.

(2) Each attack tends to be worse than the last and pain remains in the intervals.

(3) There is deep tenderness at McBurney's point.

(4) The acute attacks commence at the umbilicus and spread to the right iliac fossa, and are associated with pyrexia; this is an important distinction from visceroptosis, which we will consider next.

(5) The x-ray may reveal a kinked or fixed appendix, or barium may fail to fill it; all these

suggest appendix trouble. (6) On dilating the colon with air from an

enema pump and pressing over the distended

sigmoid, pain will be felt in the right iliac fossa in many cases of chronic appendicitis.

Visceroptosis.?This is the next cause of chronic abdominal pain to which I would direct you.

In my earlier years in India I dismissed this

subject as one applying mainly to European women and not to be considered in dealing with the Indian dyspeptic, but my attention is being drawn more and more to it. I have repeatedly operated on a spare melancholic young woman suffering from the symptoms of duodenal ulcer only to find that there was no visible palpable ulcer, that the first part of the duodenum could be delivered outside the abdomen unusually easily, and that the csecum was extremely mobile and had attached to it a very innocent looking appendix. I found that if one removed the

appendix the patient was better for a time and then came back again or went to some other

surgeon with the same symptoms. Let us consider the four factors in viscerop-

tosis and see if they throw any light on this

type of case :?

(a) abnormal mobility and dilatation of the

gastro-intestinal tract,

(6) the presence of accessary bands or mem-

branes, (c) changes in the body structure, and (d) altered mentality. All who have low viscera have not got symp-

toms and yet all who have symptoms of vis-

ceroptosis have low viscera. The principal organs affected by (a) are

(1) the stomach whose greater curvature may droop into the pelvis and the lesser curvature be kinked and U-shaped;

(2) the duodenum which may be more mobile and which is sometimes crossed in its third part by the superior mesenteric artery which will be drawn more tense by the drag of the ptosed intestines and constrict the duodenum causing duodenal ileus (figure 2);

(3) the caecum may be in the pelvis or more mobile than normal and dilated or may be restricted by unusual bands. The colon also is more mobile and may be kinked at certain

points by bands. (6) The bands are definite in their situation

and are known as Jackson's membrane, Lane's kink, Payr's membrane and Toldt's membrane

(figure 3). I once came across a case where the transverse colon was kinked into a U, and the two limbs of the U held in apposition by a membrane (figure 3). I treated this case which was suffering from the symptoms of intestinal stasis by colectomy.

(c) The changes in body structure fall into two categories, virginal ptosis and maternal

ptosis. (1) Virginal.?The patient is a young woman,

with tissues poorly developed, little fat, narrow thorax, loss of lumbar curve, and slightly pro- truding lower abdomen. These signs are present from childhood but only in adult life do symp- toms appear.

(2) Maternal.?This occurs in elderly or

middle-aged women who have borne children.

Fig. 2.?Showing ptosis of caecum causing drag on superior mesenteric artery and kinking of duodenum. Fig. 2.?Showing ptosis of caecum causing drag on superior mesenteric artery and kinking of duodenum.

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Oct., 19351 THE DYSPEPSIAS OF SOUTHERN INDIA : ORR 577

The abdomen is broad with wide thorax, loss

of lumbar curve and a marked protrusion of the lower abdomen. The signs and symptoms do

not appear till after several pregnancies and

are due to loss of muscular tone often associated

of fat /figure 4).

fj ' Y'lanf/6s in mentality.?The patient is

espondent, inclined to exaggerate her condition

can give off readily a long list of bodily

Etiology.?There are two functions of muscle, one is to produce movement and the other to maintain bodily posture. These two functions are evidently carried "out by different parts of the muscle fibre and the postural tone may be lost without the power of movement being lost or diminished. This postural tone has to be

acquired in childhood by an act of will, till it becomes second nature to stand and sit correctly and the will plays no further part. In children of poor mentality brought up in unhygienic surroundings with little or no training, as are

so many girls in this country, the will never

acts strongly enough to maintain the correct

posture and they go into adult life in the ptosis condition. In adult life with the increased strain put upon the body the ptosis becomes worse. Symptoms only appear, however, if there are present some of these congenital bands or membranes which kink the ptosed organ and eventually lead to intestinal stasis and toxic

absorption. The symptoms are very varied but are all

characterized by the fact that no matter what the nature of the pain, it is worse at the end of the day and is relieved by lying down. The

patient has a typical bodily structure and feeble mental outlook, and while the patient is usually a woman men are sometimes affected. The

symptoms may simulate the following diseases :?

