Clinical Key-nutrition Food Security and Health (NElson)

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(http://www.ugm.ac.id)

BOOK CHAPTER

Nutrition, Food Security, and Health

Harold Alderman and Meera Shekar

Nelson Textbook of Pediatrics, Chapter 43, 170-179.e1

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 (t0010)).

Table 43-1

THREE MYTHS ABOUT NUTRITION

Myth 1:Malnutrition is primarily a matter of inadequate food intake.Not so. Food is of course important. But most serious malnutrition is caused by

bad sanitation and disease, leading to diarrhea, especially among young children. Women's status and women's education play big parts inimproving nutrition. Improving care of young children is vital.

Myth 2:Improved nutrition is a by-product of other measures of poverty reduction and economic advance. It is not possible to jump-start the

process.Again, untrue. Improving nutrition requires focused action by parents and communities, backed by local and national action in health and

public services, especially water and sanitation. Thailand has shown that moderate and severe malnutrition can be reduced by 75% or more in a

decade by such means.

Myth 3:Given scarce resources, broad-based action on nutrition is hardly feasible on a mass scale, especially in poor countries.Wrong again. In

spite of severe economic setbacks, many developing countries have made impressive progress. More than two thirds of the people in developing

countries now eat iodized salt, combating the iodine deficiency and anemia that affect about 3.5 billion people, especially women and children in

some 100 nations. About 450 million children a year now receive vitamin A capsules, tackling the deficiency that causes blindness and increases

child mortality. New ways have been found to promote and support breast-feeding, and breast-feeding rates are being maintained in many

countries and increased in some. Mass immunization and promotion of oral rehydration to reduce deaths from diarrhea have also done much toimprove nutrition.

From World Bank: Repositioning nutrition as central to development, 2006 (PDF).

http://web.worldbank.org/WBSITE/EXTERNAL/TOPICS/EXTHEALTHNUTRITIONANDPOPULATION/EXTNUTRITION/0

(http://web.worldbank.org/WBSITE/EXTERNAL/TOPICS/EXTHEALTHNUTRITIONANDPOPULATION/EXTNUTRITION/0),,contentMDK:20787550~menuPK:282580~pageP

Accessed May 23, 2010.

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 appropriateinfant 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 accessby all people at all times to sufficientfood in

terms of quality, quantity, and diversity for an active and healthy lifewithout 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.Availabilityrefers to the supply of food (generally grain in the

market, reflecting economic conditions of production and trade), whereas accessis 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.
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Measurement of Food Insecurity

The most commonly used measurement of food insecurity is the Food and Agriculture Organization's (FAO's) measure of undernourishment,

expressed in terms of the number of persons who are assumed to be unable to meet daily calorie requirements necessary for light activities. In the

period 2003-2005, the FAO estimated that 848 million individuals were hungry or undernourished, and 97% of these individuals were in developing

countries, an increase of 20 million undernourished individuals in developingcountries compared to 1995-1997.

This estimate of undernourished individuals is based on country-level annual food balance sheets that take into account food production plus net

imports minus net trade. This gross availability is also adjusted for seeds used for replanting as well as grain fed to animals and an allowance for

waste. The estimates also acknowledge that the average national food availability is not uniformly distributed, and they thus make adjustments for an

assumed inequality of access based on historical patterns.

This estimate is, therefore, not based on direct measurement of household or individual consumption. However, it has the advantage of beingavailable on an annual basis for virtually all countries. Therefore, it assists in monitoring global trends. Reductions in the number of undernourished

individuals as calculated using this indicator of food access have been used as a measure of progress in reducing poverty, albeit other indicators

(percent underweight or stunted children) are better indicators for tracking changes at household and national levels.

The undernourishment measure being based on national food balance sheets cannot be disaggregated by regions or by income or other household

characteristics and is therefore not a very useful measure, especially at household or individual levels. There are often differences with estimated

levels of hunger using this indirect approach and levels derived based on surveys of consumption or expenditure recorded at the household level. Such

surveys are commonly undertaken in most countries, often with samples that are representative at regional or subregional levels and that permit

analysis of correlates of food insecurity. The surveys often are collected over rounds, and they thus allow an understanding of seasonal food

insecurity. Consumption may be based on recall or on a diary of expenditures and home consumption. There is no consensus on the relative

advantages of diary approaches compared with interviews given the level of education in food-insecure regions of the world, and there is not full

agreement on the period of recall that provides the greatest accuracy of reporting. Nevertheless, with the widespread availability and range of data

contained in these surveys, they provide the basis for substantial analysis on the determinants of household food insecurity.

Individual food insecurity is better understood using 24-hr food recall data. Such methods, preferably repeated over a period of days within a week,

allow a measure of individual intake and of intrahousehold variation of food consumption. Although these data are harder to collect and less

available, they are a better source of information on diet diversity than household or national indicators. Diet diversity is a strong predictor of child

growth and a valuable tool for understanding micronutrient intakes, a dimension of nutritional security that is generally not emphasized in data on

food security based on food balance sheets.

