Protein-Energy Malnutrition

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CHAPTER 222  PROTEIN-ENERGY MALNUTRITION  

TABLE 222-1 CLASSIFICATION OF MALDIGESTIVE AND MALABSORPTIVE DISORDERS PRIMARY ABNORMALITY Premucosal defect

PATHOPHYSIOLOGY Pancreatic insufficiency Bacterial overgrowth Rapid gastric emptying and intestinal transit

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Mucosal defect

Inadequate bowel syndrome

Intestinal resection Gluten-sensitive enteropathy Immunoproliferative small bowel disease Radiation enteritis Intestinal ischemia Crohn’s disease AIDS enteropathy

Postmucosal defect

Lymphatic obstruction

Congenital intestinal lymphangiectasia Milroy’s disease Secondary intestinal lymphangiectasia Retroperitoneal carcinoma Lymphoma Retroperitoneal fibrosis Chronic pancreatitis Tuberculosis Sarcoidosis Whipple’s disease Constrictive pericarditis Chronic congestive heart failure

SAMUEL KLEIN

DEFINITION

Normal nutritional status represents a healthy relationship between nutrient intake and nutrient requirements. An imbalance between intake and requirements over time can lead to malnutrition, manifested by alterations in intermediary metabolism, organ function, and body composition. The term protein-energy malnutrition has been used to describe macronutrient deficiency syndromes, which include kwashiorkor, marasmus, and nutritional dwarfism in children and wasting associated with illness or injury in children and adults.

PATHOBIOLOGY

Primary protein-energy malnutrition is caused by lack of access to adequate nutrient intake and usually affects children and elderly persons. The functional and structural abnormalities associated with primary protein-energy malnutrition are often reversible with nutritional therapy. However, prolonged primary protein-energy malnutrition can cause irreversible changes in organ function and growth. Secondary protein-energy malnutrition is caused by illnesses that alter appetite, digestion, absorption, or nutrient metabolism and can be divided into three general, but often overlapping, categories: (1) diseases that affect gastrointestinal tract function, (2) wasting disorders, and (3) critical illness. Gastrointestinal disease can cause protein-energy malnutrition by premucosal (maldigestion), mucosal (malabsorption), or postmucosal (lymphatic obstruction) defects (Table 222-1). The nutritional status of patients with protein-energy malnutrition caused by gastrointestinal tract dysfunction can often be restored to normal if adequate nutritional support can be provided by dietary manipulations, enteral tube feeding, or parenteral nutrition. Wasting disorders, such as cancer, acquired immunodeficiency syndrome (AIDS), and rheumatologic diseases, are characterized by involuntary loss of body weight and muscle mass in the setting of a chronic illness. These patients often experience wasting because of (1) inadequate nutrient intake related to anorexia and possibly gastrointestinal tract dysfunction and (2) metabolic abnormalities caused by alterations in regulatory hormones, cytokines, and systemic inflammation. The alterations in metabolism are responsible for the greater loss of muscle tissue observed in these patients than in those with pure starvation or semistarvation. Restoration of muscle mass is unlikely with nutritional support unless the underlying inflammatory disease is corrected. Weight gain that occurs after nutritional support is started is usually caused by increases in fat mass and body water, without significant increases in muscle tissue. Patients with critical illness exhibit marked metabolic alterations, manifested by increased energy expenditure, altered endogenous glucose production and lipolytic rates, and protein breakdown. Therefore, protein and energy requirements are increased in critically ill patients. However, providing aggressive nutritional support may ameliorate but does not prevent net lean tissue losses without correction of the underlying illness or injury.

REPRESENTATIVE DISORDERS Chronic pancreatitis Cystic fibrosis Pancreatic duct obstruction Motility diseases Blind loop syndromes Small intestine diverticula Post–gastric surgery syndrome

AIDS = acquired immunodeficiency syndrome.

