Digestion and nutrition.

Introduction
History Where growth or nutrition problems are suspected, take a careful feeding history. Ask the parent to tell you everything the child has eaten and drunk in the last 24 hours, talking them through the meal times and asking about snacks and drinks between meals. Ask specifically for quantity of milk and squash drunk and how many portions of fruit and vegetables are eaten daily. Are there battles over the child s eating! "oes the child eat alone or with other family members! A food diary kept by the parents over a # or 4 day period is sometimes useful.

Table 1 History Which milk

Infant feeding history Comments $reast or formula. If formula note which one and details of reconstitution. In breast fed infants does mother have a good milk supply! In formula fed infants note volumes

%ow much feed.

%ow often %ow long does the feed take to complete 'haracteristics of feeding.

offered and taken. &ote the times of feeds in the previous 24 hrs

%ungry, windy, apathetic, slow, sleepy etc.

(ey symptoms of gastrointestinal problems in children are vomiting, diarrhoea and abdominal pain. )*able 2+ 1

Table 2 Symptoms ,omiting

Symptoms of gastrointestinal problems Enquire about ,olume - dribble onto clothes or a stomach full &ature - effortless, forceful )onto child or parent+, pro.ectile )several feet away+, single vomit or run of vomits /requency 0elationship to feeds and posture.

"iarrhoea

1resence of blood or bile in vomit. %ow often - a bowel action after each feed is common if breast fed 'onsistency - pure liquid, porridgey or mi2ed te2ture, undigested food 'olour

'onstipation

1resence of blood or mucus %ow often, is wind passed between times %ow difficult - straining to go or with3hold, painful 4oiling

Abdominal pain

'hild s attitude to the problem 4ite5radiation! 1attern of onset and relationship to food, stress, medication 'olicky or constant duration Waking the child at night )this implies an organic cause+

62amination
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4tart by looking generally at the child and their nutrition. "o they look thin! Are there loose folds of skin in the groin or around the buttocks! &ote the health of hair, skin, nails and teeth and look for .aundice and pallor 7ently e2amine the abdomen. 62plain what you are going to do and get the child to tell you if it hurts. Watch the child s face for signs of discomfort as you e2amine. "on t forget to e2amine hernial orifices and the genitalia in boys with acute abdominal pain. *he following scheme is recommended8

General points Assess the child s growth - is there poor weight gain! 9ook for .aundice or anaemia Assess the child s muscle bulk - wasting of the gluteal muscles is seen in coeliac disease. Is there any finger clubbing )see *able #, p:+ Any evidence of assisted feeding such as a nasogastric tube or a gastrostomy

Inspe tion 9ook for abdominal distension. If present is it symmetrical! Are there any operative scars! 9ook for hernias Inspect the genitalia. "o they look normal. Are there any signs of puberty!

!alpation 9ook at the child s face while palpating the abdomen. 4tart palpating at a point furthest away from any tenderness. A reluctant child may be put at ease if their own hand is used, with the e2aminer s hand overlying. /eel for any tenderness. Is there any rebound tenderness or guarding! Identify any enlargement of the liver, kidneys or spleen. *he liver should be felt for along a path from the right iliac fossa to the right hypochondrium. *he spleen should be felt for on a path from the right iliac fossa to the left hypochondrium. It is common to feel the liver edge and the tip of the spleen in younger children. ;any children have a more prominent liver edge with concurrent respiratory disease as hyperinflation pushes the liver down.

*he lower pole of each kidney may be felt by palpating with both hands 3 one behind the flank pressing forwards towards the other .

/eel for other masses. 'ommonly faeces are palpable in the left iliac fossa. 'onstipation is common, and may be associated with tenderness over the caecum

due to gaseous distension. In severe constipation the whole lower abdomen may be distended.

!er ussion 'an be useful in delineating the edge of the liver or spleen and in e2amining for ascites.

"us ultation 9isten for bowel sounds in the acutely unwell child. 0ectal e2aminations in childhood *his is never a routine e2amination. It is rarely helpful. 'areful thought must be given to undertaking this e2amination in any child.

"ssessment of Gro#th Well infants are often weighed regularly to reassure parents and professionals. 0esults are recorded in the 1ersonal 'hild %ealth 0ecord - usually a 0ed $ook in the <nited (ingdom.

/ailure to gain weight is a cause of stress and an2iety. Infants may take up to =4 days to regain their birth weight. /ailure to regain birth weight by =4 days, or a loss of over =>? of birth weight needs assessment. $irth weight usually doubles by 4 months and trebles by =2 months. 0eview the child s growth in length, head growth and weight gain. /ailure to grow in any of the parameters is of concern, but weight loss needs urgent investigation at any age. A child whose weight crosses

two centile lines is @failing to thrive and nutritional, physical or psychological causes should be sought.

