CEDEMA AND SCABIES IN A FAMINE

HOSPITAL

By B. N. BHANDARI MAJOR, IA.M.C.

Oedema

These cases formed a large majority of the total admissions. Amongst them the death rate was particularly high, one out of each seven

admissions not leaving the hospital alive. The

observations that follow are based on over 300

cases of oedema admitted. It is a remarkable fact that seldom was there

available a history of true starvation; nor

was a single case of true beriberi seen, whether inside the hospital or in the outpatients' depart- ment. Some cases showed

'

dys-sebacia' and

phrynoderma as a minor evidence of vitamin B or vitamin A deficiency, but more gross signs of avitaminosis such as cheilosis, glossitis, photo- phobia with corneal vascularization or pellagra were rare. A few cases, however, did have

spongy gums and scattered areas of subcu- taneous haemorrhage.

In the absence of laboratory facilities, it is not possible to be sure of the true aetiology of these cases. Clinically, they roughly fell into the following sub-groups :?

Per cent

(?) (Edema following malaria .. 20

(?) (Edema following bowel upset .. 25

(c) Subacute nephritis .. .. 7

(d) Lipoid nephrosis .. .. 1

(e) Portal cirrhosis '

.. .. 3

(/) Anaemia .. ? ? ? 8

(g) Chronic heart failure .. .. 1

(h) Other causes .. .. .. 35

(a) (Edema following malaria

People of all ages were affected. There was a history of low-grade pyrexia of several months' duration, but for the last fortnight or so there had been a gradual onset of cedema of the feet and legs. Splenic enlargement was present, and also a moderate degree of anaemia and emacia- tion. The bowel action was usually normal, and the urine was clear with only a trace of albumin.

These patients gave very little trouble and did well on rest and a cou^se^of quinine and ferrous sulphate. They were^kept on ordinary diet. The more severe cases of this series were given postural treatment in addition by raising

the foot end of the bed. Their average stay in hospital was about a week, after which they were usually sent to a convalescent home for

feeding up.

(6) CEdema following bowel upset

Usually there was a history of passing blood and mucus some months previously, and al-

though this had got better within a couple of weeks, the bowels had never been quite normal since. There had been attacks of diarrhoea

alternating with constipation.. At the time of

admission, oedema of the lower extremities was

usual and of about a week's duration. The main

complaint, however, was of incessant diarrhoea and marked debility. The stools were invariably watery with only a small amount of faecal matter and bile. There was never any vomiting.

This group was the cause of a very high rate of mortality, about 25 per cent dying, no matter how enthusiastic the treatment. Glucose-saline was invariably administered intravenously in

copious amounts, and large quantities of kaolin and glucose were given by mouth. Sulpha- guanidine (or sulphapyridine) appeared to do

good in cases with a "definite history of dysen- tery, although no blood or-mucus was at the time discerned in the stools. Quinine was often used in cases showing splenic enlargement but with doubtful benefit. Vitamin B1 (and in later cases vitamin B compound tablets) was given to most cases as a matter of routine, but I doubt whether it did any good at all.

Protein hydrolysates.?At this stage, I may mention the use of glucose-peptone. It was cer-

tainly a life-saving measure in at least some of these cases. With such profuse diarrhoea feed- ing of these patients was a problem. Rice water with plenty of glucose and common salt was given, but in the stage of inanition in which most of them were, on account of prolonged purgation, the quantity they took by mouth was hopelessly inadequate. Orange juice and citrated milk were also tried, but in Bengal it appears that there is an intrinsic distaste for milk. Glucose-peptone solution (protein hydrolysates) as supplied by the All-India In- stitute of Hygiene, Calcutta, was often tried, and I think it pulled round some of the patients who were, according to previous experience, considered hopeless. In very few cases was

there any severe reaction ; only two or three

patients died with a rigor about three hours after an intravenous administration of the

hydrolysates. To patients who showed improve- ment, up to 600 c.cm. were given in three doses of 200 c.cm. each, at an interval of 5 or 6 hours. In these cases improvement was often rapid, and even the diarrhoea somehow came under control within the next couple of days (was this due to vitamin B?). During this period peptone administration was continued till the patient could be safely put on more substantial diet such as milk or even rice. Needless to say,

Dec., 1944] (EDEMA AND SCABIES IN A FAMINE HOSPITAL : BHANDARI 575

kaolin was also invariably given by mouth to all these cases.

