Gastroenterology... Pocket Paediatrics

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Vomiting CAUSES Gastrointestinal 1.



4. 5.

Reflux: Reflux: ‘normal ‘normal’’ possetti possetting: ng:   significant GOR   hiatus hernia. Infecti Infective: ve: viral viral gastroen gastroenteri teritis: tis:

• •

infection: see Box 9.1   toxin food poisoning. •  bacterial Immunol Immunologic ogical: al: coeliac coeliac disease: disease: milk intolerance •  cow’s   other specific food allergies (e.g. fish, strawberries). •Inflamm Inflammator atory: y: appendic appendicitis itis::   mesenteric adenitis. •Obstruct Obstructiv ive: e: pyl pyloric oric stenosis: stenosis: intussusception •    volvulus •   strangulated hernia •

Box 9.1

Infective Infective causes of diarrh diarrhoea oea and vomiting vomiting



Rotavirus Adenovirus Coronavirus Astrovirus Calicivirus Parvovirus Echovirus Following oral polio vaccine

Enteroinvasive E. coli  Campylobacter jejuni  Salmonellosis (esp. S. typhimurium ) S. typhi  and  and S. paratyphi  Shigella  (usually  (usually Sh. sonnei ) Vibrio cholera  Yersinia enterocolitica 


‘food poisoning’) Bacterial toxins (usually  

Giardia lamblia 

Enterotoxic E. coli  Staph. aureus   Bacillus cereus   Clostridium 

Cryptosporidium Entamoeba histolytica Malaria




• • • • • •

inguinal umbilical epigastric Hirschsprung’’s disease Hirschsprung tumour post-operative ileus.

Systemic 1.




Infe Infecctive: any fe febril brilee il illness ness:: UTI in infants following paroxysms of whooping cough acute hepatitis. Neurological: increased ICP: — trauma — meningitis or abscess — tumour migraine. Metab etabol olic ic:: diab diabet etic ic ketoa etoaci cido dosi sis: s: Reye syndrome

• • • •

• • many inborn errors of metabolism. Inge In gest drugss (e (even ven at at the thera rape peut utic ic dose doses) s):: • stioion:n: drug • poisons • post GA.

ASSESSMENT History A dietary/feeding history is paramount: Has vomiting been a problem since birth? Does vomiting only occur soon after food? Has vomiting only been a problem since weaning or the recent introduction of a new food into the diet? Is there diarrhoea? Do other family members have vomiting or diarrhoea? Has the child or a family member been abroad (within the last year)? Is the vomit green (Fig. 9.1)?

• • • •• • •

Constipation occurs in many febrile illnesses but is also a feature of obstruction. Steatorrhoea (s (sme mell lly y st stoo ools ls,, dif  dif ficult to flush) suggests malabsorption. Abdominal pain is not specifi specific for a surgical cause of vomiting. Pain also occurs in: gastroenteritis peptic ulceration and oesophagitis renall tract infect rena infection ion (ask (ask about dysuria dysuria,, haematu haematuria, ria, enuresis enuresis)) hepatitis (travel abroad or recent contacts) migraine (family (family history history,, or history history of of recurrent recurrent abdominal abdominal pain)

•• •





Malrotation ± volvulus High small bowel atresia


Palpable mass

Duplication cyst, meconium ileus tumour

No mass

Meconium normal

Meconium abnormal

Hirschsprung’s disease Septicaemia Delayed passage

Hirschsprung’s disease

Mucus   only


Necrotising enterocolitis, intussusception, volvulus Atresia, Hirschsprung’s disease

Fig. 9.1otherwise. Green vomit in an infant suggestsstools mechanical obstruction until proved In duodenal obstruction, may not be pale because of a Y-termination of the common bile duct (10%).

• •

diabetic ketoac diabetic ketoacidos idosis is (polydips (polydipsia, ia, polyuria polyuria,, weight weight loss) iron ingestion (ask about drugs in the house or at the grandparents’’). grandparents

Examination A full examination is necessary in all children. Look for fever (infect (inf ection) ion),, anaemia anaemia (acute (acute or or chronic chronic blood blood loss loss or chronic chronic malabsor mala bsorpti ption), on), jaundic jaundicee (pyloric (pyloric stenosis, stenosis, hepatiti hepatitis). s). 1. Abdo Abdomi mina nall di dist sten ensi sion on may may occu occurr in in:: chronic constipation gastroenteritis

• •



disease • coeliac • obstruction •Onlyileus. in the latter case are bowel sounds diminished. 2.

3. 4.


6. 7.

Tendern enderness ess is is more more like likely ly to to be the the result result of of a surgi surgica call cause cause the more localis localised ed it it is, the more reproduc reproducible ible it is, is, and the the further from the umbilicus it is. Don’t forget the hernial orifi orifices and genitalia. Rect Rectal al exami xamina nati tion on to look look for: for:   fissures exacerbating constipation lax sphincter and loaded rectum of chronic constipation. Faecal ‘rocks rocks’’ may also be be felt per per abdomen, abdomen, especially especially on the left side tight sphincter and empty rectum of Hirschsprung’ Hirschsprung’s disease. When Wheneever pos possi sibl ble, e, exami xamine ne the the sto stool olss for for bloo blood, d, diar diarrh rhoe oeaa or steatorrhoea. steatorr hoea. Test Test the urine for blood blood or protein: if positive, positive, urgent microscopy is required. If an abdo abdomi mina nall cau cause se seem seemss unli unlike kely ly,, look look at the the ear ears, s, thro throat at and fundi. Measu Measure re the the hei height ght and weigh weightt of the the chi child ld for for evid evidenc encee of a

• •

chronic problem.

Investigations If the cause cause of vomiting vomiting is still still not clear clear,, consider: urine microscopy and culture FBC U & E for evidence evidence of dehydration, dehydration, hyponatraemia hyponatraemia or or hypokalaemic alkalosis (pyloric stenosis) blood sugar blood cultures if febrile stool specimens for both viral and bacterial culture erect and supine AXR if there is localised tenderness or dis-

• • • • • • •

tention and constipation. Air–fl Air–fluid uid levels may be seen in: — gastroenteritis — malabsorption — obstruction — ileus in an infant infant between 2 and 10 weeks, consider a test feed to look for pyloric stenosis, stenosis, even even if the vomiti vomiting ng is not projectile.