METABOLIC RESPONSE TO STARVATION

The adaptive response to starvation involves a series of metabolic alterations that enhance the chance for survival by increasing the use of body fat as a fuel, sparing the use of glucose, minimizing body nitrogen losses, and decreasing energy expenditure. A marked shift in fuel use occurs during the first day of starvation. By 24 hours of fasting, the use of glucose as a fuel has decreased; only 15% of liver glycogen stores remain, and the rates of hepatic glucose production and whole body glucose oxidation have decreased. Conversely, endogenous fat stores become the body’s major fuel, and the rates of adipose tissue lipolysis, hepatic ketone body production, and fat oxidation are increased. After 3 days of fasting, the rate of glucose production is reduced by one half, and the rate of lipolysis is more than double the value found at 12 hours of fasting. The increase in fatty acid delivery to the liver, in conjunction with an increase in the ratio of plasma glucagon to insulin concentration, enhances hepatic ketone body production. Ketone bodies provide a watersoluble fuel, derived from water-insoluble adipose tissue triglycerides, which can be safely transported through the circulation and which readily cross the blood-brain barrier. By 7 days of fasting, plasma ketone body concentrations have increased 75-fold, and ketone bodies provide 70% of the brain’s energy needs. In addition, body energy requirements are substantially decreased by 7 days of fasting because of fatigue-induced decrease in physical activity and a 15% reduction in resting metabolic rate. The use of ketone bodies by the brain greatly diminishes glucose requirements and thereby reduces the need for muscle protein degradation to provide glucose precursors. Furthermore, thyroid hormone inactivation and plasma ketones inhibit muscle protein breakdown and prevent rapid protein losses. If postabsorptive protein breakdown rates were to continue throughout starvation, a potentially lethal amount of muscle protein would be catabolized in less than 3 weeks. As fasting continues, the kidney becomes an important site for glucose production; glutamine, released from muscle, is converted to glucose in the kidney and accounts for almost half of total glucose production. Adaptation is maximum during more prolonged starvation (>14 days of fasting). At this time, adipose tissue provides more than 90% of daily energy

CHAPTER 222  PROTEIN-ENERGY MALNUTRITION  

requirements. Total glucose production has decreased to about 75 g/day, providing fuel for glycolytic tissues (40 g/day) and the brain (35 g/day). Muscle protein breakdown has decreased to less than 30 g/day, which causes a marked decrease in urea nitrogen production and excretion. The diminished urea load to the kidneys decreases urine volume to 200 mL/day, thereby minimizing fluid requirements. Resting energy expenditures decrease by approximately 25%. Prolonged starvation causes a marked decrease in body fat mass, muscle protein, and the sizes of most organs, whereas the weight and protein content of the brain remains relatively stable.

UNDERNUTRITION-INDUCED ALTERATIONS IN TISSUE MASS AND FUNCTION

body composition.  All body tissue masses are affected by undernutrition, but fat mass and muscle mass are the most severely affected. In lean adults, these two tissues account for almost two thirds of body weight. Therefore, the loss of weight that occurs in malnourished patients is principally the result of a loss in muscle and fat mass. Body adipose tissue can be almost completely depleted and up to half of muscle mass can be consumed before death from starvation occurs. body water.  Many patients who are malnourished have intravascular volume depletion because of inadequate water and sodium intake. However, the percentage of body weight that is composed of water may be increased. Decreased plasma proteins, leaky capillaries, leaky cells, and increased interstitial ion content may cause intravascular volume depletion and expansion of the interstitial space. Therefore, malnourished patients may have diminished intravascular volume in the presence of whole body fluid overload. skin.  The skin is a large organ that regenerates rapidly: a basal cell of the dermis reaches the cornified layer and dies in 10 to 14 days. Frequently, undernutrition causes the skin to be dry, thin, and wrinkled, with atrophy of the basal layers of the epidermis and hyperkeratosis. Severe malnutrition may cause considerable depletion of skin protein and collagen. Patients with kwashiorkor experience sequential skin changes in different locations. Hyperpigmentation occurs first, followed by cracking and stripping of superficial layers, leaving behind hypopigmented, thin, and atrophic epidermis that is friable and easily macerated. hair.  Scalp hair becomes thin and sparse and is pulled out easily. In contrast, the eyelashes become long and luxuriant, and there may be excessive lanugo hair in children. Children with kwashiorkor experience hypopigmentation with reddish brown, gray, or blond discoloration. Adults may lose axillary and pubic hair. gastrointestinal tract.  Starvation and malnutrition cause structural and functional deterioration of the intestinal tract, pancreas, and liver. The total mass and protein content of the intestinal mucosa and pancreas are markedly reduced. Mucosal epithelial cell proliferation rates decrease, and intestinal mucosa becomes atrophic with flattened villi. The synthesis of mucosal and pancreatic digestive enzymes is reduced. Intestinal transport and absorption of free amino acids are impaired, whereas hydrolysis and absorption of peptides are maintained. Gastric and biliary secretions are diminished. The abdomen may become protuberant because of hypomotility and gas distention. Hepatomegaly is common in severe malnutrition because of excessive fat accumulation caused by decreased very low density lipoprotein synthesis and triglyceride export. Synthesis of most hepatic proteins is decreased. heart.  Chronic undernutrition affects cardiac mass and function. Cardiac muscle mass decreases, and the decrease is accompanied by fragmentation of myofibrils. Bradycardia (heart rate can decrease to less than 40 beats/minute) and decreased stroke volume can cause a marked decrease in cardiac output and low blood pressure. For example, a hypocaloric diet in physiologically normal volunteers that caused a 24% decrease in body weight was associated with a 38% decrease in cardiac index. lungs.  Respiratory function is altered because of decreased thoracic muscle mass and electrolyte imbalances, which cause a decrease in vital capacity, tidal volume, minute ventilation, and ventilatory response to hypoxia. kidneys.  Renal mass and function are relatively well preserved during undernutrition, provided adequate water is consumed to prevent a severe decrease in renal perfusion and acute renal failure. However, when malnutrition is severe, decreases are noted in kidney weight, glomerular filtration rate, the ability to excrete acid, the ability to excrete sodium, and the ability to concentrate urine. Mild proteinuria may also occur.

