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Cure rate (%) = (Number cures / Number treated) * 100
This is usually estimated in a clinical trial.
An epidemiologist will focus on effectiveness at both the individual and at the program level.
For the CMAM protocol, the cure rate (treatment efficacy) is close to 100% in uncomplicated incident cases (i.e. in cases with MUAC at or just below the admission criteria and cases with mild oedema). There is, therefore, little room for large improvements in the efficacy of the CMAM protocol.
We cannot significantly change the efficacy of the CMAM protocol. We can, however, change the effectiveness of the CMAM protocol.
The effectiveness of the CMAM protocol can be defined as "the cure rate in a beneficiary cohort under program conditions". Effectiveness depends, to a large extent, on:
Severity of disease : Early treatment seeking and timely case-finding and recruitment of severe acute malnutrition (SAM) cases will result in a beneficiary cohort in which the majority of cases are uncomplicated incident cases. The cure rate of the CMAM protocol in such a cohort is close to 100%. Late treatment seeking and weak case-finding and recruitment will result in a cohort of more severe and more complicated cases. The cure rate in such a cohort may be much lower than 100%.
Compliance : Programs in which the beneficiary and the provider adhere strictly to the CMAM protocol have a better cure rate than programs in which adherence to the CMAM protocol is compromised. Poor compliance can be a problem with the beneficiary (e.g. sharing of ready-to-use therapeutic food [RUTF] within the household) or a problem with the provider (e.g. RUTF and drug stock-outs), and both have a negative impact on effectiveness.
Defaulting : This is the ultimate in poor compliance.
An effective program must, therefore, have:
(1) Thorough case-finding and early treatment seeking. This ensures that the beneficiary cohort consists mainly of uncomplicated incident cases that can be cured quickly and cheaply.
(2) A high level of compliance. This ensures that the beneficiary receives a treatment of proven efficacy.
(3) Good retention from admission to cure (i.e. little or no defaulting). This also ensures that the beneficiary receives a treatment of proven efficacy.
Coverage is one factor (the other being effectiveness) in the capacity of a program to meet need. It can be expressed as:
Coverage (%) = (Number in the program / Number in need) * 100
Coverage depends on:
(A) Thorough case-finding and early treatment seeking. This ensures that the majority of admissions are uncomplicated incident cases, which leads to good outcomes.
(B) A high level of compliance. This ensures that the beneficiary receives a treatment of proven efficacy.
(C) Good retention from admission to cure. This is the absence of defaulting.
Note that that the "123" of achieving high individual effectiveness and the "ABC" of achieving high coverage in CMAM programs are the same.
Program effectiveness (met need) is:
Met need = effectiveness * coverage
Coverage and effectiveness depend on the same things and are intimately linked to each other. Good coverage supports good effectiveness. Good effectiveness supports good coverage. Maximizing coverage maximises effectiveness and met need. An effective program is built upon individual effectiveness and coverage.
Let us see how this plays out. We can look back at the CMAM vs. TFC debate of the previous decade. At the time this was a heated debate with many harsh words spoken. I think we can be more measured ...
In terms of clinical effectiveness the high dependency inpatient therapeutic feeding (TFC) model does very well. Cure-rates of 90% were achievable even with very severely malnourished caseloads. Weight velocities were also high (e.g. > 10 g/kg/day). This good performance was achievable without high coverage because care was delivered in high dependency units (HDU) using appropriate treatment products and protocols. It seems likely that the low coverage of TFC programs meant that they tended to treat mostly very severe cases and that TFC proponents believed that the case they saw were typical SAM cases and that all SAM cases needed treatment in HDUs. This is an example of drawing wrong inferences from a self-selected sample.
In comparison, CMAM programs do not look so good. Cure-rates may be lower (e.g. 80%) and weight velocities are typically half that achieved in TFCs even when the severity of SAM in most cases is not as sever as those seen in TFCs.
From a purely clinical perspective the TFC would be the program of choice. This conclusion changes when we look at the problem from an epidemiological perspective and factor in coverage.
