TB patients : nutrition recommendation
Nutrition recommendations for TB patients Francesco Branca 15.08.97
Re: Nutrition recommendations for TB patients Saskia van der Kam 15.08.97
Re: Nutrition recommendations for TB patients David Brewster 17.08.97
Nutrition of TB patents Michael H.N. Golden 18.08.97
diagnosis of TB in the malnourished Michael H.N. Golden 19.08.97
Re: Nutrition of TB patents Saskia van der Kam 19.08.97
The Diagnosis of TB in the Malnourished David Brewster 22.08.97
no title steve collins 30.08.97
RE: The Diagnosis of TB in the Malnourished in particular ascites in severe malnutrition steve collins 30.08.97
Tb and malnutrition Patrick Kolsteren 03.09.97
Diagnosis of TB in the malnourished Francis Varaine 03.09.97


Fri, 15 Aug 1997 08:10:44 +0100 (BST)

From: Francesco Branca, F.Brancaatagora.stm.it

Subject: Nutrition recommendations for TB patients

 

Dear colleagues,

 

can anybody advise on the energy and protein requirements of TB patients? Are TB patients currently admitted to suplementary feeding? Thank you.

Francesco Branca


Date: Fri, 15 Aug 1997 17:01:30 +0100

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

Subject: Re: Nutrition recommendations for TB patients

 

Dear Francesco,

MSF has quite some experience with running TB programmes. We noticed that once a TB patient gets treatment (for TB) the patient grows fast provided there is enough food.

In general our policy is to treat TB patients similarly as others, in terms of feeding programmes: If the TB patient meets the 'normal' malnutrition criteria they are enrolled in the nutrition programmes. On the other hand if a TB patient has a nutritional good state we don't enrol the TB patient. In practice the non-malnourished TB patient gets some food or milk for a period of time in order to soften the burden to swallow nasty pills, and to improve compliance.

In the feeding centres we try to separate the TB patients from the other malnourished in fear for cross-infection. (TB wards) Nutritionally spoken they get the same diet as the others: rich in vitamins and minerals, and enough energy and proteins etc.. The diets for malnourished are anyway trying to cover the needs of people with infections like the vitamin C and vitamin A content. (Therapeutic milk, enriched porridges, supplementation with oral vitamin C dose)

The TB patient grows rather fast on these diets, so we don't see reason for a change.

However we keep our eyes and ears open for further suggestion for improvement.

with kindest regards,

 

Saskia van der Kam

MSF-Holland, Amsterdam, Saskia_vd_Kamatamsterdam.msf.org


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

Sun Aug 17 23:22 BST 1997

Subject: Re: Nutrition recommendations for TB patients

 

The question is a bit ambiguous in that it is unclear whether it is a practical or basic science quesion, referring to a milk or cereal-based diets and whether you are referring to children or adults. I will take it as a practical paediatric question.

The presence of infection clearly increases energy and protein requirements in nutritional rehabilitation, but this is anticipated in the use of high energy milk in standard regimes for rapid catch up growth. Once commenced on treatment, TB patients demonstrate rapid catch up on this diet (see Waterlow's 1992 text, chapter 12). Once discharged, they usually do not need further nutritional intervention unless there are also primary nutritional risk factors.

The real problem is: 1) the accuracy of the diagnosis and 2) HIV infection. Many cases of malnutrition in children are diagnosed as TB on flimsy evidence. This is a complex question beyond the scope of this discussion, but TB diagnosis (disease, not only infection or primary

TB) in children is difficult and controversial, but nutritional status alone is a poor indicator of TB in poor countries. In most TB cases there should be a known sputum-positive adult contact in the household. There is no doubt if the child is wasted, he/she would benefit from supplementary feeding of a preferably milk-based diet in hospital, but a targetted community-based program after discharge should be unnecessary in most cases, particularly for older children.

Children under about 18 months with AIDS (usually wasted, stunted and microcephalic) do not usually benefit from nutritional rehabilitation. In poor countries with a high prevalence of HIV infection, there seems little point of keeping them on nutritional rehabilitation if they are not gaining weight.

These comments may have raised more questions than they answered.

 

David Brewster,Associate Professor of Paediatrics

Darwin, Australia


Mon, 18 Aug 1997 17:50:10 +0100 (BST)

Subject: Nutrition of TB patents

From: "Michael H.N. Golden" <m.goldenatabdn.ac.uk>

 

Francesco, asks what are the nutritional requirements for TB patients. I agree with Saskia and David, that once on treatment they do very well and should not be treated differently from patients that are malnourished with other infections.

