- Clinical science
Malnutrition is a significant cause of morbidity and mortality worldwide, leading to ∼ 45% of all deaths in children under the age of five. Approximately 52 million children have wasting with one-third (17 million) suffering from severe acute malnutrition. Even more children (∼ 154.8 million) have stunted growth, indicating widespread chronic malnutrition. In severe cases, primary protein-energy malnutrition (PEM) can develop, which has two major clinical forms: kwashiorkor and marasmus. Kwashiorkor is characterized by muscle atrophy, pitting edema, and distended abdomen with an enlarged fatty liver. It is caused by a deficiency of dietary protein despite sufficient calorie intake (e.g., from carbohydrates). Marasmus is the diffuse loss of muscle and fat tissue (without edema or distended abdomen) due to a severe state of total calorie deficiency of all macronutrients. Secondary PEM occurs due to illnesses affecting appetite, digestion, absorption, metabolism, and/or increased energy/protein demand. In addition to muscle atrophy, it is possible for patients to have clinical features of either marasmus or kwashiorkor. All PEMs are primarily clinical diagnoses; for primary PEM, WHO diagnostic criteria involve a child's weight-for-length/height and mid-upper arm circumference (MUAC). Thorough laboratory testing should also be conducted to evaluate for severity and complications. Treatment involves managing complications, rehydration, and careful nutritional rehabilitation to avoid refeeding syndrome. In the case of secondary PEM, underlying conditions should also be treated.
- Protein-energy malnutrition (PEM) is a term that describes pathological conditions resulting from a deficiency of dietary protein and/or total calories.
- Primary PEM: due to inadequate intake
- Secondary PEM: due to chronic illnesses or drugs disrupting appetite, digestion, absorption, metabolism, and/or increased energy/protein demand
|Main types of PEM|
|Calorie intake|| || |
|Key clinical features|| |
Protein-deficient KWick MEALS lead to Kwashiorkor → Malnutrition, Edema, Anemia, fatty Liver, Skin lesions!
Marasmus causes Muscle wasting but no edema!
- Description: A form of PEM caused by illnesses affecting appetite, digestion, absorption, metabolism, and/or increased energy/protein demand rather than a lack of calorie intake.
Epidemiology: usually observed in
- Chronically ill, hospitalized patients
- Chronic alcoholics
Etiology: decreased appetite/food intake, increased energy and protein demand, and/or malabsorption due to illnesses and medications
- Cachexia/wasting syndrome due to:
- Gastrointestinal dysfunction
- Increased metabolic demands
- Clinical features
PEM is primarily a clinical diagnosis. Laboratory testing should be conducted to assess the severity and complications. Additional testing may be required to determine the underlying condition for secondary PEM.
Clinical diagnosis 
- H&P: Take a thorough history and physical exam, focusing on nutrition/potential child maltreatment and typical clinical features.
- Anthropometrics: Assess the degree of malnutrition.
- WHO diagnostic criteria: for primary PEM in children aged 6–60 months 
- Clinical diagnosis based on history, body composition (e.g., low BMI), and underlying condition
- If etiology is unclear, determine the cause, e.g.:
- Thorough laboratory testing (CBC, electrolyte panel, inflammatory markers, organ function tests) should be conducted to evaluate for severity and any complications.
- Typical findings
- ↓ Total lymphocyte count, ↓ CD4+ count
- Electrolyte abnormalities, especially:
- ↓ Serum albumin and transferrin (especially in Kwashiorkor)
- ↓ Blood glucose
- ↓ BUN and creatinine (unless concurrent renal failure)
- ↑ CRP if associated with an inflammatory condition
- Test for ova and parasites in stool culture.
- Hydration (typically oral)
- Nutritional rehabilitation: Must occur slowly to prevent refeeding syndrome
- Treat complications (e.g., infection)
- For secondary PEM
Refeeding syndrome is a frequent complication if nutritional rehabilitation occurs too rapidly (sudden shift from a catabolic to an anabolic state): It is characterized by fluid retention, hypophosphatemia, hypomagnesemia, and hypokalemia.