Severe Acute Malnutrition: Clinical Case and Q&A
Clinical Case of Protein-Energy Malnutrition (SAM)
A 2-year-old boy, Rahul, is brought to the pediatric emergency department by his mother. She reports that Rahul has been lethargic, irritable, and has had poor appetite for the past few weeks. His condition has worsened in the last 3 days with the onset of diarrhea.
History:
- Exclusive breastfeeding for 2 months, followed by irregular feeding with diluted cow's milk and occasional solid foods
- Recent history of measles infection 1 month ago
- Low socioeconomic background with limited access to healthcare
Physical Examination:
- Weight: 6.5 kg (severe underweight, below -3 SD on WHO growth chart)
- Height: 75 cm (stunted, below -2 SD on WHO growth chart)
- Visible severe wasting of muscles, especially in the buttocks and thighs
- Skin changes: dry, scaly skin with areas of hyperpigmentation and depigmentation
- Hair changes: sparse, thin, and easily pluckable hair with reddish discoloration
- Bilateral pitting edema up to the knees (+2)
- Abdominal distension with hepatomegaly
- Signs of dehydration: sunken eyes, decreased skin turgor
Laboratory Findings:
- Hemoglobin: 8.5 g/dL
- Serum albumin: 2.1 g/dL
- Blood glucose: 58 mg/dL
- Serum electrolytes: Hypokalemia (2.8 mEq/L) and hyponatremia (128 mEq/L)
Diagnosis:
Based on the clinical presentation and anthropometric measurements, Rahul is diagnosed with Severe Acute Malnutrition (SAM) with complications, specifically Kwashiorkor-Marasmus mixed type.
Management Plan:
- Immediate stabilization: Treat dehydration, hypoglycemia, and electrolyte imbalances
- Initiate F-75 therapeutic milk for initial nutritional rehabilitation
- Monitor for refeeding syndrome
- Treat infections: Broad-spectrum antibiotics and antimalarial if endemic
- Gradual transition to F-100 milk and RUTF (Ready-to-Use Therapeutic Food)
- Provide supplements: Vitamin A, Folic acid, Zinc, and other micronutrients
- Educate the mother on proper feeding practices and hygiene
- Plan for long-term follow-up and community-based management
Clinical Presentations of Protein-Energy Malnutrition (SAM)
Clinical Presentations of Severe Acute Malnutrition
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Marasmus
- Severe wasting of muscles and subcutaneous fat
- Appearance of "old man" face
- Skin hangs in loose folds, especially around the buttocks ("baggy pants")
- Alert and irritable behavior
- Absence of edema
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Kwashiorkor
- Generalized edema, often starting in the feet and legs
- "Moon face" appearance due to facial edema
- Skin changes: Hyperpigmentation, hypopigmentation, desquamation, and "flaky paint" dermatosis
- Hair changes: Thin, sparse, and easily pluckable hair with color changes (flag sign)
- Hepatomegaly due to fatty infiltration
- Apathetic and irritable behavior
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Marasmic Kwashiorkor (Mixed SAM)
- Features of both marasmus and kwashiorkor
- Severe wasting with some degree of edema
- Skin and hair changes similar to kwashiorkor
- Variable behavior, often apathetic
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Nutritional Dwarfism (Stunting)
- Chronic malnutrition leading to significantly reduced height-for-age
- Delayed motor and cognitive development
- Relatively normal body proportions, but overall small stature
- May not show acute signs of malnutrition
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Cachexia
- Severe wasting with significant loss of muscle mass
- Often associated with chronic diseases (e.g., HIV, tuberculosis, cancer)
- Disproportionate loss of lean body mass compared to fat mass
- Biochemical inflammation markers are often elevated
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Micronutrient Deficiency Syndromes
- Vitamin A deficiency: Night blindness, Bitot's spots, keratomalacia
- Iron deficiency: Pallor, koilonychia, glossitis
- Zinc deficiency: Growth retardation, delayed wound healing, dermatitis
- Iodine deficiency: Goiter, cretinism in severe cases
- Often coexist with protein-energy malnutrition
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Refeeding Syndrome
- Occurs when nutrition is reintroduced too quickly in severely malnourished individuals
- Characterized by severe electrolyte imbalances, particularly hypophosphatemia
- Can lead to cardiac arrhythmias, seizures, and respiratory failure
- Requires careful monitoring during initial phases of nutritional rehabilitation
Viva Questions and Answers on Protein-Energy Malnutrition (SAM)
Viva Questions and Answers on Severe Acute Malnutrition
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Q: What are the diagnostic criteria for Severe Acute Malnutrition (SAM) in children aged 6-59 months?
