Adult malnutrition    
severely malnourished adults Saskia van der Kam 24.08.98
Severely malnourished adults with diarrhoea Michael Golden 21.08.98
Re: severely malnourished adults Steve Collins 31.08.98
severely malnourished adults Michael Golden 30.08.98
adult malnutrition continued Saskia van der Kam 18.09.98
adult malnutrition -Sudan Michael Golden 22.09.98
adult malnutrition -Sudan steve collins 10.10.98
Dietary Treatment of Severe Malnutrition in Adults David.Brewster 15.10.98
Re: adult malnutrition -Sudan Saskia van der Kam 15.10.98
dietary treatment of severe malnutrition in adults Barbara Elaine Golden 16.10.98
Adult malnutrition : proteins vs Na André Briend 30.10.98
Re: Adult malnutrition : protein Barbara Elaine Golden 30.10.98
Re: Adult malnutrition : proteins vs Na Steve Collins 18.12.98


Date: Mon, 24 Aug 1998 15:22:41 +0100

From: sakatamsterdam.msf.org (Saskia VD KAM)

Subject: Ngonut: severely malnourished adults To: ngonutatabdn.ac.uk

 

Dear Mike,

One of our projects in South Sudan brought up the problem of severely

malnourished adults, with persistent diarrhoea.

Severely malnourished adults means a BMI < 12, weights of 25kg are

not uncommon.

Diarrhoea does not respond on any antibiotic.

The diarrhoea is probably related to mal-absorption.

I suggested the team that it could be due to pancreatic insufficiency

(an old suggestion of André Briend). Therefor the use of F-75 for the

first 3 days (45kcal/kg) might be a proper solution. After this F-100

for a period defined by rpogress (free of diarrhoea, and then

progresively introduction of meals)

However the field doctor suggests it might be an osmotic diarrhoea and

consequently the sugar content of the food should be reduced (by

diluting the milk and resomal). Additionally the doctor fears that

the protein content in the F-75 is too high.

The other question of the field is whether 3 days of F-75 is enough,

or too long.

It must be noted that the number of malnourished adults is

overwhelming (300 severely malnourished cases), and the capacity of

the project is limited. Therefore intensive individual monitoring and

follow up is difficult. This stresses the need for clear protocols

applicable for the majority of the patients.

My questions are:

-do you support the protocol of 3 days on F-75, 45 kcal / kg

- is the fear for osmotic diarrhoea still valid when using F75 and

resomal? If yes, what are the solutions?

Saskia van der Kam, nutritionist Médecins Sans Frontières Holland


Date: Fri, 21 Aug 1998 16:24:26 +0100

From: Michael Golden <m.goldenatabdn.ac.uk>

Subject: Ngonut: severely malnourished adults with diarrhoea

 

Dear Saskia,

Quick answers are given directly to your questions - a full answer and comments are given after your message.

you wrote:

> Dear Mike,

> One of our projects in South Sudan brought up the problem of severely

> malnourished adults, with persistent diarrhoea.

> Severely malnourished adults means a BMI < 12, weights of 25kg are

> not uncommon.

> Diarrhoea does not respond on any antibiotic.

*** see below.

>

> The diarrhoea is probably related to mal-absorption.

*** see below

> I suggested the team that it could be due to pancreatic insufficiency

> (an old suggestion of André Briend). Therefor the use of F-75 for the

> first 3 days (45kcal/kg) might be a proper solution. After this F-100

> for a period defined by rpogress (free of diarrhoea, and then

> progresively introduction of meals)

Unlikely to be due to pancreatic insufficiency unless the stools are characteristic and a relatively small proportion of cases thus affected.

Nevertheless, F75 (45kcal/kg = 60ml/kg) is the correct way to go! Change to low-osmolality F100 after 3 days, or if you only have conventional F100 when the diarrhoea eases or stops and the patients feel hungry (MEAN of about 3.2 days but much longer in some patients - if you are going do it absolutely by time instead of appetite [which I do not think is easier, and is certainly not clinically sensible] then I would give the F75 for slightly longer - 4 or 5 days routine and less if the appetite improves.

> However the field doctor suggests it might be an osmotic diarrhoea and

> consequently the sugar content of the food should be reduced (by

> diluting the milk and resomal). Additionally the doctor fears that

> the protein content in the F-75 is too high.

No! F75 is isotonic (280mOsm/l) and the protein content is very low already - it is not recommended that F75 be diluted at all - there is some justification for diluting old style F100 - please check with your supplier to see if you have got the "low-osmolality" version of F100 in which case it should not be diluted - if you have got the high-osmolality version then dilute it by 3/4 and give an additional 25% (put one packet into 2700 ml instead of 2000 ml).

> The other question of the field is whether 3 days of F-75 is enough,

> or too long.

This depends upon the response - you cannot grow on F75, but you can maintain yourself for a very long time - we have had patients on F75 for over 10 days on rare occasions - for routine use I would go to 4 or 5 days and then "stop early" - this is much easier to manage in the mass treatment by protocol setting, than setting the time at a short time and having to prolong it for failures or having to return a lot of patients to phase 1.

> It must be noted that the number of malnourished adults is

> overwhelming (300 severely malnourished cases), and the capacity of

> the project is limited. Therefore intensive individual monitoring and

> follow up is difficult. This stresses the need for clear protocols

> applicable for the majority of the patients.

I agree absolutely - close monitoring seems to be a luxury almost no patient with malnutrition gets no matter the setting (research units excepted) - there must be simple and easily learned protocols - and, depending upon the products that you have available, I hope that what I've said can be translated into quite a simple protocol - only a different product for phase 1 and phase 2.

> Saskia van der Kam

> nutritionist Médecins Sans Frontières Holland

>

The diarrhoea of adults has not been extensively studied, however there is no real reason to suspect that it is different from that of childhood, youth or adolescence - for the presenting features and the characteristics of the stool itself seem to be the same.

There are a number of possible reasons for the malabsorption.

First, a direct effect of nutritional deficiency on gut physiology

a) The intestinal mucosal absorptive cells have a very high turnover rate (life span about 2 days) and "mature" life much less than that - they are susceptible to any factor that interferes with protein synthesis or cell division, which is itself a hall-mark of very sever malnutrition.

b) There are some nutrients whose deficiency is particularly associated with malabsorption and diarrhoea -

1) Zinc- probably the most important in this situation (zinc deficient diarrhoea has a different stool composition from non-zinc deficient diarrhoea -much lower Na and higher K concentrations) - zinc deficiency is very common in this situation and any patient with diarrhoea or skin lesions should get additional zinc. Often the persistent diarrhoea will respond to zinc alone!

2) Riboflavine - deficiency is very common (about 90% of malnourished patients in Jamaica and 40% of "normal" subjects) - this will give rise to diarrhoea as well.

3) Folic acid deficiency - again very common and will give rise to diarrhoea.

c) deficiencies associated with losses during diarrhoea which lead to persistence

1) magnesium deficiency is very common in all with persistent diarrhoea due probably to prolonged unreplaced losses. This is the main nutrient deficiency in Chrone's disease and other chronic diarrhoeal diseases of adults (and children) - and the diarrhoea will not stop until Mg is adequately replaced.

