Definition and epidemiology
Malnutrition broadly includes undernutrition (wasting, stunting, underweight, micronutrient deficiencies) and overnutrition (overweight, obesity), but in clinical and exam contexts E46 typically refers to protein-energy malnutrition (PEM) of unspecified type.
- Globally, undernutrition remains a leading cause of child mortality, concentrated in low- and middle-income countries (WHO/UNICEF data).
- In high-income countries, malnutrition is common in hospitalized patients, nursing home residents, and those with chronic disease, cancer, or eating disorders.
- Two classic pediatric syndromes are tested repeatedly: kwashiorkor (edematous malnutrition) and marasmus (non-edematous wasting). A mixed picture, marasmic kwashiorkor, also occurs.
- Severe acute malnutrition (SAM) in children is defined by WHO using weight-for-height z-score, mid-upper arm circumference (MUAC), and/or bilateral pitting edema.
- Kwashiorkor = protein deficiency with adequate calories → edema, hypoalbuminemia, fatty liver, flaky skin.
- Marasmus = total caloric deficiency → severe wasting, no edema, wizened facies.
- Bilateral pitting edema in a malnourished child = kwashiorkor regardless of weight.
- Refeeding syndrome hallmark is hypophosphatemia, driven by insulin-mediated intracellular shifts.
- Give thiamine before/during refeeding to prevent Wernicke encephalopathy and wet beriberi.
- WHO SAM treatment starts with F-75 (stabilization) then F-100/RUTF (catch-up growth).
- Iron supplementation is delayed until the child is stabilized in acute malnutrition management.
- Albumin reflects chronicity/severity but is confounded by inflammation — not a standalone diagnostic marker.
Etiology and risk factors
Primary (inadequate intake)
- Food insecurity, poverty, famine, war
- Poor breastfeeding practices or early weaning
- Restrictive diets, eating disorders (anorexia nervosa)
Secondary (increased need, loss, or impaired utilization)
- Malabsorption: celiac disease, cystic fibrosis, short bowel syndrome, chronic pancreatitis
- Increased catabolic demand: sepsis, burns, trauma, cancer, hyperthyroidism
- Chronic disease: CKD, chronic liver disease, heart failure, COPD
- Psychosocial: depression, dementia, neglect, elder abuse
- Alcohol use disorder (compounds micronutrient deficiency, especially thiamine)
Risk factors: extremes of age, poverty, chronic illness, polypharmacy, social isolation, recent hospitalization or surgery.
Pathophysiology
In marasmus, prolonged inadequate total caloric and protein intake forces the body into an adaptive starvation response: fat and muscle are catabolized for energy, albumin synthesis is relatively preserved, and there is no edema. The patient appears severely wasted with a "wizened" or old-man facies.
In kwashiorkor, protein intake is disproportionately low relative to calories. This impairs hepatic synthesis of albumin and other transport proteins, lowering plasma oncotic pressure and causing dependent and generalized edema. Impaired lipoprotein synthesis also leads to hepatic fat accumulation (fatty liver). Classic features include a protuberant abdomen, hypopigmented/depigmented hair, dermatitis with flaky skin, and apathy or irritability.
Across both syndromes, there is impaired cell-mediated immunity, reduced lymphocyte counts, loss of lean muscle mass (including respiratory and cardiac muscle), and multiple micronutrient deficiencies (iron, zinc, vitamin A, folate, thiamine). Thiamine deficiency can precipitate wet beriberi or high-output cardiac failure during refeeding.
Clinical features
Marasmus
- Severe muscle wasting and loss of subcutaneous fat
- No edema
- "Old man" or wizened facies, prominent ribs
- Normal or low albumin
Kwashiorkor
- Bilateral pitting edema (legs, face, hands)
- Protuberant abdomen (hepatomegaly, ascites)
- Thin, sparse, hypopigmented hair; flag sign (alternating bands of pigmentation)
- Dermatosis: flaky, peeling skin ("flaky paint" dermatosis)
- Apathy, irritability, poor appetite
- Low serum albumin
General/shared features
- Growth failure (stunting, wasting) in children
- Fatigue, muscle weakness, poor wound healing
- Hypothermia, bradycardia, hypotension in severe cases
- Immune suppression leading to recurrent infections
- In adults: unintentional weight loss, sarcopenia, pressure ulcers, delayed recovery from illness or surgery
Diagnosis
Diagnosis combines history, anthropometry, and selected labs; it is largely clinical.
