Malnutrition as the Intersection of Food Security and Health Security

Undernutrition is usually an outcome of 3 factors: household level food security, access to health and sanitation services, and child caring practices. A mother with few economic resources who knows how to care for her children and is enabled to do so can often use available food and health services to produce well-nourished children. If food resources and health services are available in a community, but the mother does not access immunizations or does not know how or when to properly add complementary foods to her child’s diet, that child might become malnourished (Table 43-1).

Undernutrition is not simply a result of food insecurity, although food security is often a necessary but insufficient condition for nutrition security. Many children in food-secure environments and from better-off families are underweight or stunted because of inappropriate infant feeding and child care practices, poor access to health services, or poor sanitation. In many countries where malnutrition is widespread, food production or even access to food might not be the most limiting factor. The most important causes of undernutrition are often inadequate knowledge about the benefits of exclusive breast-feeding and complementary feeding practices, the role of micronutrients, and the lack of time women have available for appropriate infant care practices and their own care during pregnancy. The situation is different in famine and emergency settings, where food insecurity is often among the most important factors.

Economic growth and food production as well as birth spacing and women’s education are also important but less-direct routes to improving nutrition outcomes in developing countries. Shorter routes to nutrition improvements often come through the provision of health, sanitation, and nutrition education and counseling services, including the promotion of exclusive breast-feeding and appropriate and timely complementary feeding, coupled with prenatal care and basic maternal and child health services. In many contexts, micronutrient supplementation and fortification are also key elements of a public health strategy aimed at addressing undernutrition.

Food Insecurity

Governments seek to promote the food security of their population both for its intrinsic value and for its instrumental value as well. The former refers to the fact that individuals value food security in its own right, whereas the latter acknowledges the contribution that food security makes toward improved nutrition. But what is food security? One prevalent definition of food security views it as access by all people at all times to sufficient food in terms of quality, quantity, and diversity for an active and healthy life without risk of loss of such access. To achieve food security, it is necessary to look at 3 dimensions of food security: availability, access, and utilization. Availability refers to the supply of food (generally grain in the market, reflecting economic conditions of production and trade), whereas access is at the household level, reflecting purchasing power as well as transfer programs. Access also has an intrahousehold dimension, because food is not necessarily shared equitably within a household. The utilization pillar reflects the fact that even when a household has access to food, it does not necessarily achieve nutritional security.

Undernutrition

The greatest risk of undernutrition occurs during pregnancy and in the first 2 years of life (Fig. 43-1); the effects of this early damage on health, brain development, intelligence, educability, and productivity are potentially irreversible (Table 43-2). Governments with limited resources are therefore best advised to focus publicly funded actions on this critical window of opportunity, between preconception and 24 mo of age. Folate deficiency also increases the risk of birth defects; this particular window of opportunity is before conception, as it is with iodine. Iron deficiency anemia is another dimension of undernutrition that has measurable risks that extend outside of the early years of life, with particular risks to the health of a mother as well as for the birth weight of her child. Anemia can also reduce physical and cognitive function and economic productivity of adults of both sexes.

Figure 43-1 The window of opportunity for improving nutrition is very small: prepregnancy until 18-24 mo of age.

(From The World Bank’s Human Development Network: Better nutrition = less poverty: repositioning nutrition as central to development: a strategy for large scale action, 2006 [PDF]. http://siteresources.worldbank.org/NUTRITION/Resources/281846-1114108837888/RepositioningNutritionLaunchJan30Final.pdf. Accessed May 23, 2010.)

Consequences of Undernutrition

The most immediate consequence of undernutrition is premature death. The global estimates conclude that stunting, severe wasting, and IUGR jointly contributes to 2.2 million deaths of children <5 yr of age. This accounts for 35% of all child mortality globally, even though this estimate is lower than those previously reported. The earlier and widely cited estimate had suggested that undernutrition was associated with nearly 53% of all child deaths. The risk of death increases even with mild undernutrition, and as the severity of undernutrition increases, the risk increases exponentially; the probability of mortality for a child <5 yr of age with a z score of weight for age below −3 is nearly 4 times the elevated risk for a child with a z score between −3 and −2. Because there are more children with less-severe malnutrition, it is this category that contributes the greater share of the global burden of malnutrition. After controlling for the occurrence of multiple nutritional deficits, deficiencies of vitamin A and zinc are estimated to be responsible for an additional 0.6 million and 0.4 million child deaths, respectively. More than 3.5 million mothers and children under 5 years die every year due to undernutrition-related causes, and many millions more are disabled or stunted for life. By the time children reach their first birthday, if undernourished, they could suffer irreversible physical and cognitive damage, thereby impacting their future health, welfare, and economic well being. These consequences continue into adulthood, and the cycle of undernutrition is passed on to the next generation when undernourished women give birth to low birth weight babies.

