09_McClure_09.indd 289 11/14/2012 2:34:57 PM CHAPTER 9 Respiratory medicine 290 Pneumonia Pneumonia is an infection of the lower respiratory tract and lung paren- chyma th at leads to consolidation. Viruses alone account for 14 \200\22335% of all community acquir ed pneumonia in childhood. In 20 \200\22360% of children a pathogen is not found. Common in fecting bacterial agents by age are: \200 Neonates: Staphylococcus aureus. Infants: School streptococcus, Bordetella pertussis, Mycop lasma pneumoniae. group B streptococcus, Escherichia coli, Klebsiella, \200 Streptoccus pneumoniae, Chlamydia. age: Streptococcus pneumoniae, Staphylococcus aureus, gr oup A Certain groups of children are at risk of pneumonia, e.g. those with: \200 \200 \200 \200 \200 \200 congenital lung cysts; chronic lung disease ( immunode \201 ciency ( cystic \201 brosis ( sickle cell disease ( tracheostomy b p.276); b pp.295, 724); b p.270); b p.620); in situ. Diagnosis History The patient may have had a recent URTI and may also be complaining of ple uritic chest pain or abdominal pain. The typical history will have: \200 \200 \200 (cid:2)38.5*C; temperature shortness of breath; cough; with sputum production in older children ( >7yrs). Examination Check for the following: \200 Signs use of accessory muscles for breathing. A resting respiratory rate of 70breaths/min i n infants or >50breaths/min in children indicates severe illness. Desaturation every child admitted to hospital with pneumonia. SpO2 \211 92% in room air indicates severe illness. h ealth and lethargy. General Auscultation decreased breath sounds; tactile vocal fremitus; b ronchial breathing. of respiratory distress: tachypnoea; grunting; intercostal recession; and cyanosis: pulse oximetry should be performed in \200 signs of lobar pneumonia: dullness to percussion; crackles; Investigations The investigations that help in diagnosis include: \200 \200 \200 culture may be of limited value. Sputum: Nasopharyngeal Blood: pneumonia (not necessary in community-acquired pneumonia). CX R: Pleural \202 uid: when there is a signi \201 cant pleural effusion, an aspirated samp le should be sent for culture and antigen testing once a drain is inserted. aspirate: viral immuno \202 uorescence in infants. culture should be done in all children with severe bacterial \200 not as routine (see b p.291). 09_McClure_09.indd 290 11/14/2012 2:34:57 PM PNEUMONIA 291 Viral titres: save a sample of blood for acute titre testing, which can be assayed the same time as the convalescent sample if a microbiological diagnosis is not made. See Box 9.2 for summary of investigations. Chest X-ray There are a variety of changes ranging from lobar consolidation to the mere pre sence of patchy bilateral in \201 ltrates. In general, routine CXR is not needed in childr en with mild uncomplicated LRTI. In other cases, look for pleural effusions, \202 uid lev els, apparent round pneumonia, cavitation, hilar adenopathy, and any calci \201 cation. At follow-up, patients with history of signi \201 cant acute X-ray change (e.g. lobar collap se, apparent round pneu- monia, empyema) or continuing symptoms will require repeat X-ray. Box 9.2 Investigations to consider in children with chronic or recurrent pneumonia Step 1: initial blood tests \200 \200 Hematology: Immunology: response to immunizations (tetanus and pneumococcus), rheumatoid fa ctor Antibodies: Genetics: FBC, complement screen, ESR IgA, IgE (and aspergillus RAST), IgG, IgM, antibody \200 aspergillus precipitins, antinuclear antibodies CF genotype Step 2: other tests \200 test \200 \200 \200 Sweat Microbiology: Lung Radiology: sputum culture function: spirometry, lung volumes, and reversibility CXR, barium swallow for vascular ring, sinus radiography Step 3: further investigations \200 Hematology: subsets, and cellular immune function Imaging: pH study: Video \202 uoroscopy : Nasal ciliary there is a normal nasal nitric oxide) Bronchoscopy: microbiological sample collection neutrophil and monocyte function, lymphocyte \200 \200 \200 high resolution CT scan of the chest for gastro-oesophageal re \202 ux for silent aspiration biopsy: microscopy and function (may be unnecessary if visualization of dynamic airway function, as well as 09_McClure_09.indd 291 11/14/2012 2:34:57 PM CHAPTER 9 Respiratory medicine 292 Pneumonia: