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Malnutrition in developing countries
SYMPOSIUM: NUTRITION
Malnutrition in developing countries
Malaria Measles Injuries AIDS 3% 3% 3% 3%
Neonatal 37%
Emily Walton Stephen Allen
Abstract Over a third of all deaths are attributable to undernutrition
Although now rare in industrialized countries, severe acute malnutrition is unfortunately still common throughout the developing world and is a key contributor to both global childhood morbidity and mortality. This review describes the epidemiology of malnutrition and the presentation and pathophysiology of the severe syndromic forms e marasmus and kwashiorkor. The gold standards for diagnosis and management are detailed and the challenges of implementation in the basic healthcare systems of the developing world are discussed. As the leading cause of ill health in the world today, more effective treatment and prevention of malnutrition must be a priority for the global healthcare community. Other 10%
Keywords kwashiorkor; marasmus; protein-energy malnutrition; severe acute malnutrition; underweight
Diarrhoea 17%
Pneumonia 19%
Based on data of the Child Mortality Estimation Group used in the UNICEF report ‘The State of the World’s Children 2008’
Figure 1 Global cause specific mortality in children under 5 years of age.
Underweight: the leading cause of ill health in the world today In 2008, of the 8.8 million global deaths of children under 5 years of age, 93% occurred in the developing countries of Africa and Asia. The highest rates of childhood mortality are found in sub-Saharan Africa where one in seven children die before their fifth birthday. Outside the neonatal period, the most common primary causes of death are pneumonia (19%) and diarrhoea (17%) but over a third of all deaths can be attributed to underlying undernutrition (see Figure 1). It is estimated that there are 148 million underweight children: 78 million live in South Asia and 36 million in sub-Saharan Africa. In the developing world, 20% of children are underweight and 3.5% (19 million) are severely malnourished. Millennium Development Goal 4 (a reduction in global under-5 mortality by 2/3 between 1990 and 2015) will only be achieved if significant gains in both the prevention and management of malnutrition are made. As well as causing loss of life, malnutrition results in substantial morbidity and loss of quality of life; long-term developmental problems and educational underachievement diminish the ability to work thereby reducing potential for national development. When calculated as disability-adjusted life years, underweight in childhood is the leading global risk factor for ill health in the world today.
Definitions and diagnosis The diagnosis of malnutrition is based on measurement of body size (anthropometry) and clinical signs (see Box 1). Based on the 2006 WHO Child Growth Standards, underweight is defined as a weight that is greater than 2 standard deviations (or “z scores”) below the median expected weight for age. This could be due either to stunting (low height for age) or wasting (low weight for height). Moderate wasting is weight for height z score (WHZ) less than 2 and severe wasting WHZ less than 3. Stunting is a result of chronic undernutrition and these children require multiple interventions to improve their health and well-being. Wasting and/or nutritional oedema signifies acute malnutrition and requires immediate and intense intervention. All degrees of malnutrition impact negatively on health. Because of the large numbers affected, the great majority of malnutritionassociated deaths occur in mild and moderately underweight children. However, compared with children with a WHZ greater than 1, the odds ratio for mortality is estimated to be 3.0 for
Criteria for the diagnosis of severe acute malnutrition One or more of:Weight for height z score of less than 3 C Presence of bilateral pitting pedal oedema C Mid upper arm circumference (MUAC) of less than 11.5 cm
Emily Walton MB BS MRCPCH is ST4 in Paediatrics at the West Middlesex University Hospital, Middlesex, UK. Conflict of interest: none.
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Stephen Allen MB ChB MRCP(UK) Diploma of Tropical Medicine and Hygiene MD is Professor of Paediatrics and International Health at the Swansea Medical School, Swansea UK. Conflict of interest: none.
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Box 1
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WHZ less than 2 and 9.4 for WHZ less than 3. Therefore, severely wasted children are the focus of in-patient treatment programmes. In the resource limited settings where malnutrition is common, accurate measurement of weight and height may not be possible and calculation of age and access to, and correct use of, the reference norms may also be difficult. MUAC (mid upper arm circumference) may be more appropriate in these situations as it can be measured more easily. MUAC is relatively constant from 6 months to 5 years avoiding the requirement for accurate calculation of age. MUAC of less than 11.5 cm and WHZ of less 3 identify similar proportions of children and are associated with similar risks of mortality. In the most basic settings where no measurements are possible, diagnosis is based on the presence of visible signs of severe wasting and nutritional oedema. There are two wellrecognized malnutrition syndromes. Children with marasmus (see Figure 2) have severe muscle wasting and minimal adipose tissue; they are often noted to be irritable. Children with kwashiorkor (see Figure 3) present with oedema and may show other classical features including dermatitis, sparse depigmented hair and hepatomegaly; they are typically described as apathetic. Nutritional oedema (i.e. pitting oedema of both feet with no identifiable cause such as nephrosis) increases weight and, therefore, may result in a misleadingly high WHZ score. Many children present with clinical features of both syndromes. Whichever diagnostic criteria are used, they must be applied consistently. All children who present to a health facility, whatever the reason, should have their nutritional status assessed. If treatment is prescribed for the presenting condition but there is a failure to identify and address underlying malnutrition then an opportunity to reduce long-term mortality has been lost.
Figure 3 Child with kwashiorkor (lower limb oedema, sparse depigmented hair, dermatitis with areas of hypo- and hyperpigmentation, angular stomatitis).
of infection e especially enteric infections. It is usually difficult to determine the exact sequence of events in any one child; rather, malnutrition and infection appear to exist in a vicious circle with each increasing susceptibility to the other. Several specific pathological mechanisms have been identified in malnourished children. Even in the absence of overt infection, micro-organisms may still play a crucial role. In unhygienic environments, it is postulated that small bowel bacterial overgrowth leads to a T-cell mediated enteropathy with variable degrees of villous atrophy and crypt hyperplasia. This enteropathy impairs nutrient digestion and absorption and, as a result of increased mucosal permeability, may result in persistent stimulation of the systemic inflammatory response and sepsis from bacterial translocation. Although the nutritional oedema of kwashiorkor was first described in the 1930s, the underlying pathological mechanism is still not fully understood. The long held assumption was that children with kwashiorkor had a disproportionate lack of protein in their diet resulting in lower plasma albumin concentrations and reduced oncotic pressure. This caused fluid leak into the interstitium and the contracted intravascular volume triggered salt and water retention by the kidney, so further worsening the oedema. However, the diets of children with marasmus and kwashiorkor have not been found to be significantly different and a low protein diet has not consistently produced a kwashiorkor-like syndrome in animal models.
Aetiology and pathophysiology Impaired growth may result from a combination of inadequate nutrient intake, increased losses (diarrhoeal episodes, vomiting) and increased energy expenditure (usually due to infections). Kwashiorkor is from the Ghanaian Kwa language meaning ‘the deposed child’ and relates to the child being displaced from the breast by a newborn sibling. Indeed, malnutrition often presents around the time of weaning. This is a critical period when breast milk no longer provides adequate calories for growth but weaning foods may be nutritionally incomplete and also a source
Figure 2 Child with marasmus (marked wasting, prominent ribs, increased axillary skin folds, ‘old man’ face).