Hunger and undernutrition have substantial consequences for survivors and their families by requiring them to spend additional resources on health care and by affecting the productivity of malnourished persons. There is substantial evidence that early child malnutrition is detrimental to productivity in adulthood. The consequences of malnutrition can be identified and quantified in 5 categories: excess costs of health care, either neonatal care for LBW babies or excess costs of infant and child illness for malnourished children; productivity losses associated with stunting; productivity losses from reduced cognitive ability and achievement; increased costs of chronic diseases associated with fetal and early child malnutrition; and consequences of impaired maternal nutrition on future generations.

There is a 2-way causality from malnutrition to infections and vice versa. Deficiencies of both macro- and micronutrients impair the immune system, with well-documented consequences. Conversely, helminthic and other infections lead to reduced nutrient absorption, and fevers lead to catabolism and anorexia and thus contribute to malnutrition. Additionally, caregivers might respond to episodes of diarrhea by withholding food.

In many low-income settings, the consequence of malnutrition leads to reduced lifetime earnings. These effects can come about through impaired cognitive development, late school entrance leading to delayed entry into the labor force, fewer completed years of schooling, less learning per year of schooling, or a combination of these.

The evidence base for the impact of nutrition on earnings is substantial and growing. While separating the factors that lead to undernutrition from the constraints of poverty that will independently affect cognitive ability and limit schooling regardless of nutritional status can be problematic, studies confirm that the impact of improved nutrition is distinct from the contribution of poverty reduction. One study assessed the earnings of adults in Guatemala up to 42 years of age who received nutritional supplements as children or whose mothers received them during their pregnancy. The men who received nutritional supplements before reaching age 3 earned wages that were 46% higher than the wages earned by men who were not supplemented. Evidence from Africa confirms that children who are under 2 years old when a drought hits their community in Africa are likely to be shorter and to complete fewer years of school than their siblings or in contrast to children in different age cohorts in the village. Elsewhere, spikes in the price of food during these critical years lead both to stunting and to diminished schooling.

In addition to the association of stunting and cognitive impairment, some micronutrient deficiencies lead to loss of cognitive potential. Individuals with an iodine deficiency have, on average, 13.5 points lower IQs than comparison groups. Interventions have shown that provision of iodine to pregnant women can reduce this gap. In the case of iron deficiencies, anemia is regularly associated with impaired cognitive development. Moreover, supplementation trials for school-age children confirm this conclusion because they regularly indicate improved cognition, although this is less regularly observed with interventions aimed at deficient younger children.

Tracking the consequences of fetal or childhood deprivation for adult chronic illness imposes additional challenges given the long latency. The hypothesis that early nutritional challenges are part of the etiology of diabetes and cardiovascular disease has first proposed on the basis of epidemiological evidence, including tracking cohorts that suffered from famines in Holland and China. This hypothesis has been bolstered by studies with animal models that help define a mechanism of embryonic development that provides a conceptual basis for the epidemiological evidence. The increased risk of adult chronic disease from this malnutrition in early life is estimated to be a particular challenge to low-income countries with rapid economic growth such as China and India, leading to premature death as well as substantial economic costs from medical expenses and lost productivity.

Quantifying the magnitude of such losses of potential for malnourished children who survive is, of course, context specific, but various studies have shown that investments in nutrition—that is, preventing these losses—can yield considerable economic returns. These preventive investments cover a broad range, including nutrition as well as a diverse set of interventions in education, water and sanitation, trade reform, and private sector deregulation. Addressing micronutrient deficiencies has the highest rate of economic return. For example, every $1 of expenditures on vitamin A supplementation is likely to produce $100 of benefits. To be fair, such estimates are based on a variety of assumptions, such as the value of future benefits compared to current benefits; economists generally view a dollar today as worth more than a dollar sometime in the future.

Nutrition, Food Security, and Poverty

Household food security tracks income closely. This is not the case for malnutrition, which is often observed even within better-off households in Asia and Africa. Data from household surveys as well as from cross-country comparisons confirm that income growth, even when evenly distributed over a population, has a modest impact on malnutrition rates, even though this impact is statistically significant and positive. On a global average, a 10% increase of national income per capita would lead to a 10% decline in the poverty rate in the country but only a 5% decline in the rate of malnutrition as measured by low weights for age. Global evidence indicates that such a rate of income growth would lead to only a 2.5% decline in anemia.

