Gizi Buruk

01Pathophysiology

Severe acute malnutrition arises from a sustained imbalance between nutrient intake and the body's metabolic demands. Two classical clinical phenotypes exist: marasmus (non-edematous) and kwashiorkor (edematous), though mixed forms are common. The distinction matters less for treatment protocols and more for understanding the different physiologic derangements at play.

In marasmus, the body enters a state of prolonged energy conservation. Caloric deprivation forces extensive catabolism of both adipose tissue and skeletal muscle to sustain gluconeogenesis and basal metabolic functions. This explains why these children appear emaciated with visible ribs, loss of the buccal fat pad ("old man facies"), and generalized muscle wasting. The body effectively cannibalizes itself to survive.

Kwashiorkor is more complex and less fully understood. The traditional "protein deficiency" explanation has been partially replaced by theories involving oxidative stress and free radical damage to cell membranes, leading to increased capillary permeability and fluid shifts into the interstitial space. This produces the hallmark bilateral pitting edema that begins at the feet and can progress to generalized anasarca. The liver becomes fatty (hepatic steatosis) because the liver lacks adequate protein to synthesize lipoproteins for fat transport, resulting in hepatomegaly. The skin undergoes characteristic "flaky paint" dermatosis because of impaired cell turnover and zinc deficiency.

At the metabolic level, several critical derangements occur simultaneously. Reductive adaptation means the body downregulates metabolic rate, cardiac output, renal blood flow, and immune function. The sodium-potassium ATPase pump becomes dysfunctional, leading to intracellular sodium accumulation and total body potassium/magnesium depletion, even when serum sodium may appear normal or low. This is why edema in SAM must never be treated with diuretics and why sodium administration is dangerous.

The immune system becomes profoundly compromised. Thymic atrophy occurs early, leading to T-cell dysfunction. This is the reason why malnourished children frequently harbor infections without mounting the usual clinical signs such as fever, elevated white cell count, or localized inflammation. The guideline therefore mandates that all children with SAM be presumed infected and treated with empiric broad-spectrum antibiotics on admission.

Hypoglycemia (blood glucose < 54 mg/dL or < 3 mmol/L) occurs because glycogen stores are depleted and gluconeogenesis is impaired. This is a direct cause of death if not treated within hours of admission. Hypothermia co-occurs because the child lacks subcutaneous fat for insulation and has insufficient metabolic fuel to generate heat. The co-existence of hypoglycemia and hypothermia is a clinical marker of severe underlying infection.

Understanding reductive adaptation is the single most important pathophysiologic concept for management. It explains why aggressive refeeding is lethal: the heart, kidneys, and intestinal mucosa have atrophied and cannot handle sudden increases in osmotic load, fluid volume, or caloric intake. Rapid feeding causes fluid shifts, electrolyte crashes (particularly phosphate depletion), cardiac failure, and death. This is the basis of refeeding syndrome, and it is why the stabilization phase uses the low-calorie, low-protein F-75 formula rather than the calorie-dense F-100.

02Classification and Clinical Manifestation

Clinical Phenotype

Edema Severity

Complication Status

Diagnostic Criteria

03Diagnostic Workup

The best initial screening tool at the community level is the MUAC measurement, because it requires no scale, no height board, and can be performed by trained community health workers. A MUAC below 11.5 cm in children aged 6-59 months flags the child for immediate referral.

The confirmatory anthropometric test is the weight-for-height/length Z-score plotted against WHO growth standards. A score below -3 SD confirms severe wasting. However, a child can meet SAM criteria by MUAC alone, by WFH alone, or by the presence of bilateral pitting edema alone. These are independent criteria; any one of them is sufficient for diagnosis.

On arrival at a health facility, every child with SAM should have an immediate blood glucose check. If point-of-care glucose testing is unavailable, the guideline instructs clinicians to assume hypoglycemia and treat empirically with 50 mL of 10% glucose solution orally or via nasogastric tube (NGT), followed immediately by F-75. This is a high-yield principle: in resource-limited settings, the inability to confirm a diagnosis does not delay treatment.

The appetite test is a critical gatekeeper for outpatient versus inpatient routing. The child is offered RUTF in a calm environment with the caregiver present. If the child eats willingly and reaches the minimum portion threshold (1/4 packet for 4-6.9 kg, 1/3 packet for 7-9.9 kg, 1/2 packet for 10-14.9 kg), the appetite is classified as "good" and outpatient care is appropriate. A poor or absent appetite indicates possible underlying complications and mandates inpatient admission.

Edema assessment must be bilateral to qualify. Unilateral edema suggests other etiologies (lymphatic obstruction, cellulitis, DVT) and does not count toward the SAM diagnosis. The edema must be pitting in character, tested by pressing the dorsum of the foot firmly for 3 seconds.