TFC coverage was usually low (i.e. typically between 5% and 15%. The early CTC (CMAM) programs achieved coverage of 70% to 80%. If we take the best coverage for TFCs and the worst coverage for CMAM programs we get:
Met need (TFC) = 15% * 90% = 13.5%
Met need (CMAM) = 70% * 80% = 56.0%
The clinically inferior program turns out to be four times more effective that then the clinically superior program. Even "bad" CMAM programs with (e.g.) 75% cure rates and 20% coverage (met need = 15%) outperform the best TFCs. All but the very worst CMAM programs outperform the best TFC programs.
I have gone into this detail to make the point that to make the right choice in terms of delivering effective programming requires us to consider more than one factor. In the TCF vs. CMAM debate (e.g.) narrow clinical considerations compounded by inferences drawn from self-selected samples would have led to us making the wrong decision. We would still be treating and curing tens of thousands of children rather that hundreds of thousands of children.
I also wanted to make the point (a golden rule in public health medicine) that coverage is the most effective route (the "Royal Road") to program effectiveness. Any discussion of CMAM admission criteria needs, therefore, to consider coverage very carefully.
There is considerable evidence favouring MUAC as the best criteria for admission into CMAM programs. This has been covered on this forum and elsewhere. In brief, MUAC is the better predictor of mortality, low MUAC children respond well to treatment with the CMAM protocol, and MUAC is cheap and practicable. The data are reviewed [url=http://www.brixtonhealth.com/FNB.27.3.Myatt.pdf]here[/url].
I will suspend my disbelief for a moment and treat MUAC and WHZ as equally valid case-definitions for SAM.
The practicability of MUAC means that case-finding with high spatial and temporal coverage of screening is possible. This is something that is very definitely not feasible with WHZ. The ability to achieve high case-finding coverage is, IMO, a key reason to favour MUAC as a primary admission criteria. Many proponents of "strong" mixed MUAC / WHZ programming ignore this. They often take SMART survey data and apply case-definitions and tabulate MUAC cases against WHZ cases and find a number of "discordant" cases (i.e. cases with WHZ < -3 and MUAC > 114 mm). They then point to the discordant cell and say "We must use WHZ on an equal or superior footing to MUAC". Such an analysis leads us into error as it assumes that case-finding and recruitment is 100% exhaustive (i.e. has 100% coverage) or is equal for both MUAC and WHZ (equality or exhaustiveness may be present in very bad programs where it approaches zero - I have seen programs like this!). 100% or equal coverage of screening is extremely unlikely to be the case. Looking at data that I have to hand regarding a bottleneck analysis of MoH-run CMAM programming in a west African state I find that coverage of screening by MUAC of 50% per quarter (i.e. 50% of children have their MUAC taken in their homes in any three month period) is routinely achievable. Such a figure is not achievable for WHZ outside of special settings (e.g. well ordered camps). It is, in fact, unlikely to exceed a very small percentage. If we take coverage into account then the number "discordant" cases (we might call this "WHZ cases missed by MUAC") is greatly diminished. That is, if you properly account for the practicability of what is being proposed then the problem can bee seen in proper proportion.
Also, we must not ignore the impact of the considerable additional cost and staff required to achieve anything but very low screening coverage for WHZ. What tends to happen is that the extent of screening by both MUAC and WHZ contracts as WHZ eats the resources available for case-finding. Coverage of screening in "strong" mixed programming suffers and the programs ability to meet need also suffers. Again, we must consider the practicability and practical consequences of what is being proposed.
I think a "strong" mixed MUAC / WHZ program cannot be effective and that introducing WHZ into MUAC programming can be counterproductive.
We might want to consider using a "weak" mixed MUAC / WHZ programming model. Such a model would concentrate on MUAC-based community-based case-finding. It would also use MUAC in all health service contacts (e.g. at clinics and during EPI extension activities, IYCF activities, &c.). WHZ could be applied in clinical facility settings. If clinical staff saw MUAC below 135 mm they could measure weight and height and calculate WHZ. Any child with MUAC < 135 mm and WHZ < -3 would be referred to / admitting into CMAM services. In my experience care would need to be taken to avoid WHZ taking resources away from community-based screening, sensitisation, and mobilisation activities. You need to note that height boards are not usually available at many health facilities and are not part of essential clinic supply packs. Also, height / length measurement is not part of the IMCI syllabus. We must be careful that we do not allow the (vestigial) WHZ tail to wag the MUAC dog.