2) Potassium deficiency is also very common - partly because of the associated magnesium deficiency (there will not be K retention in the face of Mg deficiency probably because the sodium pump is Mg dependent - experiments by Inge Dorup and Torben Clausen have clearly shown that a K deficit can often be corrected by Mg alone). and also because of the high K in zinc deficient stools.

3) Copper deficiency is quite common in those who have persistent diarrhoea - its role in the genesis of the diarrhoea is unclear at the moment.

However, Cu deficiency seems only to be common in those with persistent diarrhoea - so the relationship between this deficiency and persistent diarrhoea is very close.

 

Second, an indirect effect due to small bowel microbial overgrowth.

All the mechanisms that normally suppress microbial overgrowth are deficient in severe malnutrition.

1) Motility is probably the most relevant - anything that interferes with motility (e.g. blind loops, strictures etc) is always associated with malabsorption. The peristalsis is sluggish and mouth to caecum transit time greatly prolonged - often the patients even present with a sort of "pseudo-obstruction" - diagnosed clinically as abdominal distension: if it is severe then an audible "splash" can be heard from the abdomen when the patient is shaken - probably caused by the electrolyte abnormalities.

2) Deficient bile salt production (Snieder and Viteri showed this well at INCAP)

3) Deficient gastric acid secretion, IgA output, Lysozyme etc.

There is not only overgrowth with bacteria but also fungi. We found that we could culture candida from 100% of children's faeces on admission, whether or not they had oral thrush - and candida is frequent in gastric washings.

Also the immune suppression leads to overgrowth with some abnormal organisms as well as normal organisms - thus, in examination of the stool of malnourished children with diarrhoea we usually were able to see cryptosproidium for which there is no treatment except to feed the patient to the stage when their gut immunity recovers. (cf paper by Christie et al)

Third, Bile salt deficiency and de conjugation of bile salts by bacteria.

The fatty liver disease leads to poor bile salt production and there is bile duct stasis (in post mortem samples there is frequently cholestasis) This again is common (see Snieder and Viteri). it causes fat malabsorption and fat soluble vitamin deficiency die to lack of sufficient bile salt to get above the critical-micellar-concentration and the free bile salt which then enters the colon causes a chemical dysentery and malabsorption of salt and water - typically patients get malabsorption when they are fed frequently (not sufficient newly synthesized bile salt) and diarrhoea after a fast, such as first thing in the morning (newly synthesized bile causes salt and water malabsorption). The stool will tend to be pale with frequent feeds and green with infrequent feeds.

Treatment is by suppression of small bowel flora and feeding the patient - no replacement treatment is advised!

Fourth, pancreatic insufficiency

Yes, this will cause malabsorption - but not usually diarrhoea because the malabsorbed parts of food that depend upon pancreatic enzymes for digestion are not osmotically active - fat mainly and some protein. The stool has a very "high" smell and is greasy (when put into a plastic bag and felt through the plastic). The original descriptions of kwashiorkor describe very severe pancreatic atrophy at post-mortem. The electron-microscopy of the pancreas confirm that the protein synthesis is very severely curtailed. The normal presentation is that these patients fail to put on weight with the standard treatment until replacement pancreatic enzyme is added to the feed for a few days until there is enough absorbed to break the malnutrition/pancreatic insufficiency cycle - this occurs to a clinically relevant extent in about 2% of paediatric patients in my experience.

Fifth, specific infections. In persistent diarrhoea these are an unusual cause. Sometimes giardia can be the cause. Could Andrew Tomkins please comment on the latest on "tropical sprue", and whether this research is likely to be relevant here - it used to respond in some patients to folic acid or tetracycline but not to any other specific treatments!

 

What to do!

1) Clearly, the nutrients that are likely to be deficient in this patient group have to be replaced systematically - Zn, Mg, K, Folate, riboflavin, copper being the most important. All these are present in F75 and F100 in amounts that are probably adequate for replacement in this situation - possibly some additional zinc would be useful.

2) a diet that is easily absorbed and isotonic is needed:

- F75 has been designed to have much less fat in it than F100 (32% against 53%) because fat is the most fastidious nutrient for absorption and these patients desperately need maintenance energy to be absorbed.

-It has a higher amount of carbohydrate in it (63% of energy) to help to prevent hypoglycaemia, a common cause of death in these patients. The high carbohydrate is also necessary at this stage because we are giving a low protein diet and need to supply sufficient carbohydrate to suppress gluconeogenesis.

-it has much less protein in it. Only 4.8% of energy is derived from protein (the patients are NOT supposed to gain weight on F75 - only to repair their metabolism and correct deficits). Whereas F100 has 11.3% of energy from protein. Your staff are correct that in this situation a high protein diet can be dangerous (amino acid metabolising enzymes are deficient so the patients are like acquired "inborn" errors of metabolism) - but F75 is designed as a LOW protein diet that will not stress the liver

- it is also a LOW sodium diet. This is because of its use in sick patients with kwashiorkor, endotoxic shock and incipient heart failure.

High sodium diets will kill such patients - however, for patients with persistent diarrhoea it may be prudent to increase the sodium intake somewhat - say by 0.5 or 1 mmol/kg/d - if their diarrhoea does not abate quickly - the best source of this sodium will be a small amount of resomal (which also has potassium, magnesium and zinc in it) - but only give very restricted amounts.

There has been a slight change in the recommended formula of F75 from the draft WHO manual that many of you have. This is because when the formula is "home-made" it was impossible to get the osmolality down to acceptable levels by addition of complex carbohydrate without the diet becoming unacceptably viscous. There has thus been a compromise to allow the formula to be made from local ingredients by increasting the fat energy from 24% to 32%. This now allows the reduction of starch to an acceptable level. The revised formula is < DSM 25g, Oil 27g, Starch 35g, sugar 70g, mineral/vitamin mix> this gives a diet with an osmolality of 333mOsm/l and a renal solute load of 119 mOsm/l (Zeigler and Foman formula).

The commercial formula which you probably have in stock, has the old formula where 24% of energy comes from fat and 71% from carbohydrate - this is possible because the carbohydrate is in the form of dextrimaltose which is freely soluble (unlike the starch) - and these formulae have an osmolarity of about 280 mOsm/l - in other words they are isotonic and should not cause osmotic diarrhoea.

F100, of course is used for a quite different purpose - to promote catch up growth! This is why it has such a high fat content and an adequate protein content for this purpose. However, the home-made F100 <80g DSM, 60g oil, 50g sugar, mineral/vitamin mix> has an osmolality of about 427 mOsm/litre.

The older stocks of commercial F100 also have this high osmolality and may cause osmotic diarrhoea when it is first used (this is another reason why we do not start most patients on F100 immediately).

Action Contre la Faim had a problem with bloating, induced diarrhoea and children becoming obtund in Mogadishu, and tested a batch of low osmolality (circa 280 mOsm/l) F100 in these children - the results are not yet analysed in terms of stool frequency and growth rate etc, but there were no cases of bloating or induced diarrhoea clinically observed during this trial. The major commercial manufactures of F100 are now producing a low-osmolality version at the same price as the original version - if there is a problem with persistent diarrhoea in any of your patients, then I urge you to get your logistics department to specify the low-osmolality F100 when it is being ordered.