The international development community has collectively agreed upon 8 Millennium Development Goals (MDGs). The first of these 8 goals refers to poverty and hunger. The recognition of the close relation of food insecurity and poverty is evident in the definition of this first MDG, which aims to eradicate extreme poverty and hunger. The two targets originally proposed (a third on employment was added later) are to halve, between 1990 and 2015:

The proportion of people whose income is less than $1 a day

The proportion of people who suffer from hunger

Two measureable indicators of progress are used for the second target, the percentage of individuals who cannot meet their calorie requirements as measured by the estimate of undernourishment and by the percentage of children under 5 who are underweight as measured in nationally representative household surveys.

While prior to the global financial crisis, the prognosis in general had been that most countries were on track for achieving the poverty goal. But of 143 countries, only 34 (24%) were on track to achieve the nutrition MDG goal. No country in South Asia, where undernutrition rates are the highest, is likely to achieve this MDG—although Bangladesh was most likely to come close to achieving it, and Asia as a whole was likely to achieve it because of the improvements in China. Nutrition status was actually deteriorating in 26 countries, many of them in Africa, where the nexus between HIV and undernutrition is particularly strong and mutually reinforcing. And in 57 countries, no trend data were available to tell whether progress is being made. A renewed focus on this non-income poverty target is clearly central to any poverty reduction efforts.

Key Interventions

There is substantial consensus regarding which interventions work to address child undernutrition based on accumulated field evidence (Fig. 43-2). Many of these interventions lie within the responsibility of the health sector, albeit investments in other sectors may be necessary to sustain the benefits from the health sector interventions. Key interventions that have been proved to be cost effective in reducing infant and child mortality, improving underweight rates, and reversing micronutrient deficiencies include:

• Promoting exclusive breast-feeding

• Promoting adequate and timely complementary feeding (at ~6 mo of age)

• Promoting key hygiene behavior (e.g., hand-washing with soap)

• Providing micronutrient interventions such as vitamin A and iron supplements for pregnant and lactating women and young children

• Presumptive treatment for malaria for pregnant women in endemic malarial regions and promoting long-lasting insecticide treated bednets

• Deworming in endemic parasitic areas and oral rehydration in high-diarrhea regions

• Fortifying commonly eaten foods with micronutrients (such as salt fortified with iodine) and staple foods like wheat, oil, and sugar with iron, vitamin A, and zinc

Figure 43-2 Key interventions. SAM, severe acute malnutrition.

(From World Health Organization and Lancet Global Nutrition Series. www.who.int/nutrition/topics/lancetseries_maternal_and_childundernutrition/en/index.htm.)

Birth-spacing and family planning interventions, as well as strategies to address women’s empowerment and gender, also have strong impacts on nutrition and child health outcomes. Additionally, community growth promotion programs can provide an opportunity to impart knowledge on a face-to-face basis—hence the stress on community mobilization in many programs. Many growth promotion programs also facilitate the provision of immunizations, vitamin supplements, and deworming medicine as well as being a platform to promote behavioral change.

The emergence of HIV/AIDS as a public health concern has introduced new issues for public health nutrition. One issue is the increased requirements for both macro- and micro-nutrients of individuals with HIV/AIDS, especially those who are able to access anti-retroviral treatment (ART). In addition, there is a particular concern for the prevention of maternal child transmission from HIV-positive mothers. In 2007, an estimated 1.5 million pregnant women in low- and middle-income countries were living with HIV. Seventy-five percent of these were concentrated in 12 countries, which include South Africa, Nigeria, United Republic of Tanzania, and Mozambique.

Even if the mother is able to receive nevirapine or other ART during pregnancy and delivery, she faces a dilemma regarding breastfeeding. The overall risk of mother-to-child HIV transmission by a non-breastfeeding mother is 15-25% (without interventions to reduce transmission) and of a breastfeeding mother is 20-45%. However, the risk is less when the mother is exclusively breastfeeding and increases with duration; the majority of the transmission after delivery occurs after 6 months of breastfeeding. Breast milk substitutes are costly and risky in low-income settings; an outbreak of diarrheal disease linked to formula feeding in Botswana where substitutes are provided free by the government proved fatal to more than 30 children in 2007. Thus, in most low-income settings, HIV-positive mothers are advised to continue with exclusive breastfeeding for 6 months and to wean more abruptly than is otherwise recommended.

Severe Acute Malnutrition (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. Protein-energy 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. PEM is almost always accompanied by deficiencies of other nutrients.