Infant feeding $reast /eeding *he is no doubt that Abreast is bestB and with the correct support, advice and encouragement the ma.ority of babies will thrive on breast feeding until at least 4 months of age. *he milk is easily digested with low antigenicity and anti3infective properties. $reast feeding is good for mother child bonding, convenient and free.

1roblems and 'ontraindications to breast feeding are very few )see table #+

Table $

!roblems #ith breast feeding %anagement 4upport mother )%ealth ,isitor, ;idwife, support groups+ 0are, require specialist advice 'areful monitoring of infant 'ontraindication in developed countries 'heck safety in $&/ or with pharmacist 62pressed breast milk given via &7 tube 'ontraindicated

!roblem /eeding difficulties Inborn errors of metabolism ;aternal drug5alcohol abuse ;aternal %I, ;aternal medication 1rematurity *uberculosis

$reast fed babies feed Aon demandB. *his will be at least every 23# hours for the first few weeks, gradually increasing to every #34 hours by day and :3C hours overnight by a few months of age. $abies who are getting enough breast milk settle after feeds, have :3C wet nappies per day, tend to pass soft stool quite often, may be after every feed, and show growth on their centile charts.

$reast milk is nutritionally complete for term infants until 43: months of age. ;others who are unable or choose not to breast feed directly should be actively encouraged to e2press. 62pressing should be started as soon as possible after delivery to take advantage of the normal physiological changes that occur after the birth.

$ottle3fed infants should be fed on demand, to start with a term infant will take D>3 E>mls E or C times per day, increasing to =C>322>mls D times a day by # months of age. *eats are available and different types suit different babies.

Alternative milks 'ows milk based formulae are modified to resemble breast milk as closely as possible. 4tandard /ormula are 4>? casein :>? whey and those marketed for A%ungrier InfantB are C>? casein 2>? whey. 4tandard formulae are suitable up to =2 months of age and the casein based feeds have no proven benefit. 4oy milks are not recommended under : months of age due to concern about levels of naturally occurring plant oestrogens. /urthermore, 2>? of infants with cows milk allergy show cross reactivity with soy protein.

7oat or sheep milk is not recommended due to high solute load, similar immunogenic potential to cows milk and concerns about sterility.

%ypoallergenic formulae are recommended for infants with milk allergy or considered at risk for developing it. *hey are either highly hydrolysed cow s milk )hydrolysed feeds+ or composed of amino acids )elemental feeds+.

Infant weaning *he best time for weaning appears to be 43: months of age, even if the baby was born prematurely. 0enal and gastrointestinal immaturity means earlier weaning is inadvisable, and delaying longer seems to increase the risk of feeding difficulties. *he World %ealth Frganisation guidelines suggest e2clusive breast feeding until : months, which is appropriate to developing countries where risk of infection is greater.

Weaning foods should be introduced gradually, a new one every few days, starting with very simple vegetable purees or baby rice. *he comple2ity and range of tastes and te2tures are gradually increased. *here should be no added salt or sugarG gluten and eggs may be introduced from : months. 'ows milk is not used as the main drink until = year of age but it may be incorporated into solids from : months. It is recommended that full fat milk is given until at least 2 years of age. Alternative formula milks )Afollow onB milks+ are available with higher levels of iron, vitamin " and protein content.

Diet for older hildren *he principles of healthy eating are a diet that is roughly 4>? carbohydrate, #D? fat and =D? protein, and includes five portions of fruit and vegetables per day, plenty of fluids, ideally water rather than squash and other soft drinks, and refined carbohydrate in moderation.

,itamins

,itamin deficiency syndromes are very rare in the developed world e2cept for children with malabsorption. ,itamin A deficiency is still the most important cause of blindness in the world. ,itamin A supplementation can also reduce the risk of death from infectious disease.

,itamin " deficiency causes 0ickets. In the <(, this is seen primarily in children from ethnic minorities, often with little skin e2posure to sunlight, and diets low in calcium. 'hildren may present with neurological features of hypocalcaemia, or with failure to thrive and hypotonia, or with weak bones manifesting as knock knees or bow legs.

Iron deficiency Iron deficiency is common and may have developmental, educational and growth consequences. 1oor nutrition, chronic disease and blood loss all contribute.

Fbesity Fbesity is a rapidly growing problem for children, their families and society. In the vast ma.ority there is a simple imbalance between energy ingested and energy consumed. /actors contributing include high energy snack and fast foods, tendency for larger portion siHes, decreased levels of activity amongst children at school and social and cultural pressures.

6ducation about the short and long term risks of obesity and constructive advice on diet and e2ercise are important, but need to include other family members. 4upport groups may help but drugs are inappropriate. *he aim is to maintain weight, rather than weight loss, whilst height growth continues. 9

1arenteral &utrition
Intravenous feed containing carbohydrate, fat, protein, minerals, vitamins and trace elements are used primarily as an ad.unct to enteral feeds or short term replacement for those who cannot tolerate enteral feeds, for e2ample after bowel surgery. /ive to ten per cent of children will have complications from the

intravenous feeding line, including sepsis, blockage and embolic phenomenon. 1rogressive impairment of liver function may occur with long3term parenteral nutrition, and may culminate in cirrhosis and liver failure.