Anthropometric criteria (children, WHO)
- Weight-for-height z-score less than -3 SD = severe wasting
- MUAC less than 115 mm = severe acute malnutrition
- Bilateral pitting edema = kwashiorkor regardless of weight
- Height-for-age z-score less than -2 SD = stunting
Adults
- Unintentional weight loss (commonly greater than 5-10% over 3-6 months)
- Low BMI, reduced mid-arm circumference, reduced grip strength
- Validated screening tools: MUST (Malnutrition Universal Screening Tool), NRS-2002, MNA (elderly), SGA (Subjective Global Assessment)
- GLIM criteria (Global Leadership Initiative on Malnutrition) combine phenotypic (weight loss, low BMI, reduced muscle mass) and etiologic (reduced intake, disease burden/inflammation) criteria
Laboratory workup
- Albumin and prealbumin: reflect severity/chronicity but are confounded by inflammation (acute phase reactants) — not diagnostic alone
- CBC (anemia), electrolytes, glucose (risk of hypoglycemia), phosphate, magnesium, potassium (baseline before refeeding)
- Micronutrient levels as indicated: iron studies, vitamin A, zinc, thiamine, folate, vitamin B12
- Consider underlying cause workup (celiac serology, HIV testing, TSH, stool studies) based on clinical context
Differential diagnosis
- Nephrotic syndrome — edema and hypoalbuminemia mimic kwashiorkor; distinguished by proteinuria
- Cirrhosis/chronic liver disease — ascites, edema, low albumin from synthetic dysfunction rather than intake
- Heart failure — edema from volume overload, not hypoalbuminemia
- Anorexia nervosa — severe wasting resembling marasmus but with distinct psychiatric features and often normal albumin until late
- Malignancy (cachexia) — weight loss and wasting driven by catabolic cytokines rather than pure caloric deficit
- HIV wasting syndrome — chronic infection-associated weight loss
- Malabsorptive disorders (celiac disease, cystic fibrosis) — malnutrition secondary to nutrient loss despite adequate intake
Management
Management follows WHO protocols for severe acute malnutrition in children and general nutrition support principles in adults; both emphasize gradual, monitored refeeding.
Children with severe acute malnutrition (WHO approach)
- Stabilization phase: treat/prevent hypoglycemia, hypothermia, dehydration (cautious rehydration, avoid standard IV fluids if possible due to heart failure risk), and infection (broad-spectrum antibiotics are routinely given even without overt signs of infection)
- Therapeutic feeding: start with low-protein, low-calorie formula (F-75) during stabilization, then transition to higher-energy formula (F-100) or ready-to-use therapeutic food (RUTF) for catch-up growth
- Correct micronutrient deficiencies: vitamin A, folic acid, zinc, copper, multivitamins; iron is typically withheld initially until the child is stabilized and gaining weight (iron can worsen infection/oxidative stress early on)
- Community-based management with RUTF for uncomplicated SAM without edema or complications; inpatient care for complicated cases (edema with complications, very severe wasting, inability to feed)
Adults and hospitalized patients
- Multidisciplinary nutrition support (dietitian-led), oral nutritional supplements first-line when possible
- Enteral tube feeding if oral intake is insufficient; parenteral nutrition reserved for non-functional or inaccessible GI tract
- Treat the underlying cause (e.g., manage malabsorption, psychiatric care for eating disorders, optimize chronic disease management)
- Avoid aggressive overfeeding — start at a conservative caloric intake and advance gradually
Refeeding syndrome prevention (high-yield across settings)
- Occurs when reintroducing nutrition after prolonged starvation causes an insulin surge, driving potassium, phosphate, and magnesium intracellularly
- Hallmark: hypophosphatemia, also hypokalemia and hypomagnesemia, which can cause arrhythmias, cardiac failure, respiratory failure, and death
- Prevention: start feeding at low caloric rates, replete thiamine before/during refeeding (prevents Wernicke encephalopathy and cardiac beriberi), monitor and correct electrolytes daily during the first week
- High-risk patients: BMI less than 16, greater than 15% weight loss in 3-6 months, little/no intake for more than 10 days, or low baseline potassium/phosphate/magnesium
