Paediatrics — Nutrition and Growth, NMC MBBS licence examination syllabus (Nepal Medical Council).
Nutrition and growth: the malnourished child
These children die of the treatment as often as of the disease.
Severe acute malnutrition is one of the few conditions where the instinctive management is actively dangerous. A child who is starving, dehydrated and infected seems to call for fluid, food and antibiotics given generously — and giving fluid and food generously is precisely what kills them. Understanding why is the whole point of this chapter, and it turns on a single physiological idea.
The other half of the subject is quieter but affects far more children: growth faltering picked up on a chart, and the micronutrient deficiencies that cause preventable blindness, anaemia and intellectual disability. Neither is dramatic. Both are enormously consequential.
🩺 Where this lives: Undernutrition is an underlying factor in a large share of child deaths that are formally attributed to infection. The death certificate says pneumonia, measles or diarrhoea; the reason the child could not survive it was nutritional. That is why the malnutrition–infection cycle matters so much, and why treating a malnourished child's infection without treating the malnutrition — or the reverse — addresses only half of what is happening.
💡 A note on numbers. This chapter gives no doses, no cut-off values and no feed volumes. Severe acute malnutrition is managed strictly by protocol: MUAC and weight-for-height thresholds, therapeutic feed volumes, vitamin A dosing and antibiotic choice are all specified in the WHO and national protocols and are age- or weight-specific. Getting a feed volume wrong in this group is genuinely dangerous. Learn the principles here and take every number from the protocol in front of you. Population indicators — stunting, wasting, underweight — are covered in the Maternal and Child Health chapter.
Recognising severe acute malnutrition
The point that catches people out is oedema. A child with kwashiorkor may not look thin — the swelling adds weight and fills out the limbs and face, so a weight-based assessment can appear reassuring. This is why bilateral pitting oedema alone defines severe acute malnutrition, regardless of what the weight says. It is also why mid-upper arm circumference is so useful: it needs only a tape, works in the community, and is not distorted in the same way.
MARASMUS AND KWASHIORKOR — A USEFUL CONTRAST
MARASMUS Severe wasting, no oedema. The child has
consumed their own fat and muscle. Ribs
visible, loose folds of skin, an old-looking
face. Often ALERT and HUNGRY.
KWASHIORKOR BILATERAL PITTING OEDEMA is the defining
feature. Skin and hair changes, an enlarged
liver. Characteristically MISERABLE,
APATHETIC and with a POOR APPETITE.
The appetite difference is practically important. A child
who will not eat cannot be managed on home-based
therapeutic feeding, which is why an APPETITE TEST forms
part of deciding who needs admission.
MIXED PICTURES are common, and the older teaching that
these are two entirely separate diseases with two separate
causes is not how they are understood now. Treat what is in
front of you.
Why standard treatment is dangerous
REDUCTIVE ADAPTATION — THE IDEA THE WHOLE CHAPTER RESTS ON
A severely malnourished child has adapted to survive on
very little. Every system has slowed: cardiac output,
renal function, liver metabolism, immune response,
temperature regulation, sodium and potassium handling.
This has four practical consequences.
1. FLUID CAN KILL. A weakened heart cannot handle a rapid
intravenous bolus, and heart failure from over-
transfusion or over-hydration is a recognised cause of
death in these children. Rehydrate ORALLY where at all
possible, slowly, watching for signs of overload.
Intravenous fluid is reserved for shock, given
cautiously and by protocol.
2. FEEDING MUST START SLOWLY. Rapid refeeding drives
glucose into cells and takes potassium, magnesium and
phosphate with it — REFEEDING SYNDROME, which can cause
arrhythmia and death. Start with small, frequent, low
volume feeds and build up only in the second phase.
3. INFECTION IS OFTEN SILENT. The inflammatory response is
blunted, so a seriously infected child may have NO
fever and no rise in white cells. This is why
antibiotics are given EMPIRICALLY to severely
malnourished children rather than waiting for evidence
of infection.
