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Definition Protein-energy malnutrition (PEM) is a potentially fatal0ody-depletion disorder. It is the leading cause of death in children in developing countries. -The World Health Organization (WHO) defines malnutrition as the cellular imbalance between the supply of nutrients and energy and the" body's demand for them to ensure growth, maintenance, and specific functions." The term protein-energy malnutrition (PEM) applies to a group of related disorders that include marasmus, kwashiorkor, and intermediate states of marasmus-kwashiorkor. The term marasmus is derived from the Greek word marasmos, which means withering or wasting. Marasmus involves inadequate intake of protein and calories and is characterized by emaciation. The term kwashiorkor is taken from the Ga language of Ghana and means "the sickness of the weaning." Williams first used the term in 1933 it refers to an inadequate protein intake with reasonable caloric (energy) intake. Edema is characteristic of kwashiorkor but is absent in marasmus . Studies suggest that marasmus represents an adaptive response to starvation, whereas kwashiorkor represents a maladaptive response to starvation. Children may present with a mixed picture of marasmus and .kwashiorkor, and children may present with milder forms of malnutrition For this reason, Jelliffe suggested the term protein-calori malnutrition to include both entities . Although PEM affects virtually every organ system, this article primarily focuses on its cutaneous manifestations. Patients with PEM may also have deficiencies of vitamins, essential fatty acids, and trace elements, all of which may contribute to their dermatosis .. **** Pathophysiology: In general, marasmus is an insufficient energy intake to match the body's requirements. As a result, the body draws on its own stores, resulting in emaciation. In kwashiorkor, adequate carbohydrate consumption and decreased protein intake lead to decreased synthesis of visceral proteins. The resulting hypoalbuminemia contributes to extravascular fluid accumulation. Impaired synthesis of B-lipoprotein .produces a fatty liver ..... Internationally : In 2000, the WHO estimated that malnourished children Numbered 181.9 million (32%) in developing countries. Also, an estimated measured in terms of 149.6 children younger than 5 years are malnourished when Africa, about one half of children weight for age. In south central Asia and eastern This figure is 5 times the prevalence in the .have growth retardation due to PEM western world 1 Description PEM is also referred to as protein-calorie malnutrition. It develops in children and adults whose consumption of protein and energy (measured by calories) is insufficient to satisfy the body's nutritional needs. While pure protein deficiency can occur when a person's diet provides enough energy but lacks the protein minimum, in most cases the deficiency will be dual. PEM may also occur in persons who are unable to absorb vital nutrients or convert them to energy essential for healthy tissue formation and organ function. Although PEM is not prevalent among the general population of the United States, it is often seen in elderly people who live in nursing homes and in children whose parents are poor. PEM occurs in one of every two surgical patients and in 48% of all other hospital patients. Although PEM is not prevalent among the general population of the United States, it is often seen in elderly people who live in nursing homes and in children whose parents are poor. PEM occurs in one of every two surgical patients and in 48% of all other hospital patients. 2 Kwashiorkor also called wet protein-energy malnutrition, is a form of PEM characterized primarily by protein deficiency. This condition usually appears at the age of about 12 months when breastfeeding is discontinued, but it can develop at any time during a child's formative years. It causes fluid retention (edema); dry, peeling skin; and hair Discoloration******People who have kwashiorkor often have extremely thin arms and legs, but liver enlargement and ascites (abnormal accumulation of fluid) can distend the abdomen and disguise weight loss. Hair may turn red or yellow. Anemia, diarrhea, and fluid and electrolyte disorders are common. The body's immune system is often weakened, behavioral development is slow, and mental retardation may occur. Children may grow to normal height but are abnormally thin. ******Kwashiorkor-like secondary PEM usually develops in patients who have been severely burned, suffered trauma, or had sepsis (tissue-destroying infection) or another life-threatening illness. The condition's onset is so sudden that body fat and muscle mass of normal-weight people may not change. Some obese patients even gain weight 3 Mortality\Morbidity Approximately 50% of the 10 million deaths