treatment Oral antibiotics are safe and effective in the treatment of community- acquired pneumonia. IV antibiotics are used in children who cannot absorb oral antibiotics or in those with severe symptoms. The speci \201 c choice of antibiotic is based on the f ollowing: \200 \200 \200 \200 \200 Age of the child. Host factors. Severity of illness. Information about cultures if known. C XR \201 ndings if known. Antibiotic therapy for pneumonia Under 5yrs Streptococcus pneumoniae is the most likely pathogen. The causes of atypical pne umonia are Mycoplasma pneumoniae and Chlamydia tracho- matis \200 \200 First-line Alternatives: erythromycin, clarithromycin, or azithromycin for atypical pneumon ia treatment: amoxicillin co-amoxiclav or cefaclor for typical pneumonia; Over 5yrs Mycoplasma pneumoniae is more common in this age group \200 First-line treatment: amoxicillin is effective against the majority of pathogens, but consi der macrolide antibiotics if mycoplasma or chlamydia is suspected Alternatives: macrolide, or a combination of \202 ucloxacillin with amoxicillin if Staphylococcus aureus is suspected consider using a Severe pneumonia Co-amoxiclav, cefotaxime, or cefuroxime IV Supportive therapies Consider whether any of the following are needed: \200 IV \200 \200 Antipyretics for fever. \202 uids: consider if dehydrated or not drinking. Supplemental so that SpO2 is maintained >92% (b p.46). Chest oxygen: administer oxygen via headbox or nasal cannulae drain: for \202 uid or pus collections in the chest, as in empyema. Physiotherapy Chest physiotherapy is generally not bene \201 cial in children with pneumon ia and should not be performed. 09_McClure_09.indd 292 11/14/2012 2:34:58 PM PNEUMONIA: EFFUSION, EMPYEMA 293 Pneumonia: effusion, empyema The presence, in association with pneumonia, of a small effusi on that does not cause any respiratory distress can be managed conservatively without the n eed for aspirating a sample. A \202 uid sample, however, is needed if there is: \200 \200 \200 \200 \200 a large effusion; no clear underlying diagnosis; respiratory distress; persistent fever des pite antibiotic treatment; long history (>14 days). Fluid sample After US of the chest and checking blood-clotting studies, a small chest drain (or pigtail drain) should be inserted into the pleural \202 uid unless effu- sion is sma ll. Samples should be sent for the following: \200 \200 Microbiology: Cytology: cell types. Cytology for lymphoma may give false \200\223ve result in up to 10% of cases. bacterial culture and sensitivity, acidfast bacilli. presence of pus cells and microscopic assessment of aberrant Diagnosis of empyema The diagnosis of empyema can be based on the presence of: \200 \200 Fluid: US scan: pH < 7.2, glucose <3.3mmol/L, protein >3g/L, pus cells. loculation or \201 brin strands seen. Fluid drainage After inserting the small-bore drain or pigtail catheter, \202 uid should be allowed to drain into standard commercially available systems (e.g. water- seal two-bott le system). The drain can be removed if draining <50mL in 24hrs. Urokinase for empyema In empyema, as opposed to simple pleural effusion, instillation of ur oki- nase via the chest drain is recommended. \200 Dose 12-hourly for 3 days. Method: encourage the patient to move and roll around over the n ext 4hr. Suction: use a low pressure suction device (e.g. Robert \200\231s pump) to maintai n suction of 20cmH2O between doses. Local pain. Consult the pain control team. : 40,000U urokinase in 40mL (10,000U in 10mL if <1yr) given instill via the chest drain and then clamp the drain and anesthetic: bupivacaine around the drain site may control pleural Surgical referral If the effusion or empyema fails to resolve over a period of 7 days then a surgical opinion may be sought. Sometimes a chest CT scan is needed . A de \201 nitive s urgical procedure or large bore drain and manual disruption of loculation may be needed. 