Whether there are different actual requirements for normal maintainance and growth, is a different question and I do not think we have the answer. The RDAs are set to cover most members of "a normal population", there are no RDAs for any "abnormal" population.

I am concerned by the remark that Saskia makes "In the feeding centres we try to separate the TB patients from the other malnourished in fear for cross-infection (TB wards)". Such was also the policy of ACF when I visited their TFCs. There were children shut up in isolation without any stimulation and unable to play normally: this policy then stigmatised them as needing "isolation" to the group and made the family aware that there was something very particular wrong with their child. Isolation itself was a major cause of failure to respond to treatment and of distress. First, young children do not expectorate sputum and are not a source of infection with TB; second, their mothers (who cannot be isolated effectively) are a much greater threat; third, once effective treatment has started all TB patients quickly cease to be a hazard; forth, the exposure to TB is much more likely to come from an as-yet undiagnosed source which are fairly ubiquitous in some societies. I do not think there is any good reason for having an isolation ward for TB in a TFC and there are a number of very cogent reasons for not isolating children with TB.

Incidentally, in Mogadishu, where TB prevalence is extremely high, one TB program controller refused to treat children with TB because they did not pose a "public health risk". In contrast, one good thing about the failure of children to be infective is that the arguement that "we will not start a course of treatment if we cannot be certain to complete it" - which is commonly applied to itinerants, refugees and displaced persons "because of the danger of induction of resistance" - is a false arguement. If they are not infective then any organism that develops resistance in them will not be passed on and is of no public health consequences: Children and adults are very different from the public health point of view.

To comment on David's response. HIV diagnosis confirmation is even less commonly available than TB diagnositics. To intimate that children that are failing to thrive/ not responding to treatment "because they have HIV" should not be treated is a recipe for abandoning all failures with an assumed diagnosis that will very frequently not be correct. I think that this is wrong. Certainly, in Jamaica, we did not measure HIV status until discharge - we were frequently surprised to find that a child that recovered beautifully was HIV positive.

If the diagnosis is know to the staff indeed the chidren do not do well - after this experience I think that this is more often because of the effort at treatment rather than anything intrinsic to the majority of HIV positive patients. It would be very useful to have this very limited Jamaican experience repeated in another setting.

Best wishes,

 

Prof. Michael H.N.Golden


Subject: diagnosis of TB in the malnourished

Date: Tue, 19 Aug 1997 11:58:16 +0100 (BST)

From: "Michael H.N. Golden" <m.goldenatabdn.ac.uk>

 

David raised the question fo the difficulty of diagnosing TB, particularly in children, and the differentiation of TB and HIV (or both). In most of the settings where NGOs work there is not even the poswsibility to test parent's sputum, let alone do X-ray examinations. Mantoux is sometimes possible on the other hand.

To address this problem I, with Yvonne and Pascal Grellety, drafted a paper, which is still being refined for submission. However, as it is very pertinent to the vexed question of making the diagnosis of TB in settings where the normal backup is absent, and putting it out on this list does not constitute prior publication - I append the confidential draft for comment and discussion within the list membership.

------------------------------------------------------------------------------ CONFIDENTIAL DRAFT.

The diagnosis of tuberculosis in the malnourished.

By Michael H.N. Golden

Pascal Grellety

Yvonne Grellety

 

The diagnosis of tuberculosis is difficult under ideal circumstances. It is more difficult in parts of many developing countries, were adequate microbiological and radiographic facilities may not exist within the geographic or financial reach of the sick.

The diagnosis of tuberculosis presents a particular problem in two groups of patients. First, the preschool child, because the signs of tuberculosis are often non-specific in this age group (anorexia, failure-to-thrive, etc), sputum is difficult or impossible to obtain and gastric washings are not useful, they more often present with the severe forms of tuberculosis (miliary, meningitis, spinal osteomyelitis) and the disease is more rapidly progressive with less time for diagnostic confirmation. Second, the malnourished patient. These patients have both nutritionally acquired immunodeficiency and lack a normal inflammatory response (ref to reviews). Many of the diagnostic features of any infection, including tuberculosis, are thus absent. Indeed, in some circumstances tuberculosis may only become florid during treatment of malnutrition when the host responses recover (ref Murray et al). Indeed, tuberculosis is clinically different in severely and in moderately malnourished adults (Liddle? Lancet 1947).

