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 the accompanying stress (particularly sepsis or injury) and duration of deprivation. PCM increases the risk of death from pneumonia, chickenpox, or measles.
Both kwashiorkor (edematous PCM) and marasmus (nonedematous PCM) are common in underdeveloped countries and in areas in which 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, 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 elderly people in nursing homes. 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 burns 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.
Children with chronic PCM are small for their chronological age and tend to be physically inactive, mentally apathetic, and susceptible to frequent infections. Anorexia and diarrhea are common.
In acute PCM, children are small, gaunt, and emaciated, with no adipose tissue. Skin is dry and “baggy,” and hair is sparse and dull brown or reddish-yellow. Temperature is low; pulse rate and respirations are slowed. Such children are weak, irritable, and usually hungry, although they may have anorexia, with nausea and vomiting.
Unlike marasmus, chronic kwashiorkor allows the patient to grow in height, but adipose tissue diminishes as fat metabolizes to meet energy demands. Edema often masks severe muscle wasting; dry, peeling skin and hepatomegaly are common. Patients with secondary PCM show signs similar to marasmus, primarily loss of adipose tissue and lean body mass, lethargy, and edema. Severe secondary PCM may cause loss of immunocompetence.
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 used to show lean body mass status by relating creatinine excretion to height and ideal body weight, to yield creatinine-height index.
The 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 parentally 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. Foods are introduced slowly. Carbohydrates are given first to supply energy, and then high-quality protein foods, especially milk, and protein-calorie supplements, are given. A patient who’s unwilling or unable to eat may require supplementary feedings through a nasogastric tube or total parenteral nutrition (TPN), which is given through a central venous catheter because of its higher osmolality. Peripheral parenteral nutrition, which has a lower osmolality than TPN and can be given through a peripheral I.V. line, is an alternative to TPN, but it’s given less commonly. 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 PCM to consume as much nutritious food and beverage as possible (it’s often helpful to “cheer him on” as he eats). Assist the patient with eating if necessary. Cooperate closely with the dietitian to monitor intake, and provide acceptable meals and snacks.
❑ If TPN is necessary, observe strict sterile technique when handling catheters, tubes, and solutions and during dressing changes.
❑ Watch for PCM 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 PCM in developing countries, encourage prolonged breast-feeding, educate mothers about their children’s needs, and provide supplementary foods, as needed.
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Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2008 Williams & Wilkins.
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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
» Next page: Protein-calorie malnutrition (Handbook of Diseases)
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