All these words and still no direct answer to your question!
Let me try ...
We know that MUAC is a universally good predictor of near term mortality.
We know that low MUAC kids respond well to treatment with the CMAM protocol.
We know that WHZ is a poor predictor of mortality. The clear evidence is that it performs worse than MUAC, MUAC/A, MUAC/H, H/A, and W/A. That is, it performs worse than any other commonly used anthropometric indicator. We also know that the predictive value of WHZ ranges between worse than tossing a coin to only a little better than tossing a coin.
We know that WHZ is strongly influenced by body shape. In some settings, low WHZ is associated with good H/A which suggests that low WHZ may be predictive of survival, good educational performance, high work productivity, &c. The body shape problem means that WHZ is sensitive but not-specific in warm climate / low altitude / pastoralist populations (i.e. we may treat many children who do not need it). It also means that in cold climate / high altitude settings WHZ has low sensitivity by high specificity (i.e. we fail to treat many children who need it).
We do know that MUAC and WHZ are quite strongly correlated with each other.
When we consider this in the round it is reasonable to surmise that much of the (weak) association between WHZ and mortality may be due to low MUAC. This would means that many of the WHZ+ / MUAC- children will be at lower risk of near term mortality than the MUAC+ children. I think there is some reason to believe that the discordant cases taken as a group are not at elevated mortality risk (a couple of studies do shows this). I would hesitate to conclude that no member of the discordant group is at elevated mortality risk. I think that many of the discordant cases at elevated risk may be picked up by WHZ at health facility level in the "weak" mixed MUAC / WHZ programming model. This will be, in large part, due to them being sick enough to prompt attendance at a clinical facility.
[url=http://www.brixtonhealth.com/Briend2011MCN.pdf]This article[/url] reviews the option of adding WHZ to MUAC only programs and concludes that to identify high-risk malnourished children, there is no benefit in using both WHZ less than –3 and/or MUAC less than 115 mm, and that using MUAC alone is preferable.
ineffective.
If I were very concerned about missing children I would increase the MUAC admission threshold rather than use WHZ.
At the risk of boring you ... I have started to notice articles of [url=http://www.brixtonhealth.com/Roberfroid2015NJ.pdf]this type[/url] being touted as evidence for the need for a "strong" mixed MUAC / WHZ program. This is very weak evidence as it attempts to draw inferences from a self-selected sample (see the TFC vs. CMAM discussion above). This is something that should only be done with much caution and, when done, all efforts should be made to judge the direction and magnitude of the biases inherent in the sample. To give an example, in the "weak" mixed MUAC / WHZ model we would expect the low WHZ cases found at clinical facilities to be sicker than other cases because they were recruited as sick children attending at clinical facilities. If we looked at our patient cohort we would not be surprised to see high mortality in these children. This is an effect of sampling bias. When we see this it would not be legitimate to conclude that we must use a "strong" mixed MUAC / WHZ model.
I hope this is some help.Answered:
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My last question is, are you rejecting the six recommendation
that were decided in 2012 meeting In London. One of the
recommendations shown below.
Recommendation 1:
At community level, there should be active case finding using
MUAC to identify children requiring management of SAM.
I wholeheartedly support this.
At health facility level (fixed or mobile), there should
be systematic case finding using MUAC to identify children
requiring management of SAM. If a child is not identified
by MUAC, WHZ should be measured where it is feasible (capacity
in terms of materials, time and trained human resources)
without jeopardizing other essential health services; WHZ
should be measured in particular where there are relevant
clinical conditions, visible severe wasting, maternal
concern and/or contextual factors (e.g. acute or prolonged
emergency where more older children are affected).
I support this. I do not think that WHZ has much value in CMAM programming. I would, if resources allowed, prefer to admit cases on clinical sign such as visible severe wasting and per-oedematous signs of kwashiorkor rather than waste time and money on WHZ. These signs do not need special equipment or three staff to measure. I wholeheartedly agree with the caveat "where it is feasible (capacity in terms of materials, time and trained human resources) without jeopardizing other essential health services". Since we usually operate in resource scarce settings this caveat will usually apply and we will not use WHZ.