The alternative is to dilute the F100 formula by about 3/4 and give more at each feed in order to get the osmolality down to a level where it will not cause an osmotic diarrhoea and where there will be extra water intake (important in Sudan - see a previous message about water deficiency in the Sahel - parenthetically, since changing the protocol there to give additional water the mortality rate has dropped dramatically). Such F100dil has an osmolality of 320 mOsm/l and is a possibility for those who cannot get the commercial F100 or could not get F75. It should be noted, however, that the differences between F75 and F100 are not just in terms of the osmolality and the F100dil is not "equivalent" to the F75 - even if many more patients could now tolerate the new commercial F100 immediately than the previous commercial formulation - there will still be a residue of patients with endotoxaemia, gross liver disturbance, incipient heart failure, tendency to hypoglycaemia that will require the F75 to achieve a low mortality rate.

 

Sorry that this message is so long - there is a lot of misunderstanding about the diarrhoea that occurs in severe malnutrition and antibiotics are certainly not the answer and we should not wait to see if they work.

Prof. Michael H.N.Golden

Dept of Medicine and Therapeutics - Univ of Aberdeen, Foresterhill

AB9 2ZD. Scotland, (UK)

INTERNET m.goldenatabdn.ac.uk

Tel +44 (1224) 681 818 ext 52793/53014, Tel(direct) +44 (1224) 663 123 527 93

Fax +44 (1224) 699 884


Date: Mon, 31 Aug 1998 09:08:05 -0400

From: Steve_Collins_at_po330a01atsmtplink.unicef.org (Steve Collins)

Subject: Re: Ngonut: severely malnourished adults

 

Saskia,

We had many of the same problems of persistent diarrhea in Somali

adults. There, before F100 was about, we were treating with a

DSM/Oil/Sugar HEM and adding a little KCL, magnesium sulphate, cooper

sulphate etc...Once started on this milk many of the adults developed

diarrhea and from that time our main problem was maintaining

hydration. We used to dilute the HEM to 50% for all new admissions

for three days as standard. In many however, this wasn't sufficient

and dehydration was still a real problem. With these people I found

it easy to teach the local workers that if there was profuse diarrhea

they were to dilute the milk still further. I think that we had spent

so much time reinforcing the idea of plenty of ORS for cases of

diarrhea that they found it quite natural to added more ORS to the

milk when the diarrhea was bad and it didn't seem to be a huge

organisational problem. What was interesting was that even though we

were using standard high sodium ORS...and plenty of it (not knowing

any better) we did not have a single problem with heart failure and

pulmonary oedema, and our only "refeeding" deaths appeared to be due

to a failure to maintain hydration..(in the first few days after we

started the lower protein HEM and before we had got the hang of

dilutions...these basic treatement regimes have been recently written

up and are in AJCN last month). This seems to support what Mike was

saying in his reply to you about the extra needs for Na in such cases.

In some patients the severity of the diarrhea required a dilution of

below 1/4 strength HEM, but given in fairly large quantities even in

the initial phase. Although this was too low in calories to

completely halt the nutritional decline the results were very good in

all the patients who had diarrhea but whose appetites recovered. The

very dilute milk was never needed for more than two or three days

after which we could then quickly strengthen in up. In the majority

of cases the diarrhea resolved within a few days and hydration was

easiy maintained. In adults I feel that it is reasonable to go a

little slower with treatment, with lower calories and protein during

the initial phase of treatment and that the dangers of underfeeding

during the initial phase are less than in children whereas the dangers

of overfeeding are greater. This slower approach in adults as

compared with children makes sense, mirroring the slower descent of

adults into severe malnutrition and slower rates of weight gain in

recovery.

Now obviously the situation is much easier with F75 and low osmolar

F100.

Again our experiences at Concern accord with Mike's views on the

level of protein. In Somalia we found that the amount of protein

given was very important and that with a higher protein diet (>15% of

energy from protein) appetites, particularly in oedematous patients,

didn't recover. When we lowered the protein to about 8%, the

majority of patients quickly recovered their appetites and mortality

amongst the oedematous adults dropped by 75%!!(again these data are

in the AJCN article). Lowering it further didn't appear to help

much, so I can't see that reducing the protein content of the F75

would be of any benefit.

One other thought. Are you using yogurt at all? here in the DPRK

some of the doctors have been having great success with yogurt in

cases of persistent diarrhea. On that note, does anybody know whether

it is possible to dry yogurt so that it can be transported in sacks.

Yogurt is a traditional food in the DPRK and, as they currently have

many problems of persistent diarrhea which seems to respond to yogurt,

it makes sense to promote it's use. However the targeting of supplies

to malnourished patients is not precise enough to risk supplying DSM

and getting institutions to make their own yogurt so I wondered if

dried yogurt powder is a possibility? Can you make it out of HEM and

mix the fat that settles out on the top back in before use?

Any suggestions would be welcome.

Cheers

steve collins


Date: Sun, 30 Aug 1998 09:46:44 +0100

From: Michael Golden <m.goldenatabdn.ac.uk>

Subject: Ngonut: severely malnourished adults

 

Dear Steve,

We are in agreement. It frequently happens in emergencies that there is no access to the patients from 4-5pm until 8-10 am (depends upon security, time of sunset/rise, daily distance to travel). Clearly, 24h protocols cannot be instituted if there is 8-12h care.

For those at the early life-threatening phase this presents a real dilemma and undoubtedly accounts for the higher than expected mortality in some operations. It is not clear what to do.

For example, ACF faced this problem in Maramvya, Burundi, where there was also a cholera epidemic - in the evening we would leave buckets of ORS and a drip running for the cholera patients, but is was frequently insufficient and the patient would be dead from dehydration when the team arrived 16 hours later, next morning (cholera mortality was about 25% but fell to very low levels when we had longer access). Under such circumstances it is not reasonable to expect the same results as those obtained under 24h care conditions. However, I would very much like to know how to manage such patients in a better way.

Incidentally, darkness is also a real problem in a TFC at night. One cannot see to do the things one normally takes for granted; during the day it is easy to make up and dispense food. during the night it is difficult to even find the latrine (a major hygiene problem). I think that there is a slightly lower mortality during the full-moon because of this. In this particular TFC there were over 600 patients and their caretakers (a second TFC was refused by the authorities), lamps could not be used at night because the nearby army commander ordered complete darkness (when some light was used the TFC was attacked and burned down by "unknown persons"), any dim lights were stolen, "outsiders" would invade at night to have sexual contact with the caretakers making it very insecure for caretakers who were asked to "take responsibility". How to deal with these types of real problem is not given in the manuals (the ex patriot staff are often miles away in their house or at least guarded refuge); the reality is not transmitted in the mortality statistics (just criticism for "doing a bad job"), neither is the frustration of impotence when patients die because of the insecure situation. I am sure that many who have not been in these situations do not appreciate the actual problems of applying protocols in situations such as Somalia or Liberia during the fighting, Burundi, or South Sudan at the present time.

For these patients, I am sure that you are correct - one bends the protocols to meet the exigencies of the circumstances - and if this means giving plenty of ORS or diluting feeds then so be it. The question we should ask is the extent to which experiences from such compromises inform us about how we should act when we have 24h access.

