Nutrition & Malnutrition
Malnutrition is the commonest underlying cause of childhood death in India, and it almost never appears on a death certificate. Children die of pneumonia, diarrhoea and measles, and malnutrition is what made those illnesses fatal.
The examinable content divides cleanly into two halves that require different kinds of thinking. Measurement is arithmetic, and management is physiology. Getting the second half wrong kills children who were surviving until treatment began.
1. Three Measurements, Three Timescales
The three anthropometric indices are frequently treated as interchangeable severity grades of the same thing. They are not. They measure different processes over different periods.
| Index | Measurement | Timescale | Meaning |
|---|---|---|---|
| Wasting | Weight for height | Weeks to months | Acute, current |
| Stunting | Height for age | Years | Chronic, cumulative |
| Underweight | Weight for age | Composite | Either or both |
The organising tool is that the timescale is the diagnosis. A wasted child is losing weight now. A stunted child stopped growing in length some time ago and may be perfectly well today. An underweight child could be either.
This matters because the interventions differ entirely. Wasting responds to treatment in weeks; stunting is largely irreversible after the first two years, because linear growth potential lost in that window is not recovered later.
Underweight is the least informative of the three, since it cannot distinguish a short well-nourished child from a tall wasted one, and it is retained mainly because weight for age is the easiest measurement to take in the field.
2. Reading the Growth Indices
Anthropometric status is expressed as a Z-score, meaning the number of standard deviations from the median of the WHO reference population.
| Category | Z-score |
|---|---|
| Normal | Above minus 2 |
| Moderate | Minus 2 to minus 3 |
| Severe | Below minus 3 |
Severe acute malnutrition is defined by any one of three criteria: weight for height below minus 3 Z-scores, mid-upper arm circumference under 115 mm, or bilateral pitting oedema.
Bilateral pitting oedema alone defines severe acute malnutrition regardless of the weight, which is the point most often missed. The oedematous child may weigh more than a healthy one.
Mid-upper arm circumference is the field tool of choice in children aged 6 to 59 months, because the measurement changes little with age in this range, needs no scale or height board, and predicts mortality better than weight for height.
3. Kwashiorkor and Marasmus
The classical distinction remains examinable, though modern management barely uses it.
| Feature | Marasmus | Kwashiorkor |
|---|---|---|
| Oedema | Absent | Present, bilateral pitting |
| Weight | Severely reduced | May be near normal |
| Appearance | Old man facies, visible ribs | Moon face, distended abdomen |
| Skin and hair | Dry, thin | Flaky paint dermatosis, hair depigmentation |
| Appetite | Preserved, often ravenous | Poor |
| Mood | Alert, irritable | Apathetic, miserable |
Marasmus is adaptation that succeeded; kwashiorkor is adaptation that failed. The marasmic child has broken down fat and muscle to maintain the internal environment. The kwashiorkor child has not, and shows hypoalbuminaemia, fatty liver and oedema.
The mechanism of kwashiorkor is not settled, and pure protein deficiency is no longer accepted as a complete explanation. Aflatoxin exposure, oxidative stress and gut microbiome differences are all implicated.
Marasmic kwashiorkor exists and carries the worst prognosis, combining severe wasting with oedema.
4. Reductive Adaptation
This section explains almost every counterintuitive rule in the management of severe malnutrition, and it deserves to be understood rather than memorised.
A severely malnourished child has downregulated every energy-expensive process in the body to survive on almost nothing. This is called reductive adaptation, and it is a successful adaptation until treatment interferes with it.
| System | Adaptation | Clinical consequence |
|---|---|---|
| Cardiac | Reduced muscle mass and output | Cannot tolerate fluid loads |
| Renal | Reduced glomerular filtration | Cannot excrete a sodium or fluid load |
| Sodium pump | Downregulated | Intracellular sodium high, potassium low |
| Liver | Reduced gluconeogenesis | Hypoglycaemia within hours of not feeding |
| Immune | Suppressed | Infection without fever or leucocytosis |
| Thermal | Reduced heat production | Hypothermia |
The consequence is that the child is in danger from feeding, from fluid and from warmth applied carelessly, not only from the deficit itself.
Two facts follow directly. Infection in severe malnutrition presents without fever, without raised white cells and often without any localising sign, which is why antibiotics are given routinely rather than on clinical suspicion.