Complications and prognosis
- Infections due to impaired cell-mediated immunity (common cause of death)
- Hypoglycemia and hypothermia, especially in young children
- Refeeding syndrome during nutritional rehabilitation
- Growth stunting and long-term cognitive impairment in children if malnutrition occurs during critical developmental windows
- Fatty liver, electrolyte disturbances, cardiac atrophy and arrhythmia risk
- Pressure ulcers and poor wound healing, especially in hospitalized/elderly patients
- Prognosis depends on severity, timeliness of treatment, and underlying cause; with appropriate graduated refeeding and treatment of complications, most cases improve, but severe untreated pediatric malnutrition carries significant mortality
Kwashiorkor = "Kwashi has a Kool belly" — protein deficiency, pot-Belly (edema/ascites), ok calories. Marasmus = "Mara is a Marathon runner" — wasted, no fat, no edema, from running out of total calories.
Practice questions
1. A 2-year-old child from a famine-affected region is brought in with a swollen abdomen and bilateral pitting edema of the legs. Examination shows sparse, hypopigmented hair and flaky skin lesions. Laboratory testing shows a serum albumin of 1.8 g/dL. Which of the following best explains this child's edema?
2. A severely malnourished 3-year-old begins a supervised refeeding program in a hospital. On day 3 of feeding, she develops muscle weakness, confusion, and new-onset arrhythmia. Which electrolyte abnormality is most likely responsible?
3. A 70-year-old man with chronic alcohol use disorder is admitted after several days of minimal food intake. The team plans to start enteral feeding. Which intervention should be prioritized before or during initiation of feeding to prevent a serious neurologic complication?
Frequently asked questions
What causes malnutrition?
Malnutrition results from inadequate intake, impaired absorption, or increased metabolic demand for nutrients. Common causes include food insecurity and poverty, restrictive diets or eating disorders, malabsorptive conditions like celiac disease or cystic fibrosis, chronic illnesses such as cancer, heart failure, or kidney disease, and increased catabolic stress from infection, surgery, or burns. In children, poor breastfeeding practices and early weaning are major contributors in low-resource settings.
What are the first symptoms of malnutrition?
Early signs include unintentional weight loss, fatigue, muscle weakness, and poor concentration. In children, growth faltering (poor weight gain or linear growth) is often the earliest sign. As malnutrition progresses, patients may develop hair and skin changes, swelling (edema) in protein-deficient states, delayed wound healing, and increased susceptibility to infections due to weakened immunity.
How is malnutrition diagnosed?
Malnutrition is diagnosed clinically using history, physical exam, and anthropometric measurements such as BMI, weight-for-height z-scores, and mid-upper arm circumference. Validated screening tools (MUST, MNA, NRS-2002) and the GLIM criteria combine phenotypic findings like weight loss and reduced muscle mass with etiologic factors like reduced intake or inflammation. Labs such as albumin and electrolytes support assessment but are not diagnostic alone.
Is malnutrition curable?
Yes, malnutrition is generally reversible with appropriate, gradual nutritional rehabilitation and treatment of the underlying cause. Children with severe acute malnutrition can recover fully with timely WHO-protocol treatment, though prolonged or severe malnutrition in early childhood may leave lasting effects on growth and cognitive development. In adults, prognosis depends on the underlying disease driving the malnutrition.
Kwashiorkor vs marasmus — what is the difference?
Kwashiorkor results from protein deficiency with relatively preserved calorie intake, causing edema, hypoalbuminemia, a protuberant abdomen, and skin/hair changes. Marasmus results from an overall deficiency of calories and protein, causing severe wasting of fat and muscle without edema. Both can coexist as marasmic kwashiorkor, and bilateral edema is the key distinguishing clinical sign favoring kwashiorkor.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: E46
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.