Protein-energy malnutrition

From Wikipedia, the free encyclopedia. Jump to: navigation, search Protein-energy malnutrition ICD-10 code: E40-E46 ICD-9 code: 260-263 A deficiency syndrome caused by the inadequate intake of macronutrients. Protein-energy malnutrition (PEM), or protein-calorie malnutrition, is characterized not only by an energy deficit due to a reduction in all macronutrients but also by a deficit in many micronutrients. This syndrome is one example of the various levels of inadequate protein and/or energy intake between starvation (no food intake) and adequate nourishment. Although infants and children of some developing nations dramatically exemplify this type of malnutrition, it can occur in persons of any age in any country. Contents

1 Classification and etiology 2 Epidemiology 3 Pathophysiology 4 Symptoms and signs 5 Laboratory findings 6 Diagnosis 7 Treatment 8 Prognosis 9 See also

Classification and etiology Clinically, PEM has three forms: dry (thin, desiccated), wet (edematous, swollen), and a combined form between the two extremes. The form depends on the balance of nonprotein and protein sources of energy. Each of the three forms can be graded as mild, moderate, or severe. Grade is determined by calculating weight as a percentage of expected weight for length using international standards (normal, 90 to 110%; mild PEM, 85 to 90%; moderate, 75 to 85%; severe, < 75%). The dry form, marasmus, results from near starvation with deficiency of protein and nonprotein nutrients. The marasmic child consumes very little foodoften because his mother is unable to breastfeedand is very thin from loss of muscle and body fat. The wet form is called kwashiorkor, an African word meaning "first child-second child." It refers to the observation that the first child develops PEM when the second child is born and replaces the first child at the breast. The weaned child is fed a thin gruel of poor nutritional quality (compared with mother's milk) and fails to thrive. The protein deficiency is usually more marked than the energy deficiency, and edema results. Children with kwashiorkor tend to be older than those with marasmus and tend to develop the disease after they are weaned. The combined form of PEM is called marasmic kwashiorkor. Children with this form have some edema and more body fat than those with marasmus. Epidemiology

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Marasmus is the predominant form of PEM in most developing countries. It is associated with the early abandonment or failure of breastfeeding and with consequent infections, most notably those causing infantile gastroenteritis. These infections result from improper hygiene and inadequate knowledge of infant rearing that are prevalent in the rapidly growing slums of developing countries. Kwashiorkor is less common and is usually manifested as marasmic kwashiorkor. It tends to be confined to parts of the world (rural Africa, the Caribbean and Pacific islands) where staple and weaning foods--such as yam, cassava, sweet potato, and green banana--are protein deficient and excessively starchy. Pathophysiology In marasmus, energy intake is insufficient for the body's requirements, and the body draws on its own stores. Liver glycogen is exhausted within a few hours, and skeletal muscle protein is then used via gluconeogenesis to maintain adequate plasma glucose. At the same time, triglycerides in fat depots are broken down into free fatty acids, which provide some energy for most tissues, but not for the nervous system. When near starvation is prolonged, fatty acids are incompletely oxidized to ketone bodies, which can be used by the brain and other organs for energy. Thus, in the severe energy deficiency of marasmus, adaptation is facilitated by high cortisol and growth hormone levels and depression of insulin and thyroid hormone secretion. Because amino acids are mobilized from muscle to provide the liver with substrate for protein synthesis, plasma protein levels decrease less in marasmus than in kwashiorkor. In kwashiorkor, relatively increased carbohydrate intake with decreased protein intake leads to decreased visceral protein synthesis. The resulting hypoalbuminemia causes dependent edema, and impaired -lipoprotein synthesis causes fatty liver. Insulin secretion is initially stimulated but is reduced later in the disease. Fat mobilization and amino acid release from muscle are reduced, so that less amino acid substrate is available to the liver. In marasmus and kwashiorkor, the insulin response to a glucose load is poor, possibly due to chromium deficiency. Total body protein synthesis is about 300 g/day or 5 (g/kg)/day in the average adult male. The daily obligatory loss is only about 60 to 75 g (9 to 12 g nitrogen), because 75 to 80% is reused. The RDA of protein for an adult is about 0.8 g/kg; infants and children require 1 to 2 (g/kg)/day . Thus, infants require a higher proportion of essential amino acids in their diet than do adults. In protein deficiency, adaptive enzyme changes occur in the liver, amino acid synthetases increase, and urea formation diminishes, thus conserving nitrogen and reducing its loss in urine. Homeostatic mechanisms initially operate to maintain the level of plasma albumin and other transport proteins. The rates of albumin synthesis eventually decrease, and plasma levels fall, leading to reduced oncotic pressure and edema. Growth, immune response, repair, and production of some enzymes and hormones are impaired in severe protein deficiency. Symptoms and signs Marasmic infants have hunger, gross weight loss, growth retardation, and wasting of subcutaneous fat and muscle. Kwashiorkor is characterized by generalized edema; "flaky paint" dermatosis; thinning, decoloration, and reddening of the hair; enlarged fatty liver; and petulant apathy in addition to retarded growth. Alternating episodes of undernutrition and adequate nutrition may cause the hair to have a dramatic "striped flag" appearance. Almost invariably, infection occurs in all forms of PEM, with a variety of bacteria producing pneumonia, diarrhea, otitis media, genitourinary disease, and sepsis. Infection occurs because of obtunded immunity that resembles, in part, AIDS due to HIV infection. However, unlike the immunodefect in AIDS, the defect in primary malnutrition can be reversed by nutritional therapy.

