Investigators have searched unsuccessfully for a single cause or a specific set of causes of undernutrition and the appropriate intervention

strategies to correct that cause or set of causes. Attention has shifted from inadequate protein to inadequate energy to inadequate micronutrients, with accompanying shifts of focus concerning appropriate intervention and treatment strategies. Problems and causes of undernutrition that are debated include growth faltering, low birthweight, maternal undernutrition, deficiencies of specific nutrients (iodine, vitamin A, iron, zinc), diarrhea, HIV infection and other infectious diseases, chronic illness, inadequate infant and child feeding practices, time constraints, limited household income, limited agricultural production, food insecurity, environmental degradation, and urbanization. A wide array of solutions to these problems also is debated. These include growth monitoring, promotion of more optimal breastfeeding and complementary feeding practices, nutrition education, oral rehydration programs, child spacing, food fortification, supplementation of specific or multiple nutrients (vitamin A, iron, and/or zinc), income generation, food aid, home gardening, and agricultural intensification. To a great extent, this shifting illustrates the poor understanding of many aspects of the major worldwide problem of undernutrition. The problem of undernutrition is multifaceted, and solving it at a national level requires understanding, trust, and cooperation among diverse governmental agencies accustomed to dealing solely with health, agriculture, education, or finance issues. The frequent shifting of focus has not generated a coherent and understandable approach to the problem, but rather, has helped create the perception among many national policymakers and planners that the nutrition problem is too complicated. This, in turn, has delayed coordination of efforts across international and local governmental agencies. Equally important, it has failed to generate a consensus within the nutrition community about priority problems and the actions and strategies needed to solve them. In response to this situation, the United Nations International Children's Emergency Fund (UNICEF) has developed and is promoting an inclusive conceptual framework for organizing scientific knowledge and experience concerning undernutrition (or malnutrition), fostering a common understanding, and developing coherent strategies for addressing the problem. A key feature of this framework is the recognition that undernutrition is a biologic manifestation of the combined effects of inadequate dietary intake and disease, both of which are closely related to social and economic development. Thus, malnutrition cannot be viewed as distinct from other development problems, but rather, as a reflection of these other problems. Another feature of this framework is that the assumptions underlying various approaches to malnutrition should be stated explicitly so that they can be questioned and debated rather than assuming implicitly that malnutrition is due solely to a specific cause (lack of food, inadequate health care, limited education, poor breast-feeding practices, inadequate agricultural production). Another key feature of the UNICEF framework is that the relative importance of the underlying causes of malnutrition (inadequate food and health care) must be recognized widely across households, communities, and countries. This implies that universal causes and solutions do not exist and that constraints in providing adequate food and health care must be assessed and acted on in each setting. Rather than imposed national or global solutions, a highly decentralized approach to assessment, analysis, and action is required.

MEASUREMENT OF UNDERNUTRITION.

The traditional approach to nutritional assessment measures only the physical manifestations of the problem (clinical, anthropometric, biochemical indicators) and perhaps some of the immediate causes related to dietary intake. These indicators may be adequate for estimating the magnitude of the problem, but additional approaches are needed to assess the broader nutrition situation. These approaches include consideration not only of dietary intake but also of health care and control of resources at the household, community, and national levels. Despite the need for additional approaches, a number of anthropometric indices have been used successfully for many years to estimate the prevalence of undernutrition among preschool-aged children. These include height-for-age, weight-for-age, and weight-for-height. The 1st is an index of the cumulative effects of undernutrition during the life of the child, the 2nd reflects the combined effects of both recent and longer-term levels of nutrition, and the last reflects recent nutritional experiences. Values <8090% of expected are considered abnormally low. These indices are reasonably sensitive indicators of the immediate and underlying general causes of undernutrition, but they are not specific for any particular cause. They do not reveal the relative importance of dietary intake, infectious diseases, food insecurity, inadequate health/environmental services, low birthweight, suboptimal childcare practices, income constraints, or disparities in control of resources. These factors are part of the assessment of the overall nutrition situation and are distinct from the biochemical and/or anthropometric indicators that reflect the severity and extent of the problem, its distribution across geographic and social groups, and trends over time.
PREVALENCE OF UNDERNUTRITION.