In the child who is also malnourished a definitive diagnosis is only made in a small proportion of patients. Perhaps the most testing diagnostic situation arises with malnourished children in a refugee camp, urban slum or isolated rural village; as tuberculosis is particularly associated with poverty and overcrowding, as is HIV infection, it is in these settings that the current epidemic of tuberculosis is explosive.

Commonly, children present with malnutrition or failure-to-thrive. The diagnosis is suspected when the patient does not respond promptly to treatment of malnutrition. Where there are facilities a Mantoux test and chest X-ray are then done and attempts made to obtain suitable specimens; where these tests are not available or helpful a "therapeutic trial" of antitubercule treatment is initiated. However, such a "therapeutic trial" is structured to be identical to, and not conceptually differentiated from "blind treatment" without provision for halting treatment, except when patient initiated (non-compliance).

Thus, in guidelines for the treatment of malnutrition a typical regimen is to start with four days administration of a first line antibiotics (eg amoxicillin or penicillin & gentamicin); if the child does not improve a further four days treatment of a second antibiotic is added (eg Chloramphenicol); if there is still no improvement a presumptive diagnosis of Tuberculosis is made and a 6 month "therapeutic trial" is started following WHO or national guidelines - usually 2 months INH, rifampicin and pyrazinamide and then 4 months INH and rifampicin. In other settings failure-to-respond may be routeinly and blindly ascribed to other illnesses such as rickets or HIV.

There are major problems with the current approach. First, there are many causes of failure to respond to treatment in a malnourished patient apart from tuberculosis (ref WHO manual of PEM) making this approach highly non-specific, and presumably subjecting many patients to unnecessary treatment risks and a very high level of non-compliance. The commonest cause of failure to respond is probably giving the patient insufficient or inappropriate food. In most centres outmoded methods of management are used for malnutrition and common deficiencies such as potassium, magnesium, zinc, copper, selenium, and the vitamins A,D,E, etc are not corrected (Ashworth). Surely, a prerequisite for saying that a child has not responded to treatment of malnutrition, and therefor has tuberculosis, is to give the correct treatment for the malnutrition.

Second, even with modern treatment at least 10% of the most severely malnourished children take about 8 to 14 days to correct their metabolic defects, loose oedema and regain their appetites in the absence of tuberculosis (subsequent excellent recovery); as this time course corresponds with the recommended commencement of a trial of anti-tuberculosis treatment an apparent response with contain a lot of false positives.

Third, infections, particularly with atypical organisms, are ubiquitous in severe malnutrition and all the children have bacterial overgrowth in their small intestines: rifampicin is an excellent broad spectrum antibiotic that is effective against many infections apart from tuberculosis, such a response will lead to a false positive trial.

Fourth, INH has a non-specific appetite stimulant effect that can give rise to a improvement particularly in patients that have psychosocial deprivation.

Fifth, after starting the trial of anti-tuberculosis treatment the time course of the expected response is sufficiently long for the patient to be discharged from the malnutrition facility "to follow treatment" without adequate arrangements for monitoring the progress of the patient.

This leads to "tuberculosis" being used as a diagnostic category by which all failures are disposed, and may give a grossly inaccurate impression of the quality of treatment of malnutrition and of the prevalence of tuberculosis.

There are no data on the proportion of severely malnourished patients that have a definitive or presumptive diagnosis of TB made and how they respond to antitubercle treatment or estimates of the sensitivity and specificity of the strategies used to make the diagnosis in this group of patients.

Sixth, if the patient has tuberculosis then it would have been much better to have started treatment eight days before. During this delay the disease can progress significantly.

The problem of diagnosis of tuberculosis in the absence of diagnostic facilities will not easily be overcome and the malnourished child will remain the major challenge to researchers in this field, however, it is unclear whether a presumptive diagnosis based solely upon a response or non-response to tuberculosis treatment after 8 days is a reasonable basis for initiation of treatment.

It is our observation that the clinical skills required to examine a child for signs of tuberculosis are frequently deficient in those working in environments where there are no other methods of making the diagnosis. Such clinical acumen is also becoming atrophic in staff with ready access to modern laboratory and radiographic departments and the teaching of bedside skills is disappearing as the older clinicians who relied mainly upon these skills retire.

