Growth and nutrition are closely related, such that the mean height of a population reflects its nutritional status. Thus, in the developed world, people have become taller. Height is adversely affected by lower socioeconomic status and increasing number of children in families. Children’s size increases amongst populations emigrating from poor to more affluent countries.

Disease in adult life

Evidence suggests that undernutrition in utero resulting in growth restriction is associated with an increased incidence of coronary heart disease, stroke, non-insulin-dependent diabetes and hypertension in later life (Fig. 12.3). There is also a similar but weaker association with low weight at 1 year of age. The mechanism is unclear, but it is recognised that fetal undernutrition leads to redistribution of blood flow and changes in fetal hormones, such as insulin-like growth factors and cortisol. Alternatively, it may be the rapid, postnatal growth (catch-up) seen in babies suffering from intrauterine growth restriction that is the causal factor.

Summary

Nutritional vulnerability

Infants are more vulnerable to poor nutrition because of:

• Poor stores of fat and protein

• Extra nutritional demands for growth – the weight of a term infant doubles by 4 months and trebles by 1 year.

• More frequent intercurrent illnesses that reduce food intake and increase nutritional demands.

Advantages (see Box 12.1)

In developing countries, where the environment is often highly contaminated, breast-feeding dramatically improves survival during infancy as a result of reduced gastrointestinal infection. Consequently, breast-feeding is one of the four most important World Health Organization strategies for improving infant and child survival. The superiority of breast milk over modern adapted cow’s milk formulae is less easy to prove in developed countries. This is partly because it is impossible to conduct randomised studies and partly because of confounders such as social class, education and smoking.

However, there is convincing evidence that gastrointestinal infection is less common in breast-fed infants even in developed countries. There is also evidence that human milk feeds reduce the incidence of necrotising enterocolitis in preterm infants.

Many mothers who breast-feed find that it helps them establish an intimate, loving relationship with their baby. However, establishing breast-feeding is not always straightforward, and many mothers need help and encouragement.

Breast-feeding is associated with a reduced incidence of obesity, diabetes mellitus and hypertension in later life. There is also a reduction in breast cancer in mothers who breast-feed.

Potential complications (Box 12.2)

As one cannot readily tell how much milk a baby is taking from the breast, the baby’s weight should be checked regularly, every few days in the first couple of weeks, then weekly until feeding is well established. Successful breast-feeding of twins can be achieved, but is more difficult (Fig. 12.4). It is rarely possible to totally breast-feed triplets and higher-order births. Preterm infants can be breast-fed, but the milk will need to be expressed from the breast until the infant can suck. Maintaining the supply of milk can be a problem for mothers of preterm babies.

While two-thirds of mothers in the UK initially breast-feed, this proportion rapidly declines during the first few months (Fig. 12.5). Nearly 90% of social class I mothers start breast-feeding, but only 60% of mothers from social class V. Breast-feeding is restrictive for the mother, as others cannot take charge of her baby for any length of time. This is particularly important if she goes to work and may delay her return, which may cause financial hardship for the family. Facilities for breast-feeding in public places remain limited. Failure to establish breast-feeding will sometimes cause significant emotional upset in the mother.

Establishing breast-feeding

Colostrum, rather than milk, is produced for the first few days. Colostrum differs from mature milk in that the content of protein and immunoglobulin is much higher. Volumes are low, but water or formula supplements are not required while the supply of breast milk is becoming established.

The first breast-feed should take place as soon as possible after birth. Subsequently, frequent suckling is beneficial as it enhances the secretion of the hormones initiating and promoting lactation (Fig. 12.6).

Primates probably do not breast-feed instinctively. Monkeys bred in captivity in zoos have to be taught how to breast-feed by their keepers. It is therefore important that breast-feeding should have as high a public profile as possible. Women who have never seen an infant being breast-fed are less likely to want to breast-feed themselves. Education in schools and during pregnancy about the advantages of breast-feeding is advantageous. Advice and support from other women who have breast-fed may be important in dealing with early problems such as engorgement or cracked nipples.