In 2000, 26.7% of preschoolers in the developing world were estimated to be underweight, as reflected by a low weight-for-age and 32.5% were estimated to be stunted based on a low heightfor-age. Compared with estimates in 1980, these estimates are approximately 11% and approximately 15% lower, respectively, suggesting considerable improvement, at least in some regions, over these 2 decades. However, the population of the developing world increased during this time; thus, the total number of underweight children and children with stunted growth has not changed dramatically since 1980. Data from the USA and other developed countries indicate that the prevalence of undernutrition, as manifested by a low weight-for-age or height-for-age measure, is very low. Data from the United States National Health and Nutrition Examination Survey (NHANES) III (19881994) indicate that the prevalence of low height-for-age measure (<5th percentile) was 45% among children from 2 mo to 11 yr of age, approximately the same prevalence noted by NHANES I (19711974) 2 decades earlier. The NHANES III data also show that populations with a high prevalence of poverty do not have a higher prevalence of undernutrition than the general population, emphasizing the importance not only of adequate intake but also of adequate care, as defined in the framework of UNICEF.

In contrast to the low prevalence of undernutrition among the general population of children in the USA and other developed countries, the prevalence among hospitalized children is often as high as that in developing countries.
CONSEQUENCES OF UNDERNUTRITION.

The cumulative evidence suggests that undernutrition has pervasive effects on immediate health and survival as well as on subsequent performance. These include not only acute effects on morbidity and mortality but also longer-term effects on cognitive and social development, physical work capacity, productivity, and economic growth. The magnitude of both the acute and the longer-term effects is considerable. Prospective studies suggest that severely underweight children (<60% of reference weight for age) have more than an 8-fold greater risk of mortality than normally nourished children, that moderately underweight children (6069% of reference weight for age) have a 4- to 5-fold greater risk, and that even mildly underweight children (70 79% of reference weight for age) have a 2- to 3-fold greater risk. The high prevalence of mortality, even in children with mild and moderate undernutrition, suggests that >50% of child deaths may be caused directly or indirectly by undernutrition. Moreover, 83% of these deaths result from mild to moderate forms of undernutrition. A major factor is the potentiation of infectious diseases by undernutrition. Survivors of childhood undernutrition frequently have deficits in height and weight that persist beyond adolescence into adulthood. These deficits are often accompanied by deficits in frame size as well as muscle circumference and strength. The implications of these deficits with respect to the work capacity of both men and women and to women's reproductive performance are obvious. Survivors of childhood malnutrition also have deficits in cognitive function and school performance relative to normally nourished children from the same environment. Mean deficits in scores on standard tests of cognition range from 515 points. The fact that severely undernourished children, as assessed by low length-for-age measures, have greater deficits in cognitive performance than children with mild or moderate undernutrition strongly suggests that the intellectual deficits are related to the severity of undernutrition. The extent to which intellectual deficits can be decreased by dietary intervention alone is not clear. However, these deficits can be decreased by a combination of dietary and behavioral interventions, coupled with improvements in the overall quality of the home and/or school environment. Such interventions appear to be much more effective if instituted in early life.
PREVENTION OF UNDERNUTRITION.

Food insecurity and undernutrition are the behavioral and biologic manifestations, respectively, of problems that are rooted in the social world from the level of individuals and households to the community, national, and international levels. Thus, a wide range of scientific disciplines must be drawn on to maximize the possibility of effective, sustainable solutions. An intervention as simple as supplementing the population with vitamin A requires an understanding of the behavior of households, communities, clinical workers, program managers, and policymakers. The evolution of thought about food insecurity and undernutrition in developed and developing countries has some commonalities with significant policy implications. The major commonality

is the recognition that the causes of these problems, although strongly related globally to poverty, are highly contextual and, hence, easily misunderstood. In most developed countries, for example, not all food-insecure individuals live in poverty, and not all those living in poverty have food insecurity. Similarly, in developing countries, child malnutrition secondary to suboptimal health conditions or caring practices is common, even among households with ample food resources. Thus, food insecurity and undernutrition arise from a variety of social, economic, and ecologic situations that vary from time to time and from place to place. Therefore, the coping strategies and behaviors of individuals and households as well as communities and nations are highly responsive to a variety of micro contextual factors. Moreover, these coping strategies and behaviors are strongly influenced by the ways in which food-insecure and undernourished individuals experience reality. The risk-avoidance and risk-management strategies of poor households often discourage them from adopting new crop varieties or making other changes in their livelihood strategy, despite the fact that such changes appear desirable and rational to outsiders. Many policies and programs have been ineffective because they do not adequately assess, anticipate, and embrace the coping strategies and likely responses of the population. Some programs that do so have been initiated in communities throughout the developing world and are currently being evaluated. The results of these efforts should suggest strategies to improve the total nutrition situation and reduce the high prevalence of childhood undernutrition worldwide.
CLINICAL MANIFESTATIONS AND TREATMENT OF UNDERNUTRITION.

