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Severe and moderate acute malnutrition

SAM and MAM in childhood: definitions by MUAC and z-scores, kwashiorkor and marasmus, outpatient RUTF care, and inpatient F-75/F-100 phases.

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In one minute

  • Severe and moderate acute malnutrition (SAM and MAM) are the wasting and oedematous forms of childhood undernutrition that, together, affected more than 40 million children under 5 years at any given moment in 2024, and thousands die of them every day.
  • SAM is defined by severe wasting (weight-for-height z-score under 3, or mid-upper arm circumference under 115 mm) or by bilateral pitting oedema ("kwashiorkor"); MAM is less severe wasting (weight-for-height z-score between -2 and -3, or mid-upper arm circumference 115 to under 125 mm) without oedema.
  • Kwashiorkor and marasmus are not separate diseases; they are the two clinical pictures of the same continuum (oedematous and wasting phenotypes), and a child can move between them during illness.
  • Most children with uncomplicated SAM (good appetite, no major medical complication, no severe oedema) are treated at home with ready-to-use therapeutic food (RUTF), with intake ranging from about 130 to 220 kcal per kilogram per day, with antibiotics and deworming.
  • Children with complicated SAM (loss of appetite, severe oedema, or a medical complication) need hospital: stabilisation with F-75 milk (about 100 kcal/kg/day), treatment of dehydration with ReSoMal, then transition to F-100 or RUTF for rehabilitation, with careful avoidance of refeeding syndrome.

Learning objectives

By the end of this page you should be able to:

  1. Define SAM and MAM precisely and say how they differ from stunting and underweight.
  2. Recognise kwashiorkor and marasmus in a clinical examination and explain why the distinction is not always clean.
  3. Explain the anthropometric criteria (MUAC, weight-for-height z-score, bilateral oedema) and how to measure them.
  4. Outline the inpatient pathway (stabilisation with F-75, dehydration/ReSoMal, transition, rehabilitation with F-100/RUTF) and the outpatient RUTF pathway.
  5. Describe the medical complications of SAM (hypoglycaemia, hypothermia, dehydration and shock, infection, severe anaemia, micronutrient deficiencies, refeeding syndrome) and how each is managed.
  6. Explain the evidence gaps in the 2023 WHO guideline that still shape best practice, especially for MAM and for dehydration.

Overview

This page covers the two acute forms of childhood malnutrition that clinicians actually treat: severe acute malnutrition (SAM) and moderate acute malnutrition (MAM). It treats them as one spectrum rather than two separate diseases, because that is how guidelines and bedside practice now regard them. It is written for a medical student meeting severe undernutrition for the first time: it builds from normal growth and wasting, through recognition and assessment, to treatment at home and in hospital, and finally to prognosis and prevention. The current normative document is the WHO guideline on the prevention and management of wasting and nutritional oedema (acute malnutrition) in infants and children under 5 years, published in 2023, which superseded WHO's 2013 guideline on the management of severe acute malnutrition.

Definition and classification

DefinitionSevere acute malnutrition (SAM)

SAM in a child aged 6 to 59 months means severe wasting (weight-for-height/length z-score under 3, or mid-upper arm circumference under 115 mm) and/or the presence of bilateral pitting oedema. The term is also used interchangeably with "severe wasting and/or nutritional oedema". [6]

DefinitionModerate acute malnutrition (MAM)

MAM in a child aged 6 to 59 months means moderate wasting: a weight-for-height/length z-score between -2 and -3, or a mid-upper arm circumference from 115 mm to under 125 mm, without bilateral oedema. [4]

A child is "wasted" when the weight is low for the height. Stunting (low height for age) and underweight (low weight for age) are different problems from wasting. They often overlap with acute malnutrition but they are not the same thing and they are managed differently. [6]

Three measurements therefore sit at the centre of the diagnosis:

  • Mid-upper arm circumference (MUAC): a simple tape around the midpoint of the left upper arm; it reflects muscle and fat and takes seconds to measure.
  • Weight-for-height/length z-score (WHZ/WLZ), compared with the WHO Child Growth Standards 2006.
  • Bilateral pitting oedema, detected by pressing with the thumb for a few seconds over the dorsum of both feet (and, if needed, the legs and hands).