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One theory is that the scavenger pathways that usually protect against self-harm from the free radicals produced to destroy infectious organisms are underactive in children predisposed to kwashiorkor. A lack of the trace elements and antioxidants required to dispose of harmful free radicals allows them to damage cell membranes leading to increased vascular permeability and oedema as well as the other features of tissue damage. The finding of higher levels of iron (a catalyst for damaging free radical reactions) in children with kwashiorkor is consistent with this hypothesis. However, treatment with a variety of antioxidants has not been shown to prevent kwashiorkor. A recent theory is that children with kwashiorkor have a genetic predisposition to underexpress certain glycosaminoglycans in the intestinal mucosa, as well as in other body tissues. These polysaccharides, found in all connective tissues and basement membranes, play a role in maintaining mucosal integrity and their deficiency could result in fluid leak. Duodenal biopsies of Zambian children with kwashiorkor showed a marked deficiency of heparin sulphate proteoglycan (HSPG). As HSPG has multiple functions in the body (including roles in free fatty acid uptake and keratinocyte adhesion) other features of kwashiorkor such as fatty liver and exfoliative dermatitis could be explained and HSPG deficiency may provide a unifying hypothesis for the syndrome. In both marasmus and kwashiorkor normal physiology is deranged by a process called ‘reductive adaptation’ in which the body attempts to survive on minimal energy. It does this both by catabolizing tissue reserves of carbohydrate, fat and protein and by down-regulating certain physiological and metabolic processes. Physical activity and growth are minimized and basal metabolic rate is slowed. One outcome is a decrease in the number and function of NaeK pumps in cell membranes resulting in leakage of sodium into cells and loss of potassium into the extracellular space and thence into the urine. The net effects are an increase in total body sodium with a decrease in plasma and total body potassium. The function of all the major organs is impaired. The kidneys are less able to excrete the extra sodium. Cardiac muscle is atrophied and hypokalaemia also contributes to poor contractility and reduced cardiac function. Hepatic glucose stores are depleted and gluconeogenesis impaired. Nutrient digestion and absorption is impaired by reduced production of acid and enzymes, villous atrophy and decreased gut motility. The immune and inflammatory systems become dormant and the body does not mount normal responses to infection or injury. An understanding of these complex physiological changes is necessary for the effective management of severe malnutrition. If treatment does not take account of reductive adaptation, lives will be lost not just due to the underlying disease processes but also through faulty management.
History History of presenting complaint Appetite e recent oral intake C Recent weight change/swelling of feet C Diarrhoea (frequency, consistency, presence of blood) C Fever C Cough (acute or chronic) C
Past medical history C Pregnancy and neonatal history (preterm? low birthweight? birth asphyxia?) C Significant illnesses C Contact with TB/measles C Known/suspected HIV Drug history C Regular medications (including traditional/herbal) C Immunizations and routine vitamin A supplementation Dietary History C Infant feeding (duration of exclusive/supplementary breastfeeding, use of infant formula/non-human milk, age and diet at weaning) C Current diet (number of meals/snacks per day, type of food, protein sources, communal serving of food or designated portion) Family history C TB C HIV Social history C Family structure (number of living parents/carers, number of siblings, birth order, polygamy) C Economic (parental/carer occupation, household income, food availability) C Accommodation (crowding, water source, sanitation)
Box 2
ability to provide nutritional and other care to this child and other children in the family. This information will also be crucial in deciding whether in-patient or out-patient care is most appropriate. Examination As well as searching for the specific signs of the malnutrition syndromes (as detailed in Box 3) a thorough systemic examination should be performed to detect any co-morbidities (e.g. renal disease, congenital cardiac defects) that could predispose to malnutrition. Signs of shock, severe anaemia and hypothermia should be elicited and appropriate emergency management initiated. Accurately assessing the hydration status in a malnourished child is notoriously difficult. Atrophy of salivary and tear glands results in dry mucous membranes even when well hydrated. Loss of subcutaneous tissue gives the impression of persistently decreased tissue turgor. Poor cardiac output may prolong
Clinical evaluation History Aspects of the history to be covered in all malnourished children are listed in Box 2. A thorough dietary history is necessary to elicit inappropriate feeding practices such as supplementation of breast milk with water, early or late weaning and withholding feeds during diarrhoea. A detailed social history is also vital to obtain background information on the family and the mother’s
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these two groups is the ‘appetite test’. A good appetite is a reliable sign that the child does not have any serious hidden complications. The child is encouraged to eat an appropriate portion of ready-to-use therapeutic food (RUTF) over the course of about an hour. The child who has appetite and no obvious complications can embark immediately on an OTP. RUTFs are high energy and protein foods enriched with electrolytes, minerals and vitamins. They will keep for months at ambient temperature in the packaging they are distributed in and do not require cooking or the addition of water. This makes them microbiologically safe even in the harsh environments of the developing world. ‘Plumpy Nut’, the most widely used, is made from peanut paste, milk powder, oil and sugar with added potassium, magnesium, vitamins and minerals. Each 92 g sachet provides 500 kcal. OTPs are usually based in local health centres. At registration the child will be given a course of broad spectrum oral antibiotics. They then attend weekly for weighing and for the distribution of quantities of RUTF appropriate to their current weight. OTPs are generally popular with families but weight gain is usually not as rapid as in in-patient programmes. RUTFs are very palatable and in home based treatment there may be a temptation to share rations with other children (and adults!) in the household. OTPs are also the most appropriate setting to manage moderate malnutrition. The aim is to provide nutritious food rations, preferably based on locally available foods, and appropriate health education to promote recovery and, critically, prevent progression to severe malnutrition.
Examination C C
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Temperature: fever or hypothermia Signs of shock: cold hands with capillary refill time greater than 3 s and weak, fast pulse and lethargic or unconscious Signs of dehydration (beware: may be unreliable in the malnourished child) Oedema Signs of severe wasting (‘old man’ face, emaciated limbs, clearly visible ribs, increased axillary skin folds, buttock wasting) Pallor Localizing signs of infection (ear, throat, skin, chest) Mouth (ulcers, angular stomatitis, oral thrush) Skin (‘flaky paint’ dermatitis, areas of hypo- and hyperpigmentation in kwashiorkor; thin and flaccid in marasmus)
Box 3
capillary refill time. Decreased renal blood flow and impaired renal function decrease urine output. The most reliable measure of dehydration is current weight in comparison to a recent accurate weight. Signs of localizing infection should be searched for whilst recognizing that they may be absent even in the presence of severe infection due to impaired immune and inflammatory responses. Differentiation from HIV infection can be difficult but malnutrition alone does not typically cause generalized lymphadenopathy. Tuberculosis (TB) may co-present with malnutrition but diagnosis can be a challenge e particularly because the Mantoux test may be falsely negative. Where malnutrition does not respond to standard care, a trial of anti-TB treatment may be necessary.
