Dear Spencer,

Thanks for bringing up this very good question.

In my experience oedema often begins in the face before it is evident in the feet. In children under about 4 years old you can sometimes see it around the eyes and then the cheeks. In children a little bit older, I don’t see it as often around the eyes, but I do see it in the cheeks. These signs are more difficult to measure definitively than in the feet so I think they might be ignored. In slow on-set cases, many times there are also hair changes visible before edema in the feet.

Gopalan, in a longitudinal study in the 1960s noted this edema in the face sometimes preceded edema in the feet and called it “moon face” because the children’s faces became round.
(Gopalan, C. (1992). Classics in Indian Medicine: Kwashiorkor and Marasmus: Evolution and Distinguishing Features (reprint). The National Medical Journal of India, 5(3), 145-151.)

In eastern DRCongo, when asking community health workers to show me cases of kwashiorkor in their communities, they often take me to children with edema in the face but not in the feet and explain that the child is “starting to be malnourished”. When mothers in these same areas are asked how they knew their child is becoming malnourished, they often say a child becomes lethargic or irritable in combination with edema in the face, but the clinic won’t admit the children until the condition progressed to the point there was edema in the feet.

The signs of kwashiorkor look a bit different in different places. In some areas there is more fatty liver than others. After sudden events like conflict, kwashiorkor can develop rapidly and there may not be time for the hair to show changes. In Malawi it is more prevalent in children near the weaning age but in the DRCongo it is more prevalent in 3 and 4 year-olds. Before 1970, Kwashiorkor was identified differently in different places because it appeared slightly differently. To make sure everyone was talking about the same condition, a bunch of doctors got together in 1970 to establish a simple diagnostic criteria for kwashiorkor.

“All workers seem to agree that in kwashiorkor oedema is the single clinical feature which is universally present. Hepatomegaly is not as common in many countries as it is in Jamaica, and skin and hair changes are very variable.”
(Lancet. (1970). Classification of Infantile Malnutrition. The Lancet, 2, 302-303.)

Later “oedema” was operationalized to pitting oedema in the feet, though this was not part of the original definition. This definition, with its focus on oedema and the way it was operationalized, has had the unintended consequence of making kwashiorkor appear to be a yes/no decision based on one single sign and moved treatment away from the understanding of kwashiorkor as a syndrome with many signs, some of which may indicate a less severe stage that nevertheless might indicate the child is undernourished.

Hope that helps

Hi Spencer,
Merry offers interesting historical insights into kwashiorkor syndrome. I would argue that dropping the term 'kwashiorkor' for 'oedema' was not unintended. The term oedema provides a clear diagnostic criterion for the identification and treatment of severe acute malnutrition.

To be clear, one of the diagnostic criteria that identifies children with SAM for admission into selective feeding programmes (other than wasting) is 'bilateral oedema'. (note: WHO use the term ' bilateral oedema' while footnotes clarify that the mildest form of nutritional oedema occurs in the feet).

The severity of the oedema is graded according to where-else it occurs. The progression of the oedema is upwards.

+1 Bilateral pitting oedema of the feet
+2 Bilateral pitting oedema of the feet and lower legs & may also involve bilateral pitting oedema of the hands and lower arms
+3 As above and includes periorbital oedema

For the purpose of defining an admission criterion for treatment guidelines you may change the term from 'usually' to 'always'. The use of a simple diagnostic sign allows easy identification at community level and promotes high treatment coverage.

Where outpatient treatment is available the grade of oedema may also be used to identify whether the child is treated as an outpatient or inpatient. This varies according to context, although +3 (severe) oedema is currently always treated as an inpatient in all contexts.

Other forms of (non-nutritional) oedema can occur for a variety of medical reasons, an example being nephrotic syndrome where facial oedema / 'moon-face' may occur without being evident elsewhere on the body.