Exam trapOedema can hide wasting

Bilateral oedema adds weight and can push a severely wasted child's weight-for-height above the cut-off. For this reason an oedematous child is graded as SAM even if the weight-for-height looks normal. Screening must include the thumb test, not just the tape or scale. [6]

Kwashiorkor and marasmus as two faces of the same illness

"Kwashiorkor" is the oedematous phenotype: bilateral pitting oedema, often with flaky "paint and varnish" skin changes, hair colour change, a swollen belly and an enlarged liver. "Marasmus" is the wasting phenotype: severe loss of fat and muscle, an old-looking face, prominent ribs, but no oedema. They are not separate diseases and a child may have a mixed picture (marasmic kwashiorkor). On examination the important distinction is oedema present or absent, because it changes treatment (fluid restrictions, sodium load, protein handling) more than the name does. [5] [6]

Infant and emergency definitions

Infants under 6 months with malnutrition are managed under different criteria and a different pathway (weight-for-length z-score and/or oedema, plus assessment of feeding), and the WHO 2023 guideline expanded its scope to support these younger infants, centred on protecting exclusive breastfeeding. That pathway is beyond the scope of this page. [2]

Epidemiology

In 2024, an estimated 42.8 million children under 5 years were wasted at any given time, of whom 12.2 million were severely wasted, and more than 30 million had moderate wasting. [7] Nutritional oedema is not captured in these estimates but is thought to number in the hundreds of thousands. More than two thirds of wasted children have moderate rather than severe wasting. Wasting and oedema contribute, directly or through the infections they worsen, to roughly 45 percent of all deaths in children under 5. [3] [4] [6]

Geographically, most wasted children live in South Asia, South-East Asia and sub-Saharan Africa. Wasting is more common under 2 years (about 14 percent) than at 2 to 4 years (about 9 percent). Severe wasting in children 6 to 59 months was estimated at 13.7 million in 2023. [3] [6]

Aetiology and risk factors

The fundamental cause is inadequate dietary intake relative to need, usually over weeks, superimposed on repeated infection and on poverty, food insecurity, poor sanitation and limited care. Infection both causes and is caused by malnutrition. MAM and SAM share the same drivers; SAM is usually the end-stage of the same process when intake has been very low or infection has been severe or prolonged.

Risk factors a clinician should look for include inadequate breastfeeding or inappropriate complementary feeding, recent acute diarrhoeal illness or pneumonia, HIV, tuberculosis, congenital heart disease, severe chronic disease, and family food insecurity. Inadequate breastfeeding is the single most important nutrition problem in infants under 6 months. [1] [5]

Pathophysiology

In acute malnutrition the body moves through predictable stages. Glycogen stores are consumed within hours. Fat is then mobilised, so that the child becomes visibly thin. When fat and muscle are depleted, adapted fasting metabolism slows heart rate, temperature and activity to conserve energy. Total body water changes, plasma proteins fall, and oedema forms when albumin and oncotic pressure are low enough. Functional consequences follow in every organ system: impaired cardiac output (small heart, bradycardia, hypotension), impaired thermogenesis (hypothermia), a small shrunken liver with reduced gluconeogenesis (hypoglycaemia), gut atrophy with malabsorption and a fragile mucosa, and immune collapse (lymphocyte depletion, low complement, poor wound healing). Iron, zinc, potassium and phosphate shift between compartments, so that "normal-looking" blood results can hide serious deficits; refeeding too quickly can produce fatal refeeding syndrome. [5] [6]

Clinical features

History

The mother's account is often the most useful test. Ask about duration of poor intake and of weight loss; stool frequency and consistency (diarrhoea is both a cause and a complication); fever and cough; which foods are offered and how much is actually eaten; breastfeeding; immunisation and recent infections; and any death or illness in siblings.