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bone marrow.  Severe undernutrition suppresses bone marrow red blood cell and white blood cell production and leads to anemia, leukopenia, and lymphocytopenia. muscle.  Muscle function is impaired by malnutrition because of both a loss of muscle mass and impaired metabolism. Decreased sodium pump activity causes an increase in intracellular sodium and a decrease in intracellular potassium, which affects myocyte electrical potential, contributing to fatigue. brain.  The weight and protein content of the brain remain relatively stable during long-term starvation. Therefore, the integrity of the brain is preserved at the expense of other organs and tissues. However, data from one study found that cerebral atrophy was associated with protein-energy malnutrition in children, a finding suggesting that the brain is not completely protected from malnutrition during childhood. immune system.  Severe undernutrition causes atrophy of all lymphoid tissues, including thymus, tonsils, and lymph nodes. Cell-mediated immunity is diminished more than antibody production. Alterations in cell-mediated immunity cause impaired delayed cutaneous hypersensitivity and anergy. The ability to kill bacteria is diminished because of decreased complement and impaired neutrophil function. Gastrointestinal immunoglobulin A secretion is also decreased. Malnourished patients are at increased risk for opportunistic infections and should be considered immunocompromised. endocrine system.  Decreased plasma insulin concentrations and glucose intolerance are common in severe malnutrition. Growth hormone is usually increased and is much greater in the kwashiorkor type than the marasmic type of protein-energy malnutrition. Serum thyroxine levels are low, and the conversion of thyroxine to triiodothyronine is decreased, with increased conversion to reverse triiodothyronine. Plasma cortisol concentration is usually greater than normal. The decrease in plasma leptin concentration that occurs early during energy restriction may be an important initiator of the neuroendocrine response to fasting. energy metabolism.  Starvation and undernutrition decrease basal energy expenditure because of diminished organ size and function, increased conversion of active thyroid hormone to its inactive form, decreased sodium pump activity, decreased protein turnover, decreased body core temperature, absence of shivering and nonshivering thermogenesis, and suppression of sympathetic nervous system activity. Energy is also conserved by the onset of fatigue, which leads to decreased physical activity.

DEATH FROM STARVATION

At the terminal phase of starvation, body fat mass, skeletal muscle mass, and the size of most organs are markedly decreased. During this final phase of starvation, body fat stores are nearly depleted, energy derived from body fat decreases, and muscle protein catabolism is accelerated. The mechanism responsible for death from starvation in humans is not well understood, but many patients ultimately succumb to infection. It has been suggested that there are lethal levels of body weight loss (loss of 40% of body weight), of protein depletion (loss of 30 to 50% of body protein), of fat depletion (loss of 70 to 95% of body fat stores), or of body size (body mass index of 13 kg/ m2 for men and 11 kg/m2 for women) in humans. The duration of survival depends on the amount of available endogenous fuels and the amount of lean tissue. Data from Irish Republican Army hunger strikers demonstrate that death occurs in lean men after approximately 2 months of starvation when more than 35% (∼25 kg) of body weight is lost. Obese persons can survive much longer periods of starvation because of their increased fat stores and lean tissue mass. The longest reported fast is that of a severely obese (207 kg) man who safely lost 61% (126 kg) of his initial weight after completing a 382-day fast in which he ingested only acaloric fluids, vitamins, and minerals.