Technique.?I have come across some medical officers who have been, working in other famine relief hos-

pitals, and it appears that none of them are conversant with the right technique of the use of the protein hydrolysate set (Haye's pattern) as supplied by the All-India Institute of Hygiene, Calcutta. The tech-

nique described in the Indian Medical Gazette of

February 1944 in the article on ' Treatment and

Management of Starving Sick Destitutes' by the com- mittee of the Indian Research Fund Association can be

improved upon by using the following method (see figures 1 and 2). On removing the paper wrapper from the mouth of

the bottle two holes (A and B) at once come into view in the tin lid. The rubber membrane stretching across under the lid will be seen sucked in towards the inside of the bottle. With a swab of tincture of iodine

completely wipe the surface of the lid and of the membrane. A very fine bore hypodermic needle (C) ia then pushed in through the membrane at hole (A). There will be a roar of suction of air and the rubber membrane will soon be seen to rise up close to the tin lid. Next, sterilize over a flame one of the points of a pair of scissors (or any other sharp instrument). Push it through the hole (B) so as to pierce the rubber underneath. Withdraw the scissors. Now the glass cannula (D) is pushed through this hole. Stop-cock (F) is put into position and the far end of the rubber tubing (E) is connected to another fine hypodermic needle (G). The bottle is now suspended upside down. Stop-cock (F) is opened. The fluid at once starts

flowing through the tube and bubbles of air are seen passing through the needle (C) into the bottle to

replace this fluid. By raising and lowering the tube

(E) all air bubbles are removed from the length of the tube. The height of the bottle is now adjusted to allow roughly 60 drops of fluid per minute to flow

through needle (G). The set is now ready for intra- venous use. Needless to mention all the accessories are previously sterilized by boiling. As soon as the needle (G) has been introduced into

the vein bubbles of air will start passing upwards through needle (C). If it does not so happen, then either one of the needles is blocked or you are not

inside the vein.

Special points (i) Needle (C) must be fine. One of large

bore will not work, and the fluid will keep on dripping through it.

(ii) Large cannulae supplied in the transfu- sion set are useless and are not to be used.

They are far too large in size to push into a

vein.

I was using the metal cannula, not for intra- venous purposes, but for performing paracen- tesis abdominis in cases of respiratory distress from large ascites.

(Hi) Keep an eye at the bubbles moving up through the needle (C). Should the bubbling stop it is almost a certainty that the needle

(G) is no longer inside the vein. This often

happens when the patient is very restless and is flinging his limbs about.

cm D

C

G

Fig. 1. Fig. 1.

Fig, 2.

576 THE INDIAN MEDICAL GAZETTE [Dec., 1944

It will be seen that no extra complicated apparatus is required. With the sets previously- sterilized it has taken me less than 5 minutes to get the fluid running into the vein, starting from scratch.

Essential oils (cholera mixture) were also tried in a few cases but the result was dis-

appointing. It put the patients right off taking any fluids by mouth and in a few instances gave rise to actual vomiting.

(c) Subacute nephritis Cases were typical with a recent history of

anuria or slight hsematuria. Since then, a

general cedema of the body, eyelids, and sacrum had gradually developed. These cases usually improved on potassium citrate and sodium bicarbonate mixture with restrictions of salt and fluid intake.

(d) Lipoid nephrosis This was an interesting group. All cases

ranged between the ages of 3 and 16. There was an enormous cedema of the whole body with a very large degree of ascites. One child of 13 had an abdominal girth of 40 inches which after a month of treatment in hospital gradually sub- sided to 21 inches. It was a common sight to see the skin on the dorsum of the feet, scrotum or the penis sloughing off from distension. In all these cases the urine was scanty and full of albumin. Mucous membranes were pale. Blood pressure (systolic) was invariably below 100 mm. Hg. There was no complaint of visual disturbances. The treatment of these cases was particularly

gratifying. Practically all improved on intra- venous protein hydrolysates. The explanation is obvious. It was a simple case of replacing the proteins in the blood which had been lost in the urine.

In these cases salt was restricted, and com- plete rest was advocated. Residual cedema took a long time (3 weeks or more) to clear and was greatly assisted by oral administration of theocin sodium acetate in the usual doses. Ad- ministration of iron and liver extract was later useful in putting up the haemoglobin.

It may be mentioned that the child with an abdominal girth of 40 inches had to be tapped immediately on admission as he was suffering from acute respiratory distress.

(e) Portal cirrhosis

All these cases were men. Their ages ranged between 30 and 55. Practically all had massive ascites with respiratory distress. Besides they also had cedema of the lower extremities (from cardiac embarrassment ?). They were all brought to hospital on stretchers. In each case the cedema, though of gradual

onset, had been present for months. One of the cases was in his second attack, having recovered from the first about a year previously. AH these patients had to be tapped, and a

maximum amount of ascitic fluid removed. They

were immediately put on ammonium chloride and neptal (1 c.cm.) given intravenously. Initial improvement was rapid following a

marked diuresis, but at least two such patients never got quite free from their ascites after treatment lasting for over a month.

