A 2-year-old girl from a slum in Delhi presents with a 9-month history of progressive weight loss, chronic diarrhoea, and recurrent respiratory infections. On examination, weight is 8 kg (expected 12.5 kg), height 78 cm (expected 87 cm), with severe muscle wasting, loose skin folds, and absence of subcutaneous fat. Serum albumin is 3.2 g/dL, total protein 5.8 g/dL, and blood glucose 55 mg/dL. There is no oedema. What is the most likely diagnosis?

## Clinical Diagnosis: Marasmus ### Key Clinical Features Present **Key Point:** Marasmus is total caloric deficiency with relatively preserved protein intake, characterized by severe wasting, absence of oedema, and preserved (or near-normal) serum albumin. This child presents with the classic picture: 1. **Severe muscle wasting and loss of subcutaneous fat** — "skin and bones" appearance 2. **Chronic onset over 9 months** — indicates prolonged caloric insufficiency 3. **Absence of oedema** — critical distinguishing feature from kwashiorkor 4. **Serum albumin 3.2 g/dL (low-normal to low)** — less severely depressed than in kwashiorkor 5. **Hypoglycaemia (55 mg/dL)** — reflects depleted glycogen stores and impaired gluconeogenesis ### Differential Diagnosis: PEM Subtypes | Feature | Marasmus | Kwashiorkor | Marasmic-Kwashiorkor | |---------|----------|-------------|----------------------| | **Onset** | Chronic (months–years) | Acute (weeks–months) | Mixed | | **Oedema** | Absent | Present, bilateral | Present | | **Albumin** | 3.0–3.5 g/dL (mild ↓) | <2.5 g/dL (severe ↓) | <2.5 g/dL | | **Wasting** | Severe (BMI/age <70%) | Mild–moderate | Severe | | **Appearance** | Wizened, old-looking | Moon face, pot belly | Wasted + puffy | | **Alertness** | Alert, irritable, "old man" look | Apathetic, withdrawn | Variable | | **Skin lesions** | Minimal | Peeling dermatitis | Present | | **Hair changes** | Sparse, thin | Sparse, depigmented | Sparse | ### Biochemical Rationale **High-Yield:** In marasmus, total protein and albumin are relatively preserved because protein catabolism is proportional to caloric deficiency. The body spares visceral protein at the expense of somatic (muscle) protein. Hypoglycaemia occurs due to: - Depleted hepatic glycogen - Impaired gluconeogenesis (inadequate substrate and cofactors) - Reduced counter-regulatory hormone response **Clinical Pearl:** The absence of oedema in a severely wasted child is the single most reliable clinical sign of marasmus. Oedema indicates kwashiorkor (protein deficiency with relative caloric adequacy). ### Pathophysiology of Marasmus 1. **Prolonged inadequate caloric intake** — common in poverty, food insecurity, chronic diarrhoea 2. **Preferential catabolism of muscle and fat** — body preserves vital organs 3. **Metabolic adaptation** — reduced basal metabolic rate, hypothermia 4. **Impaired immune function** — T-cell mediated immunity severely compromised 5. **Hypoglycaemia and electrolyte derangements** — life-threatening complications **Mnemonic:** **MARASMUS** = **M**ass loss, **A**cute or chronic, **R**educed fat, **A**lbumin near-normal, **S**evere wasting, **M**uscle loss, **U**nder-nutrition, **S**kin and bones. ### Clinical Complications - **Hypoglycaemia** (as seen here, 55 mg/dL) → seizures, coma, death - **Hypothermia** — impaired thermoregulation - **Infections** — severe immunosuppression - **Electrolyte disturbances** — K^+^, Mg^2+^, phosphate depletion - **Refeeding syndrome** — if nutrition is reintroduced too rapidly ## Management Priorities 1. **Immediate:** Correct hypoglycaemia (10% dextrose IV), maintain warmth 2. **Feeding:** Gradual refeeding with micronutrient supplementation 3. **Monitoring:** Serial glucose, electrolytes, signs of infection 4. **Rehabilitation:** Catch-up growth over 6–12 months with adequate nutrition **Warning:** Rapid refeeding in marasmus can precipitate fatal cardiac arrhythmias and pulmonary oedema due to electrolyte shifts — start with 50–75 kcal/kg/day and increase gradually.