For those over the acute life-threatening phase of their illness, it is not so difficult. They are left with food to take overnight. This can be a dry product (most people use BP5 in this situation) or formula milk can be made up distributed and left for the time when staff are absent - there have been arguments between myself and Andre Briend about how long feeds can be left in this situation without the problem of significant bacterial contamination with estimates ranging from 1 (Andre) to 6h (me) - but the experiments have not been done to see - requires good microbiology in a situation where there is none.

We recognized this problem some time ago and ACF I has been working with two manufacturers to develop new products that have the same basic composition as F100 but are "dry" so that they can be used for over-night feeding, can be used in areas of greater insecurity for "take-home" management of the severely malnourished, can be used for patients whose caretakers refuse to come into a TFC because of competing demands for a whole variety of cogent reasons including personal insecurity (good examples are in the camps in northern Uganda), and can be used for those who are discharged "early" because of space pressure in a facility. It is also hoped that we will be able to use these products to manage severe malnutrition from health centres without kitchen facilities or staff where overnight and weekend feeding will always be required, and try to get the treatment out of hospitals. Also we have found that these products are much more acceptable to adults and adolescents who frequently do not consider that they have been fed unless the food is solid - so we anticipate that it will make the management of the malnourished adult much simpler. The two products are "Plumpy-Nut" by Nutriset and "BP100" by Compact. They are at the moment not freely available because they are "experimental" and are being field tested in TFCs by ACF. (Despite this, I understand that one manufacturer has already sold some for field use because of the exigencies of the emergency). In the experimental testing, first we have substituted one meal of F100 with these products to see acceptability and measure the impact on the F100 feed before and the feed after the test feed, (and measuring water intake with the dry product - because water and food are going in separately we will use this experiment to determine the desirable calorie density for F100) - these experiments are completed. Next we are giving half of the feeds as the experimental product and measuring intake and rates of weight gain, water intake, diarrhoeal incidence etc (not complete - experiments on-going). If the latter is successful, we will test to see if children can be fully rehabilitated on these products alone and then recommend them for general use, under the circumstances for which we have been developing these new product, to all who treat severe malnutrition. We may even find that these products replace much of the F100 now in use in emergency situations - but this will require careful analysis of data from thousands of patients in several centres - and a major reduction in the price of the products vis-a-vis F100 (which should be possible).

When we have got these experiments completed, we would then which to work with the manufacturers to develop the same type of substitute product for F75, which will be much more tricky from a manufacturing, formulation, dosing, testing and practical use point of view - however, we would hope that this type of product would overcome some of the problems of overnight management of the patient to whom we have no access and is in a life-threatening state.

In the mean time I would encourage those who look after these patients to follow the tried and tested established protocols wherever this is possible. And not do be dismayed at getting less-than perfect results (high mortality or low rates of weight gain) when circumstances are such that little else can be expected. We are in the midst of the Sphere Project (setting standards of care in relief settings) - I am particularly worried that setting such standards will lead agencies to fail to act when they know that the circumstances are such that they will get results that do not meet the Sphere Project targets. This is a real danger of the Sphere project and I hope that it will not lead to many more unnecessary deaths than it is trying to prevent - I know of two different NGOs that did not institute programs or help beneficiaries because the circumstances were such that they would get poor results and thus "damage" their professional reputation - and this was before the Sphere project targets, which will be used to "judge" whether a program is good or bad, were distributed. In my opinion to fail to act in such circumstances and allow people to die unaided is totally against any humanitarian charter -with me their reputation could not be lower - and I think that we should all be vigilant to ensure that the Sphere project targets is not used as a reason not to mount a relief operation.

Lactose intolerance is not, in practice, a real problem for those treating severe malnutrition with milk products. We have found though that different commercial milk formulae do seem to be different in their diarrhoeagenic potential! Lower than necessary zinc content or availability is one potent cause of prolonging persistent diarrhoea for example.

Any food which overloads the absorptive mechanism will have the same effect. In small bowel perfusion studies with double lumen tubes the degree of diminution of lactose absorption was of the same degree as of sucrose or glucose malabsorption.

The % of energy coming from Lactose in the different feeds that we use is:

Lactose Sucrose/glucose

Human Breast milk 41% 0

DWM 32% 0

DSM 60.8% 0

F100 16.6% 19.6%

F75 7.0% 52.2%

The figures speak for themselves!

With F75 any diarrhoea is more likely to be due to sucrose/glucose malabsorption rather than lactose: the only way to

As you can see there is 6 times the lactose in human milk than F75 - human milk does not cause diarrhoea in the malnourished child, so if there is a problem then it is due to something else. Adults in Africa do not seem to get diarrhoea with these milk based products due to lactose intolerance - indeed Steve Collins also states that once the adults are over their initial life-threatening phase they can take plenty of milk - our experience with over 1000 severely malnourished Hutu adults in Burundi is similar - they can be fully rehabilitated on milk based diets, after the initial few days, in the same way as a malnourished child without diarrhoea.

With F100 the diarrhoea is almost certainly related to the hyperosmolality of the conventional formulation

Yoghurt has many other attributes that make it desirable in this situation apart from having its lactose converted to lactic acid.

 

Peace and love

Mike


Date: Fri, 18 Sep 1998 19:27:38 +0100

From: sakatamsterdam.msf.org (Saskia VD KAM)

Subject: Ngonut: adult malnutrition continued

 

Dear NGONUTS,

First of all I (and the teams involved) really appreciate all thoughts on treatment of severe malnutrition among adults.

I have just returned from Wau, South Sudan, where MSF has a 24 hour care feeding programme (including milk at night) for severely malnourished adults. Admission criteria are 'unable to stand' and 'BMI<12 plus medical complications'.The facility is a last referral for all other feeding programmes implemented in Wau.

The main constraint for improving the programme is staff management. Of the local staff, most speak Arabic (expats don't) and most cannot read nor write (think about kitchen personnel and feeding assistants, nurse-aids). The level of the medical staff, of whom the better educated speak English, is low. Besides, the motivation of the staff is low; in principle the tribes are each other enemies (patient versus staff).

At this moment I want to bring up 4 issues.

1. RESOMAL.

How harmful is resomal?

During admission and during the treatment of the severely malnourished RESOMAL is given and consumed like limonade. Without any assessment of the state of dehydration, nor assessment of the physical state of the patient RESOMAL is given in full cups of 300 ml. The patients drink it all at once and ask for more.

It is impossible to implement the ideal treatment schedule: we cannot weigh the patients and the feeding personnel cannot read the cards. Besides the patients want more RESOMAL themselves.

I wonder how harmful this practise is. It might be better to put the resomal where it belongs, in the medicine cupboard, and to have regular water hand outs. However, before the introduction of this approach a refreshment training in recognition of signs of dehydration is required.

2. Emaciation versus oedem

The clinical picture of severe malnutritoin in adults changed dramatically in Wau. The emergency started with severely emaciated people; after two months, within a weak time the majority of the cases show oedema in feet, legs and face.

The WFP had been able to provide a full ration for the beginning: 400 g sorghum, 15 g oil and 60 g lentils. The people have hardly access to other food, Wau is a besieged city in the middle of a swamp.

The emaciated population lives now for 1- 2 moths on this diet.

My feeling says that these people are completely depleted in any vitamin or mineral. When food is consumed the body will try to grow, but because of the lack of the healthy nutrients, the growth will be unbalanced: it might be that cell walls etc. are incomplete, thus leaking (oedema) and that the metabolic pathways lack certain co-factors. Consequently it is impossible to produce the right tissues.