Look for visible peristalis and feel (fro (from m the left left side, side, palpate palpate the the right upper quadrant immediately lateral to the rectus sheath) for a pea-sized pyloric mass. Often this mass is felt best immediately after a vomit when the muscle is in spasm. NB. One negative test feed or normal biochemistry does not exclude exclu de this diagnosis. diagnosis. Ultrasound Ultrasound examinati examination, on, in experienc experienced ed hands, may be very helpful helpful in in making the diagnosis. diagnosis.




MANAGEMENT Treat the Treat the cause if possible. possible. Howev However er,, two common common and nonspecifi speci fic presentations which the junior doctor frequently has to manage are: 1. Chronic vomiting in a baby presenting to casualty or outpatient pat ients. s. Exclude Exclude cleft cleft palate, palate, Pierre Pierre Robin Robin sequence sequence and neurological abnormality.

If the infant infant is well, well, growing growing along along a centile, centile, and the vomits vomits are small, small, reassure the parents parents and explain explain that refl reflux will improve with time. If vomiting is still a problem pr oblem at followup, try: — Carobel 1 scoop to 100 ml milk  — infant Gaviscon 1 dose (1 ⁄ 2 dual sachet) < 4.5 kg; 2 doses (1 dual sachet) > 4.5 kg with feeds — earlier introduction of solids and propping upright for 1 hour after feeds. If the infant infant is falling falling away away from the centiles, centiles, despite adeadequatee intake, quat intake, and no cause cause can can be found, found, start start Carobel Carobel and and add infant Gaviscon to every feed but if the child has not regained regai ned the centile after 6 weeks of treatment, treatment, seek the advice of a more senior colleague or arrange admission. A barium swallow or oesophageal pH monitoring may elucidate a cause: — oesophagitis secondary to severe refl reflux — true sliding hiatus hernia — small tracheo-oesophageal fistula — oesophageal stricture — achalasia — vascular ring or mediastinal mass causing compression. Acute diarrhoea and vomiting. Few children with gastroenteritis require hospital admission. If the child is < 10% dehydrated, dehydrat ed, stop all foods foods and drinks drinks and give give a water/de water/dexx-


trose/electrolyte mixture (e.g. Dextrolyte or Dioralyte) orally and frequently using volumes calculated as on p. 22. If there is no vomiting after 4 hours of rehydration with this therapy, restart normal diet but continue to give supplementary drink  of Dioralyte with each loose motion in a volume of 10 ml/kg. Reintroduction of milk (or a light diet in an older child) should be based on cessation cessation of vomiting, vomiting, not diarrhoea. diarrhoea. Advise the parents that: loose stools may continue for 2 weeks the child is infectious to others scrupulous handwashing is essential while diarrhoea persists a breastfeeding mother must express to maintain her milk  supply while the infant is restricted to the electrolyte/  dextrose mixture.

• • • •



If the child is ≥ 10% dehydra dehydrated ted,, admit admit for for rehydr rehydrati ation on and and measure electrolytes. Intravenous rehydration is essential in the very ill and severely dehydrated child (see Ch. 3) but should otherwise be reserved for children who have failed a 6-hour trial of water/dextrose/electrolyte mixture.

Diarrhoea It is dif ficult to defi define an absolute threshold of normality; breastfed infants infants have have looser and more frequent frequent stools, sometimes sometimes after every feed.

A. ACU ACUTE TE DIA DIARRH RRHOEA OEA Whether or not not there is vom vomiting, iting, the commonest commonest cause is gastr gastrooenteritis (Box 9.1). Fever may accompany gastroenteritis.

1. Gastrointes Gastrointestinal tinal bleeding bleeding

• • • • • • •

Blood in the stools jejuni strongly suggests one of:   Campylobacter shigella amoebae intussusception (3 months– months–3 years) HUS Meckel’’s diverticulum Meckel ulcerative colitis. Small haemate Small haematemese meses, s, relati relative vely ly common common after after vomiting vomiting,, are prepresumably due to a small Mallory– Mallory –Weiss tear or gastritis. Check Hb and clotting but no further investigation.

2. the Flu Fluid id replac replaceme nt t of gastroenteritis, For suppor supportiv tiveeement treatment treatmen gastroenteritis, see the sections on vomiting (p. 145) and on fluid balance in Ch. 3 (p. 22). 3. Spe Specifi cificc che chemot mother herapy apy Kaolin or antispasmodics should be discouraged and antibiotics are only indicated as follows: erythromycin or ciprofl ciprofloxacin for prolonged C. jejuni infection ciprofl cipro floxacin or trimethoprim for Salmonella bacteraemia or severe Shigella metronidazole for Giardia lamblia or  Entamoeba histolytica hi stolytica oral vancomycin for Clostridium difficile.

• • • •

4 . P re v e n t i o n

Advise the parents of measures to reduce cross-infection in the home. If the child child is admitted, barrier nurse nurse in an isolation cubicle. cubicle.




5. Complications

• •

Recurrence of diarrhoea: Recurrence diarrhoea: warn the pare parents nts that loose stools may persist for 2 weeks. Diarrhoea persisting beyond 2 weeks: — transient lactose intolerance can occur after gastroenteritis. Stool is positive with ‘Clinitest Clinitest’’ tablets (i.e. reducing substances). Try a lactose-free milk (e.g. Pregestimil or Wysoy). There may be a generalised disaccharidase defi de ficienc ciency y, in which case case Pregestimil Pregestimil is better better — transient protein intolerance. Normal stool pH and no reducing substances. Try a hydrolysed casein milk  (Pregestimil) or soya-based milk (e.g. Wysoy Wysoy or Formula S). Soya-protein intolerance may co-exist with cow’ cow’s milk  intolerance.