Symptoms the patient describes in their own words include loss of appetite, irritability then lethargy, diarrhoea, fever, and, in kwashiorkor, swelling of the feet.

Examination

Measure first, then look:

  • Anthropometry: weight, length/height, MUAC, and oedema by the thumb test on both feet.
  • General: wasted face, loose skin over the buttocks, visible ribs and scapulae, apathy and irritability; in kwashiorkor, bilateral pitting oedema of the feet (graded mild/moderate/severe), skin desquamation, hair depigmentation.
  • Vital signs: hypothermia or fever (both carry worse prognosis in SAM), bradycardia, slow capillary refill.
  • Abdomen: distension, hepatomegaly (fatty liver in kwashiorkor).
  • Mouth: oral thrush, signs of vitamin A deficiency, cheilosis.
  • Eyes: conjunctival pallor, corneal changes of vitamin A deficiency.
  • Ears, skin and hair: the classic hair colour change of kwashiorkor.

Differential diagnosis

SAM is usually obvious once you have looked, but mild and moderate wasting overlap with several other conditions. The table compares the main ones.

Differential diagnosis of a wasted child
ConditionHow it differs from acute malnutrition
Chronic diarrhoea or malabsorption (coeliac disease, cystic fibrosis, inflammatory bowel disease)Linear growth may also be affected; weight loss precedes or outpaces wasting; malabsorption signs (bulky stools, fat in stool).
Congenital heart diseaseFeeding difficulty from infancy, breathlessness on feeding, cardiac findings, poor weight gain despite adequate intake.
HIV infectionWeight loss with chronic features; recurrent infections; lymphadenopathy; confirmed by testing.
TuberculosisChronic cough, fever, night sweats, contact history; growth faltering over months.
Cerebral palsy or neuromotor disorderFeeding difficulties and oral-motor incoordination from birth; normal birth weight followed by poor gain; abnormal tone.
Renal or endocrine disease (chronic kidney disease, hypothyroidism)Poor growth with relatively preserved weight-for-height; biochemical clues.
Neglect or non-organic failure to thriveNormal appetite when observed, often in a particular caregiver context; social clues.
A teaching summary; many children have more than one problem.

Investigations

SAM is diagnosed clinically by anthropometry, so testing is for complications and for the underlying cause, not to "confirm" malnutrition. Useful investigations in a child with complicated SAM include:

  • Hypoglycaemia: bedside glucose, or a strip, in any child who is drowsy or has convulsions; aim to nurse glucose, not wait for the laboratory.
  • Malaria and infection: thick/thin films or rapid test where malaria is endemic; chest radiograph if pneumonia is suspected; urinalysis.
  • Anaemia: full blood count and peripheral smear; severe anaemia needs transfusion.
  • Tuberculosis and HIV: tested routinely in settings where they are common.
  • Electrolytes and renal function: urea, creatinine, sodium and potassium are often disturbed; hyponatraemia and hypokalaemia are common.
  • Stool microscopy and culture when diarrhoea is severe or persistent.
  • Vitamin A levels are rarely measured; treatment is given on clinical grounds.

Diagnostic criteria and grading of severity

Severity maps directly to the definitions and to whether medical complications are present.

  • MAM: WHZ/WLZ between -2 and -3, or MUAC 115 to under 125 mm, with appetite preserved and no medical complication.
  • Uncomplicated SAM: SAM criteria (WHZ under -3, or MUAC under 115 mm, or bilateral oedema) with good appetite, no medical complication, and only mild or no oedema.
  • Complicated SAM: SAM plus any danger sign or medical complication (loss of appetite, severe oedema, or a complication such as hypoglycaemia, hypothermia, severe dehydration or shock, visible severe wasting with severe oedema, general condition).