Historically, the most severe forms of malnutrition, marasmus (nonedematous malnutrition with severe wasting) and kwashiorkor (edematous malnutrition), were considered distinct disorders. Nonedematous malnutrition was believed to result primarily from inadequate energy intake or inadequate intakes of both energy and protein, whereas edematous malnutrition 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 malnutrition, is common in children with both edematous and nonedematous malnutrition.

In the USA, severe malnutrition 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, protein-calorie malnutrition 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 Severe Protein Calorie Malnutrition

Nonedematous malnutrition (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 they can 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 (Table 43-4).

Table 43-4 CLINICAL SIGNS OF MALNUTRITION

SITE	SIGNS
Face	Moon face (kwashiorkor), simian facies (marasmus)
Eye	Dry eyes, pale conjunctiva, Bitot spots (vitamin A), periorbital edema
Mouth	Angular stomatitis, cheilitis, glossitis, spongy bleeding gums (vitamin C), parotid enlargement
Teeth	Enamel mottling, delayed eruption
Hair	Dull, sparse, brittle hair, hypopigmentation, flag sign (alternating bands of light and normal color), broomstick eyelashes, alopecia
Skin	Loose and wrinkled (marasmus), shiny and edematous (kwashiorkor), dry, follicular hyperkeratosis, patchy hyper- and hypopigmentation (crazy paving or flaky paint dermatoses), erosions, poor wound healing
Nails	Koilonychia, thin and soft nail plates, fissures or ridges
Musculature	Muscle wasting, particularly buttocks and thighs; Chvostek or Trousseau signs (hypocalcemia)
Skeletal	Deformities, usually as a result of calcium, vitamin D, or vitamin C deficiencies
Abdomen	Distended: hepatomegaly with fatty liver; ascites may be present
Cardiovascular	Bradycardia, hypotension, reduced cardiac output, small vessel vasculopathy
Neurologic	Global developmental delay, loss of knee and ankle reflexes, impaired memory
Hematologic	Pallor, petechiae, bleeding diathesis
Behavior	Lethargic, apathetic, irritable on handling

From Grover Z, Ee LC: Protein energy malnutrition, Pediatr Clin N Am 56:1055–1068, 2009.

Edematous malnutrition (kwashiorkor) can occur initially as vague manifestations that include lethargy, apathy, and/or irritability. When kwashiorkor is 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 can mask the failure to gain weight. It is often present in internal organs before it is recognized in the face and limbs. Liver enlargement can 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 (Chapter 46) not in areas exposed to sunlight. Depigmentation can occur after desquamation in these areas, or it may be generalized (Figs. 43-3, 43-4, 43-5). The hair is sparse and thin, and in dark-haired children, it can become streaky red or gray. Eventually, there is stupor, coma, and death (see Table 43-4).

Figure 43-3 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 43-4 A and B, A 7 mo old boy with diffuse erythematous papules and plaques, some scaly, and edema of the extremities.

(From Katz KA, Mahlberg MH, Honig PJ, et al: Rice nightmare: kwashiorkor in 2 Philadelphia-area infants fed Rice Dream beverage, J Am Acad Dermatol 52[5 Suppl 1]:S69–S72, 2005.)

Figure 43-5 A 14 mo old girl with a “flaky paint” dermatitis.

(From Katz KA, Mahlberg MH, Honig PJ, et al: Rice nightmare: kwashiorkor in 2 Philadelphia-area infants fed Rice Dream beverage, J Am Acad Dermatol 52[5 Suppl 1]:S69–S72, 2005.)

Noma is a chronic necrotizing ulceration of the gingiva and the cheek (Fig. 43-6). 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 manifests with fever, malodorous breath, anemia, leukocytosis, and signs of malnutrition. Untreated, it produces sever disfiguration. Polymicrobial infection with Fusobacterium necrophorum and Prevotella intermedia may be inciting agents.

Figure 43-6 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 3:419–431, 2003.)

Treatment of noma includes local wound care, penicillin, and metronidazole as well as therapy for the underlying predisposing condition.

Figure 43-7 Classification of severe acute malnutrition used in community-based therapeutic care. ICMI, integrated management of childhood illness; MUAC, mid-upper arm circumference; WHO, Word Health Organization. *Grade 1, mild edema on both feet or ankles; grade 2, moderate edema on both feet, plus lower legs, hands, or lower arms; grade 3, severe generalized edema affecting both feet, legs, hands, arms, and face. ^†IMCI criteria³⁹: 60 respirations/min children age <2 mo; 50 respirations/min for age 2-12 mo; 40 respirations/min for ages 1-5 yr; 30 respirations for age >5 yr.

(From Collins S, Dent N, Binns P, et al: Management of severe acute malnutrition in children, Lancet 368:1992–2000, 2006.)