each year in developing countries occur because of malnutrition in children younger than 5 years. In kwashiorkor, mortality tends to decrease as the age of onset increases. Race: Dermatologic findings appear more significant and occur more frequently among darkerskinned peoples. This finding is likely explained by the greater prevalence and the increased severity of PEM in Third World countries and not to a difference in racial susceptibility. Age: Marasmus most commonly occurs in children younger than 5 years. This period is characterized by increased energy requirements and increased susceptibility to viral and bacterial infections. Weaning (the deprivation of breast milk and the commencement of nourishment with other food) occurs during this high-risk period. Weaning is often complicated by geography, economy, hygiene, public health, culture, and dietetics. It can be ineffective when the foods introduced provide inadequate nutrients, when the food and water are contaminated, when the access to health care is inadequate, and/or when the patient cannot access or purchase proper nourishment. History In children, the findings of poor weight gain or weight loss; slowing of linear growth; and behavioral changes, such as irritability, apathy, decreased social responsiveness, anxiety, and attention deficit may indicate PEM. In particular, the child is apathetic when undisturbed but irritable when picked up. Kwashiorkor characteristically affects children who are being weaned. Signs include diarrhea and psychomotor changes. Adults generally lose weight, although, in some cases, edema can mask weight loss. Patients may describe listlessness, easy fatigue, and a sensation of coldness. Global impairment of system function is present. Patients with PEM can also present with nonhealing wounds. This may signify a catabolic process that requires nutritional intervention. 4 Physical In marasmus, the child appears emaciated with marked loss of subcutaneous fat and muscle wasting. The skin is xerotic, wrinkled, and loose. Monkey facies secondary to a loss of buccal fat pads is characteristic of this disorder. Marasmus may have no clinical dermatosis. However, inconsistent cutaneous findings include fine, brittle hair; alopecia; impaired growth; and fissuring of the nails. In PEM, more hairs are in the telogen (resting) phase than in the anagen (active) phase, a reverse of normal. Occasionally, as in anorexia nervosa, marked growth of lanugo hair is noted. Kwashiorkor typically presents with a failure to thrive, edema, moon facies, a swollen abdomen (potbelly), and a fatty liver. When present, skin changes are characteristic and progress over a few days. The skin becomes dark, dry, and then splits open when stretched, revealing pale areas between the cracks (ie, crazy pavement dermatosis, enamel paint skin). This feature is seen especially over pressure areas. In contrast to pellagra, these changes seldom occur on sunexposed skin. Depigmentation of hair causes it to be reddish yellow to white. Curly hair becomes straightened. If periods of poor nutrition are interspersed with good nutrition, alternating bands of pale and dark hair, respectively, called the flag sign, may occur. Also, hairs become dry, lusterless, sparse, and brittle; they can be pulled out easily. Temporal recession and hair loss from the back of the head occur, likely secondary to pressure when the child lies down. In some cases, loss of hair can be extreme. Hair can also become softer and finer and appear unruly. The eyelashes can undergo the same change, having a so-called broomstick appearance. Nail plates are thin and soft and may be fissured or ridged. Atrophy of the papillae on the tongue, angular stomatitis, xerophthalmia, and cheilosis can occur. Inflammatory bowel diseases, such as Crohn disease and ulcerative colitis, may also produce skin manifestations secondary to malnutrition. In elderly persons, an indicative sign of malnutrition is delayed healing and an increased presence of decubitus ulcers of stage III or higher. Vitamin C deficiency commonly manifests in elderly persons as perifollicular hemorrhages, petechiae, gingival bleeding, and splinter hemorrhages, in addition to hemarthroses and subperiosteal hemorrhages. Anemia may result, and wound healing may be impaired. Niacin deficiency clinically manifests as pellagra (ie, dermatitis, dementia, diarrhea) in advanced cases. The dermatitis manifests in sun-exposed areas, including the back, neck (Casal necklace), face, and dorsum of the hands (gauntlet of pellagra) initially as painful erythema and itching. Subsequently, vesicles and bullae may develop and erupt, creating crusted, scaly lesions. Finally, the skin becomes rough and covered by dark scales and crusts. Striking demarcation of affected areas from normal skin is noted. PEM is also associated with an increased likelihood of calciphylaxis, a small vessel vasculopathy involving mural calcification with intimal proliferation, fibrosis, and thrombosis. As a result, ischemia and necrosis of skin occurs. 