Although I know WFP will do everything they can, any intervention takes time. Therefor I expect a smaller or larger epidemic of this oedema. In order to be prepared on a larger case load, I wonder to what extent the oedema is lethal. In other words, can the less severe cases be treated in supplementary feeding centres, provided nutritious meals are being served? Or deserve all cases 24 hours care, with the normal procedure of small quantities of milk, medical care, RESOMAL?

I know my description of the oedema cases is not very precise; we will send some lab materials in and I have asked the doctor to make some thorough case descriptions.

3. Lactose intolerance...

All of the adults have diarrhoea during the treatment. This is a bright green one, the volume is not that much... To my opinion, a re-feeding diarrhoea.

Dinka's are nomads, living from the products of their cattle. They love milk. I don't think these adults have a lactose intolerance.

4. cause of death

The diagnostic capabilities of the medical staff is low. with this information in the back of your mind I would like to hear your opinion: frequently hypoglycaemia is given as a cause of death. This is a well known theoretical cause of death. Therefor if when some symptoms are shown the diagnoses is quickly made. I would like to have your opinion on the possibility of hyper glyceamia.......

Given that we feed 8 times a day also during the night, and alternate the feeds with RESOMAL, i have the feeling that hypoglycaemia, if occurring, should be an exception and not a frequent cause of death.

Bye bye, looking forward to your contributions,

Saskia van der Kam

nutritionist MSF Holland


Date: Tue, 22 Sep 1998 15:15:52 +0100

From: Michael Golden <m.goldenatabdn.ac.uk>

Subject: adult malnutrition -Sudan

 

Dear Saskia,

Sorry if this a long answer!

I am glad that you are using the "unable to stand criterion" , In Carlos's analysis of the 1000 adults from Maramvya, Burundi, this was by far the best prognostic feature. Yvonne Grellety took sitting heights as well as standing heights from Dinka and Nuar adults in South Sudan some time ago and the ratio is about 0.48 - if you "recalculate" their height on the basis of a ratio of 0.51 or 0.52 (which is the ratio in a Caucasian population where the BMI cut-off points were established) you reduce the height by an average of 7cm and increase the BMI by about 2 units. Can I suggest that you extend this database by also taking sitting heights from your subjects - to add to the ones that ACF are collecting. Your criterion then "translates" to a BMI-reference-population cut-off of 14 with medical complications, which is very stringent. I presume that if you extended this you would be overwhelmed -but it would be good to be able to increase your BMI cut-off to 14 as soon as possible.

>1 RESOMAL.

> How harmful is resomal?

> During admission and during the treatment of the severely

> malnourished RESOMAL is given and consumed like limonade. Without any

> assessment of the state of dehydration, nor assessment of the physical

> state of the patient RESOMAL is given in full cups of 300 ml. The

> patients drink it all at once and ask for more.

> It is impossible to implement the ideal treatment schedule: we cannot

> weigh the patients and the feeding personnel cannot read the cards.

> Besides the patients want more RESOMAL themselves.

 

> I wonder how harmful this practise is. It might be better to put the

> resomal where it belongs, in the medicine cupboard, and to have

> regular water hand outs. However, before the introduction of this

> approach a refreshment training in recognition of signs of dehydration

> is required.

This was the sort of problem that we had in Mali and Tchad when temperatures ran up to 47 degrees with very low humidity - the patients were thirsty and were given Resomal (or ORS) to drink - I found a number of patients with hypernatraemia and others that went into heart failure from the very high sodium intake with very high water turnover.

It would be useful to know if any of the patients develop the signs of hypernatraemia - the skin texture changes so that it becomes thickened and malleable like the "dough" used in bread-making (not unlike the skin of someone with hypothyroidism - or with non-pitting oedema)- followed by extreme lethargy and then convulsions. This really only occurs where ambient temperatures are over body temperature and there is a very low humidity - solution is to give water rather than resomal or ors in these conditions except where there is gastrointestinal fluid loss.

The heart failure that occurs in the malnourished can be similar to pneumonia (but they have raised veins in their necks) or, more usually, they deteriorate over a matter of a few minuets to hours to "sudden death", usually unexpected. This is induced by excess sodium intake and is a very common way for malnourished patients to meet their end by well meaning but quite inappropriate intervention.

I strongly suggest that you do give regular water hand-outs and reserve the rehydration solutions for patients with gastrointestinal fluid losses (not sweat losses). I also suggest you also put maximum-minimum thermometers into the feeding centres (very cheep from garden centres) and examine the effect of environmental temperature on mortality..

> 2. Emaciation versus oedema

> The clinical picture of severe malnutritoin in adults changed

> dramatically in Wau. The emergency started with severely emaciated

> people; after two months, within a week time the majority of the cases

> show oedema in feet, legs and face.

> The WFP had been able to provide a full ration for the beginning:

> 400 g sorghum, 15 g oil and 60 g lentils. The people have hardly

> access to other food, Wau is a besieged city in the middle of a swamp.

> The emaciated population lives now for 1- 2 moths on this diet.

> My feeling says that these people are completely depleted in any

> vitamin or mineral. When food is consumed the body will try to grow,

> but because of the lack of the healthy nutrients, the growth will be

> unbalanced: it might be that cell walls etc. are incomplete, thus

> leaking (oedema) and that the metabolic pathways lack certain

> co-factors. Consequently it is impossible to produce the right

> tissues.

Experience has shown that when the general distribution of cereal, oil, pulse is introduced to a population the type of severe malnutrition changes from marasmus to kwashiorkor even where kwashiorkor was almost unheard of in the population before. This is the latest example of this phenomenon.

The diet is very low in a number of important antioxidants, vitamins and minerals. What is of great concern is that the population as a whole will have compromised function and loose resistance to infection - the patients presenting are just the tip of the distribution.

If oedema itself is like an on-off switch (having kwashiorkor), the degree of oedema that a patient has is related more to their previous sodium intake than to their having the pathology of kwashiorkor. Thus, you can easily have a very severely ill kwashiorkor patient with a little oedema because they have had a low sodium intake and a less severely ill kwashiorkor patient with gross oedema just because they have had lots of sodium (or ORS) before they present. There is not really a good relationship between the degree of oedema and the severity of the illness.

(the excess deaths in severe oedema is probably due to the problem of mobilizing the sodium from the interstitium and the inside of the cell, to the vascular compartment and then to the bladder without getting heart failure during the process - the kidney's ability to excrete the sodium seems to recover more slowly than the other electrolyte movements). So those with mild oedema may or may not respond well to treatment.

I would try to treat walking cases with mild oedema (and BMI >14) in Supplemental Feeding Programs provided that they retain their appetites - that is the critical symptom to differentiate those that must have 24h care and those that can be managed with other feeding programs - but the quality of the food that is given is given in the SFC is then much more critical than for some programs.

For these patients I would definitely have a wet feeding program and not a dry program. The CSB/UNIMIX etc should be supplemented in the pot with a mineral-vitamin mix (such as that recommended for F100) and also with DSM (there is no phosphorus in the mineral-vitamin mix as it is supposed to come from the milk powder) - and at least 35% of energy from lipid. For overnight feeding I presume that you will send them home with some form of biscuit. The most important thing is to collect data, monitor and evaluate the program to see if it needs to be changed. It is not possible to predict at this stage if the mild oedema will or will not respond well to such a program.