Formula-feeding

Infants who are not breast-fed require a formulafeed based on cow’s milk. Unmodified cow’s milk is unsuitable for feeding in infancy as it contains too much protein and electrolytes and inadequate iron and vitamins. Even after considerable modification, differences remain between formula feeds and breastmilk (Table 12.2)

All milks currently available in the UK have been modified to make their mineral content and renal solute load comparable with that of mature human milk. Since these changes were introduced in the UK (in the 1970s), there has been an impressive reduction in the incidence of hypernatraemic dehydration in infants with gastroenteritis. There is no evidence that any one of the many brands is superior to any other.

Introduction of whole, pasteurised cow’s milk

Breast-feeding or formula-feeding is recommended until the age of 12 months, and there are advantages in continuing to 18 months of age. Pasteurised cow’s milk may be given from 1 year of age but is deficient in vitamins A, C and D and in iron, and supplementation will be required unless the infant is having a good diet of mixed solids. Alternatively, ‘follow-on’ formulae can be used. They contain more protein and sodium than infant formulae and, in contrast to cow’s milk, are fortified with iron and vitamins. Children on cow’s milk should receive full fat milk up to the age of 5 years.

Specialised infant formula

A specialised formula may be used for cow’s milk protein allergy/intolerance, lactose intolerance (primary lactase deficiency or post-gastroenteritis intolerance), cystic fibrosis, neonatal cholestatic liver disease and following neonatal intestinal resection.

In a cow’s milk-based formula, the protein is derived from cow’s milk protein, the carbohydrate is lactose and the fat mainly long-chain triglycerides. In a specialised formula, the protein is either hydrolysed cow’s milk protein, amino acids or from soya, the carbohydrate is glucose polymer and the fat a combination of medium- and long-chain triglycerides. Medium-chain triglycerides are directly absorbed into small intestine and need neither pancreatic enzymes nor bile salts for this process.

A soya formula should not be used below 6 months of age as it has a high aluminium content and contains phytoestrogens (plant substances that mimic the effects of endogenous oestrogens). There is no compelling evidence that the use of a specialised formula prevents the development of atopy (eczema, asthma, etc.).

Weaning

Solid foods are recommended to be introduced after 6 months of age, although they are often introduced earlier as parents often consider that their infant is hungry. It is done gradually, initially with small quantities of pureed fruit, root vegetables, or rice. If weaning takes place before 6 months of age, wheat, eggs and fish should be avoided. Foods high in salt and sugar should also be avoided and honey should not be given until 1 year of age because of risk of infantile botulism. After 6 months of age, breastmilk becomes increasingly nutritionally inadequate as a sole feed, as it does not provide sufficient energy, vitamins or iron.

Causes

Failure to thrive is usually classified as organic or non-organic (Fig. 12.8). Traditionally non-organic failure to thrive is believed to be associated with a broad spectrum of psychosocial and environmental deprivation. It is estimated that 5–10% of children with failure to thrive will be on a child protection register or be subjected to abuse or neglect, while in a larger proportion, socioeconomic deprivation is an important contributing factor.

The mother may be depressed, have an eating disorder herself or have poor understanding of her baby’s needs. There may be poor housing, poverty, inadequate social support and lack of an extended family, which make good child care even more difficult. However, some studies suggest that failure to thrive is not more common in deprived than in non-deprived communities, and that identification of deprivation leads to the inappropriate application of that diagnostic label. Undernutrition is the final common pathway for poor weight gain in most cases of organic and non-organic failure to thrive, and in many cases both organic and environmental factors are present.

Organic causes are listed in Figure 12.8. Less than 5% of children with failure to thrive will be found to have an organic cause.

Clinical features and investigation

Studying the growth chart in combination with the history and examination of the child is key to its evaluation. The history should focus on:

Examination should focus on identifying signs of organic disease – dysmorphic features, signs suggestive of malabsorption (distended abdomen, thin buttocks, misery), signs suggestive of chronic respiratory disease (chest deformity,clubbing), signs of heart failure and evidence of nutritional deficiencies.