5 CAUSES Worldwide, the most common cause of malnutrition is inadequate food intake. Preschool-aged children in developing countries are often at risk for malnutrition because of their dependence on others for food, increased protein and energy requirements, immature immune systems causing a greater susceptibility to infection, and exposure to nonhygienic conditions. Another significant factor is ineffective weaning secondary to ignorance, poor hygiene, economic factors, and cultural factors. The prognosis is worse when PEM occurs with HIV infection. Gastrointestinal infections can and often do precipitate clinical PEM because of associated diarrhea, anorexia, vomiting, increased metabolic needs, and decreased intestinal absorption. Parasitic infections play a major role in many parts of the world. In developed countries, inadequate food intake is a less common cause of malnutrition; PEM is more often caused by decreased absorption or abnormal metabolism. Thus, in developed countries, diseases, such as cystic fibrosis, chronic renal failure, childhood malignancies, congenital heart disease, and neuromuscular diseases, contribute to malnutrition. Fad diets, inappropriate management of food allergies, and psychiatric diseases, such as anorexia nervosa, can also lead to severe PEM. Populations in both acute-care and long-term facilities are at risk for clinically significant involuntary weight loss (IWL) that can result in PEM. IWL is defined as a loss of 4.5 kg or greater than 5% of the usual body weight over a period of 6-12 months. PEM occurs when weight loss of greater than 10% of normal body weight occurs. Elderly persons often develop malnutrition, common causes of which include decreased appetite, dependency on help for eating, impaired cognition and/or communication, poor positioning, frequent acute illnesses with gastrointestinal losses, medications that decrease appetite or increase nutrient losses, polypharmacy, decreased thirst response, decreased ability to concentrate urine, intentional fluid restriction due to fear of incontinence or choking if dysphagic, psychosocial factors such as isolation and depression, monotony of diet, higher nutrient density requirements, and other demands of age, illness, and disease on the body. Elderly patients are often at risk for PEM because of inadequate nutrition, which has been determined to be a common comorbid factor for increased morbidity and mortality in elderly burn victims. Patients with liver cirrhosis are also at risk for PEM, which is a risk factor that portends a poor prognosis for survival. This risk correlates with the degree of liver injury and the etiology of liver injury, with the risk of PEM being more severe in persons with alcoholic cirrhosis than in those with nonalcoholic cirrhosis. Patients on long-term hemodialysis also may develop PEM; this is associated with increased morbidity and mortality. Patients with squamous cell carcinoma of the esophagus are at risk for PEM. Complications Hypoglycemia Hypothermia Hypokalemia Hyponatremia Heart failure Infections (bacterial, viral & thrush) Dehydration & shock 6 Causes &symptoms Primary PEM results from a diet that lacks sufficient sources of protein and/or energy. Secondary PEM is more common in the United States, where it usually occurs as a complication of AIDS, cancer, chronic kidney failure, inflammatory bowel disease, and other illnesses that impair the body's ability to absorb or use nutrients or to compensate for nutrient losses. PEM can develop gradually in a patient who has a chronic illness or experiences chronic semi-starvation. It may appear suddenly in a patient who has an acute illness ***Secondary PEM symptoms range from mild to severe, and can alter the form or function of almost every organ in the body. The type and intensity of symptoms depend on the patient's prior nutritional status and on the nature of the underlying disease and the speed at which it is progressing. Mild, moderate, and severe classifications have not been precisely defined, but patients who lose 1020% of their body weight without trying are usually said to have moderate PEM. This condition is also characterized by a weakened grip and inability to perform high-energy tasks. **Losing 20% of body weight or more is generally classified as severe PEM. People with this condition can't eat normal-sized meals. They have slow heart rates and low blood pressure and body temperatures. Other symptoms of severe secondary PEM include baggy, wrinkled skin; constipation; dry, thin, brittle hair; lethargy; pressure sores and other skin lesions. Values Commonly Used to Grade the Severity of Protein-Energy Malnutrition Measurement