The &omiting Infant

,omiting in infancy is a fact of lifeI Almost every baby will posset, bringing up a small amount of milk after a feed, often with wind. It is necessary to distinguish this from significant gastro3oesophageal reflu2 or vomiting due to obstruction, or from neural causes. *he case scenarios describe some characteristic histories and their causes.

7astro oesophageal reflu2 Anna, a six month old infant presented with a history of vomiting since birth. What had initially seemed to be harmless positing of small amounts after feeds has progressed to bother the whole family. The vomiting was worse after feeds or if she was being moved or carried but could occur at any time. It seems effortless with enough produced to stain everyones clothes and the floor in the vicinity. The vomit containing partly digested milk. The clinical picture of a fraught family with a cheerful well nourished thriving baby was characteristic!

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7astro oesophageal reflu2 is usually a benign disorder which resolves spontaneously between si2 and =2 months of age as infants spend more time upright, solids are introduced and natural anti3reflu2 mechanisms develop. 0eassurance is the mainstay of treatment. 1arents can try smaller volumes of milk given more frequently and positioning the infant with head elevated after feeds. /eed thickeners may help.

9ess commonly, reflu2 is severe and infants may fail to thrive. Fesophagitis may develop. 0eflu2 is commonly troublesome in infants with cerebral palsy, broncho3 pulmonary dysplasia and milk intolerance.

Investigation A barium swallow and meal will usually confirm reflu2 and may identify abnormalities of oesophageal motility, strictures or hiatus hernias. 6ndoscopy will enable confirmation of oesophagitis, and stricture formation. It is useful for diagnosis of reflu2 associated with allergy )eosinophilic oesophagitis+ which may not be associated with significant acid reflu2. A p% study will confirm the severity of reflu2 by demonstrating the duration of acid reflu2 into the lower oesophagus.

*reatment options include dietary substitution, antacid therapy, prokinetic drugs or surgery )fundoplication+.

1yloric stenosis Adam, a six week old infant presents with a " day history of progressive and dramatic vomiting which does not contain bile. This occurs during or after meals 11

and the vomit is pro#ected across the room so carers have learned to keep their distance. $espite the vomiting the baby seems hungry, feeding avidly until the vomiting occurs. %n examination the baby has lost weight, is constipated and mildly dehydrated.

1yloric stenosis describes a pathological thickening of the pyloric sphincter, which hypertrophies over the first few weeks of age. *his causes obstruction of the gastric outlet. It affects =8=D> males and =8ED> female infants. It is more common in first3born children and in those with an affected parent.

"iagnosis can be made by a Atest feedB. *he hypertrophied muscle is palpable during a feed. ,isible gastric peristalsis may be seen through the abdominal wall. <ltrasound or barium e2amination will usually confirm the diagnosis. *he loss of large amounts of hydrochloric acid from the stomach leads to high plasma bicarbonate and chloride deficiency with a resultant hypochloraemic alkalosis.

'areful resuscitation is needed before pyloric stenosis is corrected by 0amstedt s pyloromyotomy. *his involves longitudinally dividing the pyloric muscle but not the mucosa under general anaesthetic. Infants usually tolerate milk within a few hours of the operation.

$ilious ,omiting in Infancy &ade, a six day old baby presented with bile stained vomiting. 'he was not feeding and her bowels have not been open for () hours. The abdomen was soft with minimal distension. There was minimal tenderness, and no evidence of a hernia.

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*eeding was stopped, a nasogastric tube sited, and intravenous fluids commenced. As she had previously passed meconium, an intestinal atresia was excluded. 'he had an urgent abdominal + ray which showed a paucity of bowel gas, suggesting upper small bowel obstruction. 'he was transferred urgently to a paediatric surgery centre, where, after a diagnostic contrast study showed malrotation, she underwent urgent surgery with fixation of the caecum to the posterior abdominal wall, and appendicectomy.

$ile stained vomiting is an indicator of serious surgical pathology, and requires urgent assessment. Abdominal J3rays may reveal evidence of obstruction with fluid levels and dilated small or large bowel, or may show a displaced caecum indicating malrotation as in this case. <pper or lower 7I contrast studies will clarify the picture. *his congenital anomaly results in the mid3gut twisting on its mesentery causing a volvulus, and potentially, infarction from the mid3duodenum to the mid3transverse colon.

'ongenital intestinal atresias most commonly affect the small bowel, particularly the duodenum. A significant number of affected infants have "own s 4yndrome. *reatment is with resection of the atretic segment.