Further information about the child and family from the health visitor, general practitioner or other professionals involved with the family can be particularly helpful. Investigations to be considered are listed in Box 12.3.

In some children who are failing to thrive, a full blood count and serum ferritin may be helpful to identify iron deficiency anaemia. This is usually secondary to inadequate iron intake and correcting it may improve appetite. In most instances, no investigations are required.

Management

The management of most non-organic failure to thrive is multidisciplinary and is carried out in primary care. The health visitor is well placed to make home visits to assess eating behaviour and provide support. Direct practical advice following observation may well be beneficial. A paediatric dietician may be helpful in assessing the quantity and composition of food intake, and recommending strategies for increasing energy intake and a speech and language therapist has specialist skills with feeding disorders. Input from a clinical psychologist and from social services may also be appropriate. Nursery placement may be helpful in alleviating stress at home and assist with feeding.

Hospital admission is usually only necessary in children under 6 months with severe failure to thrive, requiring active refeeding. While hospital admission may offer the opportunity to observe and improve the mother’s method and skill in feeding, this rarely transfers from the artificial hospital environment to home. In extreme cases, hospital admission can be used to demonstrate that the child will gain weight when fed appropriately.

Outcome

Follow-up studies suggest that children with non-organic failure to thrive continue to under-eat (see Case History 12.1). Although there is usually a gradual improvement in the preschool years, a lasting deficit is common and these children tend to remain underweight. In contrast, impairment of development is only short term.

Case History

12.1 Non-organic failure to thrive

Jamie, aged 11 months, was causing concern to his health visitor as he was not putting on any weight (Fig. 12.9). She arranged for him to be assessed by his general practitioner, who found that he was otherwise well. His mother was a single parent who left school at 16 years and had Jamie at the age of 18. They lived in a high-rise flat and Jamie’s mother received income support. Her own mother lived on the other side of the city.

On visiting the home, the health visitor found Jamie’s mother to be tense and anxious. In particular, she was worried about making ends meet. She fed Jamie the same food as she ate herself, together with pasteurised milk, which she had started at 6 months of age. The meals were chaotic. After a few mouthfuls, Jamie stopped eating and his mother did not coax him but became frustrated and angry.

Jamie’s health visitor suggested strategies for increasing Jamie’s food intake (Box 12.4). She continued to provide support and encouragement to his mother and arranged a nursery placement for Jamie. By 2 years of age, he had caught up by one centile line, but still ate erratically.

Box 12.4

Strategies for increasing energy intake

Dietary

• Three meals and two snacks each day

• Increase number and variety of foods offered

• Increase energy density of usual foods (e.g. add cheese, margarine and cream)

• Decrease fluid intake, particularly squash

Behavioural

• Have meals at regular times, eaten with other family members

• Praise when food is eaten

• Gently encourage child to eat, but avoid conflict

• Never force-feed.

After Wright CM. 2000. Identification and management of failure to thrive: a community perspective. Archives of Disease in Childhood 82:5–9.

Assessment of nutritional status

Malnutrition must be recognised and accurately defined for rational decisions to be made about refeeding. Evaluation is divided into assessment of past and present dietary intake, anthropometry and laboratory assessments (Fig. 12.10).

Nutritional assessment

Consequences of malnutrition

Malnutrition is a multisystem disorder. When severe, immunity is impaired, wound healing is delayed and operative morbidity and mortality increased. Malnutrition worsens the outcome of illness, e.g. respiratory muscle dysfunction may delay a child being weaned from mechanical ventilation. Malnourished children are less active, less exploratory and more apathetic. These behavioural abnormalities are rapidly reversed with proper feeding, but prolonged and profound malnutrition can cause permanent delay in intellectual development.

The role of intensive nutritional support

Children with chronic disorders who are malnourished will grow better if given supplemental nutritional support, which may be provided by the enteral or parenteral route.

Marasmus and kwashiorkor

Globally, over one-third of childhood deaths are attributable to undernutrition, which leaves the child susceptible and unable to survive common infections.