Mild Moderate Severe Malnutrition Malnutrition Malnutrition 90–110 85–90 75–85 < 75 Body mass index 19–24* 18–18.9 16–17.9 < 16 Serum albumin 3.5–5.0 3.1–3.4 2.4–3.0 < 2.4 220–400 201–219 150–200 < 150 Total lymphocyte 2000– 1501–1999 800–1500 < 800 count (per mm3) 3500 Delayed 2 2 1 0 Normal weight Normal (%) (g/dL) Serum transferrin (mg/dL) hypersensitivity index† *In the elderly, BMI < 21 may increase mortality risk. †Delayed hypersensitivity index quantitates the amount of induration elicited by skin testing using a common antigen, such as those derived from Candida sp or Trichophyton sp. Induration grade 0 = < 0.5 cm, 1 = 0.5–0.9 cm, 2 = ≥ 1.0 cm. 7 Lab Studies The WHO recommends the following laboratory tests: Blood glucose Examination of blood smears by microscopy or direct detection testing Hemoglobin Urine examination and culture Stool examination by microscopy for ova and parasites Serum albumin HIV test (This test must be accompanied by counseling of the child's parents, and strict confidentiality should be maintained.) Electrolytes Significant findings in kwashiorkor include hypoalbuminemia (1025 g/L), hypoproteinemia (transferrin, essential amino acids, lipoprotein), and hypoglycemia. Plasma cortisol and growth hormone levels are high, but insulin secretion and insulinlike growth factor levels are decreased. The percentage of body water and extracellular water is increased. Electrolytes, especially potassium and magnesium, are depleted. Levels of some enzymes (including lactase) are decreased, and circulating lipid levels (especially cholesterol) are low. Ketonuria occurs, and PEM may cause a decrease in the urinary excretion of urea because of decreased protein intake. In both kwashiorkor and marasmus, iron deficiency anemia and metabolic acidosis are present. Urinary excretion of hydroxyproline is diminished, reflecting impaired growth and wound healing. Increased urinary 3-methylhistidine is a reflection of muscle breakdown and can be seen in marasmus. Malnutrition also causes immunosuppression, which may result in false-negative tuberculin skin test results and the subsequent failure to accurately assess for tuberculosis 8 Treatment Treatment is designed to provide adequate nutrition, restore normal body composition, and cure the condition that caused the deficiency. Tube feeding or intravenous feeding is used to supply nutrients to patients who can't or won't eat protein-rich foods. In patients with severe PEM, the first stage of treatment consists of correcting fluid and electrolyte imbalances, treating infection with antibiotics that don't affect protein synthesis, and addressing related medical problems. The second phase involves replenishing essential nutrients slowly to prevent taxing the patient's weakened system with more food than it can handle. Physical therapy may be beneficial to patients whose muscles have deteriorated significantly. Prevention Breastfeeding a baby for at least six months is considered the best way to prevent early-childhood malnutrition. Preventing malnutrition in developing countries is a complicated and challenging problem. Providing food directly during famine can help in the short-term, but more long-term solutions are needed, including agricultural development, public health programs (especially programs that monitor growth and development, as well as programs that provide nutritional information and supplements), and improved food distribution systems. Programs that distribute infant formula and discourage breastfeeding should be discontinued, except in areas where many mothers are infected with HIV. Every patient being admitted to a hospital should be screened for the presence of illnesses and conditions that could lead to PEM. The nutritional status of patients at higher-than-average risk should be more thoroughly assessed and periodically reevaluated during extended hospital stays or nursing home residence. 9 Marasmus Primarily caused by energy deficiency, marasmus is characterized by stunted growth and wasting of muscle and tissue. Marasmus usually develops between the ages of six months and one year in children who have been weaned from breast milk or who suffer from weakening conditions like chronic diarrhea. Profound weakness accompanies severe marasmus. Since the body breaks down its own tissue to use as calories, people with this condition lose all their body fat and muscle strength, and acquire a skeletal appearance most noticeable in the hands and in the temporal muscle in front of and above each ear. Children with marasmus are small for their age. Since their immune systems are weakened, they suffer from ,frequent infections. Other symptoms include loss of appetite diarrhea, skin that is dry and baggy, sparse hair that is dull brown or reddish yellow, mental retardation, behavioral retardation, low .body temperature (hypothermia), and slow pulse and breathing rates The absence of edema distinguishes marasmus-like secondary PEM, a gradual wasting process that begins with weight loss and progresses to mild, moderate, or severe malnutrition (cachexia). It is usually associated with cancer, chronic obstructive pulmonary disease COPD), or another chronic disease that is inactive or progressing( Some individuals have both kwashiorkor and marasmus at the same.very slowly ,time. This most often occurs when a person who has a chronic inactive condition develops symptoms of an acute illness . 