General (4) : While I am agreeing ... André is correct ... we can have a slightly elastic boundary. It makes little sense, and may harm coverage, to send away a child with a MUAC of 115mm or 116mm.
I hope this is of some use.Answered:
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9 years agoDear all,
At this stage, I think it would be helpful to review the hypotheses of André and Mark and the extent to which they are infirmed or confirmed by recently published evidence. I agree that this recent evidence is far from perfect, yet it is good sometimes to see how observations match theory.
So, on the one hand, we have the following hypotheses which have been systematically put forward on this forum:
- Children with a MUAC<115mm have a higher risk of death in the short term than children with WHZ<-3 (which is in fact quite different from the statement that MUAC is a better predictor of mortality than WHZ according to ROC curves see here http://www.ennonline.net/fex/45/consultation for an objective explanation)
- Children with a MUAC<115mm are more in need for SAM treatment (short-term rehabilitation of acute nutritional deficits and appropriate management of clinical complications) than children with WHZ<-3
- Children with WHZ<-3 and MUAC=115mm (WHZonly) are in fact healthy older children with long legs
As expressed in the former consultation of experts mediated by EN-net http://www.ennonline.net/fex/45/consultation it is important to highlight that the evidence supporting these hypotheses is far from being conclusive for everybody.
On the other hand, we have the following recently published evidence:
- Midupper arm circumference and weight-for-length z scores have different associations with body composition: evidence from a cohort of Ethiopian infants.
Grijalva-Eternod CS, Wells JC, Girma T, Kæstel P, Admassu B, Friis H, Andersen GS.
Am J Clin Nutr. 2015 Sep;102(3):593-9. doi: 10.3945/ajcn.114.106419. Epub 2015 Jul 29.
- Inconsistent diagnosis of acute malnutrition by weight-for-height and mid-upper arm circumference: contributors in 16 cross-sectional surveys from South Sudan, the Philippines, Chad, and Bangladesh.
Roberfroid D, Huybregts L, Lachat C, Vrijens F, Kolsteren P, Guesdon B.
Nutr J. 2015 Aug 25;14(1):86. doi: 10.1186/s12937-015-0074-4.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547414/
This one had been wrongly quoted by Mark as being based on self-selected samples of children: on the contrary, it is based on cross sectional data gathered in representative samples of children
- Comparison of weight-for-height and mid-upper arm circumference (MUAC) in a therapeutic feeding programme in South Sudan: is MUAC alone a sufficient criterion for admission of children at high risk of mortality?
Grellety E, Krause LK, Shams Eldin M, Porten K, Isanaka S.
Public Health Nutr. 2015 Oct;18(14):2575-81. doi: 10.1017/S1368980015000737. Epub 2015 Mar 25.
- Comparison of Clinical Characteristics and Treatment Outcomes of Children Selected for Treatment of Severe Acute Malnutrition Using Mid Upper Arm Circumference and/or Weight-for-Height Z-Score.
Isanaka S, Guesdon B, Labar AS, Hanson K, Langendorf C, Grais RF.
PLoS One. 2015 Sep 16;10(9):e0137606. doi: 10.1371/journal.pone.0137606. eCollection 2015.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574398/
All these works challenge the aforementioned hypotheses and rather support the alternative hypotheses:
- MUAC<115mm is primarily an indicator of growth retardation in young children, rather than an indicator of acute nutritional needs (contrarily to WHZ)
- MUAC<115mm overdiagnose SAM in young stunted children and underdiagnose SAM in older children
- Children with WHZ<-3 and MUAC=115mm (WHZonly) are at similar high risk of death compared to children with MUAC<115mm, and they respond at least as well to treatment
- Among children with MUAC<115mm, those presenting with WHZ<-3 are the most at risk of immediate death, while those with WHZ>=-3 have more chronic vulnerability profiles.
Further investigations are required and are coming. In the meanwhile, it would be good to stay a bit cautious and to keep in mind both types of hypotheses.
Finally, I would like to say that, although I fully agree with the importance of the feasibility argument for SAM management programmes (especially the difficulty to detect and refer low WHZ children), feasibility is a context and time-specific concept which should not interfere with the need for a deep understanding of the needs for this type of programme.