A: The WHO criteria for SAM in children 6-59 months are:
- Weight-for-height Z-score < -3 SD, or
- Mid-Upper Arm Circumference (MUAC) < 115 mm, or
- Presence of bilateral pitting edema
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Q: What is the difference between marasmus and kwashiorkor?
A: Marasmus is characterized by severe wasting without edema, while kwashiorkor is characterized by the presence of bilateral pitting edema. Marasmus results from overall energy deficiency, while kwashiorkor is associated more with protein deficiency, although both conditions involve multiple nutrient deficiencies.
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Q: What is the "flag sign" in hair, and what does it indicate?
A: The "flag sign" refers to alternating bands of light and dark hair color. It indicates periods of adequate and inadequate protein synthesis, reflecting the cyclical nature of malnutrition in some cases.
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Q: Why is edema present in kwashiorkor?
A: Edema in kwashiorkor is multifactorial. It's primarily due to decreased oncotic pressure from hypoalbuminemia, increased antidiuretic hormone (ADH) levels, and increased oxidative stress leading to cell membrane damage and fluid shifts.
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Q: What is F-75, and why is it used in the initial phase of SAM treatment?
A: F-75 is a therapeutic milk formula containing 75 kcal/100mL. It's used in the initial stabilization phase of SAM treatment because it's low in protein and sodium, and high in carbohydrates. This composition helps to restore metabolic and physiologic functions without overwhelming the impaired systems of a severely malnourished child.
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Q: What are the dangers of rapid refeeding in SAM, and how can they be prevented?
A: Rapid refeeding can lead to refeeding syndrome, characterized by severe electrolyte imbalances (especially hypophosphatemia), fluid shifts, and cardiac complications. Prevention involves slow initiation of feeding, starting with F-75 formula, close monitoring of electrolytes, and gradual increase in nutritional intake.
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Q: What is Ready-to-Use Therapeutic Food (RUTF), and what are its advantages?
A: RUTF is a energy-dense, micronutrient-enriched paste used for outpatient treatment of uncomplicated SAM. Its advantages include:
- Long shelf-life without refrigeration
- Resistance to bacterial contamination
- No preparation required before consumption
- Allows for community-based treatment
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Q: Why are antibiotics routinely given in SAM cases, even without obvious infection?
A: Antibiotics are given routinely because:
- SAM children often have subclinical infections due to compromised immune function
- Clinical signs of infection may be masked or atypical in SAM
- Bacterial translocation from the gut is common in SAM
- Studies have shown improved outcomes with routine antibiotic use in SAM
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Q: What are the key principles of the WHO's "Ten Steps" approach to managing SAM?
A: The key principles include:
- Treat/prevent hypoglycemia and hypothermia
- Treat/prevent dehydration and restore electrolyte balance
- Treat infections
- Correct micronutrient deficiencies
- Start cautious feeding
- Achieve catch-up growth
- Provide sensory stimulation and emotional support
- Prepare for follow-up after recovery
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Q: How does SAM affect the cardiovascular system?
A: SAM affects the cardiovascular system by causing:
- Reduced cardiac muscle mass and function
- Decreased cardiac output
- Hypotension and bradycardia
- Increased risk of arrhythmias, especially during refeeding
- Peripheral circulatory failure in severe cases
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Q: What is the role of leptin in the pathophysiology of SAM?
A: Leptin levels are typically low in SAM, particularly in marasmus. This leads to:
- Increased appetite and decreased energy expenditure
- Impaired immune function
- Altered neuroendocrine function
- Delayed puberty in chronic malnutrition
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Q: How does SAM affect drug metabolism and dosing?
A: SAM affects drug metabolism and dosing by:
- Altering body composition and fluid distribution
- Reducing hepatic metabolism and renal excretion
- Decreasing plasma protein binding
- Potentially increasing toxicity of some drugs
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Q: What is the significance of dermatosis in kwashiorkor?
A: Dermatosis in kwashiorkor, often described as "flaky paint" or "crazy pavement," is significant because:
- It's a diagnostic feature of kwashiorkor
- It indicates severe protein deficiency and possibly zinc deficiency
- It increases the risk of infection due to compromised skin barrier
- Its healing can be used as a marker of nutritional recovery
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Q: How does SAM affect the gastrointestinal system?
A: SAM affects the gastrointestinal system by causing:
- Villous atrophy and reduced intestinal surface area
- Decreased production of digestive enzymes
- Impaired intestinal barrier function, leading to bacterial translocation
- Reduced gastric acid production, increasing susceptibility to infections
- Hepatic steatosis, particularly in kwashiorkor
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Q: What is the role of insulin-like growth factor-1 (IGF-1) in SAM?