Transient intolerances tend only to last for a few weeks and normal diet should be resumed after this period.

B. CHR CHRONIC ONIC DIA IARR RRHO HOEA EA (Box 9.2) Distinguishbybetween (see p. A157) andof true faecal overflow diarrhoea abdominal and rectal examination. history very frequent watery stools or soiling are both clues to spurious diarrhoea and abdominal and rectal examination looking for a megarectum full of faeces may be useful in distinguishing between this and primary diarrhoea. flammatory bowel disease is rare, rare, even even in older older child children ren Infl In and adolescents. If growth is normal, toddler diarrhoea and post-gastroenteritis/giardiasis should be distinguishable. This leaves children with malabsorption, essentia essentially lly coeliac coeliac disea dis ease, se, versu versuss ‘the rest’ rest’.

COELIAC DISEASE (gluten-sensitive enteropathy) History Anoreexia, Anor xia, abdo abdomi mina nall pain pain,, vomit omitin ing g and and freq freque uent nt,, smel smelly ly,, pale pale stools. Onset of symptoms after introduction of solids (usually 4–6 months; months; wheat wheat,, barley barley,, rye and and oats oats all conta contain in gluten; gluten; corn corn and rice are non-toxic).


• • • ••

Anaemia. Short stature. Muscle wasting (buttocks most obvious). Distended abdomen. Dermati Der matitis tis herpeti herpetiform formis is (itchy (itchy vesicular vesicular rash, rash, genitali genitaliaa or buttoc but tocks, ks, usually usually > 4 years) years)..


148 POCKET PAEDIA PAEDIATRICS TRICS Boxx 9 Bo 9.2 .2 Ca Caus uses es of ch chro roni nicc dia diarr rrho hoea ea Non-specifi Non-speci fic diarrhoea


Inflammatory bowel disease

Normal growth Well child

Abnormal growth Abdominal Anaemia symptoms Rickets Bloody diarrhoea Muscle wasting/hypotonia

1. Crohn ’’ s  disease  1. Irritable bowel syndrome  1. Mucosal abnormality  Post gastroenteritis 2. Ulcerative colitis  = ‘toddler diarrhoea’ diarrhoea’ Cow’’s milk or soya Cow 3. Chro Chroni nicc Onset 6 months– months–2 years milk protein intolerance Campylobacter  ‘Peas and carrots’ carrots’ stools Carbohydrate intolerance infection or Rarely persists into Coeliac disease dysentery school age Giardiasis Exaggerated gastrocolic Post cytotoxic drugs flex re refl 2. Pancreatic abnormality  2. Post gastroenteritis  CF See above 3. Structural abnormality  3. Giardiasis  Congenital lymphangiectasia Positive stool Blind loops microscopy or Malrotation duodenal aspirate Tumours (especially lymphoma) 4. Immunodeficiency  Hypogammaglobulinaemia Severe combined immunodefi immunodeficiency syndrome 5. Other inborn errors of absorption  Acrodermatitis enteropathica (zinc defi de ficiency) Congenital chloridorrhoea


•• •

Full blood count for evidence of anaemia. Total IgA level with endomysial or tissue transglutaminase antibody titre. Approximately 5% of people with coeliac disease are IgA defi deficient and a severe defi deficiency may produce falsely negati negative ve antibodies, antibodies, hence the importance importance of measuring the total IgA level as well as the antibody titre. Small bowel biopsy. The defi definitive test is now carried out in most centres by endoscopic duodenal biopsies obtained usually under general anaesthesia. This should be deferred only if the child is very ill or clotting is abnormal.

Differential diagnosis of abnormal small bowel biopsy (Box 9.3).

• • •

Thevarying characteristic features in coeliac disease are: degreeshistological of villous atrophy increased intraepithelial lymphocytes crypt hyperplasia.



Boxx 9 Bo 9.3 .3


Cause Causess o off an an a abn bnor orma mall jej jejun unal al bi biop opsy sy

Villous atrophy  Coeliac disease Temporary gluten intolerance Cow’’s milk protein intolerance Cow Soya protein intolerance Gastroenteritis Giardiasis Severe combined immunodefi immunodeficiency Cytotoxic chemotherapy Other abnormalities  Agammaglobulinaemia (no plasma cells) Lymphangiectasis (dilated mucosal lymphatics) Abetalipoproteinaemia (distention of epithelial cells by fat) Disaccharidase defi deficiency (absent on histochemical staining)

Giardia may be seen on microscopy (or organisms cultured) in gastroenteritis or blind-loop syndrome.

The differential diagnoses of abnormalities not in this characteristic pattern are given in Box 9.3. It is no longer recommended that three jejunal biopsies are obtained on and off the gluten-free diet in order to confi confirm the diagnosis. It is now accepted that a single abnormal biopsy at the time of diagnosis is adequate except in the following circumstances: age under 2 years when there may be a chance of transient gluten intolerance of infancy (although this is probably a rare phenomenon) when there is any doubt at all about the original diagnosis (this may be because the histological picture was not classical or because the clinical presentation is slightly unusual or the serological evidence is not strong) when the response to diet is not as expected.

Management Abnormal biopsy: follow follow the scheme in in Fig. 9.2. 9.2. Normal biopsy: other in investiga vestigations tions are necessary. necessary.

Failure to thrive

• •

Distinguish Distingu ish from acute weight weight loss, usually due to dehydration. dehydration. The cause of FTT is chronic there inadequate weight wei ght gain gain rather rather than than actual actand ual more loss. loss. often Hence, Hence, theis child ch ild ‘falls away’’ on a centile chart. Serial weights over 3 months are more away reliable than single absolute measurements.