Hyponatraemia is defined as serum sodium under 135 mmol/L and hypernatraemia as over 150 mmol/L; hypokalaemia is serum potassium under 3.4 mmol/L in children (under 4.1 in infants); hyperkalaemia over 4.7 mmol/L in children (over 5.3 in infants). Hyponatraemia occurs in 21 to 52 percent of children admitted with complicated SAM and hypokalaemia in 7 to 79 percent; hypernatraemia is less common (under 5 to 15 percent). [6]

Management

The overall approach

The two rules of treating SAM are: stabilise before you rehabilitate, and feed small amounts frequently. A child with SAM has no physiological reserve; a full feed on day one can precipitate heart failure, hypoglycaemia from a shrunken liver, or refeeding syndrome. Treatment is therefore staged (stabilisation, transition, rehabilitation) and, for uncomplicated SAM, moved entirely to the community with RUTF.

Uncomplicated SAM: outpatient care with RUTF

Children with uncomplicated SAM and a good appetite are managed at home in an outpatient therapeutic programme. Daily RUTF intake ranges from about 130 to 220 kcal per kilogram (the rehabilitation range), given as packets that the caregiver administers. A 92 g sachet provides about 500 kcal. In practice this means about 1.75 sachets per day for a 5 kg infant, 2.1 sachets for a 6 kg older infant, and 3 sachets for an 8.5 kg preschool child on the standard schedule. [6]

RUTF is a lipid-based paste (groundnut, milk powder, sugar, vegetable oil, micronutrient mix) that needs no preparation, keeps without refrigeration, and resists bacterial growth; that is why it can be used at home. Routine co-treatments are oral antibiotics (for example amoxicillin), deworming where geohelminths are endemic, vitamin A, and measles vaccination if missed. Appetite and weight are checked weekly; the child is transferred to inpatient care if appetite is lost or a complication appears. Exit from treatment is reached when the child has weight-for-height z-score at least -2 (or -1.5 in some protocols), MUAC above 125 mm, and oedema resolved for two weeks. Evidence for the optimal exit threshold is of very low certainty. [3] [6]

MAM: outpatient care

MAM is managed in the community, with the aim of preventing progression to SAM. The WHO 2023 guideline recommends nutrient-dense diets for recovery (a good practice statement) and specially formulated foods (SFFs) such as ready-to-use supplementary food (RUSF) or fortified blended foods for those at higher risk of poor outcome, prioritised by individual child factors (low MUAC for age, very young age) and by context (high food insecurity). Because of the very large number of moderately wasted children and the cost of SFFs, universal supplementation is not recommended everywhere; where SFFs are given the quantity is based on empirical estimates of energy need and catch-up growth. Counselling on breastfeeding, family foods and hygiene, plus treatment of any intercurrent infection, is given to all. [1] [4]

Inpatient care for complicated SAM

Approach to a child with severe acute malnutrition

  1. Screen by MUAC, WHZ and oedemaAny child meeting SAM criteria with danger signs or a complication needs inpatient care; uncomplicated SAM with good appetite goes to outpatient RUTF
  2. Stabilise (days 1 to 7)F-75 at 130 mL/kg/day (about 100 kcal/kg/day) in frequent small feeds; treat hypoglycaemia, hypothermia, infection and electrolytes; ReSoMal for dehydration
  3. Transition (about 1 to 2 days)Switch from F-75 to F-100/RUTF as appetite returns and oedema resolves, watching for refeeding syndrome
  4. RehabilitateF-100 (100 kcal/100 mL) or RUTF (500 kcal/92 g sachet) at 135 to 220 kcal/kg/day; treat micronutrient deficiencies and start catch-up growth
  5. Discharge to communityWhen clinically stable, oedema resolving, good appetite and weight gaining; continue RUTF at home with weekly review
A teaching outline for a medical student; follow the WHO 2023 guideline and local protocols.