And body potassium is depleted even when serum potassium is normal, because the sodium pump has failed and potassium has leaked out of cells while sodium has entered. Total body sodium is high despite hyponatraemia.
5. The Ten Steps of Management
Management is divided into a stabilisation phase, roughly the first week, in which the child is kept alive and metabolic derangements corrected, and a rehabilitation phase of several weeks in which catch-up growth is driven.
| Steps 1 to 7: stabilise | Steps 8 to 10: rehabilitate |
|---|---|
| Treat hypoglycaemia | Achieve catch-up growth |
| Treat hypothermia | Provide sensory stimulation |
| Treat dehydration | Prepare for follow-up |
| Correct electrolytes | |
| Treat infection | |
| Correct micronutrients | |
| Begin cautious feeding |
Step 7 is cautious feeding, not full feeding, and this is where children are killed. Feeding a starved child at normal energy density precipitates refeeding syndrome: insulin release drives phosphate, potassium and magnesium into cells, and cardiac failure follows in a heart that has already lost muscle mass.
F-75, containing 75 kilocalories per 100 mL, is used in the stabilisation phase, given in small frequent feeds including overnight. It is deliberately low in protein and sodium and provides only maintenance energy.
F-100, containing 100 kilocalories per 100 mL, or ready-to-use therapeutic food, is used in the rehabilitation phase once appetite returns and oedema has resolved.
Return of appetite is the signal to move between phases. It is a clinical marker of recovering physiology and is more reliable than any laboratory value.
Iron is withheld during stabilisation and started only in rehabilitation. Free iron promotes bacterial growth and generates oxidative damage in a child whose antioxidant defences are already exhausted. All other micronutrients, including vitamin A, zinc and folate, are given from the outset.
6. Fluids: Why Standard Resuscitation Kills
Dehydration in severe malnutrition is both overdiagnosed and dangerous to treat conventionally.
The clinical signs of dehydration are unreliable in a severely malnourished child, because sunken eyes and slow skin pinch are produced by loss of subcutaneous fat and skin elasticity regardless of hydration.
Oral or nasogastric rehydration is preferred, using ReSoMal, a modified solution with less sodium and more potassium than standard oral rehydration solution.
The composition follows directly from the physiology: total body sodium is already high and total body potassium is depleted, so giving standard rehydration solution adds sodium the kidney cannot excrete to a heart that cannot handle the volume.
ReSoMal is not used in cholera or profuse watery diarrhoea, where sodium losses are genuinely large and standard solution is required.
Intravenous fluid is reserved for shock alone, given slowly and in small volumes with frequent reassessment, because a rising pulse or respiratory rate during infusion means the heart is failing, not that more fluid is needed.
7. Community Management and the 2023 Guideline
Most children with severe acute malnutrition do not need a hospital bed, and treating them all as inpatients would exceed any health system's capacity.
The dividing line is appetite and complications, not the severity of the anthropometry. A child with severe acute malnutrition who has a good appetite, no oedema of the legs and no medical complication is treated at home.
The appetite test is the decisive assessment. The child is offered ready-to-use therapeutic food under observation, and a child who eats an adequate portion can be managed in the community, while a child who refuses cannot.
The reason it works so well is that appetite is an integrated marker of physiology. A child whose metabolism is failing, who is infected, or whose electrolytes are deranged does not eat, whatever the weight chart shows.
Ready-to-use therapeutic food makes community treatment possible because it is energy dense, requires no water or cooking, resists bacterial growth, and can therefore be given safely in a home with no clean water.
Discharge is not defined by weight alone. The child must have gained weight consistently, be free of oedema for a defined period, be eating well and be free of infection, and follow-up is arranged because relapse after discharge is common.
The 2023 guideline
WHO published a substantially expanded guideline in 2023 on the prevention and management of wasting and nutritional oedema, replacing the 2013 document.
Three changes are worth knowing. The scope was widened from severe acute malnutrition to the broader population of infants at risk of poor growth and development, including infants under six months, who were largely unaddressed before.
Moderate wasting received formal recommendations for the first time, having previously fallen between prevention and treatment programmes.
And psychosocial care of the child and the caregiver, and continuity of care after inpatient discharge, were brought into the guideline, recognising that relapse after discharge is a major and previously neglected cause of failure.