(/) and (g) Ancemia and chronic heart failure

These cases were easily recognized. The cases of chronic heart failure were evidently those

following hyperpiesia. Only two of the latter

group were admitted, one died on the third day during an attack of cardiac asthma followed by acute oedema of the lungs. It is a pity that neptal was not available in those days because he appeared to be a case who might have im- proved with this diuretic at an early stage. The other case absconded.

(h) Other causes

This group is rather difficult to analyse. Al-

though it formed nearly a third of the total

percentage, it was difficult to fit it into any of the sub-groups mentioned above. Some of the

patients presented themselves with rather a solid oedema of the feet along with oedema of other

parts of the body. Prolonged rest and nourish- ing diet had a beneficial effect, but the improve- ment was very slow as compared to other cases where the cause was more or less known. Pro-

longed treatment with neptal was very successful, but complete disappearance of oedema would not occur at least in some of the cases.

It was only in this sub-group that any evi- dence of avitaminosis was found. Apart from dryness of skin, some of them had dermatitis akin to pellagra. Bowel disturbances were fre-

quent. They, in most cases, reacted to vitamin medication. Some patients had cardiac haemic murmurs but

no actual evidence of valvular incompetence. The heart often showed signs of dilatation, but the blood pressure was never suggestive of hyper- piesis. The liver too was not invariably enlarged or tender. They were possibly cases

of acute beriberi without any nervous manifesta- tion. The death rate among these was again very high. In many such instances the peri- cardial sac was aspirated post mortem but never was there found any evidence of excessive fluid. Two patients with marked oedema and splenic

enlargement, and running a low-grade pyrexia, were not showing any improvement with

quinine. Both of them reacted favourably to urea-stibamine injections. One patient with marked anasarca, inter-

mittent pyrexia, tachycardia, hepatic enlarge- ment and tenderness, and palpable spleen showed no sign of improvement for over three weeks. She was eventually put on emetine. She recovered.

It would thus appear that this group was com-

posed of miscellaneous causes. Some of the

Dec., 1944] (EDEMA AND SCABIES IN A FAMINE HOSPITAL : BHANDARI 577

cases were probably atypical types of the

preceding sub-groups, and some perhaps had their origin in various'combinations of these sub- groups.. Quite a number of them with symp- toms of diarrhoea were probably cases of vita- min B deficiency in addition to other factors. Diet.-?A word may be said at this stage re-

garding special dietary adopted. Most cases of oedema were given a generous diet including milk, raw eggs, and citrus fruit. This applied in particular to cases of lipoid nephrosis. Cases with anuria were kept on milk and rice only, plus any fruit that was available. Cases with marked diarrhoea were maintained entirely on fluids till their condition started to show slight improvement in that direction.

Discussion.?Subacute nephritis, lipoid neph- rosis, portal cirrhosis, ansemia, and chronic heart failure as causes of various types of oedema

require no introduction. But what about the

sub-groups a, b, and h ? Malaria, especially quartan, has long been

known to give rise to nephritic manifestations, but I am not aware whether the quartan type of malaria is common in Bengal, indeed if it occurs at all. In any case, these patients did not show any nephritic symptoms. Malaria by itself as a cause must therefore be ruled out. To my mind there is one common feature to all those three sub-groups (a, b, and h). In each in- stance the patient has suffered from fevers, or diarrhoea, or avitaminosis. All, or any of these factors, operating for a prolonged period, are

bound to sap one's vitality ending in loss of appetite and general emaciation. It may also be remembered that this epidemic of oedema has only victimized the very poor who had but little funds to afford treatment at an early stage (even if quinine had been available in the market) and whose larder was equipped with the barest necessities of food, leaving out of con- sideration all luxury foodstuffs. It is conceiv-

able, therefore, that their oedema was really caused by inadequate supply of food which was poor in first-class proteins, and often in vita- mins as well. It is true that none of the

patients actually admitted starvation, but from the above it is reasonable to consider the origin of oedema as really lying in true inanition. I am not aware whether oedema has ever been observed among professional fasters, but such

people have usually had a good reserve of pro- teins and vitamins before they ever commenced a fast. Besides they usually did not absolutely deprive themselves of vitamins, etc., even during the course of the fast. In any case their fast did not perhaps last long enough for any of the deficiencies to show themselves in the form of oedema.

I am aware that a lot of laboratory work has been going on for some time to find out if the blood actually shows any deficiencies in its total proteins in such cases. I understand that such is the case in nearly 50 per cent of all cases of oedema. The result of estimation of

other blood constituents will also be awaited with great interest.