The WHO 10 steps protocol Admission to hospital has several disadvantages. Overcrowding permits the spread of nosocomial infections and in-patient treatment can be expensive for the family e either through direct costs of services or through loss of earnings for the caregiver. The health of other children in the family and the consequences of removing the mother from the household should also be taken into account. However, in-patient treatment is essential for the intensive management and close monitoring of children with complications. High mortality rates are common: 25e30% case fatality is found in many hospitals in Africa and rates as high as 50e70% are sometimes reported. High mortality is often attributed to incorrect management; a review in two South African hospitals in 2000e2001 ascribed 50% of deaths to doctor error and 28% to nurse error. High mortality results from a failure to take into account the abnormal physiology of severe malnutrition and to manage these children by the same principles as those of a normal weight. Doing so leads to avoidable deaths from hypoglycaemia, hypothermia, infection, heart failure and electrolyte imbalance. In an attempt to improve outcomes and reduce deaths, the WHO has produced a standard protocol for the in-patient management of both oedematous and non-oedematous malnutrition. This protocol consists of 10 steps divided between two phases e a stabilization and a rehabilitation phase (see Figure 4). In the stabilization phase, acute problems are tackled in a way that is specific for the malnourished child. The aim of this phase is not to achieve weight gain but rather to remedy the metabolic and biochemical disturbances that have developed and to allow the child to safely enter the rehabilitation phase e during which weight should be regained.
Investigations Access to investigations is likely to be limited in the resource limited settings where malnutrition is prevalent. If blood glucose cannot be measured, then presumptive treatment for hypoglycaemia should be initiated. The presence and degree of anaemia may need to be assessed clinically. In parts of the world where malaria is endemic, a blood film should be examined for malarial parasites. Even if available, measurement of plasma electrolytes may be misleading as they will not accurately reflect total body stores and, therefore, empirical management may actually be safer than using plasma levels to guide fluid therapy. Other investigations include a chest X-ray (to screen for TB) and HIV testing (discussed later). It is unlikely that a specific pathogen will be identified in persistent diarrhoea but stool culture is indicated in dysentery.
Management Where should malnourished children be managed? Current guidelines recommend integrated management involving both in-patient and community services. Children with complications (severe infections or metabolic disturbances) should begin treatment in an in-patient facility whereas those with no complications can progress directly to an out-patient therapeutic programme (OTP). A simple test to help discriminate between
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Stabilization Days 1–2 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Hypoglycaemia Hypothermia Dehydration Electrolytes Infection Micronutrients Initiate feeding Catch-up growth Sensory stimulation Prepare for follow-up
Days 3–7
NO IRON
Rehabilitation Weeks 2–6
WITH IRON
Taken from the World Health Organization’s ‘Pocket book of Hospital care for children’ 2005.
Figure 4 Outline of priorities and time frame in the management of severe acute malnutrition.
Common complications of severe malnutrition that require specific management: 1. Treat/prevent hypoglycaemia Unless blood glucose of 3 mmol/L can be demonstrated, hypoglycaemia should be presumed and treated with enteral glucose: give 10% dextrose or a milk feed immediately. Only if the child is unconscious should intravenous glucose be given. Hypoglycaemia is prevented by giving all new admissions frequent feeds (2e3 hourly) throughout the day and night. 2. Treat/prevent hypothermia Malnourished children are at high risk of hypothermia (axillary temperature less than 35 C or unrecordable) because they have minimal insulative body fat and no energy stores to produce their own heat. Hypothermia should be managed with an immediate feed and active rewarming. An effective way of rewarming is ‘kangaroo care’: skin-to-skin with the mother with a blanket covering both. 3. Treat/prevent dehydration As previously discussed, clinical signs of dehydration can be difficult to interpret. Therefore, all children with watery diarrhoea should be assumed to be dehydrated. Intravenous rehydration should be avoided (unless signs of shock are present) due to the risk of precipitating heart failure. Enteral rehydration should be slower than usual and use a modified version of oral rehydration solution (ORS) known as ReSoMal (Rehydration Solution for Malnutrition). 4. Correct electrolyte imbalance ReSoMal contains more potassium and less sodium than standard ORS and is therefore more suitable for malnourished children in view of their typical electrolyte shifts and imbalances. The initial milk formula (F75) recommended for feeding also has added potassium and magnesium and restricted sodium. The extra potassium should allow the kidney to excrete the excess sodium and fluid and oedema should gradually dissipate. Oedema should never be treated with diuretics. 5. Treat/prevent infection Infection should be assumed and all children treated empirically with broad spectrum antibiotics. Local guidelines should be
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followed (e.g. i.v. ampicillin/p.o. amoxicillin and i.v. gentamicin for 7 days). In countries where worm infestation is prevalent, a course of mebendazole should also be given. Strict handwashing and other infection control measures should be adhered to. 6. Correct micronutrient deficiencies Children should receive supplements of important trace elements (zinc, copper, selenium), folic acid and a multivitamin preparation. These may be added to the milk feeds at preparation. A standard dose of vitamin A should be given to all children and a higher dose to any with ocular signs of deficiency. Although malnourished children are usually anaemic, iron should not initially be replaced as iron storage systems are underactive and free iron can catalyze harmful free radical reactions as discussed above. Once infections have been treated and the child has entered the rehabilitation phase, iron can safely be supplemented. 7. Start cautious feeding The milk feed recommended for the rehabilitation phase is F75. This can be made from locally available ingredients (milk powder, vegetable oil, sugar and water) and contains 75 kcal/100 ml and 0.9 g protein/100 ml. Children are initially fed 130 ml/kg/ day reduced to 100 ml/kg/day in kwashiorkor to allow for the extra weight of the oedema. Total feed volume and the energy and protein (and therefore sodium) content of the feed are restricted to prevent heart failure, osmotic diarrhoea and a worsening of oedema. Poor appetite, impaired gut motility, and decreased gastric volume mean that feeding is more successful if smaller feeds are offered more frequently (2 hourly) and the interval spaced as the child improves. Children may also need a nasogastric tube for feeding early in the course of their treatment. Success in refeeding relies on the regular provision of frequent feeds, encouraging children to complete their feeds, and accurately recording feeds consumed to assess readiness to move into the rehabilitation phase. This can be a challenge in busy hospitals where staffing ratios are often poor and strict timekeeping not always part of the culture. Empowering mothers to involve themselves in the care of their children is a means of attempting to overcome these challenges.
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8. Achieve catch-up growth Once acute medical problems have been dealt with and the child’s appetite has improved they are ready to enter the rehabilitation phase. The starter F75 formula is replaced with F100 formula (100 kcal/100 ml and 2.9 g protein/100 ml) and volumes increased according to the child’s demand. The higher energy and protein content of F100 should result in rapid weight gain assessed in g/kg/day. A weight gain of greater than 10 g/kg/day is considered good; 5e10 g/kg/day moderate; and less than 5 g/ kg/day poor. At this stage of treatment, dependent on individual circumstances, children can often be transferred to out-patient care and RUTF offered instead of F100. 9. Provide sensory stimulation and emotional support Although usually unintentional, malnourished children have suffered a form of neglect. They should receive tender nursing care in a stimulating environment with opportunities for play and physical therapy as they recover. 10. Prepare for follow-up Recovery is considered to be a WHZ score of 1. This may take up to 6 weeks to achieve. Before discharge from in-patient or out-patient care, endeavours must be made to ensure the child will not relapse. Caregivers should receive health and nutrition education and be alerted to the signs of deterioration and when to seek medical care. Scheduled follow-up appointments should also be planned over at least the first 6 months.
the disease to ensure that families are not stigmatized and that children do not receive inferior care due to a belief that their demise is inevitable. HIV positive malnourished children should follow the same protocol as HIV negative children with the addition of prophylactic co-trimoxazole. Severe oral thrush can inhibit feeding and may need treatment with fluconazole. When to start antiretrovirals should be based on the level of immunosuppression (CD4 count) and stage of malnutrition treatment according to local protocols.
