Malnutrition in developing countries

Neonatal

37%

AIDS

3%

Injuries

3%

Measles

3%

Malaria

3%

SYMPOSIUM: NUTRITION

Malnutrition in developingcountriesEmily Walton

Stephen Allen

Based on data of the Child Mortality Estimation Group used in the UNICEF

report ‘The State of the World’s Children 2008’

Over a third of

all deaths are

attributable to

undernutrition

Other

10%

Diarrhoea

17%

Pneumonia

19%

AbstractAlthough 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 kwash-

iorkor. 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 malnutri-

tion must be a priority for the global healthcare community.

Keywords kwashiorkor; marasmus; protein-energy malnutrition; severe

acute malnutrition; underweight

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 under-

lying 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.

Emily Walton MB BS MRCPCH is ST4 in Paediatrics at the West Middlesex

University Hospital, Middlesex, UK. Conflict of interest: none.

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.

PAEDIATRICS AND CHILD HEALTH 21:9 418

Definitions and diagnosis

The diagnosis of malnutrition is based on measurement of body

size (anthropometry) and clinical signs (see Box 1).

Based on the 2006WHO 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) orwasting (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 chil-

dren 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 malnutrition-

associated 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:-

C 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

Box 1

� 2011 Published by Elsevier Ltd.

http://dx.doi.org/10.1016/j.paed.2011.04.004

Figure 3 Child with kwashiorkor (lower limb oedema, sparse depigmented

hair, dermatitis with areas of hypo- and hyperpigmentation, angular

stomatitis).


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 associ-

ated 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 well-

recognized 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, what-

ever 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.

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).


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 over-

growth leads to a T-cell mediated enteropathy with variable

degrees of villous atrophy and crypt hyperplasia. This enterop-

athy impairs nutrient digestion and absorption and, as a result of

increased mucosal permeability, may result in persistent stimu-

lation 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 kwashi-

orkor-like syndrome in animal models.



History

History of presenting complaint

C 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)

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 breast-

feeding, 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


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 perme-

ability 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 antioxi-

dants has not been shown to prevent kwashiorkor.

A recent theory is that children with kwashiorkor have

a genetic predisposition to underexpress certain glycosamino-

glycans 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 inflamma-

tory 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.

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


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 examina-

tion 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



Examination

C Temperature: fever or hypothermia

C Signs of shock: cold hands with capillary refill time greater than

3 s and weak, fast pulse and lethargic or unconscious

C Signs of dehydration (beware: may be unreliable in the

malnourished child)

C Oedema

C Signs of severe wasting (‘old man’ face, emaciated limbs, clearly

visible ribs, increased axillary skin folds, buttock wasting)

C Pallor

C Localizing signs of infection (ear, throat, skin, chest)

C Mouth (ulcers, angular stomatitis, oral thrush)

C Skin (‘flaky paint’ dermatitis, areas of hypo- and hyperpigmen-

tation 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 theymay be absent even in the presence of severe

infection due to impaired immune and inflammatory responses.

Differentiation fromHIV infection can be difficult but malnutrition

alone does not typically cause generalized lymphadenopathy.

Tuberculosis (TB)may co-present withmalnutrition but diagnosis

can be a challengee particularly because theMantoux test may be

falsely negative.Where malnutrition does not respond to standard

care, a trial of anti-TB treatment may be necessary.

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 hypo-

glycaemia 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 compli-

cations (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


these two groups is the ‘appetite test’. A good appetite is a reli-

able 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 appro-

priate health education to promote recovery and, critically,

prevent progression to severe malnutrition.

The WHO 10 steps protocol

Admission to hospital has several disadvantages. Overcrowding

permits the spread of nosocomial infections and in-patient treat-

ment 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 closemonitoring of childrenwith complications.

Highmortality rates are common: 25e30% case fatality is found in

many hospitals in Africa and rates as high as 50e70% are some-

times 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 malnu-

trition. 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.



Taken from the World Health Organization’s ‘Pocket book of Hospital care for children’ 2005.

1. Hypoglycaemia

2. Hypothermia

3. Dehydration

4. Electrolytes

5. Infection

6. Micronutrients

7. Initiate feeding

8. Catch-up growth

9. Sensory stimulation

10. Prepare for follow-up

NO IRON WITH IRON

Stabilization

Days 1–2 Days 3–7

Rehabilitation

Weeks 2–6

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 (axil-

lary 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 diar-

rhoea should be assumed to be dehydrated. Intravenous rehy-

dration 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 empiri-

cally with broad spectrum antibiotics. Local guidelines should be


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 prepara-

tion. 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 treat-

ment. 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 time-

keeping 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.




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 reha-

bilitation 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.

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 hyper-

natraemic 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 malnour-

ished 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, treat-

ment facilities must ensure that nursing staff are educated about


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 immuno-

suppression (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 staf-

fed 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 subop-

timal 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 devel-

oping world where breastfeeding is truly a life-saving interven-

tion. 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, non-

modified, 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



Practice points

C Children presenting to healthcare facilities should routinely

have their nutritional status assessed.

C Treatment of the 2 main forms of malnutrition should be stan-

dardized and take account of reductive adaptation to prevent

avoidable deaths.

C Treatment programmes should be community based where

possible but the most severely affected children will still need

intensive in-patient management.

C Strategies to prevent malnutrition should be aimed at both

individuals and communities and must tackle the wide range of

medical, social and economic causes.


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 preven-

tion 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 interven-

tions, 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

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Malnutrition in developing countries

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