04Management & Treatment

The 10-Step Inpatient Protocol by Phase

Nutritional Requirements by Phase

Antibiotic Protocol

Step 1: Treat and Prevent Hypoglycemia. On admission, give 50 mL of 10% glucose solution (one heaped teaspoon of sugar in 50 mL water) orally or via NGT, then start F-75 immediately. If the child is unconscious or lethargic, give 10% dextrose IV bolus at 5 mL/kg. Recheck blood glucose after 30 minutes. If still below 54 mg/dL, repeat the glucose bolus. Prevent recurrence by feeding F-75 every 2 hours for the first 24 hours, day and night, then every 2-3 hours for a minimum of 2 days.

Step 2: Treat and Prevent Hypothermia. If axillary temperature is below 36 degrees C, warm the child using kangaroo mother care (skin-to-skin contact), warm blankets covering the entire body including the head, or a radiant heater placed 50 cm away. Monitor temperature every 2 hours until it reaches 36.5 degrees C or higher. Do not use hot water bottles (risk of burns in a child who cannot move away). Feed F-75 every 2 hours to provide metabolic fuel for thermogenesis.

Step 3: Treat and Prevent Dehydration. Standard clinical signs of dehydration (skin turgor, sunken eyes) are unreliable in SAM because subcutaneous tissue loss mimics dehydration signs even when the child is euvolemic. Assume all SAM children with diarrhea or reduced urine output have at least mild dehydration. Use ReSoMal (not standard ORS, which has too much sodium and too little potassium for malnourished children). ReSoMal contains 37.5 mmol Na, 40 mmol K, and 3 mmol Mg per liter. Give 5 mL/kg every 30 minutes for the first 2 hours orally or via NGT, then 5-10 mL/kg/hour alternating with F-75 every hour for the next 10 hours. Avoid IV fluids except in frank hypovolemic shock, in which case give Ringer's Lactate mixed with 10% Dextrose (1:1 ratio, called RLG 5%) at 15 mL/kg over 1 hour.

Fluid overload is lethal in these children. Monitor respiratory rate and pulse every 30 minutes during rehydration. If respiratory rate increases by 5/min and pulse increases by 15/min, stop fluids immediately and reassess after 1 hour.

Step 4: Correct Electrolyte Imbalance. Potassium and magnesium supplementation is provided through the mineral mix added to F-75, F-100, and ReSoMal. There is no need for separate electrolyte orders if pre-mixed formulas are used. Never give sodium-heavy IV fluids (normal saline, Ringer's) except in shock. Do not treat edema with diuretics.

Step 5: Treat Infection. All SAM children receive empiric antibiotics regardless of clinical signs of infection. For uncomplicated outpatient cases, give oral amoxicillin 15 mg/kg every 8 hours for 5 days. For complicated inpatient cases, give parenteral ampicillin (50 mg/kg IV/IM every 6 hours for 2 days, then oral amoxicillin 25-40 mg/kg every 8 hours for 5 more days) plus gentamicin (7.5 mg/kg IV/IM once daily for 7 days). If appetite does not improve after completing the antibiotic course, continue for up to 10 days and perform a full reassessment.

Step 6: Correct Micronutrient Deficiency. Give Vitamin A on Day 1 (dose by age: < 6 months = 50,000 IU; 6-12 months = 100,000 IU; > 12 months = 200,000 IU). If the child has signs of Vitamin A deficiency (night blindness, Bitot spots) or recent measles within 3 months, give the dose on Day 1, Day 2, and Day 15. Give folic acid 5 mg on Day 1, then 1 mg/day thereafter. Give multivitamins (Vitamin C and B-complex) daily for at least 2 weeks.

Iron must be withheld until the Rehabilitation phase (approximately Week 2, once the child has appetite recovery and is gaining weight on F-100 or RUTF). This is because iron in the acute phase feeds bacteria and worsens infection through enhanced bacterial replication. When started, the dose is 3 mg/kg/day of elemental iron for at least 14 days until hemoglobin normalizes for 2 consecutive months.

If the child receives RUTF (which already contains all required micronutrients including iron), no additional micronutrient supplementation is needed, except for the therapeutic Vitamin A doses if deficiency signs or recent measles are present.

Step 7: Cautious Initial Feeding (Stabilization Phase). Use F-75 (75 kcal and 0.9 g protein per 100 mL). This low-calorie, low-protein formula is designed to stabilize metabolism without overwhelming the compromised organ systems. Feed every 2 hours in the first 24 hours (including through the night), then every 2-3 hours. If the child cannot finish at least 80% of the prescribed F-75 in two consecutive feeds, insert an NGT and deliver the remainder. Do not exceed 100 kcal/kg/day in this phase. For children with severe edema, restrict fluids to 100 mL/kg/day instead of the usual 130 mL/kg/day.