Prevention As detailed above, management of the severely malnourished child presents a huge challenge, especially in inadequately staffed and resourced health facilities. Even when the WHO 10 steps are applied rigorously, mortality often remains high. Therefore, prevention of malnutrition is a priority for governments and other organizations interested in reducing child mortality. As malnutrition is both a medical and socioeconomic condition, a range of interventions are necessary. An essential component of any preventive strategy is the promotion of breastfeeding. The WHO recommends exclusive breastfeeding until 6 months of age with supplementary breast milk forming an important part of the diet up to 2 years of age. Currently only 24e32% of infants in developing countries are exclusively breastfed up to 6 months. The WHO ranks suboptimal breastfeeding as the 7th most significant risk factor for global burden of disease. The uncompromising guidelines of the Baby Friendly Hospital Initiative e now familiar in many UK maternity units e were originally intended for use in the developing world where breastfeeding is truly a life-saving intervention. Infant formula milks are inferior to breast milk both in nutritional composition and lack of immunological protection against infectious diseases, in particular gastroenteritis and pneumonia. In poor societies where many mothers are illiterate and innumerate, producing appropriately concentrated and hygienic milk from instructions on a tin of powder is unlikely to be achieved. Furthermore, the cost may result in a temptation to over-dilute infant formula or to purchase a cheaper, nonmodified, animal milk. Other health education approaches include the promotion of nutrient rich weaning foods and discouraging the over-reliance on carbohydrate dense staple foods. This is combined with an active programme of routine child health surveillance with regular weight monitoring to detect children at risk of severe malnutrition and target interventions. Increasing coverage of immunization and vitamin A supplementation should help prevent the infectious diseases that can often trigger severe malnutrition in an already undernourished child. Primary care services must also be available to ensure the prompt treatment of childhood illnesses that can precipitate or worsen malnutrition. Improvement of a community’s sanitation and hygiene via the provision of toilets (currently available to only 59% of the world’s population) and the promotion of handwashing with soap will also be crucial in improving children’s nutritional status e particularly if tropical enteropathy is confirmed as a key contributing factor to malnutrition. The large family sizes common in many developing countries make it difficult for mothers both to offer optimal breastfeeding
Special groups Infants younger than 6 months: traditionally malnutrition has been considered a condition that develops after the age of 6 months and management guidelines are aimed at children greater than 6 months old. However, increasing numbers of young infants are presenting with both non-oedematous and oedematous malnutrition. Possible reasons for this include increased survival of low birthweight and premature babies and failure to exclusively breastfeed (for a variety of reasons including increased prevalence of maternal HIV). The younger the child the more likely an organic cause of malnutrition further highlighting the importance of a thorough assessment to detect any underlying medical conditions. Breast milk is the ideal nutrition for these infants but is often not available in sufficient quantities and the child may be too unwell to suckle effectively by the time they reach the attention of health services. There is currently no consensus on the optimum nutritional management in the rehabilitation phase if breast milk, or a commercial infant formula, are not available. F100 has a high potential renal solute load and its use could result in hypernatraemic dehydration e particularly in hot, dry environments. Some practitioners advocate the use of a diluted version of F100 as a safer alternative. However, studies of its use have not shown it to consistently support the rapid weight gain required. Additional guidance on the management of infants less than 6 months is anticipated in the next edition of the WHO treatment protocol. HIV positive children: there is debate as to whether malnourished children should be routinely screened for HIV infection. The increasing availability of antiretroviral medication, as well as the opportunity to access prophylactic co-trimoxazole, suggest that it will now be helpful to check HIV status. However, treatment facilities must ensure that nursing staff are educated about
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Hamer C, Kvatum K, Jeffries D, Allen S. Detection of severe protein-energy malnutrition by nurses in The Gambia. Arch Dis Child 2004; 89: 181e4. Humphrey JH. Child undernutrition, tropical enteropathy, toilets, and handwashing. Lancet 2009; 374: 1032e5. UNICEF. The State of the World’s Children; 2008. World Health Organization. Global health risks: mortality and burden of disease attributable to selected major risks; 2009. World Health Organization. Pocket book of hospital care for children. Guidelines for the management of common illnesses with limited resources; 2005. World Health Organization and United Nations Children’s Fund. WHO child growth standards and the identification of severe acute malnutrition in infants and children; 2009. World Health Organization. Severe malnutrition: report of a consultation to review current literature; 2005.
to each child, and to provide a diet, once weaned, of appropriate quantity and quality. Improving availability and accessibility of family planning services to either limit family size or to space pregnancies is therefore another important tactic in the prevention of malnutrition. For mothers to act as effective advocates for their children, the broader aim of empowering women and improving levels of female education must also be addressed. With just 5 years left to achieve the Millennium Development Goals there is a clear need to confront childhood undernutrition as the single most important risk factor for ill health in the world today. Mounting evidence for the efficacy of simple interventions, such as exclusive breastfeeding and improved sanitation, should aid governments and society in tackling this threat. A
FURTHER READING Amadi B, Fagbemi AO, Kelly P, et al. Reduced production of sulfated glycosaminoglycans occurs in Zambian children with kwashiorkor but not marasmus. Am J Clin Nutr 2009; 89: 592e600. Ashworth A, Chopra M, McCoy D, et al. WHO guidelines for management of severe malnutrition in rural South African hospitals: effect on case fatality and the influence of operational factors. Lancet 2004; 363: 1110e5. Berkley J, Mwangi I, Griffiths K, et al. Assessment of severe malnutrition among hospitalized children in rural Kenya: comparison of weight for height and mid upper arm circumference. J Am Med Assoc 2005; 294: 591e7. Bhutta ZA, Chopra M, Axelson H, et al. Countdown to 2015 decade report (2000e10): taking stock of maternal, newborn, and child survival. Lancet 2010; 375: 2032e44. Black RE, Allen LH, Bhutta ZA, et al. Maternal and child undernutrition: global and regional exposures and health consequences. Lancet 2008; 371: 243e60.
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Children presenting to healthcare facilities should routinely have their nutritional status assessed. Treatment of the 2 main forms of malnutrition should be standardized and take account of reductive adaptation to prevent avoidable deaths. Treatment programmes should be community based where possible but the most severely affected children will still need intensive in-patient management. Strategies to prevent malnutrition should be aimed at both individuals and communities and must tackle the wide range of medical, social and economic causes.
