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Protein-Calorie Malnutrition (Kwashiorkor)Alternative names :- kwashiorkor, protein malnutrition One of the most prevalent and serious depletion disorders, protein-calorie malnutrition (PCM) occurs as marasmus (protein-calorie deficiency), characterized by growth failure and wasting, and as kwashiorkor (protein deficiency), characterized by tissue edema and damage. Both forms vary from mild to severe and may be fatal, depending on accompanying stress (particularly sepsis or injury) and duration of deprivation. PCM increases the risk of death from pneumonia, chickenpox, or measles. CausesBoth marasmus (non edematous PCM) and kwashiorkor (edematous PCM) are common in underdeveloped countries and in areas where dietary amino acid content is insufficient to satisfy growth requirements. Kwashiorkor typically occurs at about age 1, after infants are weaned from breast milk to a proteindeficient diet of starchy gruels or sugar water, but it can develop at any time during the formative years. Marasmus affects infants ages 6 to 18 months as a result of breast-feeding failure or a debilitating condition such as chronic diarrhea. In industrialized countries, PCM may occur secondary to chronic metabolic disease that decreases protein and calorie intake or absorption, or trauma that increases protein and calorie requirements. In the United States, PCM is estimated to occur to some extent in 50% of surgical and 48% of medical patients. Those who aren't allowed anything by mouth for an extended period are at high risk of developing PCM. Conditions that increase protein-calorie requirements include severe bums and injuries, systemic infections, and cancer (accounts for the largest group of hospitalized patients with PCM). Conditions that cause defective utilization of nutrients include malabsorption syndrome, short-bowel syndrome, and Crohn's disease. Signs and symptomsEarly symptoms of kwashiorkor are fairly non-specific. They are underweight for age. An affected child may at first appear tired, irritable and disinterested in play. The child fails to grow and loses muscle mass. As deprivation continues, the child's legs and body swell up due to the accumulation of fluid (oedema) in the tissues. A "pot-belly" develops because of lax abdominal muscles and, in some cases, an enlarged liver. The hair becomes sparse, brittle and develops a reddish hue. In severe cases patches of the skin will slough off leaving oozing sores rather like a burn wound. They are often anaemic and have heavy worm infestations. Diarrhea disease is a frequent presentation. Because of impaired immunity these children are also prone to infections such as tuberculosis and septicaemia. Final symptoms may include coma or shock. If untreated the child will die. DiagnosisClinical appearance, dietary history, and anthropometry confirm PCM. If the patient doesn't suffer from fluid retention, weight change over time is the best index of nutritional status. The following factors support the diagnosis:
TreatmentThe aim of treatment is to provide sufficient proteins, calories, and other nutrients for nutritional rehabilitation and maintenance. When treating severe PCM, restoring fluid and electrolyte balance parenterally is the initial concern. A patient who shows normal absorption may receive enteral nutrition after anorexia has subsided. When possible, the preferred treatment is oral feeding of high quality protein foods, especially milk, and protein-calorie supplements. A patient who is unwilling or unable to eat may require supplementary feedings through a nasogastric tube or total parenteral nutrition (TPN) through a central venous catheter. Accompanying infection must also be treated, preferably with antibiotics that do not inhibit protein synthesis. Cautious realimentation is essential to prevent complications from overloading the compromised metabolic system. |
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