We contend 1) that the diagnosis of tuberculosis should be based first and foremost upon a detailed and skilled clinical examination rather than on failure to respond to treatment of the associated malnutrition; 2) that there are a series of clinical signs that should be sought in all malnourished patients and, if present, should lead to a clinical diagnosis of tuberculosis and immediate commencement of treatment; 3) that training material should be prepared to teach the clinical skills necessary to elucidate these signs. That failure-to-respond should be a signal to carefully retake the history, reexamine the patient and re-evaluate the whole of the patient's management rather than to automatically assume that the cause is tuberculosis, initiate treatment and discharge the patient.

We present in the table a list of clinical features that we suggest should be specifically looked for and, if found, should lead to a clinical diagnosis of tuberculosis and immediate initiation of treatment.

(Important differential diagnoses in parentheses)

(Not in any order as yet)

The Mantoux test is often negative in the malnourished patient with tuberculosis (particularly common in patients with coincidental vitamin D deficiency) - a negative test should not be taken as proof that TB is absent particularly where there are any signs of rickets; however, it is good evidence that the patient does not have TB if other features of the patient show that he has an intact immune/inflammatory response - such features would include pus collection in skin abrasions, abscess formation, intense irritation from scabies infection, fever etc.

A Mantoux test is the most reliable test for tuberculosis available in most settings and should always be performed in those with suspected TB, and repeated during nutritional treatment if initially negative. If the Mantoux is repeatedly negative then an alternative explanation for failure to thrive/ non-response to treatment should be diligently sought before a trial of anti-tubercular treatment is instituted.

This suggests chronic unilateral lung disease and is nearly always due to tuberculosis.

The features include, unilateral a) crowding of the ribs, b) expansion of the chest (with signs of emphysema), c) Harrison's sulcus.

there are no other common causes of a friction rub, although it is uncommon.

there are no other common causes of unilateral pleural effusion. Bilateral effusion in children is must probably tuberculosis, in adults the diagnosis should only be made in the absence of a raised central venous pressure (JVP), peripheral oedema

In both adults and children one-sided upper lobe pneumonia should be treated as tuberculosis, it is less common in children.

This is due to long-standing upper lobe scaring following pneumonia. It is uncommon in pre-school children

pulmonary tuberculosis is usually asymmetrical, even in the malnourished. In the malnourished lobar pneumonia is very uncommon (they nearly always get bronchopneumonia) and if present is accompanied by fever and purulent sputum. The differential of unilateral pneumonia is inhalation pneumonia (foreign body or food).

Bilateral tubercular pneumonia is usually part of miliary spread of tb and there should be other signs present

Any history or observation of fresh (red) blood in the sputum should be treated as tuberculosis.

In adults pericarditis is usually due to tuberculosis - the differential diagnosis is viral carditis which rarely gives rise to a friction rub in the malnourished.

Not seen in children. In adults a history suggestive of heart failure WITHOUT orthopnoea is very suggestive. Quite heart sounds, undisplaced quite apex beat, raised JVP with an appearance of an increased jugular pulse (increased and rapid y-descent).

In children ascites is very uncommon even in oedematous kwashiorkor (most congenial liver diseases that give rise to ascites will lead to early death in these populations). In adults ascites without jaundice and/or liver enlargement is usually abdominal TB. Abdominal TB is usually associated with constipation rather than diarrhoea. Cirrhosis and schistosomiasis are differential diagnostic problems.

This is uncommon but critical as it is almost pathognomonic and the consequences of non-treatment are devastating. Thoracic spinal tenderness or any deformity should be treated as Pott's disease unless there is a definitive history of trauma (all ages).

This should only be used to diagnose TB in the absence of local dental/oral/pharyngeal/salivary gland/scalp infection (when the glands are usually very tender). TB glamds can be tender, but the tenderness is usually less than one would suspect from the clinical appearance. HIV generally gives symmetrical lymphadenopathy.

This also occurs in carcinoma and syphilis.

discharging sinuses in the neck should be treated as TB, particularly if they are mal-odorous.

This lesion arises from an abbess in the psoas muscle "pointing" at the insertion in the groin. The differential is lymphogranuloma inguinale etc etc.

Tubercle on the retina (particularly the peripheral retina) are a sign of miliary spread and should be looked for - they are pathognomonic.

