Marasmus
Overview
Plain-Language Overview
Marasmus is a form of severe malnutrition that occurs when the body does not get enough calories and protein over a long period. It most commonly affects infants and young children, especially in areas with limited food availability. People with marasmus appear extremely thin and weak because their bodies have used up fat and muscle for energy. This condition can lead to serious health problems, including a weakened immune system and delayed growth. Without treatment, marasmus can be life-threatening.
Clinical Definition
Marasmus is a severe form of protein-energy malnutrition characterized by a significant deficiency in both calorie and protein intake, leading to marked wasting of adipose tissue and skeletal muscle. It primarily affects infants and young children in resource-limited settings. The pathophysiology involves prolonged inadequate nutrient intake resulting in catabolism of fat stores and muscle mass to meet energy demands. Clinically, patients present with severe weight loss, muscle wasting, and subcutaneous fat depletion, but without edema, distinguishing it from kwashiorkor. Other features include growth retardation, hypoglycemia, hypothermia, and immunodeficiency. Laboratory findings often show low serum albumin, anemia, and electrolyte imbalances. The condition impairs multiple organ systems and increases susceptibility to infections. Early recognition and nutritional rehabilitation are critical to prevent morbidity and mortality associated with marasmus.
Inciting Event
- Prolonged inadequate dietary intake of calories and protein is the main inciting event.
- Episodes of acute illness causing decreased appetite or increased metabolic demand can precipitate marasmus.
Latency Period
- The latency period varies but typically develops over months to years of sustained malnutrition.
Diagnostic Delay
- Delayed recognition may occur due to overlap with other causes of failure to thrive or chronic illness.
- Limited access to healthcare in resource-poor settings contributes to diagnostic delay.
Clinical Presentation
Signs & Symptoms
- Severe weight loss and failure to thrive.
- Marked muscle wasting and loss of fat.
- Irritability and lethargy.
- Hunger and increased appetite despite malnutrition.
- Delayed growth and developmental milestones.
History of Present Illness
- Progressive weight loss and muscle wasting despite adequate or reduced food intake.
- Symptoms of fatigue, irritability, and decreased activity are common.
- Parents may report poor appetite and recurrent infections.
Past Medical History
- History of chronic infections such as tuberculosis or HIV may be present.
- Previous episodes of malnutrition or gastrointestinal diseases affecting absorption increase risk.
Family History
- No specific hereditary pattern is associated with marasmus.
- Family history may reveal socioeconomic factors contributing to malnutrition.
Physical Exam Findings
- Severe muscle wasting with loss of subcutaneous fat.
- Prominent ribs and bony prominences due to fat and muscle loss.
- Dry, thin, and wrinkled skin.
- Sunken eyes and a shrunken, wasted appearance of the face.
- Normal or slightly reduced edema (unlike kwashiorkor).
Diagnostic Workup
Diagnostic Criteria
Diagnosis of marasmus is based on clinical evidence of severe wasting with a weight-for-height measurement less than 60% of the median or a body mass index (BMI) below 16 kg/m² in children. There is marked loss of subcutaneous fat and muscle mass without the presence of edema. Laboratory tests may reveal hypoalbuminemia, anemia, and electrolyte disturbances, but these are not required for diagnosis. The absence of edema helps differentiate marasmus from kwashiorkor. A history of prolonged inadequate caloric and protein intake supports the diagnosis.
Pathophysiology
Key Mechanisms
- Marasmus results from a severe deficiency of both calories and protein, leading to generalized energy depletion.
- The body responds by catabolizing muscle and fat stores to meet energy demands, causing severe wasting.
- There is a marked reduction in basal metabolic rate and impaired immune function due to nutrient deficiency.
| Involvement | Details |
|---|---|
| Organs | Liver: Decreased glycogen stores and impaired protein synthesis. |
| Heart: Reduced cardiac muscle mass can lead to decreased cardiac output. | |
| Kidneys: May suffer from hypoperfusion and electrolyte imbalances. | |
| Tissues | Skeletal muscle: Undergoes severe atrophy due to protein depletion. |
| Adipose tissue: Significantly reduced due to fat loss. | |
| Gastrointestinal mucosa: Atrophies leading to malabsorption and diarrhea. | |
| Cells | Adipocytes: Depleted fat stores characterize energy deficiency in marasmus. |
| Muscle cells: Marked muscle wasting occurs due to protein catabolism. | |
| Immune cells: Impaired function leads to increased susceptibility to infections. | |
| Chemical Mediators | Cortisol: Elevated levels promote protein breakdown and gluconeogenesis. |
| Cytokines: Increased pro-inflammatory cytokines contribute to catabolic state. | |
| Insulin: Decreased insulin activity reduces anabolic processes. |
Treatment
Pharmacological Treatments
Multivitamins
- Mechanism: Replenish essential vitamins and minerals deficient in malnutrition
- Side effects: Rare allergic reactions
Antibiotics
- Mechanism: Treat secondary infections common in malnourished patients
- Side effects: Gastrointestinal upset, allergic reactions
Non-pharmacological Treatments
- Initiate gradual nutritional rehabilitation with calorie-dense, protein-rich foods to restore body mass.
- Provide psychosocial support to address underlying causes and improve feeding behaviors.
- Ensure hydration with oral rehydration solutions to correct electrolyte imbalances.
Prevention
Pharmacological Prevention
- Supplementation with multivitamins and minerals (e.g., vitamin A, zinc, iron).
- Use of therapeutic foods enriched with essential nutrients.
Non-pharmacological Prevention
- Promotion of exclusive breastfeeding for the first 6 months of life.
- Ensuring adequate caloric intake with balanced macronutrients.
- Improving food security and access to nutritious foods.
- Education on proper infant and child feeding practices.
- Sanitation and hygiene measures to reduce infection risk.
Outcome & Complications
Complications
- Immunodeficiency leading to severe infections.
- Electrolyte imbalances causing cardiac arrhythmias.
- Hypothermia due to loss of fat insulation.
- Hypoglycemia from depleted glycogen stores.
- Multi-organ failure in severe cases.
| Short-term Sequelae | Long-term Sequelae |
|---|---|
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Differential Diagnoses
Marasmus versus Anorexia Nervosa
| Marasmus | Anorexia Nervosa |
|---|---|
| No psychiatric history or intentional food restriction | Psychiatric history of body image distortion and intentional food restriction |
| Absence of amenorrhea and lanugo hair | Presence of amenorrhea and lanugo hair in adolescent females |
| Laboratory findings consistent with protein-energy malnutrition without electrolyte disturbances | Laboratory findings of hypokalemia and metabolic alkalosis due to purging behaviors |
Marasmus versus Chronic Disease Cachexia
| Marasmus | Chronic Disease Cachexia |
|---|---|
| No evidence of underlying chronic illness or systemic inflammation | Presence of underlying chronic illness such as cancer, CHF, or COPD |
| Normal or low inflammatory markers | Elevated inflammatory markers like CRP and cytokines |
| Weight loss primarily due to nutritional deficiency without systemic symptoms | Weight loss accompanied by fatigue and systemic symptoms related to chronic disease |
Marasmus versus Kwashiorkor
| Marasmus | Kwashiorkor |
|---|---|
| Severe muscle wasting and loss of subcutaneous fat without edema | Presence of edema and ascites due to hypoalbuminemia |
| No significant skin changes or hair depigmentation | Characteristic flaky paint dermatosis and hair changes (depigmentation, easily pluckable) |
| Markedly decreased weight and body mass index | Relatively preserved weight with swollen appearance despite malnutrition |