8.1 Protein-Energy Malnutrition (PEM) & Micronutrient Deficiencies

Protein-Energy Malnutrition (PEM) & Severe Acute Malnutrition (SAM)

Protein-Energy Malnutrition (PEM) represents a spectrum of clinical conditions caused by relative or absolute deficiency of proteins and calories. In pediatric clinical practice and UPSC CMS examinations, PEM is classified according to WHO criteria, Gomez classification, and Wellcome trust classification.

Diagnostic Criteria & Definitions

WHO Classification of Acute Malnutrition (6 to 59 Months)

• Moderate Acute Malnutrition (MAM):
  • Weight-for-Height Z-score (SD score): between -2 SD and -3 SD
  • Mid-Upper Arm Circumference (MUAC): 11.5 cm to 12.4 cm
  • Bilateral Pitting Oedema: Absent
• Severe Acute Malnutrition (SAM) (Any ONE of the following criteria):
  • Weight-for-Height Z-score: < -3 SD
  • MUAC: < 11.5 cm (measured with a non-stretchable Shakir's tape at the midpoint between acromion and olecranon)
  • Presence of Bilateral Pitting Oedema of nutritional origin (nutritional oedema automatically categorizes the child as SAM, regardless of WFH Z-score)

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Clinical Comparison: Kwashiorkor vs. Marasmus

Marasmic-Kwashiorkor: Combined form displaying features of severe wasting (WFH < -3 SD) alongside bilateral pitting nutritional edema.

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Pathophysiology of SAM & Reductive Adaptation

Children with SAM undergo reductive adaptation, a physiological downsizing to survive starvation:

1. Cellular Pump Dysfunction: The Na+/K+ ATPase pump activity slows down, leading to intracellular accumulation of Sodium and loss of Potassium and Magnesium.
2. Metabolic Downregulation: Basal metabolic rate (BMR), protein synthesis, and cardiac output decrease.
3. Hepatic Steatosis: In Kwashiorkor, impaired synthesis of apolipoproteins prevents export of triglycerides from hepatocytes, resulting in severe fatty liver.
4. Immunodeficiency: Severe atrophy of the thymus, lymph nodes, and mucosal barrier leads to subclinical sepsis without typical signs like fever or leukocytosis.

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WHO 10-Step Inpatient Management Protocol for SAM

Inpatient management of complicated SAM is divided into Stabilization Phase (Days 1–7) and Rehabilitation Phase (Weeks 2–6).

Stabilization Phase (Steps 1 to 7)

1. Treat/Prevent Hypoglycemia: Defined as Blood Glucose < 54 mg/dL (3.0 mmol/L). Give 50 mL of 10% Glucose/Sucrose orally or via NGT immediately. Feed F-75 every 30 minutes for 2 hours.
2. Treat/Prevent Hypothermia: Axillary temperature < 35.5°C (95.9°F). Warm the child (Kangaroo Mother Care, radiant warmer, clothing). Ensure room temperature is 28–32°C.
3. Treat/Prevent Dehydration: Standard WHO ORS should NOT be used because of its high sodium content (75 mmol/L), which causes fluid overload and heart failure in SAM. Use ReSoMal (Rehydration Solution for Malnutrition: Sodium 45 mmol/L, Potassium 40 mmol/L, Magnesium 3 mmol/L). Give 5 mL/kg every 30 minutes for 2 hours, then 5–10 mL/kg/hr for up to 10 hours.
4. Correct Electrolyte Imbalances: Intracellular K+ and Mg2+ are depleted. Supplement Potassium (3–4 mmol/kg/day) and Magnesium (0.4–0.6 mmol/kg/day) for at least 2 weeks. Do NOT treat edema with diuretics or rapid sodium administration!
5. Treat Infections: Assume all complicated SAM children have microvascular bacteremia/sepsis. Administer broad-spectrum antibiotics: Ampicillin (50 mg/kg IV/IM q6h) + Gentamicin (7.5 mg/kg IV/IM OD) for 7 days (or oral Amoxicillin if uncomplicated).
6. Correct Micronutrient Deficiencies: Administer Vitamin A on Day 1 (unless given in past month). Give Folic Acid 5 mg on Day 1, then 1 mg/day. Supplement Zinc (2 mg/kg/day) and Copper.
   • CRITICAL CONTRAINDICATION: Do NOT give Iron in the stabilization phase! Free iron facilitates bacterial growth, worsens oxidative stress, and impairs intestinal mucosa. Iron is started ONLY in the rehabilitation phase when the child gains appetite.
7. Cautious Feeding (F-75): Feed starter formula F-75 (75 kcal and 0.9 g protein per 100 mL). Energy intake target: 100 kcal/kg/day and protein 1.0–1.5 g/kg/day in small, frequent feeds every 2–3 hours.

Rehabilitation Phase (Steps 8 to 10)

1. Achieve Catch-up Growth: Transition from F-75 to F-100 (100 kcal and 2.9 g protein per 100 mL) or Ready-to-Use Therapeutic Food (RUTF). Energy target: 150–220 kcal/kg/day and protein 4–6 g/kg/day.
2. Sensory Stimulation & Emotional Care: Tender loving care, structured play, and stimulating environment.
3. Prepare for Discharge & Follow-up: Ensure immunizations are up to date, educate caregiver on feeding, and link to Community-Based Management of Acute Malnutrition (CMAM) / Nutrition Rehabilitation Centre (NRC).