Please refer to WHO updates on the management of SAM (2013).

https://apps.who.int/iris/bitstream/handle/10665/95584/9789241506328_eng.pdf?ua=1

Regards,
Paul

There are about 40 different nutrients that are essential for health. If any one of these is deficient in the diet the person will not be fully healthy and able to resist the agents of disease. The nutrients are divided into two classes. Type I nutrients are the functional nutrients that are required for the hormonal, immunological, biochemical and other processes of the body to function normally. Most of the micronutrients fall into this category. Individuals can be very deficient in these nutrients and not have any anthropometric abnormalities (i.e. they can have grown normally and have a normal body weight). Anthropometric surveys do not give us information about the prevalence of type I nutrient deficiencies. Their deficiency does cause major illness and increased likelihood of death (e.g. iron, iodine and vitamin A deficiency). Deficiency of several of these nutrients, particularly the anti-oxidant nutrients, is the probable cause of oedematous malnutrition (kwashiorkor). Type II nutrients are the growth nutrients that are required to build new tissue. They have been deficient when there has been failure to grow, to repair tissue that is damaged, to replace rapidly turning over cells (intestine and immune cells) or to gain weight after an illness and have a normal convalescence. Deficiency of these nutrients (nitrogen, essential amino-acids, potassium, magnesium, sulphur, phosphorus, zinc, sodium and chloride) leads to stunting and wasting. Replenishment of all these nutrients, in the correct balance, is essential for recovery from malnutrition and convalescence from acute illness. More than half of all deaths in children have stunting and wasting as the underlying cause: that is, they are too thin or too short for their age because they have not had sufficient type II nutrients to grow properly and many have lost weight. These children would have recovered from other illnesses if they had not been malnourished, but because they are malnourished they die. To this toll must be added the deaths of children with type I nutrient deficiencies. Thus, most deaths in childhood have some form of malnutrition as the underlying cause. vi Acute Malnutrition is classified according to the degree of wasting and the presence of oedema. It is acute severe malnutrition (SAM) 1 if the wasting is severe (W/H < -3 Z score WHO standards or a low MUAC) or there is oedema. These guidelines address the treatment of SAM. Malnutrition is defined as moderate acute malnutrition (MAM) if the wasting is less severe (W/H between -2 and -3 Z-score WHO standards); oedematous cases are always classified as severe. Stunting is due to chronic malnutrition. Although there is some initial response to treatment according to these guidelines, the treatment has to be continued for a sufficiently long time to make it inappropriate to treat stunting according to these guidelines. Other approaches that ensure the long-term improvement in the quality of the family diet are used (e.g. positive deviance programs and family economic support such as micro-credit) as well as managing the convalescent phase of acute illnesses. The community mobilization part of these guidelines can usefully provide a starting point for such programs. In many health facilities the mortality rate from severe malnutrition is at present over 20%; this is unacceptable. If these guidelines are carefully followed the mortality rate should be less than 5%, even in areas with a high prevalence of HIV/AIDS although there is a higher mortality in patients with a low CD4 count. With this management the products (F75, F100, RUTF) and other treatment usually leads to very rapid reversal of the clinical features of SAM. Unfortunately, this entails large movements of electrolytes and water between the various compartments of the body. This temporary electrolyte disequilibrium makes the patients even more vulnerable to misdiagnosis and mismanagement of such conditions as dehydration or severe anaemia that can lead to death from heart failure. Thus, it is very important that the whole guideline is implemented along with the introduction of the therapeutic products, particularly the diagnosis and management of the complications during inpatient care. It is only appropriate to refer SAM patients to facilities where the proper training in the care of the severely malnourished has been accomplished; in particular, the staff in emergency wards need to understand that the standard treatment of complications given to non-malnourished children can lead to the death if the patient is severely malnourished.

All patients that fulfil any of the criteria in the following table have severe acute malnutrition (SAM).
They should be offered therapeutic feeding in one of the available settings.
AGE ADMISSION CRITERIA
6 months to 12 years ¾ W/H or W/L <-3 Z score (WHO-2005 standards) or
¾ MUAC <110 mm if Length =<65 cm or
¾ MUAC<115 mm if length/height >65cm or
¾ Presence of bilateral oedema (+ & ++ admission to OTP; +++ admission
to TFC)
12 to 18 years ¾ W/H <70% NCHS or
¾ Presence of bilateral oedema (+ & ++ admission to OTP; +++ admission
to TFC)
Adults ¾ MUAC < 180 mm with recent weight loss1 or
¾ BMI < 16 with recent weight loss or
¾ Presence of bilateral oedema (unless there is another clear cut cause)
This following shows the schema for the decision making process. First the patient is identified in the
community or health structure by anthropometry and looking for oedema. The severely ill are “fast tracked” to
treatment by the person doing triage. The appetite test is performed whilst waiting to see the nurse who looks
for the presence of medical complications. She discusses with the caretaker and decides upon the appropriate
treatment options. Those that need in-patient treatment are referred for admission to a TFC; those that can be
treated as out-patients are referred the OTP site nearest to their home.

Muchas gracias por sus respuestas. Feliz noche.