Hirs hprung's disease occurs due to congenital absence of ganglion cells in the intramuscular and submucous layers of the large intestine, e2tending pro2imally from the anus. *he affected bowel does not e2hibit peristalsis and pro2imal

obstruction or enterocolitis )severe diarrhoea and abdominal distension+ may occur. In the first instance, treatment is with a colostomy pro2imal to the

aganglionic bowel )determined by intra3operative histology of AfroHen sectionsB+, 13

followed later by restoration of bowel continuity, with a Apull3throughB procedure, typically around a year of age. 'hildren with "own s 4yndrome are also at greatly increased risk of %irschsprung s "isease. 0arely, if only a very short segment of aganglionic bowel is present, the main symptom is constipation )see below+, however in this case, symptoms will be present from very early life, usually from the neonatal period.

Strangulated hernias may also produce bilious vomiting secondary to intestinal obstruction.

/eeding problems A careful history will usually establish the cause and e2clude straightforward overfeeding. Infants with nasal obstruction, palate problems may feed messily, take in e2cess air and vomit. Irritable babies may gulp feeds and vomit. ;ilk intolerance may cause vomiting, with or without diarrhoea and pain )see below+.

7astroenteritis 'rinath, a formula fed child aged ,, months, developed acute diarrhoea and vomiting over a few hours. -e vomited all oral fluids and had four bowel actions in as many hours. This was associated with fever and listlessness. -is older brother had a similar, but less severe attack ( days previously. .xamination revealed moderate dehydration. The abdomen was soft with active bowel sounds.

7astroenteritis is a common infectious disease. ;ost cases are viral, and rotavirus causes over D>? of cases. $acterial causes include 4almonella, 'ampylobacter, 6.coli and 4higella, and may cause a dysentery3like picture, with blood and pus in 14

the stool, and high fever, commonly with abdominal pain. %owever, abdominal pain is not usually a prominent feature in viral gastroenteritis. Infection with 6. coli F=DE may lead to a very severe gastroenteritis, which may be complicated by acute renal failure.

Dehydration "ehydration results from depletion of electrolyte3rich gastrointestinal secretions through vomiting and5or diarrhoea. In response to these losses there is

redistribution of water by osmosis throughout the intra3 and e2tracellular fluid. *his leads to a reduction in plasma volume and stimulation of thirst. 'onsumption of hypotonic fluids depresses e2tracellular sodium concentrations, reduces plasma osmolality and A"% secretion, and reduces thirst, even if alimentary and other losses continue. *he renin3angiotensin system is stimulated, conserving sodium, and maintaining blood pressure. *hus in mild to moderate dehydration )D?+, there is minimal electrolyte disturbance, but the child will have reduced skin turgor and lethargy and reduced urine output.

As losses continue, severe dehydration results, with features of shock, including tachycardia and hypotension. *he e2tremities will feel cold. *he child is obtunded through severe dehydration with accompanying hyponatraemia.

'hildren who cannot drink sufficiently, or who have disproportionate loss of water - such as febrile infants, may develop hypernatraemia in response to dehydration. %ypernatraemic dehydration is associated with irritability, and in infants a full fontanelle, but tissue turgor is maintained )the skin has a doughy consistency+, and thus the severity of dehydration may not be appreciated. 15

In formula fed infants a short break from milk feeds may aid recovery - breast fed infants should continue to feed normally. If unable to do so, the mother should e2press milk to avoid impairment of subsequent lactation. ;ild and moderate dehydration is best treated with oral rehydration solutions containing glucose and sodium chloride, given little and often. In infants and young children, these may 4evere or hypernatraemic and administration of

be administered via nasogastric tube if necessary. dehydration requires prompt correction of

shock

glucose5saline solutions appropriate to the electrolyte status of the child. Acidosis is a common accompaniment of dehydration through a combination of lactic acidosis from impaired peripheral perfusion, and ketogenesis from rapid lipolysis. *ypically this responds well to simple or intravenous rehydration or although correction with sodium bicarbonate may occasionally be required.

0ecovery within 4C hours is the norm. *he development of a secondary cows milk protein intolerance or lactose intolerance may lead to persistent diarrhoea which can be managed using a non3cows milk formula, or a lactose free formula, for =32 months.

Intussusception. /asey, a child of six months presented screaming with bouts of colicky abdominal pain and pallor. The pain was so bad that the she seemed transiently distant and obtunded in the aftermath. There was some vomiting followed by the passage of bloody stool with mucous, likened to redcurrant #elly. A sausage shaped abdominal mass was palpable in the abdomen.

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Intussus eption in which the bowel partly invaginates, leading to ischaemia, characteristic Aredcurrant .elly stoolsB and severe episodes of pain with pallor, and vomiting, often causes diagnostic confusion. around :3K months of age. *he highest incidence is seen

It may mimic gastroenteritis, and even meningitis because of obtundation. 'hildren may be dehydrated or shocked. 4ometimes an identifiable lead point is found at the point of intussusception such as a polyp, ;eckel s "iverticulum, or enlarged 1eyer s patch. *his occurs more commonly in older children with intussusception.