Biochemical and physiological measurements show that these patients remain abnormal for at least 14 days after they start to loose their oedema - even if their oedema disappears. Please do not discharge previously oedematous patients earlier than this.

They will probably not recover well on CSB or unimix alone which have insufficient potassium, magnesium or available phosphorus (phosphate is mostly present as phytate). Unimix (depending upon its source and composition) contains additional zinc and vitamin C, but not in the amounts needed for treatment of the severely malnourished - it also contains iron which should not be given during the early phases unless unavoidable.

> 3. Lactose intolerance...

> All of the adults have diarrhoea during the treatment. This is a

> bright green one, the volume is not that much... To my opinion, a

> re-feeding diarrhoea.

> Dinka's are nomads, living from the products of their cattle. They

> love milk. I don't think these adults have a lactose intolerance.

This is not lactose intolerant diarrhoea. The green stool is classical of severe malnutrition - especially oedematous malnutrition - the green stool is often accompanied by some clear mucus and does not have a bad - or even typical faecal - smell. In the early stages the patients will pass orange stool which will turn green on exposure to the atmosphere (it normally takes about 30 mins and the green color starts from the surface). This is due to oxidation of the bile pigment in the faeces. Such stools clearly have very little antioxidant capacity. As the patients become more malnourished the oxidation starts to occur inside their intestine and the stool is passed as a bright green stool - so called "starvation stool". It is a sign of major antioxidant deficiency and these patients need to have a diet rich in antioxidants with additional lipid. The chemistry of these changes has not been investigated -but I'm sure that this would give us insight into how best to treat the patients.

Electrolyte analysis of these stool show that they are high in potassium and low in sodium - they also have a relatively low volume - this is NOT dehydrating diarrhoea and should NOT be treated with rehydration solutions - the management is to continue to give supra-maintenance amounts of the diets designed for severe malnutrition.

> 4. cause of death

> The diagnostic capabilities of the medical staff is low. with this

> information in the back of your mind I would like to hear your

> opinion: frequently hypoglycaemia is given as a cause of death. This

> is a well known theoretical cause of death. Therefor if when some

> symptoms are shown the diagnoses is quickly made. I would like to have

> your opinion on the possibility of hyper glyceamia.......

Hypoglycaemia is common. It is not easy to diagnose clinically as malnourished patients do not show the signs that well nourished patients show (sweating, hair erection, pallor etc) - one sign that I've found useful is that these patients often sleep with their eyes slightly open (this is because the innervation of the muscle that raises the eyelid - levator palpebrae superioris - gets its nerve supply both from the voluntary nerves and from the sympathetic system so that when the sympathetic system is stimulated the eyes take on a staring appearance when open and do not fully close during sleep) - if this sign is seen it is usually due to hypoglycaemia or toxic shock, but may be seen in simple dehydration as well. If a patient is sleeping without the eyelids close together, immediately give them treatment for hypoglycaemia.

> Given that we feed 8 times a day also during the night, and alternate

> the feeds with RESOMAL, i have the feeling that hypoglycaemia, if

> occurring, should be an exception and not a frequent cause of death.

Hypoglycaemia is also usually accompanied by hypothermia in these patients - what is the body temperature of the patients who are being diagnosed as hypoglycaemic?

Hypoglycaemia frequently occurs in patients with severe infections and is very uncommon in those without septicaemia/endotoxaemia - please make sure that all these patients have blind treatment with broad-spectrum antibiotics - this is as critical in the prevention of hypoglycaemia as giving regular feeds.

It is very difficult without actually having an experienced clinician examine the patients and witness the deaths to know if they really are due to hypoglycaemia - from what you say, I would doubt if this is the root cause of the problem. I am sure that you should not be alternating the feeds with resomal - and definitely not if there is any oedema - the deaths could easily be due to heart failure.

If there is a danger of the staff omitting some of the feeds at night, it is a good idea to have some complex carbohydrate in the diets - the prevention of hypoglycaemia by a meal containing simple sugars will last reasonably for 3-4 hours, in most patients, complex carbohydrate (starch) seems to give protection for longer - probably because of the longer time to digest and absorb or due to the lower insulin release with less danger of "rebound" (malnourished patients have low insulin response at any rate - but also very low glucagon or adrenalin responses). Perhaps you could give a biscuit at night.

I hope that this helps a little.

 

Mike


From: "steve collins" <steveatconcern1.demon.co.uk>

Subject: Ngonut: adult malnutrition -Sudan

Date: Sat, 10 Oct 1998 17:13:58 +0100

 

Hullo Saskia and Mike,

Here's a few thoughs on the starving adults and adolescents in S. Sudan, based on a short visit to Agip and comng from a slghtly different perspective:

Oedema and dysentery

In agip (10k from Wau but SPLA held) there was also a problem of adults becoming oedematous when treated. In one programme this was happening to some of the adults being given a high proportion of BP5, especialy those with SD1 dysentery. When the BP5 was stopped the proportion of patients who started to swell on therapy alos decreased, leading me to think that the 12% of protein in the BP5 might be a contributory factor. I think it is essential that such patients are given the full therapeutic diet, including the use of F75 and resomal. There was an impression that because of the dysentery these patients were being somewhat "medicalised" and treated for dysentery with malnutrition as a complication rather than malnutrition with dysentery as a compication. In my experianced this is an important distinction. For example in Somalia dysentery was NOT a significant poor prognostic factor in those admitted with severe malnutrition, whwreas the type of diet given definitely was. So I urge that the treatment of dysentry should not over-shadow the treatment of malnutriton (you know what doctors are like!) Early case finding and community rehydration are vital (see below)

Therapeutic Vs supplementary

In Agip there were great problems of access doing a wet supplementary ration ecause of the large distances, swamp and requirement for dailiy attendance.

People were spread out and there was a whole heap of swamp to wade through.

What was happening was that they were gong until they became ill and them they stopped...very unsatisfactory. I therefore think that to expand the proper therapeutic programme somewhat, using social / access criteria in addition to nutrition / clinical and to provide a very good / large weekly dry supplementary ration to the others is the way to go there. The social / accces criteria should include how many minuits it took the patient to walk to the centre, do they have relatives around or do they have a ghol leader/ sub chief arond. If the answers are that t took a long time or they have no support, the clinical / nutritional criteria should be expanded. For adults admissions into the TFC in Agip Concern will basicially use MUAC <16 0r 17 , MUAC <18.5 plus either dysentery, dehydration, in ability to stand and anorexia (I don't know how well that ne wil work in practice) plus a gd eyeball from a very experience worker. (NB I feel that in such circumstances an experience worker manageing the centre is very imprtant as the adult criteria and treatment protocols are still too young to be fool proof) The social criteria will be added to these and if there is a long way to come or no support the the MUAC cut-offs / clinical thresholds will be expanded .

Suplementary will be based upn an MUAC < 18.5 but relatively well.