CLINICAL MANIFESTATIONS

Protein-Energy Malnutrition in Children

Undernutrition in children differs from that in adults because it affects growth and development. Much of our understanding of undernutrition in children comes from observations and studies in developing nations where poverty, inadequate food supply, and unsanitary conditions lead to a high prevalence of protein-energy malnutrition. The Waterlow classification of malnutrition and subsequent modification by the World Health Organization (WHO) are used widely and take into account that undernutrition affects childhood growth. Therefore, nutritional status is assessed by comparing a child’s weight for height (wasting) and height for age (stunting) with normal standards (Table 222-2). The characteristics of the three major clinical

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TABLE 222-2 WATERLOW AND WHO CLASSIFICATIONS OF PROTEIN-ENERGY MALNUTRITION IN CHILDREN

TABLE 222-4 CLASSIFICATION OF PROTEIN-ENERGY MALNUTRITION IN ADULTS BY BODY MASS INDEX

MEASURE

BODY MASS INDEX (KG/M2) 18.5-24.9

NUTRITIONAL STATUS Normal

17.0-18.4

Mildly malnourished

15.0-16.9

Moderately malnourished

<15.0

Severely malnourished

NORMAL

MILD

MODERATE

SEVERE

80-89

70-79

<70

WEIGHT FOR HEIGHT (WASTING) Percentage of median NCHS standard Standard deviation from the NCHS median

90-110 +Z to −Z

−1.1 to −2 Z

−2.1 to −3 Z

≤−3 Z

95-105

90-94

85-89

<85

+Z to −Z

−1.1 to −2 Z

−2.1 to −3 Z

≤−3 Z

HEIGHT FOR AGE (STUNTING) Percentage of median NCHS standard Standard deviation from the NCHS median

NCHS = National Center for Health Statistics; WHO = World Health Organization; Z = 1 standard deviation.

TABLE 222-3 FEATURES OF PROTEIN-ENERGY MALNUTRITION SYNDROMES IN CHILDREN CHARACTERISTIC Weight for age (% expected)

KWASHIORKOR 60-80

MARASMUS

NUTRITIONAL DWARFISM

<60

<60

Weight for height

Normal or decreased

Markedly decreased

Normal

Edema

Present

Absent

Absent

Mood

Irritable when picked up Apathetic when alone

Alert

Alert

Appetite

Poor

Good

Good

syndromes of protein-energy malnutrition in children are outlined in Table 222-3. Although these three syndromes are classified separately, they may coexist in the same patient. The use of mid-upper arm circumference has been proposed as a useful screening tool in underserved areas because height is difficult to measure accurately in ill children and accurate assessment of weight depends on access to functioning scales. Mid-upper arm circumference of up to 11.5 cm in children 1 to 5 years old can predict subsequent inpatient mortality as reliably as the Waterlow and WHO classifications. marasmus.  Weight loss and marked depletion of subcutaneous fat and muscle mass are the characteristic features in children with marasmus. Loss of fat and muscle makes ribs, joints, and facial bones prominent. The skin is thin, loose, and lying in folds. These children are typically weak and lethargic. kwashiorkor.  The word kwashiorkor comes from the Ga language of West Africa and can be translated as “disease of the displaced child” because it was commonly seen after weaning. The presence of peripheral edema distinguishes children with kwashiorkor from those with marasmus and nutritional dwarfism (Fig. 222-1). Children with kwashiorkor also have typical skin and hair changes (see earlier sections on hair and skin changes). The abdomen is protuberant because of weakened abdominal muscles, intestinal distention, and hepatomegaly, but these children do not have ascites. In fact, the presence of ascites should prompt the clinician to search for liver disease or peritonitis. Children with kwashiorkor are typically lethargic and apathetic when left alone but become quite irritable when they are picked up or held. Kwashiorkor is not caused by a relative deficiency in protein intake, as was previously believed; in fact, protein and energy intakes are similar in children with kwashiorkor and marasmus. The pathogenesis of kwashiorkor is not clear, but it is likely related to the physiologic stress of an infection that induces a deleterious metabolic cascade in an already malnourished child. This explains why kwashiorkor is an acute illness compared with the chronicity of undernutrition alone and why marasmus and kwashiorkor overlap.

FIGURE 222-1.  Kwashiorkor and marasmus in brothers. The younger brother, on the left, has kwashiorkor with generalized edema, skin changes, pale reddish yellow hair, and an unhappy expression. The older child, on the right, has marasmus, with generalized wasting, spindly arms and legs, and an apathetic expression. (From Peters W, Pasvol G, eds. Tropical Medicine and Parasitology, 5th ed. London: Mosby; 2002, Fig. 986.)