(1) Chronic appendicitis, but instead of two or three attacks there may be a history of numerous attacks, not getting worse as does

appendix dyspepsia. Vomiting is repeated and not just at the commencement of the attacks.

Pyrexia is absent and there is no hyperesthesia over Poupart's ligament, but an area of hyper- esthesia to the right of the umbilicus. The ca?cum is dilated, splashing can be elicited and there is frequently a ptosis of the right kidney. This picture was implanted on my mind by a young unmarried woman who had had her

appendix removed by another surgeon and came complaining of the usual pain in the right iliac fossa. Suspecting some adhesions or pelvic trouble I operated again and removed a large fibroid from the uterus. She was better for a

time and then came again complaining of pain which was made worse after walking about but did not trouble her when resting. Careful pal- pation revealed a mobile right kidney and the x-ray revealed a general ptosis of the ca3cum. As she was well off I had a visceroptosis belt made for her which gave her great comfort and relief.

(2) Peptic nicer may also be simulated, but there will be no periodicity and no freedom between attacks, and pain commencing after a meal has not completely disappeared before the next meal. The patient is relieved by lying down. There is loss of desire for food, but no real fear of taking food. X-ray is typical and there may be local spasm suggesting ulcer. I have operated on many of these cases expecting to find an ulcer and instead have been con- fronted only by a duodenum which was easy to deliver and a spasm of the pylorus which might easily deceive one into thinking an ulcer existed. More careful pre-operative z-ray examination can exclude ulcer and the general

Fig. 3.?Showing the sites of bands and kinks.

(1) Jackson's membrane. (2) Payrs I??nl1 (3) Toldt's membrane. (4) Lanes kink.

nf' ??' ShowinS sites of bands and kinks. (1) Jackson's membrane. (2) Payr's membrane.

(3) Toldt's membrane. (4) Lane's kink.

Fig. 4.?(1) Normal contour. (2) Virginal ptosis. (3) Maternal ptosis.

Fig. 4.?(1) Normal contour. (2) Virginal ptosis. (3) Maternal ptosis.

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578 THE INDIAN MEDICAL GAZETTE [Oct., 1935

build of the patient ought to be a guide. Duodenal ileus to which I have already referred can also be readily diagnosed by the a>ray by noting a fullness of the second and third parts of the duodenum.

Cholecystitis and cancer of the stomach may also be simulated, but rr-ray and response to

rest and lying down, and the typical figure must be our guide.

Treatment of visceroptosis.?We must re-

member in treating this disease that there is no short cut, 110 easily-performed operation which will relieve the condition for we arc dealing with people who have faulty postural tone, faulty habits, membranes and bands, as well as ptosis or a poor mentality which makes them unable to co-operate. As the trouble in the virginal type starts in

childhood, more careful training in school and

by parents would prevent a lot of it. Until

girls arc treated with greater frankness and

given more freedom it is unlikely that the mental problems will be solved.

In the established disease we must deal first with the poor tone and faulty posture. The

first thing is rest in bed and during that time the muscles should be developed by massage and gentle exercise of gradually increasing severity. Deep-breathing exercises to develop the thorax and restore the lumbar curve must

be carried out. A diet calculated to increase the

amount of fat must be given if the patient's

means permit, and regular bowel movement by means of liquid paraffin is desirable. When the

patient's circumstances make prolonged rest im- possible a properly fitting abdominal belt often gives relief, but massage and exercise must be carried out as well. The surgical treatment is unsatisfactory, but

a mobile caecum may be fixed by a caecapexy operation, and a ptosed stomach can be hitched up by means of one of the various methods of shortening the mesentery. The bands causing kinking may be divided and duodenal ileus may be relieved by a gastroenterostomy, or duodeno- jejunostomy, but it must be remembered that such operations will not relieve a general viscerop- tosis nor will they of themselves bring relief unless combined with rest, massage and exercise as described already. If the patient is neuras- thenic never operate; it only makes matters worse.

References

Gushing, H. (1898). Bull. Johns Hopkins Hosp., Vol. IX, p. 295.

McCarrison, R. (1931). Indian Journ. Med. Res., Vol. XIX, p. 61.

McCarrison, R. (1931?). Brit. Med. Journ., Vol. I, p. 966.

Moynihan, B. G. A. (1909). Brit. Med. Journ., Vol. I, p. 830.

Or, I. M. (1933). Lancet, Vol. II, p. 575. Wilkie, I). P. D. (1911). Surg. Gyn. and Obstet.,

Vol. XIII, p. 399.