10 *Metabolic adaptation in protein-energy malnutrition ***The metabolic response to chronic undernutrition covers a wide spectrum that ranges from decreased growth velocity in mild cases to profound distortion of body silhouette and composition and functional derangements in advanced stages of the protein-energy malnutrition-infection complex. A wide gamut of molecular, enzymatic, and hormonal processes assure a temporary availability of endogenous nutrients and the maintenance of vital functions. Skin in protein energy malnutrition D. S. McLaren Department of Medicine, University of Edinburgh, Royal Infirmary, Scotland. **Protein energy malnutrition (PEM), the most widespread nutritional deficiency disorder of mankind, is a group of related disorders, with a more complex and still incompletely understood etiologic basis than its name suggests. Dermatologic and other clinical manifestations are more florid and characteristic in kwashiorkor than in marasmus. The complex of clinical syndromes that constitute PEM is best considered when using a three-dimensional model to illustrate its varying degrees (ie, mild, moderate, or severe) and the spectrumlike nature of the forms of the severe degree (ie, kwashiorkor, marasmickwashiorkor, or marasmus). Protein energy malnutrition is not confined to children in the Third *******World and is the most common form of undernutrition in hospitalized patients in Western countries. Marasmus is by far the most prevalent form. Much of the nutritional support given in hospitals is not based on an assessment of nutritional status, and little attention is paid to the different forms PEM might take. Even those who do consider this last point confuse hypoalbuminemia in patients acutely stressed or infected with kwashiorkor. Recent evidence suggests that the skin changes of kwashiorkor may be caused by zinc deficiency. Almost nothing is known about the histopathology of the skin per se in PEM but studies of the hair bulb have shown important differences among patients with kwashiorkor, marasmus, and normal skin. Erythrocyte membrane (Ca2+ + Mg2+)-ATPase in human protein-energy malnutrition. Calmodulin-free ghost membranes were prepared from erythrocytes of kwashiorkor children and from healthy children in the same age bracket. In the absence of calmodulin, the specific activity of Mg2+-dependent Ca2+-pumping ATPase (Ca2+ + Mg2+-ATPase) of kwashiorkor membranes was more than 40 percent lower than the specific activity of the normal enzymes, whose maximum velocity was increased by at least four-fold by the modulator protein. In contrast, the maximum velocity of the enzymes of kwashiorkor membranes was enhanced by calmodulin by about 1 1/2 times the basal activity of the normal enzymes and by 2 times the basal activity of the kwashiorkor enzymes. The affinity of the pump for ATP was lower in the membranes of kwashiorkor children (Km for ATP = 30.6 +/- 2.8 microM ATP) in comparison to normal membranes (Km for ATP = 21.7 +/- 2.0 microM ATP). Similarly, calmodulin-affinity of the enzymes, was lower in kwashiorkor membranes than in the normal membranes irrespective of source of calmodulin. Calmodulin from haemolysates of kwashiorkor red cells activated the enzymes of normal and kwashiorkor membranes to the same degree as calmodulin partially purified from the haemolysate of healthy children. A determination of the dependence of the activity of the pump on calcium in the absence and presence of calmodulin reveals that the affinity of the kwashiorkor enzymes for Ca2+ is at least 70 percent lower than that of enzymes of normal membranes. Altogether, these findings suggest that the Ca2+-pumping ATPase of kwashiorkor membranes is less functional than the enzymes of healthy erythrocytes 11 Effects of Malnutrition on the Gastrointestinal Tract and Pancreas ******Protein-energy malnutrition may produce major structural and functional changes in the gastrointestinal tract and pancreas, which, in turn, may aggravate the underlying poor nutritional condition. In severe protein-energy malnutrition, for example, acinar cell atrophy occurs and exocrine cells have decreased numbers of zymogen granules. Pancreatic secretion may be reduced following stimulation with cholecystokinin and/or secretin. With malnutrition, the activities of