09_McClure_09.indd 293 11/14/2012 2:34:58 PM CHAPTER 9 Respiratory medicine 294 Pulmonary tuberculosis Worldwide, tuberculosis of the lung is a major health problem. TB sh ould always be considered in children from endemic areas, as well as those at risk of immun ode \201 ciency or taking immunosuppressive agents. Once diagnosed, TB is a noti \201 abl e disease and contact tracing is required so that those exposed to the patient undergo tube rculin testing and CXR screen- ing. BCG vaccination appears to be protective against miliar y spread, but is no longer routinely given. Mycobacterium tuberculosis is spread from person to person by droplet infection. Once inhal ed, some bacilli remain at the site of entry and the rest are carried to regional lymph nod es. The bacilli multiply at both sites; the primary focus along with the regional lymph nod es are collectively described as the primary focus. Organisms can then spread via the blood and lymphatics. The pathological sequence after infection is as follows. \200 4 \200\2238wks: \200 \200 \200 6 \200\2239mths: \200 \200 \200 \200 \200 \200 \200 febrile illness; erythema nodosum; phlyctenular conjunctivitis. in most cases progressive healing of primary complex; effusion: focus may rupture into pleu ral space; cavitation: focus may rupture into bronchus; coin lesion on CXR: focus may enlar ge; regional lymph nodes may obstruct bronchi; regional lymph nodes may erode into bronchus or pericardial sac; miliary spread. Drug management See also b p.722 Pulmonary \200 2mths: as a 4th drug. Then 4mths: isoniazid, rifampicin, and pyrazinamide. Often ethambutol added isoniazid and rifampicin. Miliary spread \200 \200 3mths: Then 12 \200\22318mths: isoniazid, rifampicin, ethambutol and pyrazinamide. isoniazid and rifampicin. 09_McClure_09.indd 294 11/14/2012 2:34:58 PM OTHER DISORDERS 295 Other disorders Aspiration syndromes \200 Acute at any age and the typical presentation is choking and coughing. In infants, some asp iration episodes may go unrecognized in the acute phase. These babies may present later wit h consolidation that fails to improve. Chronic lobes at different times. Airway anomalies s hould be sought as an underlying cause (see b pp.846 \200\223849). Also swallowing abnormal ities need to be excluded with a video \202 uoroscopy done by an experienced speech and l anguage therapist. aspiration of \202 uid or particulate matter into the lungs may occur aspiration may present with recurrent pneumonia \200\224different Interstitial lung disease A rare group of disorders in childhood and children (usually infa nts) pre- sent with progressive tachypnoea and hypoxia. The CXR shows wide- spread reticula r shadowing but a high resolution CT scan is needed for diagnosis. Treatment should be unde rtaken in specialist centers as these children will require lung biopsy and may need treatm ent with steroids or chloroquine. A requirement for supplemental oxygen is common. Lymphoid interstitial pneumonitis (LIP) See also b p.726. LIP has the appearance of \201 brosing alveolitis, but it is a pulmonary feature of HIV infection that responds to steroid s. Immunode \201 ciency See also b pp.724 \200\223727. Recurrent infection of the lower airwa y is com- mon in patients with immunode \201 ciency such as: \200 \200 \200 IgA de \201 ciency. IgG subclass de \201 ciency. Defective cell-mediated immunity: viral or fungal infection. 09_McClure_09.indd 295 11/14/2012 2:34:58 PM This page intentionally left blank 297 Chapter 10 Gastroenterology and nutrition Healthy eating for children 298 Vomiting 300 Acute diarrhea 302 Chronic diarrhea 304 Consti pation 306 Faltering growth (failure to thrive) 308 Recurrent abdominal pain 310 Gastrointe stinal hemorrhage 312 Jaundice 314 Adverse reactions to food 316 Nutritional disorders 320 Nutritional support 322 Parenteral nutrition 324 Oesophageal disorders 326 Pancreatitis 328 Intestinal disorders 330 In \202 ammatory bowel disease 332 Malabsorption 334 Coeliac dis ease 336 Gastrointestinal infections 338 Intestinal parasites 340 Acute hepatitis 342 Chron ic liver failure 344 Alpha1-antitrypsin de \201 ciency 346 Wilson \200\231s disease 346 Li ver transplantation 347 10_McClure_10.indd 297 11/14/2012 11:28:45 PM CHAPTER 10 Gastroenterology and nutrition 298 Healthy eating for children Infants \200 \200 \200 \200 \200 \200 b p.142. See also Breast milk is the ideal feed for almost all infants. d food allergies). Solids ar e not recommended until age 6mths ( Initial solids should be based on baby rice, fruit, and vegetables. Gluten is acceptable from age 6mths. Following introduction of solids, infants should experience and progress through a wide variety of tastes and