*he infant may appear well between episodes of pain. *he diagnosis may be suggested on abdominal J3ray, and has a characteristic ultrasound appearance. *he intussusception may usually be reduced by a contrast enema using air or liquid contrast medium. *his should be performed in a paediatric surgical centre. 4urgery is indicated for failed reduction )2D?+, perforation, or recurrence )43=>?+.

4ystemic disease Almost any systemic disease can present with vomiting including upper respiratory tract infection, raised intra cranial pressure, urinary tract infection, metabolic and psychological disorders. Always e2amine the child carefully, and obtain a clean3 catch urine sample.

"bdominal pain

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Acute appendicitis 0icky, a seven year old boy had a history of vague central abdominal pain after school. -e ate little supper and spent a restless night during which he vomited once and passed a small loose stool. 1y the morning he had significant colicky central abdominal pain and would not eat. 1y the time he saw a doctor ,) hours into the illness the pain has begun to localise to the right iliac fossa. %n examination he looked unwell with a dry furred tongue, offensive breath and slightly sunken eyes. -is pulse was raised at ,22 per minute and his temperature was 3).4/. -e was holding himself awkwardly bent slightly and to one side and complained of pain on movement. -is abdomen was tense and tender all over but ex5uisite in the right iliac fossa, with rebound tenderness.

*his boy had acute appendicitis and surgery was performed as soon as possible. *he history above is typical but it can be difficult, especially in the preschool children, or if the appendi2 is unusually sited. Fther causes of acute abdominal pain must be considered, see table D.

Table ( Causes of a ute abdominal pain Appendicitis ;esenteric adenitis *onsillitis5<0*I 'onstipation. <rinary tract infection.5pyelonephritis 9ower lobe pneumonia. 'holecystitis &on3organic Infantile colic

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/rystal, a ( week old infant was taken to see her 67 because she had been crying inconsolably every evening for a week. 'he was feeding well and thriving with no other concerns. -er parents felt there must be something seriously wrong although she was well at other times of the day.

If history and e2amination reveal no worrying features it is highly likely this baby has colic. 'olic is e2cessive crying in a healthy infant which starts within the first few weeks of life and lasts until around 43D months. 4trictly speaking, this means at least # hours of crying a day, on # days a week for at least # weeks but it is used much more loosely to cover crying that parents perceive to be unacceptable. *he cause of colic is not known but painful peristalsis, trapped wind, lactose intoleranceG dietary protein intolerance and parental an2iety have all been suggested. It has also been regarded as a behaviour pattern with no pathology.

*here is no evidence that herbal remedies, gripe water or simethicone reduce colic. In bottle fed babies a =32 week trial of a cows milk protein free formula may be of benefit. 0eassurance is vital. Acknowledge how stressful the crying is, and that it will improve with age.

&on specific abdominal pain 8ibby, a 9 yr old girl attended outpatients with a 9 month history of bouts of colicky central abdominal pain. $uring attacks, which were common after school, she looked pale and miserable and had to lie down for 32 to :2 minutes. %n other days she repeatedly complained of abdominal pain. When 5uestioned she said she always had pain. 'he was missing a lot of school. %ver the counter remedies were ineffective. -er appetite was normal and there was no weight loss, vomiting 19

or alteration of bowel habit. 'he was growing normally. There were no abnormal signs on examination.

Abdominal pains like this affect =>? of children and can have a variety of labels including &4A1 )non3specific abdominal pain+, functional abdominal pain and sensitive bowels. ;any children will have no worrying features in the history or on e2amination and do not require investigations. In others inflammatory bowel disease, food intolerances or other causes )see table : may need to be e2cluded.

Table ) *ther auses of re urrent abdominal pain. Cause 0enal or ureteric pain. 7astritis or 7F0 1eptic ulceration. 4pinal or back problems. 0enal or gall bladder disease. 'onstipation. 7ynaecological problems. Abdominal migraine +ey lini al features 1ain e2perienced laterally or posteriorly. 6pigastric or chest pain. &ight pain. 9ateral pain. 4igns over the spine. )*enderness, limited movement+ 0ight hypochondrial pain. Laundice. <sually presents with constipation rather than pain, pain better if $F 4uprapubic or iliac fossa pain. 1eriodic pain. )monthly+ Acute attacks M53 pallor and vomiting

'urrent hypotheses suggest that there may be disordered motility or perception of motility. %owever many parents accept that occasional abdominal pains are stress related. 'areful history, e2amination and reassurance are often sufficient and the pains may respond to simple remedies like paracetamol or hot water bottles. 4ome of the children are more an2ious than their more care3free )and pain3free+

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peers. *he stresses in their lives are usually common ones, such as trying to work in a noisy classroom and arguments with friends. "on t forget to ask about bullying, but don t assume all children with pain are facing some huge problem in their livesI About half of these abdominal pains settle within a few months. In some the pains can be recurrent and a proportion will go on to develop irritable bowel syndrome as an adult.