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Laboratory findings Mild or moderately severe PEM may cause a slight depression of plasma albumin and a decrease in the urinary excretion of urea, due to decreased protein intake, and in hydroxyproline, reflecting impaired growth. Increased urinary 3-methylhistidine reflects muscle breakdown. In marasmus and kwashiorkor, the percentage of body water and extracellular water is increased. Electrolytes, especially potassium and magnesium, are depleted; levels of some enzymes and circulating lipids are low, and blood urea decreases. Anemia, usually due to iron deficiency, and metabolic acidosis are also present. Diarrhea is common and is sometimes aggravated by intestinal disaccharidase deficiency, especially of lactase. Kwashiorkor is characterized by low plasma levels of albumin (10 to 25 g/L), transferrin, essential amino acids (especially branched-chain), -lipoprotein, and glucose. Plasma cortisol and growth hormone levels are high, but insulin secretion and insulin-like growth factor are depressed. Diagnosis Differential diagnosis includes consideration of secondary growth failure due to malabsorption, congenital defects, renal failure, endocrine disease, or emotional deprivation. Skin changes in kwashiorkor differ from those in pellagra, in which they occur on skin exposed to light and are symmetrical. Edema in nephritis, nephrosis, and heart failure is accompanied by other features of these diseases and responds to specific treatment. Hepatomegaly from disorders of glycogen metabolism and cystic fibrosis can be differentiated. Treatment For children and adults who have severe PEM, the first step is to correct fluid and electrolyte abnormalities and to treat infections with antibiotics. The most common electrolyte abnormalities are hypokalemia, hypocalcemia, hypophosphatemia, and hypomagnesemia. The second step, which may be delayed 24 to 48 h in children (to avoid worsening the diarrhea), is to supply macronutrients by dietary therapy. Milk-based formulas are the treatment of choice. The amount is gradually increased during the first week; after a week, the full rate of 175 kcal/kg (730 kJ/kg) and 4 g of protein/kg for children and 60 kcal/kg (250 kJ/kg)and 2 g of protein/kg for adults can be given. Fluid and electrolyte therapy: Initially, children with PEM should be treated with IV fluids. Although total body water is increased, evidence of intravascular dehydration is often present, especially in children with a history of severe diarrhea. The initial rehydrating fluid is Darrow's solution, which contains 1:2:3 parts by volume of 0.17 mol/L lactate:normal saline:5% glucose, to which 50 mL of 50% D/W is added to each 500 mL. This solution supplies 78 mEq/L of sodium and 55 mmol/L of glucose. The water deficit should be replaced over the first 8 to 12 h of therapy. For example, a 5-kg child who is 10% dehydrated should receive a total of 500 mL of fluid over 12 h. After the first 12 h, potassium may be added to the infusion to attain a concentration of 20 mmol/L. A severely dehydrated child may receive as much as 20 mL/kg of the initial IV solution (2% of body weight) during the first hour of therapy to increase intravascular volume and therefore renal blood flow and urine output. On the 2nd day, if the child is unable to be fed orally or has persistent diarrhea, a 1:2:6 solution of lactate:normal saline: glucose that contains 20 mEq of potassium/L is given IV at a rate of 10 (mL/kg)/h until oral therapy is initiated, usually by the 3rd day. Supplementary magnesium 0.4 (mEq/kg)/day intramuscular is given for 7 days. Bcomplex vitamins at two times the RDA are given parenterally for the first 3 days.

