One of the most prevalent and serious depletion disorders, protein-calorie malnutrition 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. Protein-calorie malnutrition increases the risk of death from pneumonia, chickenpox, or measles.
Both marasmus (nonedematous protein-calorie malnutrition) and kwashiorkor (edematous protein-calorie malnutrition) 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 protein-deficient 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, protein-calorie malnutrition 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, protein-calorie malnutrition 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 for developing protein-calorie malnutrition. Conditions that increase protein-calorie requirements include severe burns and injuries, systemic infections, and cancer (accounts for the largest group of hospitalized patients with protein-calorie malnutrition.) Conditions that cause defective utilization of nutrients include malabsorption syndrome, short-bowel syndrome, and Crohn’s disease.
Children with chronic protein-calorie malnutritioin are small for their chronological age and tend to be physically inactive, mentally apathetic, and susceptible to frequent infections. Anorexia and diarrhea are common.
With acute protein-calorie malnutrition, children are small, gaunt, and emaciated, with no adipose tissue. Their skin is dry and “baggy,” and their hair is sparse and dull brown or reddish yellow. Their temperatures are low; their pulse rates and respirations, slowed. Such children are weak, irritable, and usually hungry; however, they may have anorexia, with nausea and vomiting.
Unlike marasmus, chronic kwashi-orkor allows the patient to grow in height, but adipose tissue diminishes as fat metabolizes to meet energy demands. Edema commonly masks severe muscle wasting; dry, peeling skin and hepatomegaly are common. Patients with secondary protein-calorie malnutrition show signs similar to marasmus, primarily loss of adipose tissue and lean body mass, lethargy, and edema. Severe secondary protein-calorie malnutrition may cause loss of immunocompetence.
Clinical features, dietary history, and anthropometry confirm protein-calorie malnutrition. 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:
❑ height and weight less than 80% of standard for the patient’s age and sex, and below-normal arm circumference and triceps skinfold
❑ serum albumin level less than 2.8 g/dl (normal: 3.3 to 4.3 g/dl)
❑ urinary creatinine (24-hour) level is used to show lean body mass status by relating creatinine excretion to height and ideal body weight, to yield creatinine-height index
❑ skin tests with standard antigens to indicate degree of immunocompromise by determining reactivity expressed as a percentage of normal reaction
❑ moderate anemia.
The aim of treatment is to provide sufficient proteins, calories, and other nutrients for nutritional rehabilitation and maintenance. When treating severe protein-calorie malnutrition, 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’s 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 don’t inhibit protein synthesis. Cautious realimentation is essential to prevent complications from overloading the compromised metabolic system.
❑ Encourage the patient with protein-calorie malnutrition to consume as much nutritious food and fluid as possible (it may be helpful to “cheer him on” as he eats). Help the patient eat if necessary. Cooperate closely with the dietitian to monitor intake and provide acceptable meals and snacks.
❑ If TPN is necessary, observe strict aseptic technique when handling catheters, tubes, and solutions and during dressing changes.
❑ Watch for protein-calorie malnutrition in patients who have been hospitalized for a prolonged period, have had no oral intake for several days, or have cachectic disease.
❑ To help eradicate protein-calorie malnutrition in developing countries, encourage prolonged breast-feeding, educate mothers about their children’s needs, and provide supplementary foods as needed.
CLINICAL TIP: If the older patient is anorectic, consider asking family members and other visitors to bring in special foods from home that may improve the patient’s appetite. In addition, encouraging the family to collaborate on feeding a dependent patient can help promote his recovery, enhance his feelings of well-being, and stimulate him to eat more.
Review other book chapters online related to Nutritional deficiency:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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