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Malnutrition in developing countries
Malaria Measles Injuries AIDS 3% 3% 3% 3%
Neonatal 37%
Emily Walton Stephen Allen
Abstract Over a third of all deaths are attributable to undernutrition
Although now rare in industrialized countries, severe acute malnutrition is unfortunately still common throughout the developing world and is a key contributor to both global childhood morbidity and mortality. This review describes the epidemiology of malnutrition and the presentation and pathophysiology of the severe syndromic forms e marasmus and kwashiorkor. The gold standards for diagnosis and management are detailed and the challenges of implementation in the basic healthcare systems of the developing world are discussed. As the leading cause of ill health in the world today, more effective treatment and prevention of malnutrition must be a priority for the global healthcare community. Other 10%
Keywords kwashiorkor; marasmus; protein-energy malnutrition; severe acute malnutrition; underweight
Diarrhoea 17%
Pneumonia 19%
Based on data of the Child Mortality Estimation Group used in the UNICEF report ‘The State of the World’s Children 2008’
Figure 1 Global cause specific mortality in children under 5 years of age.
Underweight: the leading cause of ill health in the world today In 2008, of the 8.8 million global deaths of children under 5 years of age, 93% occurred in the developing countries of Africa and Asia. The highest rates of childhood mortality are found in sub-Saharan Africa where one in seven children die before their fifth birthday. Outside the neonatal period, the most common primary causes of death are pneumonia (19%) and diarrhoea (17%) but over a third of all deaths can be attributed to underlying undernutrition (see Figure 1). It is estimated that there are 148 million underweight children: 78 million live in South Asia and 36 million in sub-Saharan Africa. In the developing world, 20% of children are underweight and 3.5% (19 million) are severely malnourished. Millennium Development Goal 4 (a reduction in global under-5 mortality by 2/3 between 1990 and 2015) will only be achieved if significant gains in both the prevention and management of malnutrition are made. As well as causing loss of life, malnutrition results in substantial morbidity and loss of quality of life; long-term developmental problems and educational underachievement diminish the ability to work thereby reducing potential for national development. When calculated as disability-adjusted life years, underweight in childhood is the leading global risk factor for ill health in the world today.
Definitions and diagnosis The diagnosis of malnutrition is based on measurement of body size (anthropometry) and clinical signs (see Box 1). Based on the 2006 WHO Child Growth Standards, underweight is defined as a weight that is greater than 2 standard deviations (or “z scores”) below the median expected weight for age. This could be due either to stunting (low height for age) or wasting (low weight for height). Moderate wasting is weight for height z score (WHZ) less than 2 and severe wasting WHZ less than 3. Stunting is a result of chronic undernutrition and these children require multiple interventions to improve their health and well-being. Wasting and/or nutritional oedema signifies acute malnutrition and requires immediate and intense intervention. All degrees of malnutrition impact negatively on health. Because of the large numbers affected, the great majority of malnutritionassociated deaths occur in mild and moderately underweight children. However, compared with children with a WHZ greater than 1, the odds ratio for mortality is estimated to be 3.0 for
Criteria for the diagnosis of severe acute malnutrition One or more of:Weight for height z score of less than 3 C Presence of bilateral pitting pedal oedema C Mid upper arm circumference (MUAC) of less than 11.5 cm
Emily Walton MB BS MRCPCH is ST4 in Paediatrics at the West Middlesex University Hospital, Middlesex, UK. Conflict of interest: none.
C
Stephen Allen MB ChB MRCP(UK) Diploma of Tropical Medicine and Hygiene MD is Professor of Paediatrics and International Health at the Swansea Medical School, Swansea UK. Conflict of interest: none.
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WHZ less than 2 and 9.4 for WHZ less than 3. Therefore, severely wasted children are the focus of in-patient treatment programmes. In the resource limited settings where malnutrition is common, accurate measurement of weight and height may not be possible and calculation of age and access to, and correct use of, the reference norms may also be difficult. MUAC (mid upper arm circumference) may be more appropriate in these situations as it can be measured more easily. MUAC is relatively constant from 6 months to 5 years avoiding the requirement for accurate calculation of age. MUAC of less than 11.5 cm and WHZ of less 3 identify similar proportions of children and are associated with similar risks of mortality. In the most basic settings where no measurements are possible, diagnosis is based on the presence of visible signs of severe wasting and nutritional oedema. There are two wellrecognized malnutrition syndromes. Children with marasmus (see Figure 2) have severe muscle wasting and minimal adipose tissue; they are often noted to be irritable. Children with kwashiorkor (see Figure 3) present with oedema and may show other classical features including dermatitis, sparse depigmented hair and hepatomegaly; they are typically described as apathetic. Nutritional oedema (i.e. pitting oedema of both feet with no identifiable cause such as nephrosis) increases weight and, therefore, may result in a misleadingly high WHZ score. Many children present with clinical features of both syndromes. Whichever diagnostic criteria are used, they must be applied consistently. All children who present to a health facility, whatever the reason, should have their nutritional status assessed. If treatment is prescribed for the presenting condition but there is a failure to identify and address underlying malnutrition then an opportunity to reduce long-term mortality has been lost.
Figure 3 Child with kwashiorkor (lower limb oedema, sparse depigmented hair, dermatitis with areas of hypo- and hyperpigmentation, angular stomatitis).
of infection e especially enteric infections. It is usually difficult to determine the exact sequence of events in any one child; rather, malnutrition and infection appear to exist in a vicious circle with each increasing susceptibility to the other. Several specific pathological mechanisms have been identified in malnourished children. Even in the absence of overt infection, micro-organisms may still play a crucial role. In unhygienic environments, it is postulated that small bowel bacterial overgrowth leads to a T-cell mediated enteropathy with variable degrees of villous atrophy and crypt hyperplasia. This enteropathy impairs nutrient digestion and absorption and, as a result of increased mucosal permeability, may result in persistent stimulation of the systemic inflammatory response and sepsis from bacterial translocation. Although the nutritional oedema of kwashiorkor was first described in the 1930s, the underlying pathological mechanism is still not fully understood. The long held assumption was that children with kwashiorkor had a disproportionate lack of protein in their diet resulting in lower plasma albumin concentrations and reduced oncotic pressure. This caused fluid leak into the interstitium and the contracted intravascular volume triggered salt and water retention by the kidney, so further worsening the oedema. However, the diets of children with marasmus and kwashiorkor have not been found to be significantly different and a low protein diet has not consistently produced a kwashiorkor-like syndrome in animal models.
Aetiology and pathophysiology Impaired growth may result from a combination of inadequate nutrient intake, increased losses (diarrhoeal episodes, vomiting) and increased energy expenditure (usually due to infections). Kwashiorkor is from the Ghanaian Kwa language meaning ‘the deposed child’ and relates to the child being displaced from the breast by a newborn sibling. Indeed, malnutrition often presents around the time of weaning. This is a critical period when breast milk no longer provides adequate calories for growth but weaning foods may be nutritionally incomplete and also a source
Figure 2 Child with marasmus (marked wasting, prominent ribs, increased axillary skin folds, ‘old man’ face).