150 POCKET PAEDIA PAEDIATRICS TRICS Jejunal biopsy shows mucosal damage

Receiving gluten

Gluten free diet

Recovery (See text for further challenge)

Not receiving gluten

Stoo St ooll re redu duci cing ng su subs bsta tanc nces es

Diarrhoea persists (See box 9.2)

Try Formula S low lactosesucrose diet


Diarrhoea persists

No re redu duci cing ng su subs bsta tanc nces es

Try Formula S Cow’’s milk protein Cow free diet

Diarrhoea persists


Disaccharide-free, cow Disaccharide-free, cow’’s milk and soya protein free diet, e.g Pregestimil


Diarrhoea persists


Notes: 1. The very ill ill child child may may need need immedia immediate te resusc resuscitati itation on with with plasm plasma/bl a/blood ood transfusion and TPN until well enough for a trial of diet. 2. Introdu Introduce ce each each new new prepara preparation tion by a grade graded d increas increasee in conce concentra ntration tion.. Diarrhoea may persist for several weeks. Try each stage for at least 1 week. Ideally, recovery should be proved by repeat biopsy. 3. Reintrod Reintroduce uce poten potential tial provo provoking king nutr nutrient ientss in the the order order lactose lactose,, protein protein,, (soya/cow’’s milk) gluten. (soya/cow Fig. 9.2 Trial of diets for chronic diarrhoea. Specifi Speci fic vitamin and mineral supplements may also be required.

• •

A common pitfall is that birthweight is an unreliable predictor of future weight and ‘physiological down regulation’ regulation’ is common in the first 12 months of life. In the older child, decreased decreased height velocity velocity is a more sensitive sensitive indicator of FTT than weight.

CAUSES Almost any chronic paediatric condition can result in FTT but all causes act via one or more of the mechanisms in Box 9.4. In over half the cases, the cause cause is poor poor dietary dietary intake. intake.




Boxx 9 Bo 9.4 .4 Ca Caus uses es of fail failur ure e to to tthr hriv ive* e* Inadequate diet offered  Too little offered Not offered often enough Offered but defi deficient in calories, protein or vitamins Inadequate intake  The ‘fussy eater’ eater’ Anorexia through an organic cause, e.g. coeliac disease Cardiovascular, respiratory or neurological disease may render intake diffi difficult despite good appetite Vomiting  Diet is taken but not absorbed. Severe refl reflux has the same consequence and may additionally cause oesophagitis Chronic vomiting or refl reflux will lead to loss of appetite also Malabsorption  Diet is taken in suffi sufficient quantities but not absorbed: specifi specific mucosal or exocrine problem Increased requirements  Cardiac failure, respiratory failure and thyrotoxicosis result in increased basal energy expenditure Decreased utilisation  Many dysmorphic children fail to thrive even with adequate intake. Endocrine FTT is due to inadequate utilisation of diet

*Several may occur simultaneously, e.g. CF.


• • • • •

Detailed history of the onset of FTT and growth prior to introduction of solids. Past medical history. Family Fa mily history history of of short short stature stature,, CF, CF, coeliac coeliac disease, disease, etc. etc. Social Social circumst circ umstanc ances: es: who feeds feeds the child? child? Pregnancy Pregna ncy history history (congenital (congenital infection infection), ), gestation gestation and birthbirthweight. Detailed dietary history, history, both offered and taken. The mean milk  intake of thriving babies is > 150 ml/kg (2.5 oz/lb) per 24 hours hour s during the first 6 month months, s, with with feeds feeds at 3–6-hour intervals.

The diet of older children should be scrutinised by a dietitian for calo ca lori ries es,, prot protei ein, n, vita vitami mins ns,, iron iron and and Ca2+ intake. Development Dev elopmental al milestones: milestones: motor delay delay is common. common. Ask specifi specifically about: — vomiting — diarrhoea

• •



— — — —

abdominal pain shortness shortn ess of breath, breath, chronic chronic cough (recurr (recurrent ent aspiratio aspiration, n, CF) tiredness/cyanosis/sweating on feeding (cardiac failure) urinary urin ary frequenc frequency y or excessi excessive ve thirst thirst (UTI, (UTI, diabetes diabetes mellitus or diabetes insipidus).


• • • •

Measure height Measure height,, weight weight and OFC OFC and plot plot on an approp appropriat riatee centile chart using the child’ child’s decimal age. Height of parents parents and siblings siblings (see Ch. 5, p. 50). Compl Com plete ete physic physical al exam examina inati tion, on, inclu includin ding g mou mouth, th, BP and and fundoscopy. Stool inspection and urinalysis.

The features in Box 9.5 suggest the child is constitutionally small. Serial weights should continue for 6 months but no other action is necessary. If the the child child is fail failing ing to thri thrive ve,, but but is well, well, simple simple dieta dietary ry advice may suf fice. Howe However ver,, if at follow-up follow-up 6 weeks later later there has been no ‘catch-up catch-up’’, admi admitt for for a trial of feeding (Fig. 9.3). A successful trial effectively excludes an organic cause for FTT and often requires hospital admission; 4 weeks may be needed to demonstrate the improvement effectively. If the trial is unsuccessful, unsuccessf ul, the period period of inpatient inpatient observation observation may may direct direct the nature of further investigations (see Fig. 9.2 and Table 9.1).

Boxx 9 Bo 9.5 .5

The The const constit itut utio iona nall llyy ssma mall ll chil child d

1. Asymptomatic 2. Low Low birt birthw hwei eigh ghtt for for gest gestat atio iona nall age age 3. Propor Proportion tionally ally small small (heigh (height, t, weigh weightt and and OFC OFC centiles centiles similar) similar) Asymmetrical growth patterns suggest particular causes: (a) OFC centile centile > height > weigh weightt suggests suggests third third trimester trimester IUGR (usually followed by ‘catch up’ up’ growth if diet is adequate) or nutritional FTT (b) OFC centile centile = weight weight > height height suggest suggestss endocrin endocrinee FTT 4. Normal Normal h heigh eightt and weight weight ve veloci locities ties (i.e. (i.e. growing growing parallel parallel to but but below below the third centile) 5. Small parents If not, look for evidence of: congenital infection fetal alcohol syndrome chromosomal abnormality dysmorphic features skeletal dysplasia