Pediatric Micronutrient Deficiencies

Micronutrient deficiencies ('hidden hunger') significantly impair physical growth, neurodevelopment, and immune function in infants and children.

1. Vitamin A (Retinol) Deficiency & Prophylaxis

Vitamin A is essential for visual pigment synthesis (rhodopsin), epithelial tissue integrity, and immune resistance.

WHO Classification of Xerophthalmia

• XN: Night blindness (first clinical symptom, often noticed by mothers at twilight)
• X1A: Conjunctival xerosis (dryness and loss of transparency of bulbar conjunctiva)
• X1B: Bitot's spots (pathognomonic: triangular, foamy, silvery-white plaques on temporal bulbar conjunctiva consisting of keratinized epithelium and Corynebacterium xerosis)
• X2: Corneal xerosis (hazy, dry, non-wetting cornea)
• X3A: Corneal ulceration / Keratomalacia involving < 1/3 of corneal surface
• X3B: Corneal ulceration / Keratomalacia involving > 1/3 of corneal surface (emergency; leads to perforation and blindness)
• XS: Corneal scar (healed end-stage lesion)
• XF: Xerophthalmic fundus (pale spots on retina)

National Vitamin A Prophylaxis Schedule (India UIP)

Under the National Programme for Prevention of Blindness due to Vitamin A Deficiency, a total of 9 doses (17 lakh IU) are administered orally from 9 to 60 months of age:

Therapeutic Management of Active Xerophthalmia / Measles / SAM: Administer high-dose oral Vitamin A immediately on Day 1, Day 2, and Day 14:

• Age < 6 months: 50,000 IU per dose
• Age 6–12 months: 100,000 IU per dose
• Age > 12 months: 200,000 IU per dose

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2. Vitamin D Deficiency & Rickets

Nutritional Rickets is caused by deficient Vitamin D, impaired 25-hydroxylation (liver), 1-alpha-hydroxylation (kidney), or target organ unresponsiveness, leading to unmineralized osteoid matrix at growth plates.

Clinical Manifestations

• Head & Cranium:
  • Craniotabes: Softening of skull bones (ping-pong ball sensation on pressure over parietal/occipital bones; earliest sign, seen in infants < 6 months).
  • Delayed closure of anterior fontanelle (normally closes by 12–18 months; remains wide open > 18 months).
  • Frontal bossing and parietal bossing giving the skull a 'caput quadratum' (box-like) shape.
  • Delayed dentition and enamel hypoplasia.
• Thorax:
  • Rachitic Rosary: Palpable, non-tender, rounded enlargement of costochondral junctions.
  • Harrison's Groove / Sulcus: Horizontal groove along the lower border of the chest corresponding to diaphragmatic insertion.
  • Pigeon Chest (Pectus carinatum): Sternum protrudes anteriorly.
• Extremities:
  • Widening of wrists and ankles: Epiphyseal expansion of distal radius, ulna, tibia, and fibula.
  • Bow Legs (Genu varum) or Knock Knees (Genu valgum) once the child starts weight-bearing.
  • Greenstick fractures due to cortical thinning.

Radiological Findings (X-Ray Wrist AP View)

• Fraying: Indistinct, brush-like margin of the metaphysis.
• Cupping: Concave distension of the metaphyseal margin.
• Splaying: Lateral widening of the metaphyseal end.
• Increased Joint Space: Distance between epiphysis and metaphysis is widened.

Laboratory Diagnosis & Stoss Therapy

• Biochemical Panel: Serum Calcium is normal/low, Phosphate is low, Serum Alkaline Phosphatase (ALP) is markedly elevated (best indicator of disease activity and healing).
• Stoss Therapy: Single oral/IM dose of 600,000 IU (or 300,000–600,000 IU) Vitamin D3 (Cholecalciferol) OR daily oral administration of 2,000–5,000 IU/day for 4–6 weeks, supplemented with elemental Calcium (50 mg/kg/day).

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3. Vitamin C Deficiency (Infantile Scurvy)

• Pathophysiology: Impaired hydroxylation of proline and lysine residues in procollagen, causing vessel wall fragility and defective osteoid matrix.
• Clinical Presentation: Age 6–24 months. Irritability, subperiosteal hematomas causing extreme pain (child assumes a 'frog-leg position' with pseudoparalysis of lower limbs), scorbutic rosary (sharp, tender, subluxated costochondral junctions), and swollen, spongy, bleeding gums.
• Radiological Signs: Trümmerfeld zone (scurvy line/zone of destruction), Frankel's line (dense zone of calcification at metaphysis), Wimberger's ring (calcified ring surrounding radiolucent epiphysis), and Pelkan's spur.

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4. Zinc Deficiency & Iron Deficiency Anemia

• Zinc Deficiency: Causes Acrodermatitis Enteropathica (triad of periorificial/acral vesicobullous dermatitis, chronic diarrhea, and alopecia), growth failure, and impaired cell-mediated immunity. Standard pediatric diarrhea therapy requires 10 mg/day (for infants < 6 months) or 20 mg/day (for children ≥ 6 months) of elemental Zinc for 14 days.
• Iron Deficiency Anemia (IDA): Most common hematological disorder in children (peak age 6–24 months). Presents with pallor, irritability, pica, breath-holding spells, and impaired cognitive development. Peripheral smear shows microcytic hypochromic RBCs with low serum ferritin and elevated Total Iron Binding Capacity (TIBC). Dose: 3–6 mg/kg/day of elemental iron divided BD for 3 months after Hb normalizes.