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One theory is that the scavenger pathways that usually protect against self-harm from the free radicals produced to destroy infectious organisms are underactive in children predisposed to kwashiorkor. A lack of the trace elements and antioxidants required to dispose of harmful free radicals allows them to damage cell membranes leading to increased vascular permeability and oedema as well as the other features of tissue damage. The finding of higher levels of iron (a catalyst for damaging free radical reactions) in children with kwashiorkor is consistent with this hypothesis. However, treatment with a variety of antioxidants has not been shown to prevent kwashiorkor. A recent theory is that children with kwashiorkor have a genetic predisposition to underexpress certain glycosaminoglycans in the intestinal mucosa, as well as in other body tissues. These polysaccharides, found in all connective tissues and basement membranes, play a role in maintaining mucosal integrity and their deficiency could result in fluid leak. Duodenal biopsies of Zambian children with kwashiorkor showed a marked deficiency of heparin sulphate proteoglycan (HSPG). As HSPG has multiple functions in the body (including roles in free fatty acid uptake and keratinocyte adhesion) other features of kwashiorkor such as fatty liver and exfoliative dermatitis could be explained and HSPG deficiency may provide a unifying hypothesis for the syndrome. In both marasmus and kwashiorkor normal physiology is deranged by a process called ‘reductive adaptation’ in which the body attempts to survive on minimal energy. It does this both by catabolizing tissue reserves of carbohydrate, fat and protein and by down-regulating certain physiological and metabolic processes. Physical activity and growth are minimized and basal metabolic rate is slowed. One outcome is a decrease in the number and function of NaeK pumps in cell membranes resulting in leakage of sodium into cells and loss of potassium into the extracellular space and thence into the urine. The net effects are an increase in total body sodium with a decrease in plasma and total body potassium. The function of all the major organs is impaired. The kidneys are less able to excrete the extra sodium. Cardiac muscle is atrophied and hypokalaemia also contributes to poor contractility and reduced cardiac function. Hepatic glucose stores are depleted and gluconeogenesis impaired. Nutrient digestion and absorption is impaired by reduced production of acid and enzymes, villous atrophy and decreased gut motility. The immune and inflammatory systems become dormant and the body does not mount normal responses to infection or injury. An understanding of these complex physiological changes is necessary for the effective management of severe malnutrition. If treatment does not take account of reductive adaptation, lives will be lost not just due to the underlying disease processes but also through faulty management.
History History of presenting complaint Appetite e recent oral intake C Recent weight change/swelling of feet C Diarrhoea (frequency, consistency, presence of blood) C Fever C Cough (acute or chronic) C
Past medical history C Pregnancy and neonatal history (preterm? low birthweight? birth asphyxia?) C Significant illnesses C Contact with TB/measles C Known/suspected HIV Drug history C Regular medications (including traditional/herbal) C Immunizations and routine vitamin A supplementation Dietary History C Infant feeding (duration of exclusive/supplementary breastfeeding, use of infant formula/non-human milk, age and diet at weaning) C Current diet (number of meals/snacks per day, type of food, protein sources, communal serving of food or designated portion) Family history C TB C HIV Social history C Family structure (number of living parents/carers, number of siblings, birth order, polygamy) C Economic (parental/carer occupation, household income, food availability) C Accommodation (crowding, water source, sanitation)
Box 2
ability to provide nutritional and other care to this child and other children in the family. This information will also be crucial in deciding whether in-patient or out-patient care is most appropriate. Examination As well as searching for the specific signs of the malnutrition syndromes (as detailed in Box 3) a thorough systemic examination should be performed to detect any co-morbidities (e.g. renal disease, congenital cardiac defects) that could predispose to malnutrition. Signs of shock, severe anaemia and hypothermia should be elicited and appropriate emergency management initiated. Accurately assessing the hydration status in a malnourished child is notoriously difficult. Atrophy of salivary and tear glands results in dry mucous membranes even when well hydrated. Loss of subcutaneous tissue gives the impression of persistently decreased tissue turgor. Poor cardiac output may prolong
Clinical evaluation History Aspects of the history to be covered in all malnourished children are listed in Box 2. A thorough dietary history is necessary to elicit inappropriate feeding practices such as supplementation of breast milk with water, early or late weaning and withholding feeds during diarrhoea. A detailed social history is also vital to obtain background information on the family and the mother’s
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these two groups is the ‘appetite test’. A good appetite is a reliable sign that the child does not have any serious hidden complications. The child is encouraged to eat an appropriate portion of ready-to-use therapeutic food (RUTF) over the course of about an hour. The child who has appetite and no obvious complications can embark immediately on an OTP. RUTFs are high energy and protein foods enriched with electrolytes, minerals and vitamins. They will keep for months at ambient temperature in the packaging they are distributed in and do not require cooking or the addition of water. This makes them microbiologically safe even in the harsh environments of the developing world. ‘Plumpy Nut’, the most widely used, is made from peanut paste, milk powder, oil and sugar with added potassium, magnesium, vitamins and minerals. Each 92 g sachet provides 500 kcal. OTPs are usually based in local health centres. At registration the child will be given a course of broad spectrum oral antibiotics. They then attend weekly for weighing and for the distribution of quantities of RUTF appropriate to their current weight. OTPs are generally popular with families but weight gain is usually not as rapid as in in-patient programmes. RUTFs are very palatable and in home based treatment there may be a temptation to share rations with other children (and adults!) in the household. OTPs are also the most appropriate setting to manage moderate malnutrition. The aim is to provide nutritious food rations, preferably based on locally available foods, and appropriate health education to promote recovery and, critically, prevent progression to severe malnutrition.
Examination C C
C
C C
C C C C
Temperature: fever or hypothermia Signs of shock: cold hands with capillary refill time greater than 3 s and weak, fast pulse and lethargic or unconscious Signs of dehydration (beware: may be unreliable in the malnourished child) Oedema Signs of severe wasting (‘old man’ face, emaciated limbs, clearly visible ribs, increased axillary skin folds, buttock wasting) Pallor Localizing signs of infection (ear, throat, skin, chest) Mouth (ulcers, angular stomatitis, oral thrush) Skin (‘flaky paint’ dermatitis, areas of hypo- and hyperpigmentation in kwashiorkor; thin and flaccid in marasmus)
Box 3
capillary refill time. Decreased renal blood flow and impaired renal function decrease urine output. The most reliable measure of dehydration is current weight in comparison to a recent accurate weight. Signs of localizing infection should be searched for whilst recognizing that they may be absent even in the presence of severe infection due to impaired immune and inflammatory responses. Differentiation from HIV infection can be difficult but malnutrition alone does not typically cause generalized lymphadenopathy. Tuberculosis (TB) may co-present with malnutrition but diagnosis can be a challenge e particularly because the Mantoux test may be falsely negative. Where malnutrition does not respond to standard care, a trial of anti-TB treatment may be necessary.