Causes of death.?-As usual, children and old people produced the highest mortality. Cases with marked diarrhoea just sank gradually ; their blood pressure continuing to fall till the pulse became imperceptible. Giving extra glucose-saline would often cause venous en-

gorgement without reviving the heart. A small

percentage of such cases had a little rise of

temperature just before death. An inspection of their bed clothes sometimes showed the pres- ence of little blood and mucus, in the diarrhceic stools. Were these cases of dysentery ? In view of the fact that no signs or symptoms of dysentery were previously noted I am inclined to believe that it was a fresh attack of dysen- tery contracted from other patients through the agency, and the careless habits, of the un- trained civilian staff in spite of most1 careful vigilance. And this attack was usually the last straw.

Another cause of death among cases with diarrhoea was the onset of cerebral thrombosis. It occurred in about 5 per cent of the series.

In cases without diarrhoea, a couple of hours before death, the main symptom complained of was a feeling of extreme debility and exhaus- tion. Even though the pulse was perceptible the tension was always low. Listlessness and

prostration of the patient were most pathetic. He gradually went into coma before death.

Injections of camphor in ether or administra- tion of intravenous glucose made no material difference to the outcome.

During the first week of starting the hospital, a young girl in her early twenties was admitted with oedema of the lower extremities. She had walked up to the hospital. On the third morn-

ing of her stay she walked to the outside of the ward and sat in the sun, her oedema apparently having slightly improved. Half an hour later she walked back to her bed, but now she was in a state of collapse. Ten minutes later she was dead. Was she a case of beriberi ? After this

incident, a complete rest was enjoined on all

patients, but similar cases continued to occur

nevertheless. An onset of ursemic coma was uncommon

even among nephritic cases. No case of evi- dent cerebral haemorrhage was seen. Some of the patients who died of cerebral thrombosis or

gradual heart failure may have belonged to this group, but a typical case of chronic nephritis with high blood pressure ending in heart failure was not met with. A. fair number of deaths were accounted for by a terminal attack of

broncho-pneumonia. Scabies

In ordinary circumstances, one has got to con- sider each patient individually. Is he suffering from dermatitis herpetiformis or lichen planus as there is so much itching complained of? There is no such difficulty in famine times in Bengal. In this area 80 per cent of the very

578 THE INDIAN MEDICAL GAZETTE [Dec., 1944

poor population are suffering from skin troubles; 95 per cent of these are cases of scabies, the remainder of impetigo, eczema, or dhobi's itch. Patients suffering from malaria are usually dis- appointed if they cannot get quinine, but cases of scabies are actually quarrelsome if they are denied an adequate amount of sulphur oint- ment.

Why is scabies so common ? It is now an

established fact that the infestation with Acarus

scabiei occurs mainly through close personal contact. In this connection let me recall the

famous experiment in which 25 healthy volun- teers were made to sleep under blankets

recently used by persons infected with scabies. No infection occurred. Then 32 volunteers were made to wear infected underclothing, only two got infected. Then volunteers were made to

sleep with scabies cases, all with pyjamas on, 3 out of 4 got the infection. This is rather a

startling fact which will probably make us re- vise our opinion with regard to the routine followed in military hospitals of disinfecting all personal and hospital clothing' used by scabies patients. The famine has hit the poor rather badly.

Lack of clothing means more and more people sleeping huddled together under one blanket

exactly reproducing the conditions in the experi- ment quoted above. The result is obvious. But this perhaps is not the whole explanation

for such a wide spread of scabies. Half of the

superior nursing staff and the medical officers

(including myself) also got infected. No doubt we were all in close contact with the patients but hardly ever in such intimate and prolonged contact as to get infected in such a high per- centage. And there was no question of inade- quate provision of clothing. I am inclined to believe that the condition of the skin has some-

thing to do with it. Let me explain. Water in Madaripur is extremely hard, and it '

is immaterial whether you draw it from the river or the tube-well. Each time soap is used, a thick scum rises to the water surface. You

wipe your hands on a towel afterwards, there is a yellow stain left on the cloth. This neces-

sarily means a dry skin. Now, the worst cases of scabies have almost

invariably a very dry skin. Dry skin is

obviously what the scabies mite wants. It is much easier for the acarus to find small cracks to burrow into. This to my mind is one of the additional factors affecting the spread of itch. Again, owing to famine conditions, phryno-

derma as an evidence of vitamin A deficiency has been very common. This, in ordinary par- lance, means a dry skin. That again means a

greater susceptibility to scabies. A suggestion has been made that scabies and

cedema have both been very .common during this famine, and therefore there may be some relationship between the two diseases. Neph- ritis (which formed only 7 per cent of the series of hospital admissions due to cedema) finds

only one thing in common with scabies, and that is they are both liable to occur more in the cold weather rather than in the hot. Inadequacy of clothing favoured suitable conditions for both diseases.

I cannot see any relationship between scabies and oedema due to causes other than nephritis except the famine and non-availability of medical attention in the early stages of various diseases that followed it.