Benjamin
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9 years agoWe keep coming back to tangentially relevant or misleading evidence:
Givjalva-Eternod et al. (2015) - Interesting but not, I think, directly relevant as the "outcome" measure is of body composition (not mortality). The finding of this paper are at odds with other papers that address this issue. Further work is probably needed although I am not sure if it will be relevant to CMAM programming.
Roberfroid et al. (2015) - Showing that MUAC and WHZ select different children is exactly the point. WHZ perform badly at what we need it to do. MUAC performs better that WHZ at what we need it to do. If MUAC and WHZ selected the same children then MUAC and WHZ would perform equally well as what we need then to do. I avocate for the use of MUAC exactly because because it is different from WHZ (which does very badly at what we need it to do). Please point me to the post where I misrepresent the Roberfroid et al. (2015) paper. I will check and, if needed, write a correcting note.
Grellety et al. (2015) - This has been discussed at length above. This is not appropriate or useful evidence.
Isanaka et al. (2015) - Here we have evidence that children with low MUAC respond to treatment. This is supports using MUAC for admission. We already knew this. The article does not address the issue of mortality risk in untreated cohorts which is what we need to decide whether the discordant MUAC-/WHZ+ children need the full CMAM protocol or could be treated in (e.g.) TSFP type programs. Clinical studies miss the point somewhat (see above re Grelley et al. (2015)).
It does seem that we need more evidence (although I fear that it will be ignored by those with a "dogmatic attitude in favour of low WFH children"). What you have presented above is not the evidence we need. At best these articles present tangentially relevant evidence. Grellety el al. (2015) is so inappropriate and biased as to be misleading. Your "Further investigations ... " suggest more of the same pseudo-evidence.
I am not sure where the evidence for some of the statements about MUAC and WHZ comes from. We know from the CTC research program that (e.g.) low MUAC kids in SFP die at five or six times the the rate as the same kids in OTP. This was a key piece of evidence for allowing MUAC to be used in OTP programs. I cannot understand the logic behind classifying the identification and admission of children who need and can benefit from the program as over-diagnosis. This is the sort of "logic" that gives rise to the sort of programming described in Grellety et al. (2015).
Please ... rather than keep producing and flaunting tangentially relevant or misleading evidence why not start collecting so useful and appropriate evidence?
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9 years agoDear Mark,
You wrote: "I am not sure where the evidence for some of the statements about MUAC and WHZ comes from."
These hypotheses are in my opinion quite well supported by the papers I quoted, as well as by the evidence reviewed here, and by Roberfroid et al. for WHO. They also cope quite well with the evidence (not talking here about the comments) you usually present. The reverse is not true: your usual hypotheses are challenge by the recent evidence.
Indeed :
- Knowing that mortality risk decreases with age, a parameter like MUAC, which is strongly related to age, and which is also strongly related to stunting, can be expected to be a good predictor of mortality. It does not need to be an indicator of acute nutritional needs to display this characteristic.
- Young and stunted children without acute nutritional needs, as would be children misdiagnosed as SAM by MUAC, can be expected to display some weight or MUAC gains, especially when treated with high caloric foods. You can even call this recovery if weight or MUAC gain is the only recovery criteria you are interested in measuring.
- However, young and stunted children without acute nutritional needs can hardly achieve the short term rates of weight gain demonstrated by children with acute nutritional needs.
Mark, with the data you have in hands, can you tell us how weight gains of MUAC only children in the short term, let’s say at 2 weeks, compare with weight gains in the two other SAM categories (i.e children with both MUAC<115mm and WHZ<-3; and children with MUACabove115mm and WHZ<-3)?
I am sure you will be interested in the observation made on this point by Isanaka et al.
It is true however that the hypothesis that MUAC-only children are rather chronic than acute could be challenged by the observation of a high immediate mortality risk in these children. Published evidence of this is however not there. I only retrieved a citation of a “natural experiment” observing mortality in children with MUAC<110mm and height below 75cm and WHZ above 70%of the mean (NCHS) in one of your publications, Mark (Myatt 2006). Can you have a look at your files and tell us how many of these children where MUAC<115mm and WHZabove-3, how many were MUAC<115mm and WHZ<-3, and what was their mortality rate?
That would be definitely an interesting piece of information.
Benjamin
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9 years agosorry there is a problem with the link I wanted to add above: I was referring to the great EN-net mediated review on this issue.