4. THEY BECOME COLD AND HYPOGLYCAEMIC QUICKLY. Minimal fat
and glycogen, poor temperature control. Keep the child
warm and feed frequently, INCLUDING OVERNIGHT — a long
unfed night is a recognised danger.
ALSO: sodium is relatively high and potassium low in body
stores despite what the blood may show, which is why the
rehydration and feed formulations used in this group are
specifically designed rather than standard ones.
Management
💡 Exam angle: the two-phase structure is examined because getting the order wrong is harmful. Stabilisation treats hypoglycaemia, hypothermia, dehydration, electrolytes and infection, with cautious feeding and no attempt to gain weight. Only once the child is stable does rehabilitation push catch-up growth. A question describing high-energy feeding started immediately in a shocked, hypothermic child is describing an error.
Micronutrients
Vitamin A deficiency remains a leading preventable cause of childhood blindness, and the sequence — night blindness, then conjunctival and corneal changes, then irreversible corneal damage — is worth knowing because the early stages are treatable and the late stage is not. It also worsens measles and diarrhoea, which is why vitamin A supplementation is part of measles management in deficient populations and why it features in national supplementation programmes.
Growth monitoring
💡 Exam angle: the growth chart question almost always tests trend versus single point. A child who is small but tracking steadily along a line is usually constitutionally small and well. A child crossing centile lines downwards has a problem, even if the current weight is still within the normal range. When faltering growth is found, work through the causes in order: is enough food offered, is it taken, is it absorbed, and is it being used up by chronic infection — with tuberculosis and HIV worth active consideration.
Clinical reasoning: four presentations
🔍 Case 1 — the swollen child who looks well-fed
PresentationAn 18-month-old has swollen legs and a puffy face. His weight is near the expected range, and staff comment that he does not look thin. He is miserable, apathetic and refuses food. Hair is sparse and pale.
TrapBeing reassured by the weight.
ReasoningBilateral pitting oedema defines severe acute malnutrition regardless of weight, because the oedema masks the deficit. Apathy, poor appetite and hair changes fit kwashiorkor.
AnswerManage as severe acute malnutrition per protocol. His poor appetite means he needs inpatient stabilisation rather than home-based therapeutic feeding.
🔍 Case 2 — generous fluid and a deteriorating child
PresentationA severely malnourished child with diarrhoea is given rapid intravenous fluid as would be standard for dehydration. Within hours he becomes breathless with a raised respiratory rate and an enlarging liver.
What happenedFluid overload and heart failure.
ReasoningReductive adaptation leaves a weakened myocardium that cannot handle rapid volume. Over-hydration is a recognised cause of death in this group, and standard rehydration protocols do not apply.
AnswerStop the infusion and manage overload per protocol. Rehydrate malnourished children orally and slowly wherever possible, using the specified formulation, reserving intravenous fluid for shock.
🔍 Case 3 — no fever, but not well
PresentationA child with severe acute malnutrition is lethargic and feeding poorly. He is afebrile with a normal white cell count, so infection is considered unlikely and antibiotics are withheld.
ErrorApplying normal markers of infection to an abnormal immune system.
ReasoningThe inflammatory response is blunted in severe malnutrition, so serious infection frequently occurs without fever or leucocytosis. Lethargy and poor feeding are themselves the warning signs.
AnswerGive empirical antibiotics as the protocol directs for severe acute malnutrition, alongside warming, glucose and cautious feeding. Absence of fever is not evidence of absence of infection here.
🔍 Case 4 — small, but is she falling?
PresentationTwo toddlers are both below the expected weight for age. One has tracked steadily along the same low line since birth. The other was previously average and has crossed two centile lines downwards over six months.
Key questionWhat is the trend?
ReasoningThe first child is likely constitutionally small and growing normally. The second has faltering growth, and the change over time is the abnormality — whatever the absolute figure.
AnswerAssess the second child: is food offered, taken, absorbed, or being used up? Take a feeding and social history, examine thoroughly, and consider chronic infection including tuberculosis and HIV.
Commonly confused
Confusion
The distinction
Why it matters
Normal weight vs not malnourished
Oedema masks the deficit
Bilateral pitting oedema alone defines SAM.