;esenteric adenitis 'entral abdominal pain which is associated with tenderness, occurring at the same time as an <0*I is often labelled as ;esenteric adenitis. It is thought to be due to inflamed mesenteric lymph nodes with a peritoneal reaction although pathological evidence of this is often lacking. 6pisodes of pain may be recurrent.

'onstipation &emima, a 3y old girl was opening her bowels every " ; days. 'he was distressed for 4( hours beforehand and was frightened to sit on the toilet. The stools were hard and very painful to pass, with fresh blood on wiping. -er appetite was poor particularly when she had not opened her bowels for a few days. 'he was otherwise well. The problems stated : months previously after she had been ill with chickenpox.

'onstipation is common and causes a much distress to children and families. *here may be a genetic tendency but poor fluid and fibre intake, fear of defecation and development of a mega3rectum e2acerbate the problems. ;ega3rectum develops when the rectum remains over distended and the sensations of needing to defecate are lost. Involuntary soiling may then occur as liquid stool escapes 21

passed the hard impacted stool, and through a stretched anal sphincter. *his is very demoralising to child and families and the risks of social isolation and school avoidance are real. 'onstipation is rarely due to a food intolerance, endocrine causes, such as hypothyroidism, or neurological causes. In short3segment

%irschprung s disease, symptoms date back to the neonatal period. 'onstipation is manageable with enthusiastic and supportive therapy. A combination of good diet, stool softeners and osmotic la2atives will produce a soft stool. 4timulant la2atives and behavioural modification will produce regular emptying.

Chroni Diarrhoea
'hronic diarrhoea in children has diverse causes ranging from toddler diarrhoea to inflammatory bowel disease.

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Table , Clini al Chara teristi s of Different Causes of Chroni Diarrhoea Abdominal ,omiting 1ain *oddler 3 "iarrhoea /ood M Allergy 'oeliac MM "isease 'rohn s MM "isease <lcerative MM 'olitis M53 M affected MMM M M 3 M if colon MM MM MM 3 mucous M <nusual $lood Fccasional /ailure 3 ;ucous or 7rowth

Toddler diarrhoea Nuite often loose or variable te2ture stools are passed #3D times per day in a well =3# year old who is unaware or untroubled by it are very common. Also called @peas and carrots diarrhoea identifiable food is a characteristic which can cause alarm to parents. In some investigations may be necessary. It is due to rapid gastrointestinal transit. *riggers may be high fibre foods such as wheat biscuit breakfast cereals, fruit .uices, and sometimes an inadequate fat intake, due to mistaken use of AhealthyB low3fat foods, inappropriate for young children. It is a benign condition and most children grow out of it by school age. A careful history and e2amination will e2clude coeliac disease, food allergy and sugar intolerance in most cases.

-ood intoleran e 23

/ood intolerance may be caused by allergy, )cows milk protein+, immune mediated disease eg coeliac disease, enHyme deficiency eg lactose intolerance, or chemical irritation )chilliesI+

Allergy 'ows milk protein allergy is the most common food allergy, but allergic reaction can develop to other antigenic proteins including 4oya, eggs, peanuts, tree nuts, cereals and fish. 0isk of allergic reactions increases if there is a strong family history of atopy. 4ymptoms include urticaria, stridor, anaphyla2is, vomiting, diarrhoea, abdominal pain and behavioural changes.

Investigations are rarely of value although eosinophilia, raised food3related blood Ig6 levels or positive skin prick tests may be found. A therapeutic trial of food withdrawal, with symptoms reccurring on subsequent challenge is the gold standard for diagnosis.

;anagement is to strictly e2clude offending antigens from the diet.

*wenty

percent of children with cows milk protein intolerance, also develop symptoms with soya, so hypoallergenic formulae are advised. ;ost children will outgrow the allergy by 2 3D years, although in very few it is lifelong. If there is a history of severe allergic reactions, particularly anaphyla2is, food challenges should be done in hospital.

Sugar intoleran e

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*hese are due to enHyme defects and fermentation of undigested sugars causes e2plosive frothy stools with flatus, with or without abdominal pain and distension. 9actase deficiency is the most common and is usually transient )after severe gastroenteritis or untreated coeliac disease+ or due to a progressive fall in lactose production )common in non3'aucasians, who have increasing intolerance with age+. ,ery rarely, it may be congenital, when it is inherited as an autosomal recessive trait.