There is a prodromal history of change of mood, behaviour, appetite, malaise and vomiting over several weeks. The diagnosis should be considered in children with vomiting without diarrhoea. The disease evolves with a much slower time course than bacterial meningitis or encephalitis (days rather than hours). It is nearly always associated with a bulging fontanelle in young children and there is usually papilloedema (occasionally optic atrophy). Signs of cranial nerve involvement occur at a much earlier stage and are more common than with other forms of meningitis. In children the head circumference is frequently larger than predicted from the height.

Other signs, that occur in tuberculosis, are NOT sufficiently specific to tuberculosis to warrant a diagnosis to be made and treatment started when they are found to be present, however, they should prompt a through search to be made for other signs including, for example, examination of the retina under mydriasis in the dark. These signs include:

----------------------------------------------------------------------------

 

Best wishes,

 

Prof. Michael H.N.Golden


Date: Tue, 19 Aug 1997 12:00:07 +0100

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

Subject: Re: Nutrition of TB patents

 

Thanks Mike for the excellent explanation.

I must react on your remark that it is not desirable to shut TB patients up in isolation.

First of all we don't do that. We separate the TB children but not in isolation. I must confess that the reason I gave: 'fear for cross infection' is not right. For purely management reasons children are put in a different corner in order to be able to keep a close eye on the tb, medical and nutritional treatment.

 

Saskia van der Kam, MSF-H, Amsterdam

Saskia_VD_KAMatamsterdam.msf.org


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

Date: Fri, 22 Aug 1997 12:51:09 +0930

Subject: The Diagnosis of TB in the Malnourished

 

Dear Dr Golden

Thank you for sending the copy of "The Diagnosis of Tuberculosis in the Malnourished". This is very important paper dealing with the difficult paediatric issue of TB diagnosis in the developing country situation. Clinical paediatric practice of TB diagnosis various very considerably even between Teaching Hospital settings. For example when I arrived at the Royal Victoria Hospital in the Gambia, most malnourished children ended up on TB treatment due to a failure to respond to one week of penicillin and one week of chloramphenicol. The real problem was the nutritional rehabilitation regime and the compliance with TB treatment on discharge from hospital was <10% because the infrastructure for TB management in communities was overwhelmed by paediatric nutrition cases, nearly all of whom in fact did not have TB.

In my rural visits in Zimbabwe, The Gambia, Malawi and Solomon Islands, one of the most frequent consultations by nurses and District Medical Officers was whether a malnourished child had tuberculosis. It indicated to me that most clinicians are very uncomfortable about saying that a malnourished child does not have TB in case they are wrong. This difficulty is compounded by anecdotal case reports with children with no cough, a normal chest x-ray and a negative Mantoux responding dramatically to TB treatment and therefore definitely having tuberculosis. In addition many junior doctors and nurses do not have a clear idea about the spectrum of disease in tuberculosis so are unwilling to say that a particular child does not have TB. I have found that a therapeutic trial of TB treatment in a primary nutritional problem is not usually very helpful because one is not very sure if the catch-up growth is due to the TB treatment itself or improved diet + natural history of the non-TB disease (and antibacterial effect of the drugs). On the other hand I do agree that catch-up growth is a very important feature of tuberculosis treatment in definite TB cases. Nearly all TB cases present with a history suggestive of tuberculosis rather than primarily a child with malnutrition.

In terms of specific TB diagnoses, miliary TB has a distinct radiological picture which requires prompt initiation of therapy. These children generally appear very unwell with rapid heart rate and frequently hepatosplenomegaly but with a clear chest on auscultation in most circumstances. There sick enough to get to hospital and will usually get a chest x-ray which would make the diagnosis obvious. The finding of choroid tubercles in the retina (not Roth spots) is an interesting finding but not usually helpful for diagnosis since this is only found in about 10% of cases.

Tuberculous lymphadenopathy is also a distinct clinical picture which should not be confused with primary malnutrition. Occasionally it can be confused with a lymphoma or HIV infection.

I have found that axillary lymph glands are characteristic of HIV infection and extremely uncommon with TB. The glands of a lymphoma tend to grow more slowly and are firmer in consistency. The Mantoux test is never negative with tuberculous lymphadenitis, so Mantoux test is crucial in assessing TB lymphadenitis. Note the PNG report on Mantoux testing in hospitalised TB cases (ref 1 below).