8. Infant and Young Child Feeding
Breastfeeding is initiated within one hour of birth, and colostrum is given rather than discarded. It is rich in immunoglobulin A and provides passive mucosal protection at the point of first exposure.
Exclusive breastfeeding is recommended for six months, meaning no water, no honey, no ritual feeds. Breast milk supplies sufficient water even in hot climates.
Complementary feeding begins at six months, because breast milk alone can no longer meet energy, iron and zinc requirements after that point, while breastfeeding continues to two years and beyond.
The window from six to twenty-four months is where stunting is determined. Growth faltering in Indian children begins around six months and is largely established by two years, which is why interventions after that age recover so little.
The complementary feeding rules are frequency, amount, thickness, variety and responsive feeding. Thickness matters more than people expect, because a thin gruel fills a small stomach with water and delivers little energy.
9. Micronutrient Deficiencies
| Deficiency | Presentation | Note |
|---|---|---|
| Vitamin A | Night blindness, Bitot spots, xerophthalmia, keratomalacia | Leading preventable cause of childhood blindness |
| Iron | Microcytic anaemia, impaired cognition | Commonest deficiency worldwide |
| Iodine | Goitre, cretinism, impaired development | Cretinism is preventable and irreversible |
| Vitamin D | Rickets, hypocalcaemic seizures | Common despite abundant sunlight |
| Zinc | Diarrhoea, poor growth, impaired healing | Given in every diarrhoeal episode |
| Vitamin B12 | Megaloblastic anaemia, developmental regression | Vegetarian and exclusively breastfed infants of deficient mothers |
| Vitamin C | Scurvy: bleeding gums, subperiosteal haemorrhage, pseudoparalysis | Refusal to move a limb from pain |
Vitamin A deficiency progresses in a defined order, and knowing the order is what the examiner tests. Night blindness comes first and is reversible. Bitot spots, which are foamy triangular patches of keratinised conjunctiva, come next. Corneal xerosis, then ulceration, then keratomalacia follow, and keratomalacia destroys the eye.
India's programme gives 100,000 IU at nine months with measles-rubella vaccine, then 200,000 IU every six months to five years, giving nine doses in total.
Vitamin A is also given in every case of measles, on two consecutive days, because measles depletes stores at the moment they are most needed.
Iodine deficiency in pregnancy causes cretinism, with severe intellectual disability, deafness and spasticity, and universal salt iodisation is the intervention that prevents it.
Anaemia
Anaemia is the most widespread nutritional problem in Indian children and is mostly iron deficiency, though folate, vitamin B12 and chronic infection all contribute.
Infants are vulnerable from six months onwards because iron stores acquired in the third trimester are exhausted by then, and breast milk, though its iron is highly bioavailable, contains little of it. Preterm and low birth weight infants exhaust their stores earlier.
The consequences reach beyond haemoglobin. Iron deficiency impairs cognitive development and attention, and the deficit may persist after the anaemia is corrected, which is the argument for prevention rather than treatment.
A revealing detail of NFHS-6 is that all seven anaemia indicators were removed from the survey, after the previous round recorded anaemia in children under five rising from 58.6 to 67.1 percent. The measurement was contested, but the absence of the indicator is itself worth noting.
10. Rickets
Rickets is failure of mineralisation at the growth plate, so it occurs only in growing bone and its signs cluster where growth is fastest.
The features are craniotabes in infancy, a widened anterior fontanelle, frontal bossing, the rachitic rosary at the costochondral junctions, Harrison sulcus, widened wrists and ankles, and bowing of the legs once the child begins to walk.
The radiograph shows cupping, splaying and fraying of the metaphysis, with a widened growth plate.
Nutritional rickets is due to vitamin D deficiency and responds to vitamin D. Biochemistry shows low or normal calcium, low phosphate, raised alkaline phosphatase and raised parathyroid hormone.
Rickets that does not respond to vitamin D is not nutritional, and the commonest cause is X-linked hypophosphataemic rickets, in which renal phosphate wasting is the primary defect and parathyroid hormone is not raised. Renal tubular acidosis and chronic kidney disease are the other causes to consider.
Vitamin D deficiency remains common in India despite abundant sunlight, because of skin pigmentation, covering clothing, urban living and air pollution.