Coelia Disease 'oeliac disease is a small bowel enteropathy due to intolerance to the protein gluten in wheat, barley, rye and possibly oats. It can occur at any time after the introduction of gluten into the diet. *here is a very strong genetic susceptibility. *he disease affects between = in #>> and = in =>>> people. *he risk is higher with a family history, autoimmune disorders, diabetes and "own syndrome. ;ost infants and children with coeliac disease have diarrhoea, which is typically pale, fatty, offensive and Aporridge3likeB in nature. Fther symptoms are described in *able E.

Table . Symptoms of oelia disease Type of presentation 'lassical presentation )K3=C months+ 6arly presentation )OK months+ 9ate presentation )childhood3adult life+ 4creening )In patients with insulin dependent diabetes or a strong family 25 Signs and Symptoms 1ale, irritable, failure to thrive, Abdominal distension, buttock wasting ,omiting or constipation Iron deficiency anaemia, short stature, fatigue, abdominal pain, 4ubtle symptoms or none at all

history+ 'oeliac disease is a permanent condition and should not be confused with transient wheat or gluten intolerance, which may occur in children under 2y, especially after gastroenteritis.

'linical history and positive blood antibody testing )anti3gliadin, anti3endomysial, tissue tranglutaminase antibodies+ may suggest coeliac disease but a small bowel biopsy is essential to confirm the diagnosis. *ypical histology shows subtotal villous atrophy with increased lymphocytes in the lamina propria and epithelium.

*he management of coeliac disease is with a strict gluten free diet e2cluding all wheat, rye and barley. Fats may be tolerated later but are usually e2cluded to begin with. 4taple foods can be prescribed by 71s. 4upport of a paediatric dietitian is essential, and the 'oeliac 4ociety is an invaluable source of up3to3date information on gluten3free products. &on3compliance with diet risks osteoporosis, infertility and small bowel lymphoma.

Crohn's disease 'rohn s "isease affects = in =>>> adults, = in 4 of whom present in adolescence. It causes a inflammation of the whole bowel wall )transmural involvement+G anywhere from mouth to anus, with the terminal ileum being most often affected. *he presentation is often delayed with non specific symptoms such as growth failure, delayed puberty, anore2ia, poor concentration, lethargy, malaise and deteriorating school or sport performance. If colitis is present, diarrhoea and abdominal pain may be a feature. 62amination may show evidence of malnutrition, linear mouth ulcers and perianal skin tags. *enderness or abdominal masses are 26

variable. Inflammatory markers such as 640 usually parallel disease activity, but the nature and e2tent of inflammation need to be demonstrated. *his is usually by upper gastrointestinal endoscopy and colonoscopy with biopsy.

;anagement begins with induction of remission using nutritional therapy )elemental or hydrolysed feed and food e2clusion+ or systemic steroids. Fn3going maintenance treatment with D Amino34alicylate derivatives )4alaHopyrine, mesalaHine+, immunosupression )aHathiaprine, methotrea2te+ or immune therapy )monoclonal anti3*&/ alpha+ may be needed. 4urgery should be avoided whenever possible but may be needed for complications such as obstruction, fistulas or failed medical treatment. *ypically the course is relapsing into and throughout adult life.

/l erati0e olitis <lcerative 'olitis is rarer than 'rohn s disease, in children, but the disease is more likely to be a pan3colitis in contrast to adults. <lcerative colitis typically presents with cramping abdominal pain with diarrhea containing blood and5or mucous. <rgency of stool is often a feature and may be very distressing. Anore2ia, weight loss or e2tra intestinal manifestations may be present such as erythema nodosa, arthritis, liver disease or eye lesions. 'olonoscopy and biopsy are required to confirm the diagnosis. *ypical histology shows mucosal inflammation with crypt abscesses and goblet cell depletion.

*reatment involves the Induction of remission with systemic steroids. *his is followed by maintenance treatment with D3amino3salicylate derivatives, low dose steroids or immunosupression )aHathiaprine, methotrea2te+. *otal colectomy may 27

be needed for complications such as to2ic megacolon, hemorrhage or failed medical treatment. 4urveillance colonoscopy is performed annually when disease has been active for => or more years to reduce the very real risk of carcinoma.

1aundi e in Children
Laundice arises from elevation of bilirubin. %aemolytic disorders cause .aundice, or it may arise from impaired clearance of bilirubin in hepatocellular dysfunction, as occurs with hepatitis, or from biliary obstruction, such as biliary atresia.