Stabilisation: F-75

F-75 is a low-protein, low-sodium, high-carbohydrate milk (75 kcal/100 mL) given at 130 mL/kg/day, providing about 100 kcal/kg/day, in frequent small feeds day and night during stabilisation. The aims are to meet basal energy needs without stressing a fragile heart, to replace electrolytes gently, and to avoid refeeding syndrome. High-protein feeds are avoided initially because the recovering liver cannot handle a large urea load and because protein can worsen oedema. [6]

Dehydration and ReSoMal

Dehydration is hard to recognise in SAM: sunken eyes and reduced skin turgor occur in wasting itself, and oedema can mask dehydration or mimic fluid overload. ReSoMal (Rehydration Solution for Malnutrition) has a lower sodium and higher potassium concentration than standard WHO low-osmolarity ORS.

FluidSodium (mmol/L)When to use
ReSoMal45Dehydration without shock in complicated SAM or oedematous malnutrition
Standard low-osmolarity ORS75Dehydration without shock in MAM, or in SAM with cholera or profuse watery diarrhoea
Intravenous fluids (for example half-strength Darrow's, or Ringer's lactate with 5% dextrose)per solutionShock or severe dehydration only; give carefully with monitoring

Dehydration without shock is treated with oral or nasogastric ReSoMal in frequent small sips; standard ORS is used when ReSoMal is unavailable, and always in cholera or profuse watery diarrhoea, where sodium losses are high. Intravenous fluids are reserved for shock or severe dehydration. The Integrated Management of Childhood Illness (IMCI) and DHAKA (Dehydration: Assessing Kids Accurately) algorithms both have high false-positive rates for dehydration in malnourished children (about 41 and 35 percent for moderate dehydration, and 76 and 82 percent for severe dehydration respectively), so clinical judgement matters. [3] [6] [8]

Shock

A child in shock with SAM is given intravenous fluids cautiously with close monitoring of the pulse, breathing and (where possible) central venous pressure, because over-hydration risks heart failure. Boluses of 10 to 15 mL/kg of an appropriate solution (half-strength Darrow's or Ringer's lactate with 5% dextrose) can be repeated, up to 30 to 40 mL/kg, with reassessment; isotonic saline is avoided because of its sodium load. Blood transfusion is given for severe anaemia or if shock does not respond. [5] [6]

Hypoglycaemia, hypothermia and infection

Hypoglycaemia and hypothermia are emergencies in SAM and both respond to warmth, frequent feeding and treating infection. Every child with these signs should receive oral or nasogastric glucose immediately, or intravenous dextrose if unconscious, kept warm (skin-to-skin, warm room) and fed 2-hourly. A broad-spectrum antibiotic (for example benzylpenicillin plus gentamicin, or ceftriaxone where indicated) is given to every child with complicated SAM, because infection is often silent. Albendazole or mebendazole is given once clinically stable. [5] [6]

Refeeding syndrome and electrolyte handling

Refeeding syndrome is the central danger of the rehabilitation phase. Starved children are total-body depleted of phosphate, potassium and magnesium even when blood levels look normal; when calories are reintroduced, insulin drives these ions into cells, producing hypophosphataemia, hypokalaemia, fluid retention and cardiac failure. It is prevented by the slow start with F-75, by giving daily oral potassium (and magnesium if deficiency is suspected), and by restricting sodium in the first week. It is treated by stopping rehabilitation feeds, giving potassium and phosphate, and restarting more slowly once stable. [5] [6]