Ascites can be present with severe kwashiorkor once the serum albumin is below 15 g/L. I know the traditionally teaching is that ascites is rare with kwashiorkor, but this was not the case in Malawi in older children. I believe that the presence of ascites in kwashiorkor may only indicate a very low level of albumin with low oncotic pressure. However, I agree that the presence of ascites certainly would make one consider abdominal TB or liver disease in the older child, although bilharzia would be unlikely to present with cirrhosis under 5 years of age.

In terms of pneumonia, tuberculosis should always be considered in the presence of the right middle lobe collapse syndrome due to enlarged hilar glands. The crucial differentiation of bacterial pneumonia from tuberculous pneumonia is prompt response to penicillin in pneumococcal pneumonia and the need for a follow up chest x-ray in suspicious cases of TB. As mentioned, the presence of a pleural effusion is highly suggestive of tuberculosis and is distinctly uncommon in primary nutritional problems. Similarly enlarged hilar glands should lead to a Mantoux test, which if positive is likely to be related to TB.

The emergence of HIV has further complicated the diagnosis of TB in children. HIV infection has resulted in a pronounced increase in adult TB, but I do not believe that this has led to such an increase in paediatric TB associated with HIV infection, except in the children of sputum positive adults. For example the study by Lucas quoted in reference 2 below from Ivory Coast confirmed that pneumocystis carinii pneumonia was extremely common in HIV infected infants, but TB was very uncommon at post mortem of HIV cases.

Finally and most importantly, I think the paper should reflect the importance of TB contact in making a diagnosis in malnourished children. Basically paediatric TB is a disease transmitted by a sputum positive adult living in the household. I am aware that such a case cannot always be found due to various factors, but the importance of contact tracing of sputum positive adults cannot be over emphasised. Most paediatric TB can be picked up by tracing the contacts, particularly children under 5 of sputum positive adults. It was not our practice in developing world countries to isolate children with TB because it is sputum positive adults - not tuberculous lymphadenitis or other forms of TB that transmit the disease. Thus, case finding directed to contacts of sputum positive adults is much more cost effective than case finding on a clinical basis. In my experience, TB contact is frequently denied until the diagnosis is made and then miraculously the TB contact emerges. So I would emphasis the importance of contact tracing and chasing sputum positive adults in the diagnosis of paediatric TB along with the clinical diagnosis features.

Yours sincerely

 

David Brewster, Associate Professor of Paediatrics

Darwin Clinical School, Northern Territory, Australia

 

1. Murtagh K. Unreliability of the Mantoux test using 1 TU PPD in excluding childhoodtuberculosis in Papua New Guinea. Arch.Dis.Child. 1980 Oct;55(10):795-9

Abstract: 139 children with bacteriological or histological proof of active tuberculosis were given the Mantoux tuberculin test while they were inpatients at Port Moresby General Hospital. Only half (70) of the children had positive results (induration of at least 5 mm). Of the 35 children under 2 years, 25 (71%) showed no reaction whatsoever. Malnutrition, assessed by weight for age, did not appear to influence the response although nearly all children under 5 weighed less than the Harvard mean. Previous BCG immunisation had no significant effect on the reaction to tuberculin. General debility, recent measles, treatment with corticosteroids, or early stage of illness may account for some negative reactions, but whatever the cause, the high proportion of negative results means that the tuberculin test as currently practised in Papua New Guinea cannot be relied on to exclude active tuberculosis in children.

2. Lucas SB, Hounnou A, Koffi K, Beaumel A, Andoh A, De Cock KM. The pathology of paediatric HIV infection in Cote D'Ivoire. J Pathol 1993;170:342A (Abstract)

3. Brewster DR. Tuberculosis in malnourished children [letter]. Trop Doct 1991;21:124-125.

4. Wilkinson D. Tuberculosis and malnourished children [letter]. Trop Doct 1992;22:88

5. Wilkinson D. Tuberculosis in malnourished children [letter]. Trop Doct 1992;22:35


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

Subject:

Date: Sat, 30 Aug 1997 16:17:50 +0100

 

I always separate out ? TB patients because I am frightened of cross infection. Could somebody explain why that isn't a valid reason

yours

 

Steve Collins


30 Aug 97 16:54 BST

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

Subject: RE: The Diagnosis of TB in the Malnourished in particular ascites in severe malnutrition

 

Hullo there,

I was interested in David Brewster's observation that :