The Infant #ith *bstru ti0e 1aundi e 7eter was referred by his 67 at 4" days of age, after his health visitor noticed that he was still #aundiced. -is weight gain was poor, and he had dark urine with putty coloured stools. urobilinogen. <rine testing was positive for bilirubin, but negative for

-is bilirubin level was ,()=mol>l, the ma#ority of which was

con#ugated. -e had abnormal coagulation. 1iliary atresia was suspected and he was urgently referred to a tertiary specialist centre. subse5uently confirmed, and he underwent surgery. 1iliary atresia was

*he young infant with obstructive .aundice requires urgent evaluation to e2clude biliary atresia. In biliary atresia, there is progressive obliteration of the e2tra3 and intra3hepatic bile ducts, leading to hepatocellular in.ury, with cirrhosis and portal hypertension. 4urgery to construct a bile conduit )(asai procedure+ is performed as soon as possible. If surgery is unsuccessful, then liver failure results, requiring liver transplantation. If bile drainage is achieved, then the progression of liver disease may be slowed, although ascending cholangitis, malnutrition due to fat

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malabsorption, and portal hypertension leading to oesophageal varices and consequent gastro3intestinal haemorrhage are common complications.

*he differential diagnosis of obstructive .aundice includes congenital holedo hal yst affecting the e2trahepatic biliary tree, and neonatal hepatitis. &eonatal

hepatitis presents with prolonged obstructive .aundice and evidence of hepatocellular dysfunction. It is usually idiopathic, but infective, endocrine and metabolic causes - notably galactosaemia and alpha3=3antitrypsin deficiency must be e2cluded.

A baby with prolonged jaundice 1ridget was a term baby who had difficulty establishing feeds. 'he presented with sepsis at ,: days of age. 'he had vomiting, diarrhoea, and hypoglycaemia, and was lethargic and #aundiced. .xamination revealed hepatomegaly. The liver en?ymes were elevated, with an elevated con#ugated bilirubin, and abnormal coagulation studies. 1lood cultures were positive for 6. coli. 0educing substances were present in the urine and 1ridget was found to have reduced levels of galactose , phosphate uridyl transferase @6A8 , 7<TA, confirming the diagnosis of galactosaemia.

7alactosaemia results from an inability to metabolise galactose. *o2ic metabolites accumulate with resultant hepatic and renal to2icity and cataracts. %igh levels of galactose3=3phosphate provide an ideal substrate for 6. coli sepsis, which complicates half of cases. It is treated by elimination of all sources of lactose and galactose, which includes breast and bottled milks. *his rare condition is inherited in an autosomal recessive manner. "espite early treatment, learning difficulties 29

are common, notably verbal dyspra2ia. 7irls are almost always infertile due to premature ovarian failure.

Hepatitis
%epatitis is characterised by .aundice with dark urine containing bilirubin and urobilinogen, sometimes with other features of hepatocellular dysfunction.

Hepatitis " is a common infectious disease. *he virus spreads by the faeco3 oral route and cause infectious .aundice. *he ma2imum period of infectivity occurs in the two weeks prior to onset of .aundice. *here is little systemic upset but often abdominal pain, vomiting and loss of appetite which may last several weeks. *ravellers to endemic areas, or e2posed contacts, such as other family members at risk of infection, may receive hepatitis A immunisation.

Hepatitis 2 or C may be acquired from contaminated body fluids, or more often, from congenital infection. 'hronic hepatitis $ and ' may cause cirrhosis and hepatocellular carcinoma. 4creening of children Aat riskB of hepatitis $ is recommended in the <(, with e2posed children receiving %epatitis $ vaccine. 'hildren with chronic hepatitis secondary to hepatitis $ or ' may respond to interferon and other antiviral therapy.

Epstein32arr 0irus, the cause of glandular fever, is also commonly associated with a mild, often sub3clinical hepatitis.

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"utoimmune hepatitis and s lerosing

holangitis are often associated with

inflammatory bowel disease. *he liver problems may be the first manifestation of this. Autoimmune hepatitis is characterised by elevated autoantibodies,

particularly anti3nuclear, and liver3kidney3microsomal antibodies. 'irrhosis is often present at diagnosis, and indicates a poorer prognosis. aggressive immunosuppressive therapy. *reatment is with

*bstru ti0e 1aundi e in Childhood Fbstructive .aundice in older children is seen with choledochal cyst )see above+, and gall stones secondary to chronic haemolysis or hypercholesterolemia. 'hildren requiring long3term parenteral nutrition are at high3risk of progressive liver disease and resultant liver failure.

-ulminant Hepati -ailure /ulminant %epatic /ailure )/%/+ is fortunately rare, and manifests with encephalopathy, hepatocellular dysfunction )impaired coagulation,

hypoalbuminaemia with oedema, acidosis, hypoglycaemia+ renal failure and sepsis. *he commonest cause in the <( is para etemol poisoning, followed by fulminating viral infections. Fther causes include metabolic diseases such as

Wilson s disease, 0eye s syndrome and disorders of fatty acid metabolism. Wilson s disease is an autosomal recessive disorder presenting with severe liver disease, typically /%/, or in teenagers with neurological manifestations. 0eyes syndrome is an acute encephalitis with liver failure and renal damage. *he cause is not known but aspirin increases risk, especially in association with chicken po2, and should not be given to children under the age of =2y.

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