enzymes contained in pancreatic juice (i.e., trypsin, chymotrypsin, lipase, amylase) are reduced. With reversal of malnutrition these can return to normal levels, but this may require several weeks. In addition to pancreatic exocrine changes, the entire wall and mucosal lining of the stomach and intestine may be reduced in thickness. This change appears to be reversible, as a more normal macroscopic appearance can follow nutritional repletion. Microscopically, marked changes may develop, including severe "flattening" of the small intestinal mucosa, similar to celiac disease. In contrast to celiac disease, however, reduced numbers of crypt mitoses are seen; the mucosa is hypoplastic rather than hyperplastic. In this setting, correction of the nutritional state per se can produce a complete reversion to normal. Nonspecific ultrastructural changes also occur, including epithelial cell lipid droplets. Changes may be present throughout the small intestine in an irregular patchy distribution, although the jejunum appears to be most severely affected. Qualitative and quantitative changes in the intestinal microflora, particularly anaerobes, also occur in protein-energy malnutrition. However, their role in altering mucosal structure and function requires definition. Some brush-border enzymes (i.e., disaccharidases) may be reduced; as a result, malabsorption of a variety of substances (e.g., lactose) may be observed. Altered uptake of glucose and D-xylose has also been reported, and steatorrhea may be present with impaired absorption of fat and some fat-soluble vitamins. In addition, there may be increased protein loss from the gut, leading to increased fecal nitrogen loss. Finally, specific nutrients may be deficient and cause alterations in certain tissues. For example, folic acid and vitamin B12 deficiencies have well-recognized effects on rapidly dividing hematopoietic precursor cells in the bone marrow; for similar reasons, as shown in Table 5, analogous changes may be anticipated in the small intestinal epithelium. 12 SOURCES Balint JP: Physical findings in nutritional deficiencies. Pediatr Clin North Am 1998 Feb; 45(1): 245-60 Beers MH, Berkow R, eds: Nutritional Disorders: Malnutrition. The Merck Manual. 17th ed. 1999:28-32: Available at: http://www.merck.com/pubs/mmanual/section1/chapter2/2c.htm. Caksen H, Kendirci M, Kandemir O, Patiroglu T: A case of malignant histiocytosis associated with skin involvement mimicking kwashiorkor. Pediatr Dermatol. 2001; Nov-Dec;18(6): 545-6. Collins N: Protein-energy malnutrition and involuntary weight loss: nutritional and pharmacological strategies to enhance wound healing. Expert Opin Pharmacother 2003 Jul; 4(7): 1121-40. Constans T, Alix E, Dardaine V: [Protein-energy malnutrition. Diagnostic methods and epidemiology] . Presse Med 2000; Dec 16;29(39): 2171-6 Delahoussaye AR, Jorizzo JL: Cutaneous manifestations of nutritional disorders. Dermatol Clin 1989 Jul; 7(3): 559-70. Demling RH: The incidence and impact of pre-existing protein energy malnutrition on outcome in the elderly burn patient population . J Burn Care Rehabil 2005; Jan-Feb;26(1): 94-100. Gehri M, Stettler N, Di Paolo ER: Marasmus. eMedicine Journal [serial online]. 2004. Available at: http://www.emedicine.com/ped/topic164.htm .. Glaser, KL: Pediatrics: Malnutrition. 2001; Available at: http://www.medstudents.com.br/pedia/pedia1.htm. Golden MHN: Severe malnutrition. In: Weatherall DJ, Ledingham JGG, Warrell DA, eds. Oxford Textbook of Medicine. 3rd ed. 1996:1278-96. Goskowicz M, Eichenfield LF: Cutaneous findings of nutritional deficiencies in children. Curr Opin Pediatr 1993 Aug; 5(4): 441-5. Grigsby DG: Malnutrition. eMedicine Journal [serial online]. 2003. Available at: http://www.emedicine.com/ped/topic1360.htm.. Gupta MA, Gupta AK, Haberman HF: Dermatologic signs in anorexia nervosa and bulimia nervosa. Arch Dermatol 1987 Oct; 123(10): 1386-90. Gurski RR, Schirmer CC, Rosa AR, Brentano L: Nutritional assessment in patients with squamous cell carcinoma of the esophagus. Hepatogastroenterology 2003 Nov-Dec; 50(54): 19437. Harris CL, Fraser C: Malnutrition in the institutionalized elderly: the effects on wound healing. Ostomy Wound Manage 2004 Oct; 50(10): World Health Organization, Dept of Nutrition for Health and Development: Nutrition for health and development: a global agenda for combating malnutrition . Geneva World Health Organization 2000; Available at: http://whqlibdoc.who.int/hq/2000/WHO_NHD_00.6.pdf. 13 INDEX Definition00000000000000000000000000001 Discribition0000000000000000000000000002 Kwashiorkor0000000000000000000000000 Mortality\Morbidity& History000000000000000 CAUSES& Complications000000000000000 Causes &symptoms00000000000000000 Lab Studies00000000000000000 Prevention& Treatment000000000000000000000000 Marasmus000000000000000000000000 Effects of PEM0000000000000000000000 14