Undernutrition

The greatest risk of undernutrition occurs during pregnancy and in the first 2 years of life ( Fig. 43-1 (f0010)) the effects of this early damage on

health, brain development, intelligence, educability, and productivity are potentially irreversible ( Table 43-2 (t0015)). 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 deficiencyanemia 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

(http://siteresources.worldbank.org/NUTRITION/Resources/281846-1114108837888/RepositioningNutritionLaunchJan30Final.pdf). Accessed May 23, 2010.)

Table 43-2

WHY MALNUTRITION PERSISTS IN MANY FOOD-SECURE HOUSEHOLDS

Pregnant and nursing women eat too few calories and too little protein, have untreated infections, such as sexually transmitted diseases that lead

to low birthweight, or do not get enough rest.

Mothers have too little time to take care of their young children or themselves during pregnancy.

Mothers of newborns discard colostrum, the first milk, which strengthens the child's immune system.

Mothers often feed children


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Caregivers start introducing complementary solid foods too late.

Caregivers feed children


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measurement. Height for age is particularly difficult to measure for the most vulnerable children


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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 nutritionthat is, preventing these lossescan 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 MDGalthough 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

(f0015)). 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:
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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

(http://www.who.int/nutrition/topics/lancetseries_maternal_and_childundernutrition/en/index.htm).)

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

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 basishence 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 overallrisk 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.

Clinical Manifestations and Treatment of Undernutrition

Treatment of vitamin and mineral deficiencies is discussed in Chapter 45, Chapter 46, Chapter 47, Chapter 48, Chapter 49, Chapter 50, Chapter 51.

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 adeficiency 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
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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 listlessnessuntil 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 (t0025)).

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 l iver 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 56:10551068, 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 (t0025)).

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.)
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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]:S69S72, 2005.)

Figure 43-5

A 14 mo old gir l with a flaky pa int 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]:S69S72, 2005.)

Nomais a chronic necrotizing ulceration of the gingiva and the cheek ( Fig. 43-6 (f0035)). 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 necrophorumandPrevotella intermediamay 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 3:419431, 2003.)

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

Pathophysiology of Severe Protein-Calorie Malnutrition

Why edematous malnutrition develops in some children and nonedematous malnutrition develops in others is unknown. One factor may be 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 nonedematous malnutrition 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 malnutrition are
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aflatoxin poisoning as well as diarrhea, impaired renal function and decreased Na +/K +-ATPase activity. Free radical damage has been proposed as

an important factor in the development of edematous malnutrition. 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 nonedematous malnutrition.

Treatment

The usual approach to the treatment of severe acute malnutrition includes 3 phases ( Table 43-5 (t0030)and Fig. 43-7 (f0045)). The initial phase (1-7

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 rehydrationtherapy is preferred ( Chapter 55, Chapter 332). 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 high-calorie formula (see Fig. 43-7 (f0045)and Table 43-6 (t0035)), 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 kJ/100 mL). The rehabilitation diet is with the F100 diet

(100 kcal or 420 kJ/100 mL). Feedings are initiated with higher frequency and smaller volumes over time, the frequency is reduced from 12 to 8 to 6

feedings per 24 hr. The initial caloric intake is estimated at 80-100 kcal/kg/day. In developed countries, 24-27 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 may be used.

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 criteria 39: 60 respirations/min children age 5 yr.

(From Collins S, Dent N, Binns P, et al: Management of severe acute malnutrition in children, Lancet 368:19922000, 2006.)

Table 43-5

TIME FRAME FOR THE MANAGEMENT OF A CHILD WITH SEVERE MALNUTRITION [object Object]

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

Organization.

*Malnutritionand malnourishedare used as synonyms for undernutritionand undernourished, respectively.

Table 43-6

PREPARATION OF F75 AND F100 DIETS

INGREDIENT AMOUNT

F75 * (hl0000369) F100 (hl0000372)

Dried skim milk 25 g 80 g

Sugar 70 g 50 g

Cereal flour 35 g

Vegetable oil 27 g 60 g

Mineral mix (hl0000376) 20 mL 20 mL

Vitamin mix (hl0000376) 140 mg 140 mg
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Water to make 1,000 mL 1,000 mL


Organization.

* 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 commerciallyand 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.