appropriate textures. Finger foods should be introduced from age 7mths. Continue complementary breast or formula feeds until age 1yr. Normal full fat cow \200\231s milk can then be introduced as the main drink. Avoid addition of salt and sugar to food. Low fat products are not suitable for infa nts. Supplemental vitamins A, C, and D are recommended until age 5yrs. \200 \200 \200 Age 1 \200\2235yrs A well balanced diet in early childhood is important to establish a life time pattern of healthy eating. The key recommendations for healthy eating to be achieved b y age 5yrs are the following: \200 Decrease fat to 35% energy intake by avoiding excess high fat foods and changing milk to se mi-skimmed at age 2yrs, and skimmed at age 5yrs. Include whole grain cereals and 5 portions per day of fruits and vegetables to increase \201 bre intake. Monitor for (accelerating weight velocity) and avoid obesity. Moderate salt intake, e.g. not adding salt to cooking o r at the table. Avoid iron de \201 ciency anemia by restricting milk intake to 1 pint per day and including foods rich in iron (red meat, cereals, beans, pulses, egg yolk, dark gree n vegetables, and dried fruit). Add vitamin C as fruit juice at a meal to increase iron abs orption. Drinking tea with meals decreases iron absorption. Excessive consumption of fruit juices or squashes can contribute to chronic non-speci \201 c diarrhea of childhood (toddl er diarrhea) and contribute to feeding problems. \200 \200 Older children Schoolchildren should eat a diet based on a wide variety of foods. Nutrition al guidelines relating to school meals have been set out by many UK local authorities and h ealthy eating forms part of the UK national cur- riculum. A healthy diet should include: \200 At least one starchy food at each meal time, e.g. whole meal bread, potatoes, pasta, and ri ce. Five portions per day of fruit and vegetables. Two servings of meat or alternatives eac h day. Two to three portions a day of skimmed milk, low-fat yogurt, fromage frais, or chees e (a portion = 1 yogurt, 1/3 pint milk, 30g cheese). Only small and occasional amounts of s ugar and fats. \200 \200 10_McClure_10.indd 298 11/14/2012 11:28:46 PM HEALTHY EATING FOR CHILDREN 299 10_McClure_10.indd 299 11/14/2012 11:28:46 PM CHAPTER 10 Gastroenterology and nutrition 300 Vomiting A common symptom in childhood. Three clinical scenarios are recognized (see Box 10.1): Acute: and usually associated with an acute illness. Chronic: severe, discrete episodes associated with pallor, lethargy +/ \200\223 Cyclic: abdominal pain. The child is well in between episodes. Often there is a fa mily history of migraine or vomiting. discrete episode of moderate to high intensity. Most common \200 low-grade daily pattern, frequently with mild illness. Causes \200 Acute: GI infection; non-GI infection (e.g. urinary tract infection); GI obst ruction (congenital or acquired e.g. pyloric stenosis); adverse food reaction; poisoning; r aised intracranial pressure; endocrine/metabolic disease (e.g. diabetic ketoacidosis). Chro nic (usually GI): peptic ulcer disease; gastro-oesophageal re \202 ux; chronic infection; gastritis; gastroparesis; food allergy; psychogenic (see Psychogenic vomiting); bulimia; pr egnancy. Cyclic (usually non-GI cause): migraine; endocrine (e.g. Addison \200\231s disease ); metabolic (e.g. acute intermittent porphyria); intermittent GI obstruction; fabricated i llness. idiopathic; CNS disease; abdominal Management \200 Full history: members with similar illness. Full examination: Assess for dehydration. e.g. early morning vomiting with CNS tumor, or family including ear, nose, and throat (ENT) and growth. Treatment \200 Supportive \200 Treat \200 Pharmacological: extrapyramidal reactions); prokinetic drugs, e.g. domperidone. 5-HT3 antagonists, e.g. ondansetron, are increasingly being used for treating post-operative or chemotherapy induced vomiting. 5-HT1D agonists, e .g. pizotifen, are useful as prophylaxis and treatment for cyclic vomiting syndrome. treatment as needed: e.g. oral or IV \202 uids. cause: e.g. pyloromyotomy for hypertrophic pyloric stenosis. antihistamines; phenothiazines (side-effects: Complications Dehydration, plasma electrolyte disturbance (e.g. d K+, d Cl \200\223, alkalo sis with pyloric stenosis), acute or chronic GI bleeding (e.g. Mallory \200\223Weiss tear), oesophageal stricture, Barrett \200\231s metaplasia, broncho-pulmonary as- piration, falte ring growth, iron de \201 ciency anemia. Psychogenic vomiting \200 Causes: family history of vomiting is common. Management: anxiety; manipulative behavior; disordered family dynamics. A exclude organic disease. Refer to child psychologist. 