The WHO 10 steps protocol Admission to hospital has several disadvantages. Overcrowding permits the spread of nosocomial infections and in-patient treatment can be expensive for the family e either through direct costs of services or through loss of earnings for the caregiver. The health of other children in the family and the consequences of removing the mother from the household should also be taken into account. However, in-patient treatment is essential for the intensive management and close monitoring of children with complications. High mortality rates are common: 25e30% case fatality is found in many hospitals in Africa and rates as high as 50e70% are sometimes reported. High mortality is often attributed to incorrect management; a review in two South African hospitals in 2000e2001 ascribed 50% of deaths to doctor error and 28% to nurse error. High mortality results from a failure to take into account the abnormal physiology of severe malnutrition and to manage these children by the same principles as those of a normal weight. Doing so leads to avoidable deaths from hypoglycaemia, hypothermia, infection, heart failure and electrolyte imbalance. In an attempt to improve outcomes and reduce deaths, the WHO has produced a standard protocol for the in-patient management of both oedematous and non-oedematous malnutrition. This protocol consists of 10 steps divided between two phases e a stabilization and a rehabilitation phase (see Figure 4). In the stabilization phase, acute problems are tackled in a way that is specific for the malnourished child. The aim of this phase is not to achieve weight gain but rather to remedy the metabolic and biochemical disturbances that have developed and to allow the child to safely enter the rehabilitation phase e during which weight should be regained.
Investigations Access to investigations is likely to be limited in the resource limited settings where malnutrition is prevalent. If blood glucose cannot be measured, then presumptive treatment for hypoglycaemia should be initiated. The presence and degree of anaemia may need to be assessed clinically. In parts of the world where malaria is endemic, a blood film should be examined for malarial parasites. Even if available, measurement of plasma electrolytes may be misleading as they will not accurately reflect total body stores and, therefore, empirical management may actually be safer than using plasma levels to guide fluid therapy. Other investigations include a chest X-ray (to screen for TB) and HIV testing (discussed later). It is unlikely that a specific pathogen will be identified in persistent diarrhoea but stool culture is indicated in dysentery.
Management Where should malnourished children be managed? Current guidelines recommend integrated management involving both in-patient and community services. Children with complications (severe infections or metabolic disturbances) should begin treatment in an in-patient facility whereas those with no complications can progress directly to an out-patient therapeutic programme (OTP). A simple test to help discriminate between
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Stabilization Days 1–2 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Hypoglycaemia Hypothermia Dehydration Electrolytes Infection Micronutrients Initiate feeding Catch-up growth Sensory stimulation Prepare for follow-up
Days 3–7
NO IRON
Rehabilitation Weeks 2–6
WITH IRON
Taken from the World Health Organization’s ‘Pocket book of Hospital care for children’ 2005.
Figure 4 Outline of priorities and time frame in the management of severe acute malnutrition.
Common complications of severe malnutrition that require specific management: 1. Treat/prevent hypoglycaemia Unless blood glucose of 3 mmol/L can be demonstrated, hypoglycaemia should be presumed and treated with enteral glucose: give 10% dextrose or a milk feed immediately. Only if the child is unconscious should intravenous glucose be given. Hypoglycaemia is prevented by giving all new admissions frequent feeds (2e3 hourly) throughout the day and night. 2. Treat/prevent hypothermia Malnourished children are at high risk of hypothermia (axillary temperature less than 35 C or unrecordable) because they have minimal insulative body fat and no energy stores to produce their own heat. Hypothermia should be managed with an immediate feed and active rewarming. An effective way of rewarming is ‘kangaroo care’: skin-to-skin with the mother with a blanket covering both. 3. Treat/prevent dehydration As previously discussed, clinical signs of dehydration can be difficult to interpret. Therefore, all children with watery diarrhoea should be assumed to be dehydrated. Intravenous rehydration should be avoided (unless signs of shock are present) due to the risk of precipitating heart failure. Enteral rehydration should be slower than usual and use a modified version of oral rehydration solution (ORS) known as ReSoMal (Rehydration Solution for Malnutrition). 4. Correct electrolyte imbalance ReSoMal contains more potassium and less sodium than standard ORS and is therefore more suitable for malnourished children in view of their typical electrolyte shifts and imbalances. The initial milk formula (F75) recommended for feeding also has added potassium and magnesium and restricted sodium. The extra potassium should allow the kidney to excrete the excess sodium and fluid and oedema should gradually dissipate. Oedema should never be treated with diuretics. 5. Treat/prevent infection Infection should be assumed and all children treated empirically with broad spectrum antibiotics. Local guidelines should be
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followed (e.g. i.v. ampicillin/p.o. amoxicillin and i.v. gentamicin for 7 days). In countries where worm infestation is prevalent, a course of mebendazole should also be given. Strict handwashing and other infection control measures should be adhered to. 6. Correct micronutrient deficiencies Children should receive supplements of important trace elements (zinc, copper, selenium), folic acid and a multivitamin preparation. These may be added to the milk feeds at preparation. A standard dose of vitamin A should be given to all children and a higher dose to any with ocular signs of deficiency. Although malnourished children are usually anaemic, iron should not initially be replaced as iron storage systems are underactive and free iron can catalyze harmful free radical reactions as discussed above. Once infections have been treated and the child has entered the rehabilitation phase, iron can safely be supplemented. 7. Start cautious feeding The milk feed recommended for the rehabilitation phase is F75. This can be made from locally available ingredients (milk powder, vegetable oil, sugar and water) and contains 75 kcal/100 ml and 0.9 g protein/100 ml. Children are initially fed 130 ml/kg/ day reduced to 100 ml/kg/day in kwashiorkor to allow for the extra weight of the oedema. Total feed volume and the energy and protein (and therefore sodium) content of the feed are restricted to prevent heart failure, osmotic diarrhoea and a worsening of oedema. Poor appetite, impaired gut motility, and decreased gastric volume mean that feeding is more successful if smaller feeds are offered more frequently (2 hourly) and the interval spaced as the child improves. Children may also need a nasogastric tube for feeding early in the course of their treatment. Success in refeeding relies on the regular provision of frequent feeds, encouraging children to complete their feeds, and accurately recording feeds consumed to assess readiness to move into the rehabilitation phase. This can be a challenge in busy hospitals where staffing ratios are often poor and strict timekeeping not always part of the culture. Empowering mothers to involve themselves in the care of their children is a means of attempting to overcome these challenges.
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8. Achieve catch-up growth Once acute medical problems have been dealt with and the child’s appetite has improved they are ready to enter the rehabilitation phase. The starter F75 formula is replaced with F100 formula (100 kcal/100 ml and 2.9 g protein/100 ml) and volumes increased according to the child’s demand. The higher energy and protein content of F100 should result in rapid weight gain assessed in g/kg/day. A weight gain of greater than 10 g/kg/day is considered good; 5e10 g/kg/day moderate; and less than 5 g/ kg/day poor. At this stage of treatment, dependent on individual circumstances, children can often be transferred to out-patient care and RUTF offered instead of F100. 9. Provide sensory stimulation and emotional support Although usually unintentional, malnourished children have suffered a form of neglect. They should receive tender nursing care in a stimulating environment with opportunities for play and physical therapy as they recover. 10. Prepare for follow-up Recovery is considered to be a WHZ score of 1. This may take up to 6 weeks to achieve. Before discharge from in-patient or out-patient care, endeavours must be made to ensure the child will not relapse. Caregivers should receive health and nutrition education and be alerted to the signs of deterioration and when to seek medical care. Scheduled follow-up appointments should also be planned over at least the first 6 months.
the disease to ensure that families are not stigmatized and that children do not receive inferior care due to a belief that their demise is inevitable. HIV positive malnourished children should follow the same protocol as HIV negative children with the addition of prophylactic co-trimoxazole. Severe oral thrush can inhibit feeding and may need treatment with fluconazole. When to start antiretrovirals should be based on the level of immunosuppression (CD4 count) and stage of malnutrition treatment according to local protocols.