Undernutrition ranges from a lower than desired intake of 1 or more nutrients, with either no symptoms or only vague symptoms, to severe malnutrition (discussed later). The approach to treating mild undernutrition is the same as that suggested for food insecurity of sufficient severity to result in low intake of specific nutrients. Treatment of vitamin deficiencies is discussed in Chapters 4550 [Chapter 45] [Chapter 46] [Chapter 47] [Chapter 48] [Chapter 49] [Chapter 50] , and treatment of the most severe form of undernutrition is discussed in the next section of this chapter.
SEVERE CHILDHOOD UNDERNUTRITION (PROTEIN-ENERGY MALNUTRITION).

Deficiency of a single nutrient is an example of undernutrition or malnutrition, but deficiency of a single nutrient usually is accompanied by a deficiency of several other nutrients. Proteinenergy malnutrition (PEM) is manifested primarily by inadequate dietary intakes of protein and energy, either because the dietary intakes of these 2 nutrients are less than required for normal growth or because the needs for growth are greater than can be supplied by what otherwise would be adequate intakes. However, PEM is almost always accompanied by deficiencies of other nutrients. For this reason, the term severe childhood undernutrition, which more accurately describes the condition, is preferred. The terms primary malnutrition and secondary malnutrition refer, respectively, to malnutrition resulting from inadequate food intake and malnutrition resulting from increased nutrient needs, decreased nutrient absorption, and/or increased nutrient losses. Both primary and secondary malnutrition occur in developing as well as developed countries; malnourished children often present with gastroenteritis or pneumonia.

Severe childhood undernutrition (SCU), whether primary or secondary, is a spectrum ranging from mild undernutrition resulting in some decrease in length-for-age and/or weight-for-age through severe forms of undernutrition resulting in more marked deficits in weight-for-age and length-for-age as well as wasting (a low weight-for-length measure). Historically, the most severe forms of SCU, marasmus (non-edematous SCU with severe wasting) and kwashiorkor (edematous SCU), were considered distinct disorders. Non-edematous SCU was believed to result primarily from inadequate energy intake or inadequate intakes of both energy and protein, whereas edematous SCU was believed to result primarily from inadequate protein intake. A third disorder, marasmic kwashiorkor, has features of both disorders (wasting and edema). The 3 conditions have distinct clinical and metabolic features, but they also have a number of overlapping features. A low plasma albumin concentration, often believed to be a manifestation of edematous SCU, is common in children with both edematous and non-edematous SCU. In addition, the underlying causes of this spectrum of conditions are quite similar. Among these are social and economic factors such as poverty and ignorance, social factors such as food taboos, biologic factors such as maternal malnutrition and inadequate intakes of breast milk and other foods, and environmental factors such as overcrowded and unsanitary living conditions. In the USA, SCU has been reported in families who use unusual and inadequate foods to feed infants whom the parents believe to be at risk for milk allergies and also in families who believe in fad diets. Many cases are associated with rice milk diets, a product that is very low in protein content. In addition, SCU has been noted in chronically ill patients in neonatal or pediatric intensive care units as well as among patients with burns, HIV, cystic fibrosis, failure to thrive, chronic diarrhea syndromes, malignancies, bone marrow transplantation, and inborn errors of metabolism.
CLINICAL MANIFESTATIONS OF SCU.

Non-edematous SCU (marasmus) is characterized by failure to gain weight and irritability, followed by weight loss and listlessness until emaciation results. The skin loses turgor and becomes wrinkled and loose as subcutaneous fat disappears. Loss of fat from the sucking pads of the cheeks often occurs late in the course of the disease; thus, the infant's face may retain a relatively normal appearance compared with the rest of the body, but this, too, eventually becomes shrunken and wizened. Infants are often constipated, but may have starvation diarrhea, with frequent, small stools containing mucus. The abdomen may be distended or flat, with the intestinal pattern readily visible. There is muscle atrophy and resultant hypotonia. As the condition progresses, the temperature usually becomes subnormal and the pulse slows. Edematous SCU (kwashiorkor) may initially present as vague manifestations that include lethargy, apathy, and/or irritability. When advanced, there is lack of growth, lack of stamina, loss of muscle tissue, increased susceptibility to infections, vomiting, diarrhea, anorexia, flabby subcutaneous tissues, and edema. The edema usually develops early and may mask the failure to gain weight. It is often present in internal organs before it is recognized in the face and limbs. Liver enlargement may occur early or late in the course of disease. Dermatitis is common, with darkening of the skin in irritated areas, but in contrast to pellagra (see Chapter 46 ), not in areas exposed to sunlight. Depigmentation may occur after desquamation in these areas, or it may be