• • • • •




Offer a diet appropriate to age Good intake No GI symptoms Good weight increase

Poor intake and poor weight gain

Poor weight gain despite good intake

Diagnosis  Previous diet or feeding behaviour inadequate

No GI symptoms

Genuine GI symptoms

Diagnosis  Systemic illness or hypothyroidism


Diagnosis  Malabsorption e.g. GI infection   Coeliac disease   Protein allergy   CF

Fig. 9.3

No diarrhoea or vomiting

Diagnosis  Disorder of swallowing Developmental delay CNS lesion Respiratory failure Cardiac failure Renal failure Chronic infection Malignancy Hypothyroidism Behaviour disorder

Vomiting but no diarrhoea

Diagnosis  Systemic illness e.g. Urinary infection   Renal failure   CNS lesion   Drug side-effects   Bulimia nervosa

Diagnosis  GI abnormality e.g. Reflux   Hiatus hernia   Oesophageal   stricture   Pyloric stenosis   Intermittent   obstruction

Trial of feeding for failure to thrive.

Gastrointestinall bleeding Gastrointestina In ov over er 50% of of cases in in childhood, childhood, no specifi specific cause is found. A cause should be sought more vigorously in either the newborn (vitamin K defi deficiency) or an older child (portal hypertension and oesophageal oesophageal varices), varices), or if the bleeding bleeding is severe. severe. Haematemesis Haemat emesis is more common common than than melaena, melaena, and if a small haematemesis haematem esis occurs after previous previous bloodless vomiting, vomiting, the cause is probably a small Mallory– Mallory–Weiss tear. tear. In the newborn, haematemesis haematemesis may be swal swallo lowed wed ma matern ternal al blood, blood, and in an an older older child, child, the result result of a nosebleed.



Inve Investi stiga gati tion on o off fail failur ure e to tthr hriv ive e Investigation

Probable diagnosis

Daily weights


Trial of normal diet in hospital for 2– 2–4 weeks

Inspect stools



Cysts of.Giardia  or Amoeba  Pathogenic E. coli, Shigella , Salmonella 

Reducing substances pH < 5.5

Disaccharidase deficiency

Chymotrypsin or Pancreatic elastase

Pancreatic disorder

Culture Glycosuria Proteinuria/haematuria

UTI Diabetes mellitus Renal failure

Reducing substances other than glucose (Clinitest positive, Clinistix negative) Osmolality < 200 mosmol/l Specifi Speci fic gravity < 1.005 Aminoacid and organic acid chromatography Vanyl mandelic acid




Diabetes insipidus Amino or organic aciduria Neuroblastoma

Sweat chloride > 60 mmol/l CF (40– (40 –60 mmol/l = equivocal result). Must have at least 100 mg of sweat. If doubt exists send blood for qenotype (NB: sweat does occur).test negative CF


Hb, WBC, platelets and film Folate (serum and RBC)

Iron/ferritin/transferrin/TIBC Electrolytes _

HCO3 Creatinine Ca2+, PO 43–, alkaline phosphatase Conjugated bi bilirubin, lliiver function tests, albumin Clotting studies

Anaemia Schwachmann’s syndrome Leukaemia Iron de deficiency Chronic vomiting Diabetes insipidus Chloridorrhoea Renal tubular disorder Renal failure Rickets Biliary or or liliver d diisease Dietary deficiency, malabsorption or liver disease



Table 9.1


(contd ) Investigation

Probable diagnosis

Thyroid function GH Cholesterol Immunoglobulins CF genotype Hypoproteinaemia

Hypo/hyperthyroidism Hypopituitarism Abetalipoproteinaemia Hypogammaglobulinaemia CF Dietary deficiency, liver disease, nephrotic or protein losing enteropathy

Small bowel  biopsy 

Se e p . 1 4 8

Se e B o x 9 . 3



Aspiration pneumonia, CF Cardiac failure

Erect and supine AXR Consider barium meal and follow through

Malrotation Blind loop syndrome Crohn’s disease Peptic ulcer

Left hand and wrist

Constipation Cystinosis Bo n e a g e

Fresh blood p.r. is most commonly due to an anal fissure or bacteriall enteritis. bacteria enteritis. If not, not, consider: clotting abnormality intussusception (3 months– months–3 years) volvulus dietary protein allergy infl in flammatory bowel disease haemangioma or telangiectasia sexual abuse or foreign body.

• • • • • • Melaena suggests bleeding from stomach or small bowel: abnormality • clotting ulceration or gastritis • peptic or gastric varices • oesophageal Meckel’’s diverticulum. • Meckel

In all cases: resuscitate first, if necessary. necessary. Giv Givee plasma 20 ml/kg if shocked. shocked. If the shock is severe severe and and obviously obviously due to haemorrhage, haemorrhage, give give blood, blo od, type-s type-spec peciific if possible, but in v very ery severe severe haemorrhagic haemorrhagic shock use Group O Rhesus negative

• •

look for for other bleedi bleeding ng sites, sites, signs signs of portal hypert hypertensi ension, on, skin haemangioma initial investigations: — crossmatch blood



• •

— Hb (initial Hb may not refl re flect serious blood loss) — platelet count — clotting screen — evidence of chronic liver disease (see Table 9.3) involve a surgeon early. Proctoscopy for small rectal bleeds all children with head injuries or receiving intensive care should be given ranitidine 1 mg/kg 6– 6–8-hourly as a 3– 3–5 min bolus injection.

Bleeding varices In addition to the above: low threshold for insertion of central venous catheter. Keep CVP 1–2 cm H2O relative to sternal angle. Avoid over-transfusion pass an NGT and aspirate frequently treat hepatic encephalopathy (see management of acute liver failu fa ilure, re, p. 162) 162) octreotide 25– 25–50 g per hour (or 1 g/kg/hour) as an infusion

• • • • • •

ranitidine i.v. as above together with oral sucralfate passage of a Sengstaken– Sengstaken–Blakemore tube requires expert assistance discuss with Regional Children’ Children’s Liver Unit.