A: In SAM:
- IGF-1 levels are typically low
- This contributes to growth failure and muscle wasting
- Low IGF-1 impairs protein synthesis and cell proliferation
- IGF-1 levels increase with nutritional rehabilitation, correlating with catch-up growth
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Q: How does SAM affect the immune system?
A: SAM severely compromises the immune system:
- Reduces production and function of T-lymphocytes
- Impairs phagocytic function of neutrophils and macrophages
- Decreases complement levels and antibody production
- Atrophy of lymphoid tissues, including the thymus
- Weakens mucosal barriers, increasing susceptibility to infections
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Q: What is the significance of reductive adaptation in SAM?
A: Reductive adaptation in SAM is crucial because:
- It's a survival mechanism where the body reduces its metabolic rate and energy expenditure
- It affects multiple organ systems, slowing growth and reducing physiological functions
- It necessitates cautious refeeding to prevent overwhelming these adapted systems
- Understanding this process is key to appropriate management and avoiding complications during treatment
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Q: How does SAM affect fluid and electrolyte balance?
A: SAM significantly disrupts fluid and electrolyte balance:
- Increased total body sodium despite low serum sodium levels
- Potassium depletion, which may be masked by extracellular shift
- Magnesium deficiency, affecting cardiac and neuromuscular function
- Altered fluid distribution with expanded extracellular fluid volume in kwashiorkor
- Impaired renal concentration ability, increasing risk of dehydration
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Q: What are the key differences in managing marasmus versus kwashiorkor?
A: Key differences include:
- Fluid management: More cautious in kwashiorkor due to risk of fluid overload
- Protein introduction: Slower in kwashiorkor to prevent worsening of edema
- Diuretic use: May be necessary in kwashiorkor but rarely in marasmus
- Albumin administration: Sometimes considered in severe kwashiorkor but not in marasmus
- Edema monitoring: Critical in kwashiorkor, not applicable in marasmus
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Q: How does SAM affect cognitive development, and what are the long-term implications?
A: SAM significantly impacts cognitive development:
- Impairs brain growth and myelination during critical developmental periods
- Leads to delayed motor and cognitive milestones
- Associated with lower IQ scores and poorer school performance in later life
- May cause permanent cognitive deficits if severe or prolonged, especially in the first 1000 days of life
- Long-term implications include reduced economic productivity and intergenerational effects
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Q: What is the role of zinc supplementation in SAM treatment?
A: Zinc supplementation is crucial in SAM treatment because:
- It promotes catch-up growth and protein synthesis
- Enhances immune function and reduces risk of infections
- Improves appetite and dietary intake
- Helps in resolving persistent diarrhea, common in SAM
- Aids in skin healing, particularly important in kwashiorkor
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Q: How do you assess for refeeding syndrome, and what are the management principles?
A: Assessment and management of refeeding syndrome:
- Assessment: Monitor serum electrolytes (especially phosphate, potassium, magnesium), fluid balance, and clinical signs of cardiac or respiratory distress
- Management principles:
- Start feeding at 25% of requirements and increase gradually
- Correct electrolyte imbalances before and during refeeding
- Provide thiamine before starting refeeding
- Monitor and replace phosphate, potassium, and magnesium as needed
- Be cautious with fluid administration to prevent fluid overload
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Q: What is the role of breastfeeding in the management of infants with SAM?
A: Breastfeeding plays a crucial role in managing infants with SAM:
- Encouraged to continue throughout treatment, including during F-75 and F-100 phases
- Provides immunological benefits, reducing risk of infections
- Helps maintain the emotional bond between mother and infant
- Supplements the therapeutic feeds, aiding in catch-up growth
- Crucial for long-term nutrition after discharge from treatment
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Q: How does SAM affect the endocrine system?
A: SAM has multiple effects on the endocrine system:
- Reduced thyroid hormone production and peripheral conversion of T4 to T3
- Increased cortisol levels, contributing to muscle catabolism
- Decreased insulin-like growth factor-1 (IGF-1) production, impairing growth
- Insulin resistance, affecting glucose metabolism
- Hypogonadism, potentially delaying puberty in chronic cases
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Q: What are the principles of community-based management of acute malnutrition (CMAM)?
A: Key principles of CMAM include:
- Early identification of SAM cases through community screening
- Treatment of uncomplicated SAM cases at home with RUTF
- Inpatient care only for SAM with medical complications
- Integration with existing health systems and services
- Emphasis on caregiver education and follow-up
- Addressing underlying causes of malnutrition in the community