Another approach is the use of ready to use therapeutic foods(RUTFs) ( Fig. 43-8 (f0050)). RUTFs reduce mortality in a cost-effective manner, in

part because they are less susceptible to spoilage than powdered milkbased 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 isequally 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

(http://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 (t0040)) and ongoing monitoring ( Table 43-8 (t0045)), 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

BLOOD OR PLASMA VARIABLES INFORMATION DERIVED

Hemoglobin, hematocrit, erythrocyte count, mean

corpuscular volume

Degree of dehydration and anemia type of anemia (iron/folate and vitamin B 12

deficiency, hemolysis, malaria)

Glucose Hypoglycemia

Electrolytes and alkalinity

Sodium Hyponatremia, type of dehydration

Potassium Hypokalemia

Chloride, pH, bicarbonate Metabolic alkalosis or acidosis

Total protein, transferrin, (pre)albumin Degree of protein deficiency
http://www.who.int/nutrition/publications/severemalnutrition/9789241598163/en/index.htmlhttps://www.clinicalkey.com/f0050https://www.clinicalkey.com/t0040https://www.clinicalkey.com/t0045


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C-reactive protein, lymphocyte count, serology, thick and

thin blood films

Presence of bacterial or viral infection or malaria

Stool examination Presence of parasites

From Mller O, Krawinkel M: Malnutrition and health in developing countries, CMAJ 173(3):279286, 2006. 2005 Canadian Medical Association. Reprinted with

permission of the publisher.

Table 43-8

ELEMENTS IN THE MANAGEMENT OF SEVERE PROTEIN-ENERGY MALNUTRITION

PROBLEM MANAGEMENT

Hypothermia Warm patient up maintain and monitor body temperature

Hypoglycemia Monitor blood glucose provide oral (or intravenous) glucose

Dehydration Rehydrate carefully with oral solution containing less sodium and more potassium than standard mix

Micronutrients Provide copper, zinc, iron, folate, multivitamins

Infections Administer antibiotic and antimalarial therapy, even in the absence of typical symptoms

Electrolytes Supply plenty of potassium and magnesium

Starter nutrition Keep protein and volume load low

Tissue-building

nutrition

Furnish a rich diet dense in energy, protein, and all essential nutrients that is easy to swallow and digest

Stimulation Prevent permanent psychosocial effects of starvation with psychomotor stimulation

Prevention of relapse Start early to identify causes of protein-energy malnutrition in each case involve the family and the community in

prevention

From Mller O, Krawinkel M: Malnutrition and health in developing countries, CMAJ 173(3):279286, 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 ratherthan 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

CONSTITUENT AMOUNT PER 100 mL

F75 F100

Energy 75 kcal th (315 kJ) 100 kcal th(420 kJ)

Protein 0.9 g 2.9 g

Lactose 1.3 g 4.2 g

Potassium 3.6 mmol 5.9 mmol

Sodium 0.6 mmol 1.9 mmol

Magnesium 0.43 mmol 0.73 mmol

Zinc 2.0 mg 2.3 mg

Copper 0.25 mg 0.25 mg

Percentage of energy from:

Protein 5% 12%

Fat 32% 53%

Osmolarity 333 mOsmol/L 419 mOsmol/L


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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 syndromecan complicate the acute nutritional rehabilitation of children who are undernourished from any cause ( Fig. 43-9 (f0055),

Table 43-10 (t0055)). 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 336:14951498, 2008.)

Table 43-10

CLINICAL SIGNS AND SYMPTOMS OF REFEEDING SYNDROME

HYPOPHOSPHATEMIA HYPOKALEMIA HYPOMAGNESEMIA VITAMIN/THIAMINE

DEFICIENCY

SODIUM

RETENTION

HYPERGLYCEMIA

Cardiac

Hypotension

Decreased stroke

volume

Respiratory

Impaired diaphragm

contractility

Dyspnea

Respiratory failure

Neurologic

Paresthesia

Weakness

Confusion

Disorientation

Lethargy

Areflexic paralysis

Seizures

Coma

Cardiac

Arrhythmias

Respiratory

Failure

Neurologic

Weakness

Paralysis

Gastrointestinal

Nausea

Vomiting

Constipation

Muscular

Rhabdomyolysis

Muscle necrosis

Other

Death

Cardiac

Arrhythmias

Neurologic

Weakness

Tremor

Tetany

Seizures

Altered mental status

Coma

Gastrointestinal

Nausea

Vomiting

Diarrhea

Other

Refractory hypokalemia and

hypocalcemia

Death

Encephalopathy

Lactic acidosis

Death

Fluid overload

Pulmonary

edema

Cardiac

compromise

Cardiac

Hypotension

Respiratory

Hypercapnea

Failure

Other

Ketoacidosis

Coma

Dehydration

Impaired immune

function
https://www.clinicalkey.com/f0055https://www.clinicalkey.com/t0055


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Hematologic

Leukocyte dysfunction

Hemolysis

Thrombocytopenia

Other

Death

Data from Kraft MD, Btaiche IF, Sacks GS: Review of RFS, Nutr Clin Pract 20:625633, 2005. From Fuentebella J, Kerner JA: Refeeding syndrome, Pediatr Clin N Am

56:12011210, 2009.

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