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For oral rehydration in adults, the World Health Organization solution containing 90 mEq/L sodium, 20 mEq/L potassium, 80 mEq/L chloride, 30 mEq/L bicarbonate, and 111 mmol/L glucose given in divided doses over 24 h is satisfactory. Dietary therapy: When diarrhea is severe, the patient may be kept NPO (nil per os, nothing by mouth) for up to 48 h. When diarrhea subsides (usually during the first 48 h), the IV is discontinued and oral feeding begins. In the early stages of PEM, it is easier to give the needed calories and protein in a milk-based formula, which can be given through a tube if necessary. A full-fat desiccated milk product can be fortified with additional corn oil and maltodextrin so that it contains 100 kcal (420 kJ), 4 g of protein, 5.5 g of fat, and 8.2 g of carbohydrate per 100 mL. The distribution of energy among macronutrients is 16% protein, 50% fat, and 34% carbohydrate. This formula also supplies 2.7 mEq/kg of sodium, 5 mEq/kg of potassium, 7.3 mEq/kg of calcium, 6.2 mEq/kg of phosphorus, and 1.4 mEq/kg of magnesium per day. It is fortified to meet the child's requirements for zinc, manganese, copper, iodine, fluoride, molybdenum, and selenium. After 4 weeks, the formula can be replaced with whole milk plus solid foods, including eggs, fruit, meats, cod liver oil, and yeast. A group of Thai children with PEM were fed ad libitum over a 12-week period. They reached their maximum intake of 165 kcal/kg (690 kJ/kg) and 6 g/kg of protein and their maximum growth rate after 3 weeks of therapy. Their intake then slowly declined to 125 kcal/kg (525 kJ/kg) and 4 g/kg of protein at 12 weeks. By that time, they had attained 90% of expected weight for height. Iron is important in the treatment of children with PEM. Most of them have decreased bone marrow iron stores on admission, and without iron supplementation, all bone marrow iron disappears within 4 to 6 weeks. Because absorption of oral iron is poor in PEM, the use of intramuscular (IM) iron or high doses of oral iron (100 to 200 mg/day of elemental iron) should be considered. IM iron immediately increases bone marrow iron stores. In adults with PEM, mild anemia can be treated with oral iron. Most adults with PEM can take formula by mouth from the beginning. A commercial formula for oral feeding can be used for repletion therapy. Prognosis In children, mortality varies between 5 and 40%. The lower mortality rates are observed in children given intensive care. Death in the first days of treatment is usually due to electrolyte imbalance, infection with sepsis, hypothermia, or heart failure. Stupor, jaundice, petechiae, low serum sodium, and persistent diarrhea are ominous signs. The disappearance of apathy, edema, and anorexia is a favorable sign. Recovery is more rapid in kwashiorkor than in marasmus. Long-term effects of malnutrition in childhood are not fully documented. When treatment is adequate, the liver recovers fully without subsequent cirrhosis. In some children, malabsorption and pancreatic deficiency persist. Humoral immunity is variably impaired and cell-mediated immunocompetence is markedly compromised, but they return to normal after treatment. The degree of mental impairment is related to the duration, severity, and age at onset of the malnutrition. Some prospective studies suggest that a relatively mild degree of mental retardation may persist into school age. In adults, untreated PEM can result in morbidity and some mortality, but mortality data are scarce. Except when organ failure occurs, treatment is uniformly successful.

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