The World Health Organization recommends that nutritional status is expressed as:

• Weight for height – a measure of wasting and an index of acute malnutrition (Fig. 12.11). Severe malnutrition is defined as a weight for height more than −3 standard deviations below the median plotted on the WHO standard growth chart. This corresponds to a weight for height <70% below the median.

• Mid upper-arm circumference (MUAC) – <115 mm is severe malnutrition

• Height for age – a measure of stunting and an index of chronic malnutrition

Severe protein-energy malnutrition in children usually leads to marasmus, with a weight for height more than −3 standard deviations below the median, corresponding to <70% weight for height, and a wasted, wizened appearance (Fig. 12.12). Oedema is not present. Skinfold thickness and mid-arm circumference are markedly reduced, and affected children are often withdrawn and apathetic.

Kwashiorkor is another manifestation of severe protein malnutrition (Fig. 12.13), in which there is generalised oedema as well as severe wasting. Because of the oedema, the weight may not be as severely reduced. In addition, there may be:

It is unclear why some children with protein-energy malnutrition develop kwashiorkor and others develop marasmus. Kwashiorkor is a feature of children reared in traditional, polygamous societies, where infants are not weaned from the breast until about 12 months of age. The subsequent diet tends to be relatively high in starch. Kwashiorkor often develops after an acute intercurrent infection, such as measles or gastroenteritis. There is some evidence that kwashiorkor is a manifestation of primary protein deficiency with energy intake relatively well maintained or, alternatively, that it results from excess generation of free radicals.

Malnutrition

Rickets

Rickets signifies a failure in mineralisation of the growing bone or osteoid tissue. Failure of mature bone to mineralise is osteomalacia.

Clinical manifestations

The earliest sign of rickets is a ping-pong ball sensation of the skull (craniotabes) elicited by pressing firmly over the occipital or posterior parietal bones. The costochondral junctions may be palpable (rachitic rosary), wrists (especially in crawling infants) and ankles (especially in walking infants) may be widened and there may be a horizontal depression on the lower chest corresponding to attachment of the softened ribs and with the diaphragm (Harrison sulcus) (Figs 12.15, 12.16). The legs may become bowed (see Fig. 12.15). The clinical features are listed in Box 12.6 (see also Case History 12.2).

Rickets

Box 12.6

Clinical features of rickets

• Misery

• Failure to thrive/short stature

• Frontal bossing of skull

• Craniotabes

• Delayed closure of anterior fontanelle

• Delayed dentition

• Rickety rosary

• Harrison sulcus (Fig. 12.16)

• Expansion of metaphyses (especially wrist)

• Bowing of weight-bearing bones

• Hypotonia

• Seizures (late).

Management

Nutritional rickets is managed by advice about a balanced diet, correction of predisposing risk factors and by the daily administration of vitamin D₃ (cholecalciferol). If compliance is an issue, a single oral high dose of vitamin D₃ can be given, followed by the daily maintenance dose. Healing occurs in 2–4 weeks and can be monitored from the lowering of alkaline phosphatase, increasing vitamin D levels and healing on X-rays, but complete reversal of bony deformities may take years.

Summary

Rickets

• Nutritional – has re-emerged in the UK in Asian and black infants exclusively breast-fed into late infancy

• Diagnosis – serum calcium is low or normal, phosphorus low, plasma alkaline phosphatase greatly increased, 25-hydroxyvitamin D low and parathyroid hormone elevated

• X-ray features – cupping and fraying of the metaphyses and widened epiphyseal plate.

Case History

12.2 Seizures and rickets

Mohammed, a 13-month-old Somalian boy, was admitted to the A&E department with a generalised afebrile seizure. This was initially controlled with per rectum diazepam. Some 20 minutes later he had another generalised seizure and needed intravenous anticonvulsant to control his seizure.

His mother said that he was a healthy child. He was born at term, birthweight 3.1 kg, and was still breast-fed. Some weaning foods were started at 7–8 months, but he preferred feeding at the breast. He had only recently begun to sit without support.