Kwashiorkor is characterized by leaky cell membranes that permit the movement of potassium and other intracellular ions to the extracellular space. The increased osmotic load in the interstitium causes water movement and edema. nutritional dwarfism.  The child with failure to thrive may be of normal weight for height but has short stature and delayed sexual development. Providing appropriate feeding can stimulate catch-up growth and sexual maturation.

Protein-Energy Malnutrition in Adults

The diagnosis of protein-energy malnutrition in adults is different from that in children because adults are no longer growing in height. Therefore, undernutrition in adults causes wasting rather than stunting and can be assessed by determining body mass index, defined as the patient’s weight (in kilograms) divided by the patient’s height (in meters squared) (Table 222-4). In addition, although kwashiorkor and marasmus can occur in adults, most studies of adult protein-energy malnutrition have evaluated hospitalized patients with secondary protein-energy malnutrition and coexisting illness or injury. The current methods that are used clinically to evaluate protein-energy malnutrition in hospitalized adult patients shift nutritional assessment from a diagnostic to a prognostic instrument in an attempt to identify patients who can benefit from nutritional therapy. Therefore, common nutritional assessment parameters are affected by non-nutritional factors that make it difficult to separate the influence of the disease itself from the contribution of inadequate nutrient intake. At present, no “gold standard” exists for determining protein-energy malnutrition in ill patients. The most commonly used methods include a careful history, physical examination, and selected laboratory tests.

TREATMENT Initial Evaluation

A careful clinical examination is needed to identify life-threatening complications of protein-energy malnutrition that require immediate treatment. The presence of fluid, plasma glucose, electrolyte, and acid-base abnormalities should be determined. A search for infections (e.g., obtaining a white blood cell count, urine analysis and culture, blood cultures, and chest radiograph) should be considered even in the absence of physical findings because many patients are not able to mount a normal inflammatory response. The evaluation must also include a careful analysis of the possible route for nutritional support and whether the gastrointestinal tract can be used or parenteral nutrition is needed for refeeding.

Initial Supportive Care: Resuscitate and Stabilize

Judicious resuscitation with fluids and electrolytes may be necessary before beginning feedings, with frequent evaluations to prevent congestive heart failure from fluid overload. Vitamin supplementation should be given routinely. Severely malnourished patients are poikilothermic, and a warm ambient temperature and warming blankets may be necessary to raise their core temperature slowly. However, if warming blankets are used, patients must be carefully monitored to avoid hyperthermia.

Refeeding: Nutritional Rehabilitation

The goal of feeding the severely malnourished patient can be divided into three phases: (1) to prevent further deterioration and correct life-threatening abnormalities, (2) to restore normal organ function and metabolism, and finally (3) to replete deficient nutrient stores. Oral or enteral tube feedings are preferred to parenteral feeding because of fewer serious complications and enhanced gastrointestinal tract recovery. Feedings should be given in small amounts at frequent intervals to avoid overwhelming the body’s limited capacity for nutrient processing and to prevent hypoglycemia, which can occur during brief nonfeeding intervals. Therefore, small amounts of oral feeding should be given frequently (every 1 to 4 hours), enteral tube feeding by continuous drip, or parenteral nutrition by continuous infusion. Sodium intake should be limited during early refeeding, but liberal amounts of phosphorus, potassium, and magnesium should be given to patients who have normal renal function. Daily monitoring of body weight, fluid intake, urine output, and plasma glucose and electrolyte values is critical during the first few days of refeeding so that nutritional therapy can be appropriately adjusted when necessary. Appetite will have usually improved during the second phase. Protein and energy intake should be marginally higher than estimated requirements to provide for adequate maintenance and repair. Additional protein and energy should be provided during phase 3 for repletion and synthesis of new tissue. The use of nutrient-rich, ready-to-use therapeutic foods is an easy and effective approach for treating malnutrition at home, particularly in developing nations where access to appropriate foods is limited. The manufacturing and processing of ready-to-use-therapeutic foods make it possible to add functional ingredients in an attempt to improve clinical outcome. However, adding probiotics and prebiotics to standard nutritional therapy does not have additional therapeutic effects.