generalized (Figs. 43-1, 43-2, and 43-3 [1] [2] [3]). The hair is sparse and thin, and in darkhaired children, it may become streaky red or gray. Eventually, there is stupor, coma, and death.

Figure 43-1 A, Kwashiorkor in a 2 yr old boy. Note the generalized edema, the typical skin lesions, and the state of prostration. B, Close-up view of the same child showing the hair changes and psychic alterations (apathy and misery); the edema of the face and skin lesions can be seen more clearly. (Photographs made available by the Institute of Nutrition of Central Panama, Guatemala, courtesy of Moises Behar, MD.)

Figure 43-2 Diffuse fine scale in a reticulated pattern over the abdomen. (From Liu T, Howard RM, Mancini AJ, et al: Kwashiorkor in the United States. Arch Dermatol 2001;137:630 636.)

Figure 43-3 Flaky paint dermatosis on the thighs. (From Liu T, Howard RM, Mancini AJ, et al: Kwashiorkor in the United States. Arch Dermatol 2001;137:630636.)

Noma is a chronic necrotizing ulceration of the gingiva and the cheek ( Fig. 43-4 ). It is associated with malnutrition and is often preceded by a debilitating illness (measles, malaria, tuberculosis, diarrhea, ulcerative gingivitis) in a nutritionally compromised host. Noma presents with fever, malodorous breath, anemia, leukocytosis, and signs of malnutrition. If untreated, it produces sever disfiguration. Polymicrobial infection with Fusobacterium necrophorum and Prevotella intermedia may be inciting agents. Treatment includes local wound care, penicillin, and metronidazole as well as therapy for the underlying predisposing condition.

Figure 43-4 Noma lesion. (From Baratti-Mayer D, Pittet B, Montandon D, et al for the Geneva Study Group on Noma [GESNOMA]: Noma: An infectious disease of unknown aetiology. Lancet Infect Dis 2003;3:419 431.)

PATHOPHYSIOLOGY OF SCU.

Many of the manifestations of SCU represent adaptive responses to inadequate energy and/or protein intakes. In the face of inadequate intakes, activity and energy expenditure decrease. However, despite this adaptive response, fat stores are mobilized to meet the ongoing, albeit lower, energy requirement. Once these stores are depleted, protein catabolism must provide the ongoing substrates for maintaining basal metabolism. Why edematous SCU develops in some children and non-edematous SCU develops in others is unknown. Although no specific factor has been identified, a number have been suggested. One concerns the variability among infants in nutrient requirements and in body composition at the time the dietary deficit is incurred. It also has been proposed that giving excess carbohydrate to a

child with non-edematous SCU reverses the adaptive responses to low protein intake, resulting in mobilization of body protein stores. Eventually, albumin synthesis decreases, resulting in hypoalbuminemia with edema. Fatty liver also develops secondary, perhaps, to lipogenesis from the excess carbohydrate intake and reduced apolipoprotein synthesis. Other causes of edematous SCU are aflatoxin poisoning as well as diarrhea, impaired renal function and decreased Na+ K+ ATPase activity. Finally, free radical damage has been proposed as an important factor in the development of edematous SCU. This proposal is supported by low plasma concentrations of methionine, a dietary precursor of cysteine, which is needed for synthesis of the major antioxidant factor, glutathione. This possibility also is supported by lower rates of glutathione synthesis in children with edematous compared with non-edematous SCU.
TREATMENT OF SCU.