Micronutrients

F-75, F-100 and RUTF all contain added micronutrients, but the quantities are based largely on expert opinion rather than direct evidence, and no Codex specifications exist for F-75 and F-100. F-75 has a low sodium concentration (7.4 mmol/L), providing 13 to 30 percent of the adequate intake depending on age, and a high potassium content (142 mg/100 mL), providing 37 to 107 percent of the adequate intake. F-100 and RUTF have more sodium (59 to 132 percent and 35 to 78 percent of adequate intake respectively) and more potassium (80 to 232 percent and 82 to 238 percent). ReSoMal provides 45 mmol/L sodium, lower than the 75 mmol/L in standard ORS. [6]

Supplementation outside therapeutic feeds is guided by clinical signs of overt deficiency rather than by routine high-dose programmes, because of the risk of refeeding and micronutrient excess. [6]

Rehabilitation: F-100 and RUTF

Once appetite returns and oedema begins to resolve, the child is moved to a rehabilitation feed: F-100 (100 kcal/100 mL), or RUTF (500 kcal per 92 g sachet), given at 135 to 220 kcal/kg/day (about 175 kcal/kg/day at the mid-point). The transition usually takes one to two days and the child is watched throughout for refeeding syndrome. Small, frequent feeds become larger and less frequent as the child's appetite and tolerance improve. [6]

Micronutrient deficiencies in SAM

Micronutrient deficiencies are common in severe malnutrition and often coexist. Evidence on their prevalence is limited, but the pattern is predictable from the diet of a malnourished child:

  • Vitamin A: night blindness, xerophthalmia, corneal ulceration; WHO recommends about 5,000 IU (1,500 micrograms retinol activity equivalent) daily in therapeutic foods, and clinical trials in children with SAM have used a single high dose (200,000 IU) where deficiency is suspected. [6]
  • Zinc: poor wound healing, diarrhoea; plasma levels fall, although they are hard to interpret because albumin binds zinc.
  • Iron: anaemia is almost universal; iron is given only once the child is stable and recovering, not in the acute phase, because iron can feed infection and is poorly absorbed in the starved gut.
  • Iodine, folate, vitamin B12, riboflavin, thiamine, niacin, vitamin C, calcium, phosphate and magnesium: all may be deficient; routine supplementation via RUTF/F-100 normally covers maintenance needs.
  • Sodium and potassium: as above; sodium restriction and potassium repletion are part of standard care.

Where deficiency signs are present (for example bitot spots, rickets, angular stomatitis, neurology), targeted supplementation is added on top of feeds. [5] [6]

Complications

The medical complications dominate prognosis and each has a specific treatment. In approximate order of danger:

  1. Hypoglycaemia and hypothermia (see above) - mortality if untreated.
  2. Severe dehydration and shock - treated carefully with ReSoMal or IV as above.
  3. Infection - often occult; sepsis, pneumonia, otitis media, urinary tract infection and meningitis are all common; broad-spectrum antibiotics for all complicated SAM.
  4. Severe anaemia (very low haemoglobin) - transfusion when needed, given slowly with a loop diuretic in severe wasting.
  5. Diarrhoea - oral rehydration as above; persistent diarrhoea suggests an underlying infection or lactose intolerance (lactose-free feeds can be trialled).
  6. Heart failure - from fluid overload or severe anaemia; restrict fluids and treat the cause.
  7. Vitamin A deficiency - high-dose supplementation with care for the bulging fontanelle warning sign of intracranial hypertension.
  8. Refeeding syndrome - see above.

Prognosis

Mortality in severely malnourished children during hospitalisation is 10 to 23 percent, and long-term mortality in the months after treatment ranges from 0.6 to 10.4 percent. Mortality is far higher without effective treatment. Inpatient deaths often cluster in the first 48 hours and are linked to hypoglycaemia, hypothermia, shock and infection. Survivors usually recover weight faster than linear growth, and children treated for SAM remain at higher risk of stunting, poor development and later cardiometabolic disease into adult life; long-term follow-up including neurodevelopmental support is therefore important. [6] [3]