Marasmus vs kwashiorkor
Wasting without oedema versus oedema
Appetite differs, and so does admission need.
Standard vs malnutrition rehydration
Reductive adaptation weakens the heart
Rapid fluid can cause fatal overload.
Feeding generously vs cautiously
Refeeding syndrome
Start slow; build up in phase two.
No fever vs no infection
The inflammatory response is blunted
Antibiotics are given empirically.
Stabilisation vs rehabilitation
Weight gain belongs to phase two
Pushing growth too early is harmful.
Single measurement vs trend
Crossing centiles downwards
A small steady child is usually well.
Poor intake vs chronic infection
Consider TB and HIV in faltering growth
Otherwise the cause is missed.
Rapid revision
MUST-KNOW FACTS
1. SAM is identified by weight-for-height, MUAC, or BILATERAL PITTING OEDEMA.
2. OEDEMA ALONE defines severe acute malnutrition — whatever the weight.
3. MUAC needs only a tape, so it works in the community.
4. MARASMUS: severe wasting, no oedema, often alert and HUNGRY.
5. KWASHIORKOR: oedema, skin and hair changes, APATHETIC, POOR APPETITE.
6. Poor appetite means inpatient care rather than home-based feeding.
7. An APPETITE TEST helps decide who needs admission.
8. REDUCTIVE ADAPTATION: every system has slowed to survive.
9. Therefore FLUID CAN KILL — the heart cannot handle rapid volume.
10. Rehydrate ORALLY and SLOWLY where possible; IV only for shock.
11. Fluid overload and heart failure are recognised causes of death here.
12. Feed SLOWLY at first — REFEEDING SYNDROME can be fatal.
13. Refeeding shifts potassium, magnesium and phosphate into cells.
14. INFECTION IS OFTEN SILENT — no fever, no leucocytosis.
15. Give ANTIBIOTICS EMPIRICALLY in severe acute malnutrition.
16. Lethargy and poor feeding are themselves the warning signs.
17. They become HYPOTHERMIC and HYPOGLYCAEMIC fast.
18. Keep warm and feed frequently INCLUDING OVERNIGHT.
19. PHASE 1 STABILISATION: hypoglycaemia, hypothermia, dehydration, electrolytes, infection.
20. Do NOT push weight gain during stabilisation.
21. PHASE 2 REHABILITATION: catch-up feeding, stimulation, follow-up.
22. Many children can be treated at home with ready-to-use therapeutic food.
23. VITAMIN A deficiency: night blindness → xerophthalmia → BLINDNESS.
24. Vitamin A deficiency worsens measles and diarrhoea.
25. IRON deficiency is the commonest deficiency worldwide.
26. IODINE deficiency causes goitre and intellectual disability.
27. VITAMIN D deficiency causes RICKETS.
28. ZINC reduces the duration and severity of diarrhoea.
29. GROWTH CHART: the TREND matters more than a single point.
30. CROSSING CENTILES DOWNWARDS is the abnormality.
31. Faltering growth: is food offered, taken, absorbed, or used up?
32. Most faltering growth is inadequate INTAKE.
33. But consider chronic infection — TUBERCULOSIS and HIV.
34. Take all thresholds, volumes and doses from the current protocol.
💡 Exam angle: nearly every question here tests the same insight from a different angle — that a severely malnourished child is physiologically abnormal, so normal rules do not apply. Normal fluid rates overload them. Normal feeding rates harm them. Normal markers of infection fail in them. Recognise the pattern and the answers follow.
Syllabus points
How severe acute malnutrition is identified
Why oedema alone defines it
Marasmus and kwashiorkor contrasted
Appetite and who needs admission
Reductive adaptation
Why fluid can kill
Refeeding syndrome
Why infection is often silent
Hypothermia and hypoglycaemia
Stabilisation before rehabilitation
Micronutrient deficiencies that matter
Reading a growth chart by trend
Working through faltering growth
Create a free account to tick topics off, take notes as you read, watch the video lessons and get a day-by-day study plan built around your exam date.