Abdominal pain ! 

A. ACUT ACUTE EA ABD BDOM OMIINAL NAL P PAI AIN N (Box 9.6) The single most important question is:   ‘Does this child require emergency surgery?’ surgery?’ This is a clinical decision but pointers to a surgical cause are: signs of peritonism peritonism (fev (fever er,, localised localised tenderness, tenderness, including including recrectally,, guarding, tally guarding, rigidity rigidity and absent bowel bowel sounds). sounds). Appendicitis Appendicitis is the commonest cause but is rare < 2 years. Anorexia is usual and vomiting vomiting very very common. common. The younger the the child, the more vague the signs of appendicitis signs sig ns of obstr obstruc uctio tion n (vom (vomiti iting, ng, abdomi abdomina nall diste distensi nsion on,, highhighpitched bowel sounds and constipation –  the rectum may or may not be empty) GI bleeding.

• • •

Investigations Consider: urine microscopy urinaly urin alysis sis for for glycosur glycosuria, ia, proteinu proteinuria, ria, haematu haematuria ria FBC and WBC differential. Sickling test in African and AfroCaribbean children

• • •



Boxx 9. Bo 9.6 6


Caus Causes es of ac acut ute e abd abdom omin inal al pa pain in

Require early surgical referral

Abdominal cause but does not require immediate surgical referral

Systemic cause

Appendicitis Peritonitis Intussusception Volvulus Strangulated hernia Obstruction Trauma Gl bleeding

Gastroenteritis* Infantile colic* Ingestion Constipation* Peptic ulcer (including Helicobacter pylori  associated gastritis/ulceration)* Pancreatitis, including mumps Cholecystitis/cholangitis UTI*, nephrotic syndrome Urinary calculus* Hepatitis Dysmenorrhoea*

Any febrile illness but especially ENT infection Lower lobe pneumonia Abdominal migraine* Diabetic ketoacidosis Sexual abuse* Sickle causes Porphyria Lead poisoning HSP

*More common organic causes of recurrent abdominal pain

plain AXR (erect and supine).

B. RE RECU CURR RREN ENT T ABD ABDOM OMIN INAL AL PAIN AIN All of the causes of acute abdominal pain may recur but some are more likely likely than than others others (see Box 9.6, asterisks). asterisks). Howe However ver,, at least least 90% of children with recurrent abdominal pain do not have an organic cause. Functional abdominal pain (‘ ( ‘periodic syndrome’ syndrome’, ‘abdominal migraine’ migraine’) is a positive clinical diagnosis and not a diagnosis of last resort after multiple investigations.

• • • • •

Clues are: child is otherwise healthy and thriving good appetite and no diarrhoea or vomiting episodes are relatively short and may coincide with environmental triggers pain is periumbilical; there are no abnormal physical signs family history of recurrent abdominal pain or migraine.

If still still in doubt, doubt, urine urine microsc microscopy opy,, FBC and and ESR ESR (or plasma plasma visviscosity), cosity ), and plain AXR should should suf fice to reassure you and the parents.

Constipation, soiling and encopresis While these are usually considered together, encopresis is a quite separate entity:



• • •

no organic abnormality no constipation: constipation: therefore laxati laxatives ves are not indicated indicated normal faeces are voluntarily passed in an unacceptable place, including the child’ child’s pants.

There is a signifi significant emotional disorder in the child or in the family and this must be recognised early. faeces) may be caused by:yet Soiling (involuntary ‘developmental delay’passage delay’ , i.e. the of ski skill ll of toilet toile t training has has not •   been acquired neurological abnormali neurological abnormality ty,, e.g. spina spina bifi bifida • achronic constipation and overfl overflow of liquid faeces. • The management of constipation is in two stages. First, Fir st, exclude exclude an orga organic nic cause cause (Box (Box 9.7), 9.7), and second, second, restore restore a normal bowel habit. Clues to an organic cause are: constipation since birth or delay in passage of meconium beyond 24 hours the more severe the constipation and the younger the child FTT or abnormal physical signs empty rectum or ‘toothpaste sign’ sign’ after p.r. exam (suggests Hirschsprung’’s disease). Hirschsprung

• • • •

MANAGEMENT OF CONSTIPATION CONSTIPATION WITHOUT AN ORGANIC CAUSE Response to treatment is directly proportional to the confi con fidence, enthusiasm and persistence of the paediatrician.

Boxx 9. Bo 9.7 7

Orga Organi nicc ca cause use of chr chron onic ic const constip ipat atio ion n

Gastrointestinal  Hirschsprung’’s disease (if necessary, exclude by rectal biopsy stained for Hirschsprung ganglion cells and cholinesterase) Anal stricture Anal fissure Partial intestinal obstruction Systemic  Hypothyroidism Hypercalcaemia Lead poisoning (associated with pica: anaemia and basophilic stippling on blood film) Renal tubular disorders (plasma HCO3– and urine pH) Diabetes insipidus (urine osmolality; may need water deprivation test, see p. 29) Sexual abuse

*Organic causes are more likely in infants, especially if onset is from birth.




ASSESSMENT Detailed history of the onset of constipation (e.g. febrile illness or visit to a relative), relative), whether unremitting unremitting or alterna alternating ting with period periodss of  normal norm al bowel bowel habit habit,, the age age and and pattern pattern of toilet toilet traini training, ng, and the the ambience of the domestic dome stic lavatory. lavatory. A dietary history including drinkdrin king habits may suggest a cause. A complete physical examination is essential, including rectal rectal eexaminatio xamination n and assessment assessment of anal tone. Look particularly for an anal fissure.