Table 43-6 PREPARATION OF F75 AND F100 DIETS

* 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.

^† 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 is not 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 may be used in these diets. A comparable formula can be made from 35 g whole dried milk, 70 g sugar, 35 g cereal flour, 17 g oil, 20 mL mineral mix, 140 mg vitamin mix, and water to make 1,000 mL. Alternatively, use 300 mL fresh cow’s milk, 70 g sugar, 35 g cereal flour, 17 g oil, 20 mL mineral mix, 140 mg vitamin mix, and water to make 1,000 mL. Isotonic versions of F75 (280 mOsmol/L), which contain maltodextrins instead of cereal flour and some of the sugar and which include all the necessary micronutrients, are available commercially. If cereal flour is not available or there are no cooking facilities, a comparable formula can be made from 25 g dried skim milk, 100 g sugar, 27 g oil, 20 mL mineral mix, 140 mg vitamin mix, and water to make 1,000 mL. However, this formula has a high osmolarity (415 mOsmol/L) and might not be well tolerated by all children, especially those with diarrhea. A comparable formula can be made from 110 g whole dried milk, 50 g sugar, 30 g oil, 20 mL mineral mix, 140 mg vitamin mix, and water to make 1,000 mL. Alternatively, use 880 mL fresh cow’s milk, 75 g sugar, 20 g oil, 20 mL mineral mix, 140 mg vitamin mix, and water to make 1,000 mL.

From World Health Organization: Management of severe malnutrition: a manual for physicians and other senior health care workers, Geneva, 1999, World Health Organization.

Another approach is the use of ready to use therapeutic foods (RUTFs) (Fig. 43-8). RUTFs reduce mortality in a cost-effective manner, in part because they are less susceptible to spoilage than powdered milk–based supplementary foods. F100 is water based and subject to bacterial contamination, whereas RUTF is an oil-based paste that has little water content and a similar nutrient profile but a higher calorie density and is equally palatable to F100. RUTF is a mixture of powdered milk, peanuts, sugar, vitamins, and minerals.

Figure 43-8 Severe acute malnutrition (SAM) management. RUTF, ready to use therapeutic foods.

(From World Health Organization and the United Nations Children’s Fund: WHO child growth standards and the identification of severe acute malnutrition in infants and children, 2009 (PDF). www.who.int/nutrition/publications/severemalnutrition/9789241598163/en/index.html. Accessed May 23, 2010.)

One advantage of RUTFs is that in many cases it can be used in community settings rather than in rehabilitation centers where there is a high risk of infection. Indeed, it may be hard to separate out the intrinsic advantage of the RUTF products from the advantages of the community-based management of care.

Laboratory evaluation (Table 43-7) and ongoing monitoring (Table 43-8), when available, help guide therapy and prevent complications. Fluid status must be monitored very carefully in anemic patients, who might require a packed red blood cell transfusion.

Table 43-7 LABORATORY FEATURES OF SEVERE MALNUTRITION

From Müller O, Krawinkel M: Malnutrition and health in developing countries, CMAJ 173(3):279–286, 2006. © 2005 Canadian Medical Association. Reprinted with permission of the publisher.

Table 43-8 ELEMENTS IN THE MANAGEMENT OF SEVERE PROTEIN-ENERGY MALNUTRITION

From Müller O, Krawinkel M: Malnutrition and health in developing countries, CMAJ 173(3):279–286, 2006. © 2005 Canadian Medical Association. Reprinted with permission of the publisher.

The second rehabilitation phase (wk 2-6) may include continued antibiotic therapy with appropriate changes, if the initial combination was not effective, and introduction of the F100 or RUTF diet (Tables 43-6 and 43-9) 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 can interfere with the protein’s host defense mechanisms. There also is concern that free iron during the early phase of treatment might exacerbate oxidant damage, precipitating infections (malaria), clinical kwashiorkor, or marasmic kwashiorkor in a child with clinical marasmus. Some recommend treatment with antioxidants.

Table 43-9 COMPOSITION OF F75 AND F100 DIETS

From World Health Organization: Management of severe malnutrition: a manual for physicians and other senior health care workers, Geneva, 1999, World Health Organization.

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 providing 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 preventing additional episodes.

Refeeding syndrome can complicate the acute nutritional rehabilitation of children who are undernourished from any cause (Fig. 43-9, Table 43-10). 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 they are low, phosphate should be administered during refeeding to treat severe hypophosphatemia (Chapter 52.6).

Figure 43-9 Guidelines for management.

(From Mehanna HM, Moledina J, Travis J: Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 336:1495–1498, 2008.)