Dehydration and presentation

Initial dehydration appears to be the major problem (rather than maintaining hydration once admitted). The dehydratio appeared to be not so much from crashing diarhoea but from late presentation. I therefore think that early case finding is particularlly important in the dinka poulation (in Agip it appeared that displaced people with no family contacts i the village would not be assisted to find treatment) Concern and MSF are therefore trying to improve early case finding and referral. I the dinka yo might find that singers are particularly appropriat as conduits for health information and mobilising people. Each paprmount chief has a singer, something lke the town crier that we used to have here. Well it seems as though it willbe pssible to harness these people with such catchy little numbers as "if yo have a diarrhoea stool go and drink loads of ors la di da di da". To complement this community ORS posts are important. Concern easily found many TBAs who were willing to manage such posts. These hopefully will become a focus for case finding and information dissemination. I wold also envisage the facilitation of groups (womens groups etc by paying the group to make mats etc or whatever the programme needs.....this isn't sustainable in the long run of course but that's not really the issue, it is a way to rapidly organise displaced people and gain some degree of access to them (I looked at this i Tanzania and the effect of such groups on health knowledge was very impressive.

Re experienced workers

I saw what you mean. Have yo tried to hire some of the middle level supervisors i Khartoum and moe them down. Although more expensive you might find a limited number in key roles e.g. feeding worker/ors supervisor might pay dividends. Cncern have managed to do this on the other side by hiring some key workers from an SPLA refugee camp..just a thought

Hope this is of some interest

cheers

 

steve

p.s. I'm afraid that I'm off again for a bit so I won't be able to reply to anything


From: David.BrewsteratCASRDH.HEALTH.nt.gov.au

Date: Thu, 15 Oct 1998 14:09:47 +0930

Subject: Ngonut: Dietary Treatment of Severe Malnutrition in Adults

 

The Am. J. Clin. Nutr. paper by Collins, Myatt and Golden has just

arrived here, and I realise that there has been some discussion

already on the network.

On page 96 column 2, the authors discuss the watery diarrhoea

associated with increased appetite on the low protein diet, leading to

rapid hypovolaemia. They also mention the need to dilute milk feeds up

to 1:9. Surely this is OSMOTIC diarrhoea due to lactose intolerance in

patients with tropical enteropathy and severe malnutrition. It is

certainly not consistent with starvation diarrhoea, as suggested by

citing Roediger's paper.

This hypothesis (osmotic diarrhoea) is dismissed on page 197 column 2

because of "the lower incidence of diarrhoea among patients receiving

the high protein diet" The high protein diet would have meant

ingesting 137g/day of lactose vs 95g/day for the low protein diet, but

that is misleading since those on the high protein diet were anorexic

and may not have even ingested enough of the diet to overcome the

lactase threshold. We know from Buford Nichols work that lactase is

likely to be limiting for enteropathy and malnutrition, particularly

in oedematous malnutrition. It would be simple to confirm osmotic

diarrhoea by measuring stool pH and reducing substances (Clinitest)

even in Baidoa.

Our work in Malawi on kwashiorkor and unpublished work in Australian

Aboriginal children convinces me that the gut mucosal insult (as

measured by sugar permeability testing) of poor hygienic circumstances

and malnutrition make patients very susceptible to osmotic diarrhoea.

When we compared milk and maize in kwashiorkor (Arch.Dis.Child

1997;76:242-8), we were surprised to find that our initial low lactose

intake of 1.7g/kg/day on standard phase 1 milk was still associated

with significantly more diarrhoea (34.8% vs 24.3% of hospital days)

than the lactose-free maize diet. Yet after about a week of the

initial low protein diet with clinical improvement, there was no

increase in diarrhoea on the high energy milk diet with an intake of

8.7g/kg/day of lactose. Thus, the lactase threshold must increase

rapidly during the recovery phase of kwashiorkor, as does intestinal

permeability.

I would be interested in the authors (and others) comments on the

importance of osmotic diarrhoea with milk diets in the context of

nutritional rehabilitation.

Sincerely

 

David Brewster

Northern Territory Clinical School

Darwin, Australia


Date: Thu, 15 Oct 1998 09:49:07 +0100

From: sakatamsterdam.msf.org (Saskia VD KAM)

Subject: Re: Ngonut: adult malnutrition -Sudan

 

Hello Steve and other colleagues,

Although Ajiep and Wau are near (about 20 km) the situations are very

different.

Wau, a real town (ruled by Khartoum) surrounded by swamp, relatively

well of with full rations, organised distribution and plenty of NGO's.

Ajiep, in the middle of a swamp (SPLA), relatively poor general

rations and limited NGO support.

The increasing cases of oedema in adults were in a situation of 2

months of a full ration. It is possible that those adults received BP5

meals in one of the feeding programmes of other NGO's. Something to

check maybe.

The feared epidemic of oedema has not developed. still we face high

mortality in the adult malnutritoin ward (about 25%) Keep in mind that

out facility is a last referral possibility in the line. Treatment

schedule is indeed according the best we know for now: F100 F75,

RESOMAL, ORS, water, frequent feeds, starch, virtually all on

antibiotics etc..

Our doctors want to describe several patients in detail, marasmic and

oedematous adults. Have you realistic suggestions what should

definitely in this case descriptions?

I thin kit would be useful if projects in Burundi dealing with adults

with kwashiorkor do the same. Although I have not seen these adults, I

have the feeling they have a different clinical presentation.

I fully agree with Steve that in the management, but also in the

assessment clinical criteria and insight is very important.

An unrelated additional remark:

When admission is based on MUAC, children as well as adults, keep i

mind that the increase of MUAC lags behind the increase in body

weight.

Now the situation improves in Wau we find children with a reasonable

WFH but still very low MUAC.

Well, keep you all informed (if you like),

 

Saskia van der Kam MSF - Holland


From: Barbara Elaine Golden <chl037atabdn.ac.uk>

Date: Fri, 16 Oct 1998 10:46:19 +0100

Subject: dietary treatment of severe malnutrition in adults

 

Re the AJCN paper David Brewster referred to, thank you for these interesting comments!

In response, Roediger's paper probably wasn't the best to quote as it's about 'starvation' rather than 'refeeding' diarrhoea and Steve's adults were clearly having diarrhoea related to refeeding.

In retrospect, measuring stool pH & reducing substances would have been very worthwhile. In Baidoa in 92/93, Steve had more pressing duties!

But had the patients osmotic diarrhoea? After much discussion, our conclusion was, PROBABLY not! It poured out of them but didn't 'burn their bottoms'. The adults consuming diluted LP diet probably did receive more lactose per day but as a higher flow rate of feed of lower lactose concentration. The adults offered HP diet consumed it to begin with but then refused it. Wouldn't one have expected them to have experienced osmotic diarrhoea at the start at least, when the flow rate of feed was relatively high and the lactose concentration was much higher than in the LP diet: one might have expected such diarrhoea to have started and then stopped when the feed intake fell.

Finally, in Jamaica, lactase deficiency didn't pose a problem when the lactose concentration was low to start with. And we would agree that any problem with lactase deficiency resolved VERY rapidly.

I think more research is needed 'in the field' to resolve Steve's refeeding diarrhoea problem but perhaps others can shed more light?

Barbara G

 

Barbara E Golden BSc MD FRCPI MRCPCH DCH Dept Child Health, University of Aberdeen, Medical School, Foresterhill, Aberdeen AB25 2ZD Phone 01224 681818 ext 53894 Fax 01224 663658 b.e.goldenatabdn.ac.uk


Date: Fri, 30 Oct 1998 11:27:31 +0100 (CET)

From: briendatext.jussieu.fr (Andre' BRIEND)

Subject: Adult malnutrition : proteins vs Na

 

Dear all,

I had another look at Steve's paper, and have a query re: the interpretation of the data.