• •

• • • • •

Explain that Explain that the proble problem m is common, common, treatab treatable le and not not the child’’s fault. child Recommend increased fluids (especi (especially ally fruit fruit juice juice), ), brown brown bread brea d instead instead of white white,, bran or high high fibre breakfast cereals, cooking with vegetables and pulses. Start regular faeca faecall softeners, e.g. lactu lactulose lose 5 ml 12-hourly and increase by 5 ml 12-hourly every 4 days until the stools are soft. Recommend that the child sits on the toilet for at least 5 minutes after mealtimes. Advise that a diary be kept. See the child with the diary again in 2 weeks. Be encouraging, encouraging, even even if there has be been en no result. If there there is no no respon response, se, start start regu regular lar laxati laxatives ves,, e.g. Senoko Senokott 2.5 ml 12-hourly which can be increased to 10 ml 12-hourly. If there is still still no response after a further further 4 weeks, weeks, start behavbehaviour modifi modification (star chart) with ‘rewards rewards’’ which are appropriate to the child’ child’s age, age, sex sex an and d fami family ly cir circu cums msta tanc nces. es. Follow-up at 2-week intervals and do not allow your enthusias enthusiasm m to wane. Remember that forceable use of suppositories or enemas in a resisting child is harrowing for all concerned and may hamper future treatments. If there is still no improvement, improvement, arrange an inpatient admission for nursing observation, observation, dietary manipulation, manipulat ion, behaviour behaviour assessmen assessmentt and intensive intensive behaviour behaviour therapy employing nursing staff and the hospital school. This inpatient period may include more aggressive therapy using aperients such as Movicol. After this continue vigorous outpatient follow-up including home visits.

Hepatosplenomegaly The causes are legion but many are rare. The differential diagnosis can be narrowed by ascertaining whether there is enlargement of  liver liver only only,, spleen spleen only only, or both both (Table (Table 9.2) and and whethe whetherr this is is recent or chronic.


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Table able 9. 9.3 3



Inves Investi tiga gati tion on of liver liver fail failur ure e Abnormality



Haemochromatosis or CF associated with liver damage and diabetes Galactosaemia Coagulopathy Hepatorenal syndrome Biliary obstruction

Reducing su substances Haematuria

Bilirubin but no urobilinogen Save urine for toxicology screen and chromatography for rare inborn errors of metabolism. Send for viral (CMV) and bacterial culture, and microscopy (infection may precipitate acute or chronic liver failure) Blood 

1. FBC  Hb and iron binding

WBC Platelets 2. U & E  Glucose



Iron deficiency anaemia due to chronic Gl bleeding Iron overload in haemochromatosis Haemolytic anaemia due to hypersplenism Infection may precipitate acute or chronic liver failure Low if DIC has supervened or there is hypersplenism Hypoglycaemia commonly complicates liver failure and inborn errors of metabolism Electrolyte abnormalities may precipitate liver failure or result from liver failure (usually hyponatraemia) May be low in severe liver failure (urea is synthesised in the liver) or high if ascites and vomiting cause hypovolaemia and prerenal failure

3. Tests of hepatocellular function  May be elevated in liver failure and is NH4+ not specifi specific for Reye syndrome Falsely elevated if sample is not fresh ALT or AST Transaminases are elevated with liver cell damage 4. Tests of synthetic function  Clotting studies Both intrinsic and extrinsic paths are prolonged by defi deficiency of vitamin K dependentt factors (II, VIII, IX, X) dependen May occur rapidly Albumin Synthesised in the liver but several days must elapse before levels fall ficantly signifi signi 5. Tests of excretory function  Conjugated bi bilirubin May be be el elevated in in he hepatocellular o orr obstructive jaundice (see urine)



(contd ) Abnormality


Unco Un conj njug ugat ated ed bi bililiru rubi bin n

Only Only el elev evat ated ed in very very se seve vere re lilive verr failure or co-existent hypersplenism (haemolytic anaemia) Note th thee wid wide and and age-d e-depend endent normal range High levels suggest biliary obstruction High levels suggest biliary obstruction

Alka Alkali lin ne phosph sphatas atasee

Gamma-glutamyl transpeptidase 6. Evidence of infection  Blood cultures Hepatitis antigens and antibodies Also CMV and EBV

Se e B o x 9 . 9

7. Metabolic and other disorders  Alpha-1-antitrypsin Deficiency causes cirrhosis   ↑Cu2+ and ↓caeruloplasmin in Plasma Cu2+ and caeruloplasmin Autoim toimm mune he hepatitis itis

Wilson’s disease Immunoglobulin inss aan nd auto-antibodies


8. Evidence of toxic substance ingestion, especially paracetamol  Sweat test CF leads to cirrhosis



Essential to exclude biliary obstruction and space-occupying lesion

Liver biopsy  See p. 165

of consciousness level • alteration • vomiting • hypoglycaemia bleeding diathesis •  jaundice an d electrolyte abnormalities • enlarged and and tender liver. •


• • ••

Discuss with Regional Children’ Children’s Liver Unit. Identify and treat the underlying cause (Table 9.3). Record baseline vital signs and an d Glasgow Coma Score (see Ch. 2). Avoid sedat sedation. ion. In the presence of liver liver failure, failure, the dose of all drugs must be checked (see also Table 9.4). Minimise encephalopathy: — low protein diet; avoid TPN; but 



Table able 9.4 9.4


Drugs Drugs to be used used with with cauti caution on iin n liver liver disease disease

D rug

Problems in liver disease

Magnesiu Mag esium m tr tris isci cili liccate ate Gaviscon Diuretics Beta-blockers Anticoagulants Aminophylline Aspirin Paracetamol Opiates Anticonvulsants

So Sod dium ium loa load agg aggravate vatess asci scite tess Sodium load aggravates ascites Hypokalaemia precipitates coma Reduce dose as decreased first pass metabolism Clotting already prolonged Reduce dose GI bleeding and Reye syndrome Reduce dose May precipitate coma Avoid valproate Dose of other anticonvulsant may need to be reduced Increased risk of bone marrow failure