The usual approach to the treatment of SCU includes 3 phases ( Table 43-1 ). The initial phase (17 days) is a stabilization phase. During this phase, dehydration, if present, is corrected and antibiotic therapy is initiated to control bacterial or parasitic infection. Because of the difficulty of estimating hydration, oral rehydration therapy is preferred (see Chapters 55 and 337 ). If intravenous therapy is necessary, estimates of dehydration should be reconsidered frequently, particularly during the first 24 hr of therapy. Oral feedings are also started with specialized highcalorie formula (Tables 43-2 and 43-3 [2] [3]), proposed by the World Health Organization, that can be made with simple ingredients. The initial phase of oral treatment is with the F75 diet (75 kcal or 315 kg/100 mL). The rehabilitation diet is with the F100 diet (100 kcal or 420 kg/100 mL). Feedings are initiated with higher frequency and smaller volumes; over time, the frequency is reduced from 12 to 8 to 6 feedings/24 hr. The initial caloric intake is estimated at 80100 kcal/kg/day. In developed countries, 2427 calorie/oz infant formulas may be initiated with the same daily caloric goals. If diarrhea starts or fails to resolve and lactose intolerance is suspected, a nonlactose-containing formula should be substituted. If milk protein intolerance is suspected, a soy protein hydrolysate formula can be used.

TABLE 43-1 -- Time Frame for the Management of a Child with Severe Malnutrition

TABLE 43-2 -- Preparation of F75 and F100 Diets AMOUNT INGREDIENT F75[*] Dried skim milk 25 g Sugar Cereal flour Vegetable oil Mineral mix[] 70 g 35 g 27 g 20 mL 60 g 20 mL F100[] 80 g 50 g

AMOUNT INGREDIENT F75 Vitamin mix[]

[*]

F100[] 140 mg

140 mg

Water to make 1,000 mL 1,000 mL From World Health Organization: Management of Severe Malnutrition: A Manual for Physicians and Other Senior Health Care Workers. Geneva, WHO, 1999. If cereal flour is not available or there are no cooking facilities, a comparable formula can be made from 25 g of dried skim milk, 100 g of sugar, 27 g of oil, 20 mL of mineral mix, 140 mg of vitamin mix, and water to make 1,000 mL. However, this formula has a high osmolarity (415 m0smol/L) and may not be well tolerated by all children, especially those with diarrhea. A comparable formula can be made from 110 g of whole dried milk, 50 g of sugar, 30 g of oil, 20 mL of mineral mix, 140 mg of vitamin mix, and water to make 1,000 mL. Alternatively, use 880 mL of fresh cow's milk, 75 g of sugar, 20 g of oil, 20 mL of mineral mix, 140 mg of vitamin mix, and water to make 1,000 mL.
* To prepare the F75 diet, add the dried skim milk, sugar, cereal flour, and oil to some water and mix. Boil for 5 7 min. Allow to cool,

then add the mineral mix and vitamin mix, and mix again. Make up the volume to 1,000 mL with water. A comparable formula can be made from 35 g of whole dried milk, 70 g of sugar, 35 g of cereal flour, 17 g of oil, 20 mL of mineral mix, 140 mg of vitamin mix, and water to make 1,000 mL. Alternatively, use 300 mL of fresh cow's milk, 70 g of sugar, 35 g of cereal flour, 17 g of oil, 20 mL of mineral mix, 140 mg of vitamin mix, and water to make 1,000 mL. Isotonic versions of F75 (280 m0smol/L), which contain maltodextrins instead of cereal flour and some of the sugar and which include all the necessary micronutrients, are available commercially.
To prepare the F100 diet, add the dried skim milk, sugar, and oil to some warm boiled water and mix. Add the mineral mix and

vitamin mix, and mix again. Make up the volume to 1,000 mL with water.
If only small amounts of feed are being prepared, it will not be feasible to prepare the vitamin mix because of the small amounts

involved. In this case, give a proprietary multivitamin supplement. Alternatively, a combined mineral and vitamin mix for malnourished children is available commercially and can be used in these diets.

TABLE 43-3 -- Composition of F75 and F100 Diets AMOUNT-100 mL CONSTITUENT Energy Protein Lactose Potassium Sodium Magnesium Zinc Copper F75 0.9 g 1.3 g 3.6 mmol 0.6 mmol 0.43 mmol 2.0 mg 0.25 mg F100 2.9 g 4.2 g 5.9 mmol 1.9 mmol 0.73 mmol 2.3 mg 0.25 mg 75 kcalth (315 kJ) 100 kcalth (420 kJ)

AMOUNT-100 mL CONSTITUENT Percentage of energy from: Protein Fat 5% 32% 12% 53% F75 F100

Osmolarity 333 mOsmol/L 419 mOsmol/L From World Health Organization: Management of Severe Malnutrition: A Manual for Physicians and Other Senior Health Care Workers. Geneva, WHO, 1999.