Steve makes the point that a decrease in mortality was obtained by changing the diet and lowering the protein intake. I have no doubt on his data and on the reduction of mortality he obtained by changing the diet. I consider his paper as a major contribution to reducing mortality in adult patients, and has a lot of admiration on quality of the work and its potential health impact.

I have queries though the interpretation of the data. No doubt it may be valid. It relies, however, on the asumption that patient took all the diet they were offered, or rather, that patients took equal amounts of all foods being offered.

Is this likely ? I don't know. I would suspect that critically ill patients may prefer (or rather be given preferentially) liquid food. And here is the trouble. What happens if patients took only liquid milk looking food ? I tried to figure out the Na intake of a patient taking 6000 Kj (or roughly 1500 kcal) of 'recovery milk' and of dsm oil and sugar of the 'new diet'.

The Na intake would be as follows :

Recovery milk: (42 / 4276) * 6000 = 59 mmole Na

DSM, oil + sugar: ((44/(2646+5733+2688))*6000 = 24 mmoles Na

Obviously, patients taking only milk looking food would have a much lower Na intake with the new diet. This could also be an explanation for the more rapid loss of odema on the new diet... and lower mortality only in patients with oedema... and no effect in other patients. High Na intakes in patients with oedema are known to lead to heart failure.

What about other foods ? Were the beans given with a pinch of salt ? What about unimix ? From the table, Na is said to be very low, but I don't know if the 1 Na from beans and 0 Na from UNIMIX come from food composition tables, or that strict guidelines were given not to give any salt to these patients. In absence of very strict guidelines and checks +++ to the staff and attendants (I know how difficult this may be) it may be tried to give a pinch of salt in case of anorexia. If even small amounts of salt were added to some foods, this would make the case for Na even stronger. Beans and UNIMIX are not in diet 2. Rice is often eaten with salt, but is present in the same amount in the 2 diets. Bananas are in diet 2 only and are high K but have no Na and are not eaten with salt.

I discussed Steve's paper with colleagues refeeding adult patients here in Paris following all sorts of medical / surgical complications. They are very strict on low Na intake, especially in case of odema, but don't consider very low protein intake as essential part of the treatment, even in case of minor liver dysfunction.

Any comment ?

Regards,

 

Dr. Andre' Briend


Date: 30 Oct 98 15:15 EST

From: " Barbara Elaine Golden" <chl037atabdn.ac.uk>

Subject: Re: Ngonut: Adult malnutrition : protein

 

In response to Andre''s comments on Steve Collins' paper ...

I think Steve's still abroad but I hope he'll reply himself as only he knows the 'mix' that most of his subjects consumed.

Andre''s point, that those ill patients with very poor appetites may only have consumed the liquid part of the diet offered, is important and valuable comment. It would apply particularly to the 'high protein' (HP) group but :

1. If the HP gp took everything except their biscuits, their Na intake (24mmol/6000kJ) would be similar to that of the 'low protein' (LP) group, whether the LP gp took only their milk (24mmol/6000kJ)or they took the whole diet (16mmol/6000kJ). So ... the mix is very important!

2. If the groups only took their 'milk' as Andre''s assumed for his calculations, then the protein intakes would also be very disparate - HP 77g/6000kJ; LP 35g/6000kJ.

Thus, whether it's protein or sodium that's more important remains unknown. However, sodium really only becomes a contender if the HP group only take their milk.

I do not think that what they advocate in Paris for very ill hospital patients is relevant to Steve's severely malnourished patients although I think nobody would dispute that sodium intake is important in the management of oedematous patients. Salt being added to recovery diets is of course very important.

I reiterate, I hope you're out there, Steve, with your computer, and able to answer these useful questions??

Barbara Golden (co-author)

 

Barbara E Golden BSc MD FRCPI MRCPCH DCH Dept Child Health, University of Aberdeen Medical School, Foresterhill, Aberdeen AB25 2ZD Phone: (44) 01224 681818 ext 53894

Fax: (44) 01224 663658

b.e.goldenatabdn.ac.uk


From: Steve Collins

Re: Adult malnutrition : proteins vs Na

18.12.98

 

Hullo Andre,

Sorry about the delay in replying but I was having a little trouble with

Hurricane Mitch!

I appreciate your observations re NA and protein and agree with a lot of

yours and Barbara's observations. The bottom line is that, unfortunately,

the study is insufficiently rigorous to definitively say it's protein or Na

which are the most important causes of the dramatic decreases in mortality

seen. However that said, I feel that on balance the evidence points

strongly to the protein content as being the most relevant factor. During

the initial two weeks after we introduced the LP diet in December 92, the

high incidence of refeeding diarrhoea made us dilute ALL the LP milk with

standard WHO ORS. As I mention in the article this standard dilution was

down to 1/3 strength during that time, as I was having such a difficult

time maintaining hydration in patients with severe diarrhoea (during those

first few weeks of the LP diet all of the other Concern expatriate staff

were evacuated due to the horrific fighting that broke out when the armed

gangs were given a one week warning of the imminent American operation

restore hope. This meant that supervision was insufficient to make sure

that all those with diarrhoea drank enough ORS). Given that basic

dilution, which seemed to control the diarrhoea in most patients, I also

found the concept of further diluting the LP milk at the time of delivery,

titrated against how much diarrhoea the patient reported, easy to teach to

the staff. This resulted in a few oedematous patients with severe

diarrhoea getting little more than milky ORS for the first few days (once

down to 1: 9th strength) containing frightenly large amounts of sodium).

This dilution with standard WHO ORS (same I didn't know about the ReSoMal

then) radically increased the Na intake in these patients, in your example

of 1500 Kcal of lower protein milk this would, in the early stages of

treatment have meant that over 1.5 litres of standard (90 mmol Na/litre)

ORS had been added, representing a quantity of sodium far in excess of that

in the HP diet(probably in reality most would not have taken this quantity

of calories from the milk during the early phases). Of course the HP diet

group also received 1/2 diluted milk for the first 3 days, but diarrhoea in

these patients was always much less (in fact constipation was probably more

of a problem) and the length of time patients received diluted milk never

needed to be more than the 3 days we had in the protocol. In addition none

of the HP subjects required the large quantities of oral ORS given to the

LP patient group. The increase in appetite with the LP diet was almost

immediate and a marked improvements in the clinical condition of most

oedematous patients occurred within days, whilst all were receiving 1/3

diluted milk and therefore high Na. This included may cases where oedema,

that had been present for months with the HP diet, disappeared once the

diluted LP was started. Given this it seems unlikely that Na is a central

feature. Indeed it is rather surprising that these patients lost their

oedema quite so quickly given the large amounts of Na they wee getting in

the ORS, I supposed that they were also loosing a lot of Na with the watery

diarrhoea. Maybe the difference is that the hospital patients that your

colleagues are treating have more cardiac orientated oedema rather than

true nutritional oedema ? I would be keen to communicate with your

hospital colleagues refeeding malnourished adults, so if you have a contact

e-mail I'd be grateful.

Thanks for the interesting comments

cheers

 

steve