Refeeding Complications

Refeeding can be harmful and may even cause death because of impaired organ function and depleted nutrient stores resulting from previous starvation. The adverse consequences caused by initiating feeding too aggressively are known as the refeeding syndrome and usually occur within the first 5 days. (Refeeding syndrome as a complication of parenteral nutrition is briefly discussed in Chapter 224.) Refeeding syndrome complications include fluid overload, electrolyte imbalances, glucose intolerance, cardiac arrhythmias, and diarrhea.

Fluid Overload

Severely malnourished patients are at increased risk for fluid retention and congestive heart failure after nutritional therapy because of compromised cardiac and renal function. Because the ability to excrete sodium is impaired, even normal amounts of dietary sodium intake can be excessive. In addition, carbohydrates increase the concentration of circulating insulin, which stimulates sodium and water reabsorption by the renal tubule. The presence of heart failure requires discontinuation of feeding until cardiac status is stabilized.

Mineral Depletion

Carbohydrate refeeding stimulates insulin release and intracellular uptake of phosphate, which is used for protein synthesis and glucose metabolism. Therefore, plasma phosphorus concentrations can sometimes fall precipitously to less than 1 mg/dL after initiating nutritional therapy if adequate phosphate is not given. Severe hypophosphatemia, associated with muscle weakness, paresthesias, seizures, coma, cardiopulmonary decompensation, and death, has occurred in severely malnourished patients after they received enteral or parenteral nutritional therapy.

Decreased body cell mass and decreased sodium, potassium–adenosine triphosphatase activity, or leaky cell membranes in the malnourished patient lead to depletion of the major intracellular cations, potassium and magnesium. Nonetheless, serum potassium and magnesium concentrations may remain normal or near normal during starvation because of their release from tissue and bone stores. During refeeding, increases in protein synthesis, body cell mass, and glycogen stores require generous intakes of potassium and magnesium. In addition, hyperinsulinemia during refeeding increases cellular uptake of potassium and can cause a rapid decline in its extracellular concentrations.

Glucose Intolerance

Malnourished patients are predisposed to hypoglycemia because of decreased hepatic glucose production. However, starvation and malnutrition impair insulin’s ability to suppress endogenous glucose production and stimulate glucose uptake and oxidation. Therefore, providing enteral or parenteral carbohydrates can cause hyperglycemia, glucosuria, dehydration, and hyperosmolar coma. Furthermore, because of the importance of thiamine in glucose metabolism, carbohydrate refeeding in patients who are thiamine deficient can precipitate Wernicke’s encephalopathy (Chapter 425).

Cardiac Arrhythmias

Sudden death from ventricular arrhythmias can occur during the first week of refeeding in severely malnourished patients and has been reported in conjunction with severe hypophosphatemia. A prolonged QT interval may be a contributing cause of the rhythm disturbances.

Gastrointestinal Dysfunction

Alterations in gastrointestinal tract function limit the ability of the gastrointestinal tract to digest and absorb food. Mild diarrhea after initiating oralenteral feeding usually resolves and is not clinically important if fluid and electrolyte homeostasis can be maintained. However, in some severely malnourished patients, oral feeding is associated with severe diarrhea and death. Therefore, aggressive fluid and electrolyte replacement and a search for enteric pathogens should be considered in patients with prolonged or severe diarrhea.

SUGGESTED READINGS Johansson L, Sidenvall B, Malmberg B, et al. Who will become malnourished? A prospective study of factors associated with malnutrition in older persons living at home. J Nutr Health Aging. 2009;13:855861. This longitudinal study identified the factors that increase older adult risk for malnutrition. Matilsky DK, Maleta K, Castleman T, et al. Supplementary feeding with fortified spreads results in higher recovery rates than with a corn/soy blend in moderately wasted children. J Nutr. 2009;139:773-778. Randomized controlled trial, conducted in moderately wasted Malawian children, which demonstrates ready-to-use therapeutic foods are superior than standard fortified corn and soy blended flour in treating malnutrition. Morley JE. Nutrition and the brain. Clin Geriatr Med. 2010;26:89-98. Review. Oshikoya KA, Sammons HM, Choonara I. A systematic review of pharmacokinetics studies in children with protein-energy malnutrition. Eur J Clin Pharmacol. 2010;66:1025-1035. Review of common drugs. Scrimshaw NS, Viteri FE. INCAP studies of kwashiorkor and marasmus. Food Nutr Bull. 2010;31:34-41. Review. Panteli JV, Crook MA. Refeeding syndrome still needs to be recognized and managed appropriately. Nutrition. 2009;25:130-131. Reviews the pathophysiology, clinical manifestations, and management of refeeding syndrome.