Transition Phase. When the child shows resolution of acute complications, return of appetite, and reduction of edema, transition from F-75 to F-100 (100 kcal and 2.9 g protein per 100 mL) or RUTF (545 kcal per 100 g). Replace F-75 with F-100 at the same volume for 2 days. On Day 3 of transition, increase F-100 by 10 mL per feed until the child leaves some or cannot finish, which usually happens at around 200 mL/kg/day. If using RUTF, introduce it with small frequent portions (8 times daily), supplementing with F-75 if the child cannot eat enough RUTF to meet caloric needs. If the child fails to consume at least half the required RUTF in 12 hours, stop RUTF and revert to F-75. Reattempt RUTF in 1-2 days.

Step 8: Catch-Up Growth (Rehabilitation Phase). Target 150-220 kcal/kg/day and 4-6 g protein/kg/day using F-100 or RUTF. RUTF dosing by weight: 4-4.9 kg = 1.5 packets/day; 5-6.9 kg = 2 packets/day; 7-9.9 kg = 3 packets/day; 10-14.9 kg = 4 packets/day (each packet = 500 kcal / 92 g). Target weight gain is at least 5 g/kg/day (or 50 g/kg/week). Poor weight gain (< 5 g/kg/day) requires a full reassessment for occult infection, poor compliance, or inadequate caloric delivery. Monitor for early signs of cardiac failure (respiratory rate increase by 5/min and pulse increase by 25/min sustained over two checks 4 hours apart); if detected, reduce feeding volume to 100 mL/kg/day and increase gradually (115 mL for 24 hours, then 130 mL for 48 hours, then increase by 10 mL per feed).

Step 9: Sensory Stimulation. Structured play therapy for 15-30 minutes daily using simple toys. Encourage caregiver-child bonding activities. Physical activity as tolerated once clinically stable.

Step 10: Prepare for Discharge and Follow-Up. Discharge from inpatient to outpatient care is based on clinical criteria (no complications, edema resolving, good appetite, clinically well), not anthropometric targets. The child then continues outpatient care with weekly follow-up visits, recalculating RUTF or F-100 doses at each visit based on current weight. Deworming with albendazole (200 mg for 12-23 months; 400 mg for 24 months and older; single dose) or pyrantel pamoate or mebendazole is given starting at Day 7 of treatment.

Cure criteria (must be sustained for 2 consecutive weeks): MUAC 12.5 cm or greater (green zone), and/or WFH/WFL at -2 SD or greater, and no edema, and clinically well. The anthropometric indicator used for discharge must be the same as the one used for admission.

Anthelmintic therapy is given at Day 7 if stool examination is positive. For preventive deworming in endemic areas, mebendazole 100 mg twice daily for 3 days starting on Day 7 is the standard approach for children over 12 months weighing at least 10 kg.

05Differential Diagnosis & Distractors

06Traps and High-Yield Pearls

The most common way students get SAM questions wrong falls into three categories.

First, treating SAM like a normally nourished dehydrated child. Students reflexively order IV normal saline or standard ORS for dehydration. In SAM, this is dangerous. The child already has excess total body sodium, depleted intracellular potassium, and a weakened myocardium. Standard ORS has too much sodium and too little potassium. The correct rehydration fluid is ReSoMal, and the correct route is oral or NGT, not IV. IV fluids are reserved only for frank hypovolemic shock, and even then, the volume and rate are carefully restricted (15 mL/kg over 1 hour using RLG 5%, not the 20 mL/kg boluses used in normally nourished children).

Second, giving iron too early. Iron supplementation in the stabilization phase feeds bacteria and worsens oxidative injury. Iron is withheld until the rehabilitation phase, when the child has a recovering appetite and is gaining weight. If a vignette describes a SAM child with severe anemia on Day 1, the answer is still to withhold iron and treat the underlying infection. The only exception is RUTF, which inherently contains iron, but this is given in calibrated amounts within the therapeutic food itself.

Third, confusing the formulas. F-75 is the stabilization formula (low calorie, low protein, designed to prevent refeeding syndrome). F-100 is the catch-up formula (higher calorie and protein, used in transition and rehabilitation). Giving F-100 in the stabilization phase risks refeeding syndrome, cardiac failure, and death. A vignette presenting a newly admitted SAM child with complications where the question asks about the next step in feeding should be answered with F-75, not F-100.

Other high-yield traps include: edema in SAM must never be treated with diuretics (the edema is from metabolic derangement, not volume overload); the co-occurrence of hypoglycemia and hypothermia should prompt the student to consider occult severe infection rather than treating each in isolation; and discharge criteria from inpatient to outpatient is based on clinical improvement (not anthropometric recovery), while cure from the outpatient program requires anthropometric normalization sustained for 2 consecutive weeks.

The core competency being tested is your ability to recognize that SAM is a metabolic emergency requiring a phased, cautious approach, not an aggressive one. The test-writer is evaluating whether you understand that the normal rules of pediatric resuscitation (bolus fluids, early feeding, iron for anemia) become harmful when applied to a child whose organ systems have adapted to starvation.