Chloramphenicol Erythromycin Isoniazid Rifampicin Doxorubicin Methotrexate

Avoid: increased risk of hepatosplenomegaly Reduce dose

— maintain a normal blood glucose with i.v. dextrose if necessary — purge the gut of blood and protein using oral lactulose (1 ml/kg 8-hourly) — oral neomycin (15 mg/kg 6-hourly) to reduce gut bacteria. Correct any coagulopathy. Give vitamin K1 (phytomenadione) 0.3 mg/kg i.v. slowly routinely and FFP 10 ml/kg if there ther e is active bleeding or to cover an invasive invasive procedure. Cross-matched blood should always be available if there has been haematemesis, malaena or known varices. Correct electrol electrolyte yte imbalances, imbalances, preferably preferably by altering altering intake. intake. Treat ascites by: — restricting fluid intake to 2 ⁄ 3 maintenance requirement — restricting Na+ intake to 1 mmol/kg per 24 hours — giving oral spironolactone (1– (1–2 mg/kg 12-hourly) or i.v. potassium canrenoate (1– (1–2 mg/ mg/kg kg 12-h 12-hou ourl rly y, cont contra ra-indicated in hyponatraemia) to combat hyperaldosteronism; avoid all other diuretics — considering salt-poor albumin solution i.v. if serum albumin is < 25 g/l and response to the above is poor but  do not expect to generate a negative fluid balance of more than 1% bodyweight in each 24-hour period. Avoid paracentesis unless infected ascites is suspected. Mannitol 1 g/kg i.v. i.v. may temporarily reduce ICP. ICP. If more aggressive management is deemed appropriate (ventilation, ICP monitori monitoring, ng, renal renal dialysis dialysis,, exchang exchangee trans transfusi fusion, on, charcoal charcoal



Caus Causes es of of chi child ldho hood od cirr cirrho hosi siss

Hepatic  (commonest) 1. Wilson’s disease 2. Chronic Chronic hepatitis hepatitis (followi (following ng hepat hepatitis itis B or as an autoim autoimmun munee disord disorder) er) 3. Alph Alphaa-11-an anti titr tryp ypsi sin n defi deficiency 4. Drug Drug indu induced ced (parac (paracetam etamol ol ove overdo rdose, se, ch chloro lorocarb carbon on ingesti ingestion, on, isoni isoniazid azid,, methotrexate, halothane) Post-hepatic  1. Biliary Biliary atresi atresiaa an and d other other anat anatomic omical al anoma anomalies lies of the the bilia biliary ry tree tree 2. Recu Recurr rren entt chol cholan angi giti tiss 3. Inflammatory bowel disease 4 . CF Pre-hepatic  (rarest) Budd– Budd –Chiari syndrome

haemoperfusion), haemoper fusion), consider this this early on and arrange arrange transfer transfer to a major centre.

CHRONIC LIVER FAILURE FAILURE Hepatomegaly or portal hypertension due to cirrhosis (Box 9.8) are Hepatomegaly suggested by: spider naevi palmar erythema  jaundice, anaemia or Kayser– Kayser–Fleischer ring purpura, purp ura, haemate haematemesi mesiss or malaena malaena enlarged and hard liver with non-tender splenomegaly ascites and peripheral oedema.

• • • • • •

A mixture of these features may be seen in acute on chronic liver failure and obviously there may be other signs of the underlying cause.

Management Usually as an outpatient. The following may require attention: Treatment of the underlying cause. FTT: — high high-ene -energ rgy y, high-ca high-carboh rbohydra ydrate, te, low-pr low-protei otein n diet diet — vitamin supplementation (particularly fat soluble vitamins A, D, E and and K: use Ketov etovit itee liqui liquid d 5 ml per 24 hour hourss and and Ketovite etovite tabl tablets ets orally orally,, one tablet tablet 8-hour 8-hourly ly,, unless unless serum serum monitoring demonstrates inadequate levels in which case

• •

each vitamin can be supplemented individually.



• • • • • •


Coagulopathy: monitor PT as index of adequac Coagulopathy: adequacy y of vitamin K supplementation. Iron defi deficiency anaemia suggests chronic GI bleeding. Biochemi Bioc hemical cal rickets: rickets: monitor monitor Ca2+, PO43- and alkaline phosphatase as index of adequacy of vitamin D supplementation. Jaundice: monitor levels levels of of unconjugate unconjugated d bilirubin. bilirubin. Cholestyramine may be necessary for pruritus but may exacerbate fat-soluble vitamin and folic acid defi deficiency. Monitor transaminase transaminase levels: levels: look for causes of abrupt deteriodeterioration. Ascites (see p. 163). Haematemesis Haemat emesis and melaena: melaena: advise the parents parents to see seek k urgent urgent admission. Avoid aspirin and other non-steroidal antiinfl in flammatory analgesics (see Table 9.4). Endoscopy and oesophageal variceal banding should be undertaken by an expert.

Liver biopsy Should be performed only by an expert and only when the result may aid management: 1. Wilson’s disease 2. Chronic hepatitis 3. Conjug Conjugat ated ed ja jaund undic icee wi witho thout ut evi eviden dence ce of vir viral al infec infecti tion on or anomaly of biliary tree 4. Unco Unconju njugat gated ed jau jaundi ndice ce with without out haem haemoly olysis sis (Crigl (Crigler er– –Najjar syndrome). Platelet count and PT should be checked, Platelet checked, blood crossmatched crossmatched and available av ailable,, and consent obtained. obtained. The histopathologist histopathologist must be consul con sulted ted bef before ore the procedure regarding the need for samples for: formalin fixation for light microscopy unfi un fixed core for frozen section glutaraldehyde fixation for electron microscopy snap freezing for enzyme studies fresh specimen for chemical analyses.

• • • • •

Jaundice NEONATAL See Ch. 19.



THE OLDER CHILD (Box 9.9) Mixed hyperbilirubinaemia is more common and the cause is usually infective. Hepatitis A is the commonest in the UK and rarely requires hospital admission. Elevated Elevated transaminases precede  jaundice. No longer infectious once jaundice appears. Urine is dark. Stools may be pale. Conjugated hyperbilirubinaemia (pale stools and dark urine) is rare in childhood and and always always requires investig investigation: ation: early USS to demonstrate biliary obstruction. Look for evidence of chronic liver disease (see Box 9.8).

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