Prevention and screening

Prevention of SAM is far more effective than its treatment, and it is the focus of the 2023 WHO guideline's prevention section. Effective measures include protecting and supporting exclusive breastfeeding for the first 6 months, timely complementary feeding from 6 months with nutrient-dense family foods, micronutrient fortification and supplementation where indicated, management of maternal malnutrition, and prevention and early treatment of infections (malaria chemoprophylaxis, measles immunisation, water and sanitation). Community screening by MUAC and bilateral oedema at growth monitoring and immunisation contacts, often by community health workers, detects cases early and improves coverage. [1] [4]

Special groups

Infants under 6 months are managed under the broader WHO 2023 pathway focused on poor growth and development, with exclusive breastfeeding support, and are not covered here. Pregnant and breastfeeding adolescents and women should be screened and treated for MAM/SAM in pregnancy, because maternal nutrition drives fetal and infant outcomes. Children with HIV or tuberculosis need integrated care: treat the infection alongside the malnutrition, with adjusted drug dosing and infection-control precautions. [2] [5]

Low-resource settings

Where scales, tapes or laboratory tests are unavailable, the most useful actions are: teach MUAC with a simple colour-banded tape; teach the thumb test for bilateral oedema on both feet; feed stabilisation milk F-75 made up locally to the formula, using careful measurement; give glucose orally or as sugar water for hypoglycaemia; keep the child warm with skin-to-skin contact; and reserve antibiotics and IV fluids for those who need them. RUTF allows treatment to be moved to the community, which is where the cost and coverage gains lie. Even where full treatment is not available, early referral from a sick malnourished child to a centre with inpatient capacity saves lives. [4] [5]

Key points

  • SAM is defined by severe wasting (WHZ under -3 or MUAC under 115 mm) or bilateral pitting oedema; MAM by moderate wasting without oedema.
  • Wasting, stunting and underweight are distinct and should not be confused.
  • Kwashiorkor and marasmus are two phenotypes of the same illness, classified by the presence or absence of oedema.
  • SAM and MAM share causes (inadequate intake plus infection in the setting of poverty) and represent a continuum.
  • Most uncomplicated SAM can be treated at home with RUTF (about 130 to 220 kcal/kg/day).
  • Complicated SAM needs inpatient staged treatment: F-75 at 130 mL/kg/day (about 100 kcal/kg/day) in stabilisation, then F-100 or RUTF at 135 to 220 kcal/kg/day in rehabilitation.
  • Dehydration in SAM is treated with ReSoMal (45 mmol/L sodium) unless cholera or profuse watery diarrhoea are present, in which case standard ORS is used; IV fluids are for shock only.
  • Danger signs (hypoglycaemia, hypothermia, infection, shock, severe anaemia, refeeding syndrome) are the main causes of death and must be anticipated.
  • Iron and high-protein feeds are delayed to the rehabilitation phase; sodium is restricted early; potassium is replenished.
  • MAM is managed in the community with nutrient-dense food and, for high-risk children, specially formulated foods.
  • The 2023 WHO guideline covers both SAM and MAM for children aged 6 to 59 months and has replaced the 2013 SAM guideline; important evidence gaps remain, most notably for dehydration, exit thresholds, RUTF quantity and long-term outcomes.
  • Early detection by MUAC and the thumb test, and early referral, save more lives than clever inpatient care.

Check yourself

Answer each one in your head first, then open the answer.

  1. A 20-month-old child weighs 5.9 kg, has MUAC 112 mm, bilateral foot oedema and a good appetite. Is this SAM or MAM, complicated or uncomplicated, and where should they be treated?

    Show answerHide answer

    SAM, and because there is bilateral oedema it should be treated as complicated: oedema makes this complicated SAM and the child belongs in hospital for stabilisation even though appetite is good. Uncomplicated SAM requires no oedema (or only mild oedema).

  2. Why should a child with complicated SAM not receive iron or a high-protein feed in the first week?

    Show answerHide answer

    The stabilising liver cannot metabolise a large protein load, excess protein can worsen oedema, and iron in the starved state feeds infection and is poorly absorbed. Both are deferred to the rehabilitation phase, once the child is stable and eating.