His weight and head circumference were on the 2nd–9th centile. He had marked frontal bossing, widened wrist (Fig. 12.17) and other epiphyses, Harrison sulci, wide anterior fontanelle, craniotabes and a rachitic rosary. He would not take his weight on standing.

Investigations showed a low calcium and phosphate level, a high alkaline phosphatase and parathyroid hormone level and a very low vitamin D level, confirming rickets. Liver and renal function tests were normal and coeliac screen was negative. His wrist X-ray showed characteristic features (Fig. 12.18). A detailed dietetic history revealed a diet deficient in calcium and vitamin D, confirming nutritional rickets as the cause.

Dietetic input was provided. He was started on oral vitamin D and his solid food intake was increased to ensure that he was receiving sufficient calcium and vitamin D in his diet. His rickets resolved.

Definitions

In children, the body mass index (BMI = weight in kg/height in metres²) is expressed as a BMI centile in relation to age and sex-matched population. By convention in the UK, the 1990 chart is used (Fig. 12.19). For clinical use, overweight is a BMI >91st centile, obese is a BMI >98th centile. Very severe obesity is >3.5 standard deviations above the mean; extreme obesity >4 standard deviations. For children over 12 years old, overweight is BMI ≥25, obese ≥30, very severe obesity BMI ≥35 and extreme obesity BMI ≥40 kg/m².

In 1995, 11% of males and 12.5% of females aged 2–15 years were obese. By 2006, these figures were 17.5% and 14.5%, respectively.

Prevention

There are few randomised controlled trials and most involve complex packages of interventions. Interventions include decreased fat intake, increased fruit and vegetables, reduction in time spent in front of small screens, increased physical activity, and education. Of these, a reduction in time spent on small screens appears to be the most effective single factor.

Endogenous causes

Overnutrition accelerates linear growth and puberty. Obese children are therefore relatively tall and will usually be above the 50th centile for height. An endogenous cause, i.e. hypothyroidism and Cushing syndrome should be sought in short, obese children, in whom height velocity is decreased as height remains static in these conditions.

In children who are obese with learning disabilities, or who are dysmorphic, a syndrome should be considered. The commonest of these is Prader–Willi (obesity, hyperphagia, poor linear growth, dysmorphic facial features, hypotonia and undescended testes in males; see Chapter 8 and Figure 8.19. In severely obese children under the age of 3 years, gene defects, e.g. leptin deficiency, should be considered.

Management

Most obese children are managed in primary care. Specialist paediatric assessment is indicated in any child with complications (Box 12.7) or if an endogenous cause is suspected.

In the absence of evidence from randomised controlled trials, a pragmatic approach in any individual child based on consensus criteria has to be adopted (Box 12.8). Treatment should be considered where the child is above the 98th centile for BMI and the family are willing to make the necessary difficult lifestyle changes. Weight maintenance is a more realistic goal than weight reduction and will result in a demonstrable fall in BMI on centile chart as height increases. It can only be achieved by sustained changes in lifestyle:

Drug treatment and surgery

Drug treatment has a part to play in children over the age of 12 who have extreme obesity (BMI>40 kg/m²) or have a BMI>35 kg/m² and complications of obesity. It is recommended that drug treatment should only be considered after dietary, exercise and behavioural approaches have been started (NICE 2006).

Orlistat is a lipase inhibitor, which reduces the absorption of dietary fat and thus produces steatorrhoea. Fat intake should be reduced to avoid the unpleasant gastrointestinal side-effects. Metformin is a biguanide that increases insulin sensitivity, decreases gluconeogenesis and decreases gastrointestinal glucose absorption.

If there is evidence of insulin insensitivity (Acanthosis nigricans, see Fig. 25.2), metformin should be considered. Orlistat may be appropriate if fat intake is high.

Bariatric surgery is generally not considered appropriate in children or young people unless they have almost achieved maturity, have very severe or extreme obesity with complications, e.g. type 2 diabetes or hypertension, and all other interventions have failed to achieve or maintain weight loss. American data would suggest that laparoscopic adjustable gastric banding is the most appropriate operation.