11. India's Nutrition Picture and Programmes
The sixth National Family Health Survey, conducted in 2023 to 2024, showed stunting falling from 35.5 to 29.3 percent, the largest decline recorded between two consecutive rounds.
Wasting, however, remains close to 19 percent, having barely moved from the 19.3 percent of the previous round, and underweight fell only marginally from 32.1 to 31.8 percent. Severe wasting did fall from 7.7 to 5.2 percent.
The pattern is informative. Chronic malnutrition is improving while acute malnutrition is not, which suggests that gains have come from sanitation, maternal education and household conditions rather than from treatment of the acutely wasted child.
Programmes are delivered largely through the anganwadi system. Saksham Anganwadi and Poshan 2.0 consolidates supplementary nutrition, infant and young child feeding, and the management of moderate and severe acute malnutrition.
Nutrition Rehabilitation Centres manage severe acute malnutrition with medical complications as inpatients, while uncomplicated cases with preserved appetite are managed in the community with ready-to-use therapeutic food.
The Mid Day Meal scheme, now PM POSHAN, and the Integrated Child Development Services supply the population-level component, while anaemia control operates through iron and folic acid supplementation across age groups.
12. Worked Examples
Example 1. A 3-year-old has height for age at minus 3 Z-scores but weight for height at minus 1. What is the classification and what does it mean?
The child is severely stunted but not wasted. This indicates chronic malnutrition established over years rather than a current deficit, and the child is not acutely at risk. Stunting reflects the cumulative effect of inadequate nutrition, repeated infection and poor sanitation, is largely irreversible after two years of age, and predicts reduced cognitive attainment and adult productivity.
Example 2. A child with severe acute malnutrition has bilateral pitting oedema and serum potassium of 3.9 mmol/L. Is potassium supplementation needed?
Yes. Serum potassium reflects the extracellular compartment only, and in reductive adaptation the sodium pump is downregulated, so potassium has leaked out of cells and been excreted while sodium has entered them. Total body potassium is depleted even when the serum value is normal, and total body sodium is high despite hyponatraemia. Potassium is supplemented and sodium restricted.
Example 3. A severely malnourished child with diarrhoea has sunken eyes and a slow skin pinch. Should intravenous fluids be given?
Not on these findings. Sunken eyes and a slow skin pinch are produced by loss of subcutaneous fat and skin elasticity in a malnourished child regardless of hydration, so dehydration is overdiagnosed. Oral or nasogastric ReSoMal is preferred. Intravenous fluid is reserved for shock, given slowly with frequent reassessment, because a rising pulse or respiratory rate during infusion indicates cardiac failure rather than a need for more volume.
Example 4. A 2-year-old with severe acute malnutrition is admitted, apyrexial, with a normal white cell count. Should antibiotics be given?
Yes, routinely. Immune suppression in severe malnutrition means infection presents without fever, without leucocytosis and often without any localising sign, so the usual indicators of infection are absent precisely when infection is most likely and most lethal. Antibiotics are therefore given to every child with severe acute malnutrition rather than on clinical suspicion.
Summary
Three indices, three timescales. Wasting is acute, stunting is chronic, underweight is composite and least informative.
Stunting is largely irreversible after two years, so the six to twenty-four month window determines it.
Severe acute malnutrition is defined by weight for height below minus 3, mid-upper arm circumference under 115 mm, or bilateral pitting oedema alone.
Reductive adaptation explains the management. Every energy-expensive process has been downregulated, so the child cannot tolerate fluid, cannot mount a fever, and cannot handle full feeds.
Infection presents without fever or leucocytosis, so antibiotics are routine.
Body potassium is depleted and body sodium is high, whatever the serum values show.
Feed cautiously with F-75 in stabilisation and F-100 or therapeutic food in rehabilitation, using return of appetite as the signal to progress.
Withhold iron until rehabilitation, because free iron feeds bacteria and generates oxidative damage.
Use ReSoMal, not standard rehydration solution, except in cholera.
Vitamin A deficiency progresses from night blindness through Bitot spots to keratomalacia, and the order is what is examined.
India's stunting fell to 29.3 percent in NFHS-6, but wasting remains near 19 percent, meaning chronic malnutrition is improving while acute malnutrition is not.