  3. How much F-75 should a 6 kg child with complicated SAM receive in 24 hours?

    Show answerHide answer

    780 mL in total (130 mL per kilogram), given as frequent small feeds day and night, providing about 100 kcal per kilogram per day. Exact local protocols may vary.

  4. A severely wasted child with diarrhoea has sunken eyes and reduced skin turgor. Why might this not mean dehydration, and what should you do?

    Show answerHide answer

    These signs occur in wasting itself, and oedema can mask dehydration. Reassess repeatedly; if dehydration is judged to be present and the diarrhoea is not cholera or profusely watery, give ReSoMal by mouth or nasogastric tube in small frequent amounts; use standard ORS if ReSoMal is unavailable or if cholera or profuse watery diarrhoea is present; reserve intravenous fluids for shock.

  5. A child recovers from SAM on F-75 and is moved to RUTF on day 5. On day 6 they develop lethargy, vomiting and a distended abdomen. What complication are you worried about and what is your first step?

    Show answerHide answer

    Refeeding syndrome: hypophosphataemia, hypokalaemia and fluid retention after too-rapid refeeding. First steps are to stop the rehabilitation feed, give potassium and phosphate supplementation, keep the child warm and monitored, and restart feeding more slowly once stable.

Acute diarrhoea and dehydration in children; HIV infection in children; congenital heart disease; tuberculosis in children; anaemia in children; pediatric growth and nutrition; vitamin A deficiency.

References

  1. World Health Organization. WHO guideline on the prevention and management of wasting and nutritional oedema (acute malnutrition) in infants and children under 5 years. Geneva: World Health Organization; 2023. ISBN 978-92-4-008283-0. Accessed .
  2. Daniel AI, de Polnay K, Bendabenda J, et al. Strengthening the evidence base around prevention and management of wasting and nutritional oedema in infants and children: insights from the 2023 WHO guideline. BMJ Glob Health 2025;10 (Suppl 5):e015929. doi:10.1136/bmjgh-2024-015929. Accessed .
  3. Thompson DS, Kumar P, Alsadeeq A, et al. Infants and children 6-59 months of age with severe wasting and/or nutritional oedema: evidence gaps identified during WHO guideline development. BMJ Glob Health 2025;10 (Suppl 5):e016878. doi:10.1136/bmjgh-2024-016878. Accessed .
  4. Trehan I, Bandsma RHJ, Borg B, et al. Infants and children 6-59 months of age with moderate wasting: evidence gaps identified during WHO guideline development. BMJ Glob Health 2025;10 (Suppl 5):e017228. doi:10.1136/bmjgh-2024-017228. Accessed .
  5. Titi-Lartey OA, Daley SF. Severe Acute Malnutrition: Recognition and Management of Marasmus and Kwashiorkor. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; updated 2025. Accessed .
  6. Vresk L, Flanagan M, Daniel AI, et al. Micronutrient status in children aged 6-59 months with severe wasting and/or nutritional oedema: implications for nutritional rehabilitation formulations. Nutr Rev 2024;83(1):112-145. doi:10.1093/nutrit/nuad165. Accessed .
  7. World Health Organization, UNICEF, International Bank for Reconstruction and Development/The World Bank. Levels and trends in child malnutrition: UNICEF/WHO/World Bank Group joint child malnutrition estimates, key findings of the 2025 edition. Geneva: WHO; 2025. Accessed .
  8. Tsegaye AT, Pavlinac PB, Walson JL, et al. Integrated Management of Childhood Illness (IMCI) and dehydration assessment in wasted children. PLOS Glob Public Health 2023;3:e0002520. doi:10.1371/journal.pgph.0002520. Accessed .

Educational content for medical students and doctors. It is not a substitute for clinical judgement or local guidelines.