> Ascites can be present with severe kwashiorkor once the serum albumin below 15 g/L. I know the traditionally teaching is that ascites is rare with kwashiorkor, but this was not the case in Malawi in older children. I believe that the presence of ascites in kwashiorkor may only indicate a very low level of albumin with low oncotic pressure. However, I agree that the presence of ascites certainly would make one consider abdominal TB or liver disease in the older child,>

I have found ascites to be a relatively common finding om severely malnourished adults. The appearance of ascites doesn't really seem to relate to the degree of malnutrition as the incidence varies in different geographical areas Angola > Somalia > south Sudan where I didn't see any adult ascites at all despite extreme emaciation. In Angola there was ascites even in apparently mildly malnourished adults. In Somalia it occurred in both young and old adults and was sometimes extremely severe. In Somalia ascites did not appear to be associated with a poorer prognosis once pedal oedema was introduced into the prognostic models. In many of the cases the ascites responded well to a diet with under 10% of the energy from protein but not to other diets where 16% of the energy was in the form of protein. By way of example: One 40 year old woman was admitted with severe oedema and ascites. Both ascites and oedema responded well to the lower protein diet but returned after she was changed onto the higher protein diet. She was then switched back onto the lower protein diet and was discharged apparently well and able to till her land after four week therapy. In some of the cases the ascites didn't respond to any sort of nutrition treatment combined with basic antibiotics such as penicillin/amoxil/cotrimox.

These finding seem to reflect earlier findings from researchers in prisoner or war camps / liberated concentration camps and ? the Warsaw ghetto.

Hope this was of some interest.

 

Steve Collins


Date: Wed, 3 Sep 1997 14:21:32 +0000

Subject: Tb and malnutrition

From: "Patrick Kolsteren" <pkolsterenatitg.be>

 

Dear ngonut,

It was interesting to read the reflections of Dr.Golden on tuberculosis and malnutrition.

Since we depend in the field so much on clinical signs, particularly do diagnose tb we used to payed particular attention to the food requests of the malnourished children in the field. It struck us (in Nepal) that some malnourished children had a particular craving for meet, would devour meat dishes and keep requesting for more. These children we found out, had TB. I asked some of my (much) older colleagues and some of them remembered that in the older textbooks the craving for meet was a typical sign of TB. These observations are of course, personal and come from observations on small numbers. Some of my colleagues in the field also had the impression that one found more often TB in malnourished children with this craving for meat.

Does anyone has access to old textbooks where this clinical sign is described and are there any other experiences???

Some feed for discussion

 

Dr.P.Kolsteren

Nutrition Unit, Institute of Tropical Medicine Antwerp

NAtionalestraat 155, 2000 Antwerpen, Belgium

tel 32-3-2476389 Fax 32-3-2476543


Date: Fri, 5 Sep 1997 12:20:20 +0200

From: Veronique_PRIEMatparis.msf.org (Veronique PRIEM)

Subject: Diagnosis of TB in the malnourished

Auteur : Francis VARAINE MSF-PARIS

 

Dear All,

We were much interested by the approach of TB diagnosis proposed by dr. Golden and colleagues.

First of all, according to our field experiences we agree that in case of failure to respond to the nutritional treatment the commonest cause is the insufficient or inadequate food.

One has always to keep this in mind: we had examples of sudden increase in the number of suspected TB cases in our feeding centers which were retrospectively explained by a mistake in the preparation of the meals (a change in the blended food composition had remained unoticed).

This point being ascertained, we then recommend to use the classical paediatric scores as a guidance for TB diagnosis. One of the more widely used is the clinical score developped by Edwards in Papua New Guinea.

The rational of it is that the diagnosis of Tb in a child can only be based on a network of signs, each of them with a different predictive value. Malnutrition in some places, or failure to respond to nutritional treatment are considered as part of a network of signs which could lead to suspect TB.

Some of the other elements to be taken into account are: TB case in the family (M+), tuberculine test result, large painless lymph nodes, unexplained fever, deformity of spine, etc..

Different values are given to these informations and should probably be adapted to the local context.

According to the final score obtained a flow-chart is proposed to help the decision.

We think that this systematic approach has the advantage of bringing together the various pieces of a clinical presentation and rationalize the decision.

An example of these scores and flow chart is given in "Clinical tuberculosis" J Crofton.

We recommend not to undertake any TB treatment in the absence of a properly organized TB program.

We consider isolation only for malnourished adults with suspected (or confirmed) pulmonary TB.

Regards,

 

Dr. Francis Varaine

Veronique Priem

Medical Department MSF-Paris