Prevention As detailed above, management of the severely malnourished child presents a huge challenge, especially in inadequately staffed and resourced health facilities. Even when the WHO 10 steps are applied rigorously, mortality often remains high. Therefore, prevention of malnutrition is a priority for governments and other organizations interested in reducing child mortality. As malnutrition is both a medical and socioeconomic condition, a range of interventions are necessary. An essential component of any preventive strategy is the promotion of breastfeeding. The WHO recommends exclusive breastfeeding until 6 months of age with supplementary breast milk forming an important part of the diet up to 2 years of age. Currently only 24e32% of infants in developing countries are exclusively breastfed up to 6 months. The WHO ranks suboptimal breastfeeding as the 7th most significant risk factor for global burden of disease. The uncompromising guidelines of the Baby Friendly Hospital Initiative e now familiar in many UK maternity units e were originally intended for use in the developing world where breastfeeding is truly a life-saving intervention. Infant formula milks are inferior to breast milk both in nutritional composition and lack of immunological protection against infectious diseases, in particular gastroenteritis and pneumonia. In poor societies where many mothers are illiterate and innumerate, producing appropriately concentrated and hygienic milk from instructions on a tin of powder is unlikely to be achieved. Furthermore, the cost may result in a temptation to over-dilute infant formula or to purchase a cheaper, nonmodified, animal milk. Other health education approaches include the promotion of nutrient rich weaning foods and discouraging the over-reliance on carbohydrate dense staple foods. This is combined with an active programme of routine child health surveillance with regular weight monitoring to detect children at risk of severe malnutrition and target interventions. Increasing coverage of immunization and vitamin A supplementation should help prevent the infectious diseases that can often trigger severe malnutrition in an already undernourished child. Primary care services must also be available to ensure the prompt treatment of childhood illnesses that can precipitate or worsen malnutrition. Improvement of a community’s sanitation and hygiene via the provision of toilets (currently available to only 59% of the world’s population) and the promotion of handwashing with soap will also be crucial in improving children’s nutritional status e particularly if tropical enteropathy is confirmed as a key contributing factor to malnutrition. The large family sizes common in many developing countries make it difficult for mothers both to offer optimal breastfeeding
Special groups Infants younger than 6 months: traditionally malnutrition has been considered a condition that develops after the age of 6 months and management guidelines are aimed at children greater than 6 months old. However, increasing numbers of young infants are presenting with both non-oedematous and oedematous malnutrition. Possible reasons for this include increased survival of low birthweight and premature babies and failure to exclusively breastfeed (for a variety of reasons including increased prevalence of maternal HIV). The younger the child the more likely an organic cause of malnutrition further highlighting the importance of a thorough assessment to detect any underlying medical conditions. Breast milk is the ideal nutrition for these infants but is often not available in sufficient quantities and the child may be too unwell to suckle effectively by the time they reach the attention of health services. There is currently no consensus on the optimum nutritional management in the rehabilitation phase if breast milk, or a commercial infant formula, are not available. F100 has a high potential renal solute load and its use could result in hypernatraemic dehydration e particularly in hot, dry environments. Some practitioners advocate the use of a diluted version of F100 as a safer alternative. However, studies of its use have not shown it to consistently support the rapid weight gain required. Additional guidance on the management of infants less than 6 months is anticipated in the next edition of the WHO treatment protocol. HIV positive children: there is debate as to whether malnourished children should be routinely screened for HIV infection. The increasing availability of antiretroviral medication, as well as the opportunity to access prophylactic co-trimoxazole, suggest that it will now be helpful to check HIV status. However, treatment facilities must ensure that nursing staff are educated about
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Hamer C, Kvatum K, Jeffries D, Allen S. Detection of severe protein-energy malnutrition by nurses in The Gambia. Arch Dis Child 2004; 89: 181e4. Humphrey JH. Child undernutrition, tropical enteropathy, toilets, and handwashing. Lancet 2009; 374: 1032e5. UNICEF. The State of the World’s Children; 2008. World Health Organization. Global health risks: mortality and burden of disease attributable to selected major risks; 2009. World Health Organization. Pocket book of hospital care for children. Guidelines for the management of common illnesses with limited resources; 2005. World Health Organization and United Nations Children’s Fund. WHO child growth standards and the identification of severe acute malnutrition in infants and children; 2009. World Health Organization. Severe malnutrition: report of a consultation to review current literature; 2005.
to each child, and to provide a diet, once weaned, of appropriate quantity and quality. Improving availability and accessibility of family planning services to either limit family size or to space pregnancies is therefore another important tactic in the prevention of malnutrition. For mothers to act as effective advocates for their children, the broader aim of empowering women and improving levels of female education must also be addressed. With just 5 years left to achieve the Millennium Development Goals there is a clear need to confront childhood undernutrition as the single most important risk factor for ill health in the world today. Mounting evidence for the efficacy of simple interventions, such as exclusive breastfeeding and improved sanitation, should aid governments and society in tackling this threat. A
FURTHER READING Amadi B, Fagbemi AO, Kelly P, et al. Reduced production of sulfated glycosaminoglycans occurs in Zambian children with kwashiorkor but not marasmus. Am J Clin Nutr 2009; 89: 592e600. Ashworth A, Chopra M, McCoy D, et al. WHO guidelines for management of severe malnutrition in rural South African hospitals: effect on case fatality and the influence of operational factors. Lancet 2004; 363: 1110e5. Berkley J, Mwangi I, Griffiths K, et al. Assessment of severe malnutrition among hospitalized children in rural Kenya: comparison of weight for height and mid upper arm circumference. J Am Med Assoc 2005; 294: 591e7. Bhutta ZA, Chopra M, Axelson H, et al. Countdown to 2015 decade report (2000e10): taking stock of maternal, newborn, and child survival. Lancet 2010; 375: 2032e44. Black RE, Allen LH, Bhutta ZA, et al. Maternal and child undernutrition: global and regional exposures and health consequences. Lancet 2008; 371: 243e60.
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Children presenting to healthcare facilities should routinely have their nutritional status assessed. Treatment of the 2 main forms of malnutrition should be standardized and take account of reductive adaptation to prevent avoidable deaths. Treatment programmes should be community based where possible but the most severely affected children will still need intensive in-patient management. Strategies to prevent malnutrition should be aimed at both individuals and communities and must tackle the wide range of medical, social and economic causes.
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