Laboratory evaluation ( Table 43-4 ) and ongoing monitoring ( Table 43-5 ), when available, help guide therapy and prevent complications. Fluid status must be monitored very carefully in anemic patients, who may require a packed red blood cell transfusion.

TABLE 43-4 -- Laboratory Features of Severe Malnutrition BLOOD OR PLASMA VARIABLES INFORMATION DERIVED Hemoglobin, hematocrit, erythrocyte count, mean corpuscular volume Glucose Electrolytes and alkalinity Sodium Potassium Chloride, pH, bicarbonate Creatinine C-reactive protein, lymphocyte count, serology, thick and thin blood films Hyponatremia, type of dehydration Hypokalemia Metabolic alkalosis or acidosis Renal function Presence of bacterial or viral infection or malaria Degree of dehydration and anemia; type of anemia (iron/folate and vitamin B12 deficiency, hemolysis, malaria) Hypoglycemia

Total protein, transferrin,(pre-)albumin Degree of protein deficiency

Stool examination Presence of parasites From Mller O, Krawinkel M: Malnutrition and health in developing countries. CMAJ 5; 173(3):279286. 2005 Canadian Medical Association. Reprinted with permission of the publisher.

TABLE 43-5 -- Elements in the Management of Severe Protein-Energy Malnutrition PROBLEM MANAGEMENT Hypothermia Hypoglycemia Dehydration Micronutrients Infections Electrolytes Starter nutrition Tissue-building nutrition Stimulation Warm patient up; maintain and monitor body temperature Monitor blood glucose; provide oral (or intravenous) glucose Rehydrate carefully with oral solution containing less sodium and more potassium than standard mix Provide copper, zinc, iron, folate, multivitamins Administer antibiotic and antimalarial therapy, even in the absence of typical symptoms Supply plenty of potassium and magnesium Keep protein and volume load low Furnish a rich diet dense in energy, protein, and all essential nutrients that is easy to swallow and digest Prevent permanent psychosocial effects of starvation with psychomotor stimulation

Prevention of Start early to identify causes of protein-energy malnutrition in each case; relapse involve the family and the community in prevention From Mller O, Krawinkel M: Malnutrition and health in developing countries. CMAJ 5; 173(3):279286. 2005 Canadian Medical Association. Reprinted with permission of the publisher.

The second rehabilitation phase (wk 26) may include continued antibiotic therapy with appropriate changes, if the initial combination was not effective, and introduction of the F100 diet (see Tables 43-2 and 43-3 [2] [3]), with a goal of at least 100 kcal/kg/day. This phase usually lasts an additional 4 wk. At any time, if the infant is unable to take the feedings from a cup, syringe, or dropper, administration by a nasogastric tube rather than by the parenteral route is preferred. Bottles may be contaminated in certain locales, and their use is discouraged unless cleanliness is assured. Once ad libitum feedings are allowed, intakes of both energy and protein are often substantial. Iron therapy usually is not started until this phase of treatment; iron may interfere with the protein's host defense mechanisms. There also is concern that free iron during the early phase of treatment may exacerbate oxidant damage, precipitating infections (malaria), clinical kwashiorkor, or marasmic kwashiorkor in a child with clinical marasmus. Some recommend treatment with antioxidants. By the end of the 2nd phase, any edema that was present has usually been mobilized, infections are under control, the child is becoming more interested in his or her surroundings, and his or her appetite is returning. The child is then ready for the final follow-up phase, which consists of

feeding to cover catch-up growth as well as the provision of emotional and sensory stimulation. The child should be fed ad libitum. In developing countries, this final phase is often carried out at home. In all phases, parental education is crucial for continued effective treatment as well as prevention of additional episodes. Refeeding syndrome may complicate the acute nutritional rehabilitation of children who are undernourished from any cause. The hallmark of refeeding syndrome is the development of severe hypophosphatemia after the cellular uptake of phosphate during the 1st week of starting to refeed. Serum phosphate levels of 0.5 mmol/L can produce weakness, rhabdomyolysis, neutrophil dysfunction, cardiorespiratory failure, arrhythmias, seizures, altered level of consciousness, or sudden death. Phosphate levels should be monitored during refeeding, and if low, phosphate should be administered during refeeding to treat severe hypophosphatemia (see Chapter 52.6 ). Email to Colleague Print Version