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9 years agoBenjamin
You keep referring to the 2010 WHO working document of which you are a co-author. I posted a comment on the weaknesses of of this document on the thread on MUAC for admission and discharge. Please reply to these comments before considering this can be used against my current position:
MUAC is better predictor of death than WFH. The Grellety et al paper cannot be used in any way to refute this.
Children with low MUAC respond to treatment and have a rapid weight gain when getting SAM treatment.
Now you say:
“Young and stunted children without acute nutritional needs, as would be children misdiagnosed as SAM by MUAC, can be expected to display some weight or MUAC gains, especially when treated with high caloric foods. You can even call this recovery if weight or MUAC gain is the only recovery criteria you are interested in measuring.”
We are several on this forum to plea WFH supporters to provide evidence in favour of their position or at least to tell us which kind of study will support their attitude. A claim which cannot be tested and for which there is no sound scientific rationale should be regarded as non scientific.
In the statement above you claim that the weight gain of some low MUAC children is not a criteria of improvement. How can you say this ? And test this ? Do you think any committee will allow a trial in which young stunted low MUAC children will remain un-supplemented to test your hypothesis ? And what is the rationale supporting the idea that giving a high energy high nutrient diet promoting weight gain will not be beneficial for them ?
This kind of statement is just creating confusion, and reflects a dogmatic attitude. I suggest you come back on this discussion when you have something clear to propose to support your ideas.
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9 years agoI have started a thread here.
I hope that we can come together there to work out what we need to do to move forward with an informed debate on issues around MUAC-only programming (a wider topic than has been debated here) and the appropriate treatment of children with MUAC > 115 mm and WHZ < -3.
See you there!
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9 years agoDear all,
When I said that it was good sometimes to see how observations match theory, I never meant that it would be a pleasant exercise for everybody. There is no point however in leaving the ground, losing tempers and insulting people engaged in providing more evidence, asking questions, putting forward existing and alternative hypotheses, or simply referring to balanced and collective examination of the scientific literature.
I will now go back to the scientific discussion.
André, you wrote: “MUAC is better predictor of death than WFH”
First, according to the past cohorts and their ROC curves, even age alone would be performing better than WHZ: this does not mean that all children under 2 have acute nutritional needs and should be treated for SAM. Second, this statement does not mean that children with MUAC<115mm have a higher mortality risk than children with WHZ<-3, does it? In which of your publications (or comments) have you shown this? Here I would have missed something.
Mark and André, you wrote: children with MUAC<115mm “exhibit rapid gains in both weight and MUAC usually following a typical growth curve (i.e. very rapid gains in the first few weeks slowing and approaching an asymptote)” and “children with low MUAC respond to treatment and have rapid weight gain”
In fact, it seems that not all children with MUAC<115mm exhibit this type of growth curve, only the ones presenting with both a MUAC<115mm and WHZ<-3 (and the WHZonly category as well). See the paper by Isanaka et al 2015: initial response to treatment in terms of weight gain is much lower in MUAConly SAM children than in the two other SAM categories (children with both criteria, and WHZonly children). This was also highlighted in the review by Roberfroid et al for WHO in 2013. This is also confirmed by many field observations.
Mark, you wrote: “When we don’t recruit them into OTP and put them into SFP they do not do well”, thereby referring to the “natural experiment” you mention in the 2006 paper.
Again, among these children with excess of mortality risk in SFP, what was the proportion of children with both MUAC<115mm and WHZ<-3, and what was the proportion of children with only MUAC<115mm? That would be interesting and useful information for the current discussion.
To conclude, I will not adopt a dogmatic attitude and extrapolate beyond the observations to draw high-impact recommendations restricting the target of SAM management programmes to one or the other of the criteria. I will rather go back to work, and try with my colleagues to provide the evidence we are lacking now.
Benjamin
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9 years agoDear all,
This discussion is now running on two threads, so I propose to close this one and any further comments can be posted here in the Prevention and treatment of MAM forum area under the "Only MUAC for admission and discharge?" discussion.
Alternatively, a new thread has been opened to discuss ideas for research/collection of evidence to help us move the debate forward. It can be found here .
Best wishes,
Tamsin
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