10_McClure_10.indd 300 11/14/2012 11:28:46 PM VOMITING 301 Box 10.1 Investigations for vomiting Acute (if severe) \200 \200 \200 \200 \200 \200 \200 FBC U&E Creatinine Stool for culture and virology AXR Surgical opinion if obstruction or ac ute abdomen possible Exclude systemic disease Chronic \200 FBC \200 ESR/CRP \200 U&E \200 LFT \200 Helicobacter \200 Urinalys is \200 Abdominal US \200 Small bowel enema \200 Sinus X-rays \200 Test feed or abd ominal ultrasound for pyloric stenosis \200 Brain imaging (CNS tumor) \200 Consider uri ne pregnancy testing in teenage girls \200 Upper GI endoscopy pylori serology Cyclic As for chronic vomiting, plus the following: \200 \200 \200 \200 Serum amylase Serum lipase Blood glucose Serum ammonia 10_McClure_10.indd 301 11/14/2012 11:28:46 PM CHAPTER 10 Gastroenterology and nutrition 302 Acute diarrhea Normal stool frequency and consistency vary, e.g. breastfed infants may pass 10 \200\22312 stools per day, primary school children may pass stool from three times a da y to once every three days. Diarrhea is a change in con- sistency and frequency of stools w ith enough loss of \202 uid and electrolytes to cause illness. It kills 3 million childre n per year worldwide. Acute diarrhea Causes \200 \200 \200 \200 \200 \200 \200 \200 \200 b p.338). Infective gastroenteritis. Most common cause ( Non-enteric infections, e.g. respiratory tra ct. Food hypersensitivity reactions ( b p.178). NEC ( Drugs, e.g. antibiotics. Henoch \200 \223Sch nlein purpura (HSP) ( b p.860). Intussusception (<4yrs) ( Haemolytic \200\223uraem ic syndrome ( Pseudomembranous enterocolitis. b p.316). b p.788). b p.376). Presentation \200 \200 \200 Fever +/ \200\223 vomiting (infectious gastroenteritis). Diarrhea +/ \200\223 bloody stools (colitis \200\224infectious or non-infectious). Dehydration and d consciousness. Management \200 Assess hydration and vital signs, pallor (blood loss), abdominal tenderness, signs of assoc iated illness (e.g. petechial rash in HSP). Mild/moderate dehydration: \200 \200 no tests necessary; replace \202 uid and electrolyte losses with oral glucose \200\223ele ctrolyte based rehydration \202 uid, e.g. Dioralyte (UK). Severe/shock dehydration: \200 U&E, creatinine, FBC, blood gas, stool M,C&S/virology, tests for speci \201 c disease (e.g . US in suspected intussuseption); IV \202 uid and electrolyte replacement (see b pp.65, 89 \200\22393). Anti-motility drug treatment is not recommended; it can be harmful, particularly in acute i nfection/in \202 ammation. Antibiotics are not indicated unless cause is proven, e.g. Yers inia or Campylobacter infection, parasitic infection, NEC, or proven bacteraemia/systemic i nfection. Other treatment is disease speci \201 c. Some diarrhoeal processes require remov al of the offending agent, such as in lactose intolerance or coeliac disease or allergic ga stroenteritis. Others may require bowel rest or surgery, e.g. NEC or intussusception. Once rehydrated, resume normal diet. Replace on going losses. Continue breast feeding. There is no evidence that prolonged starvation is bene \201 cial in infective gastroenteritis. 10_McClure_10.indd 302 11/14/2012 11:28:46 PM ACUTE diarrhea 303 Prevent cross-infection with strict hand washing and barrier nursing. In the less developed world, breastfeeding, provision of clean water, and adequate sanitation are also important to reduce risk of infection. Investigations See b p.301. Prognosis The majority of cases, particularly if caused by infe ctive gastroenteritis, make a complete recovery with appropriate treatment. 10_McClure_10.indd 303 11/14/2012 11:28:46 PM CHAPTER 10 Gastroenterology and nutrition 304 Chronic diarrhea Chronic diarrhea De \201 ned as diarrhea persisting for >14 days. Many of the diseases that cause acute diarrhea can lead on to chronic diarrhea. The pathophysiology may involve: Reduced GI absorptive capacity, e.g. coeliac disease. Osmo tic diarrhea, e.g. lactase de \201 ciency. In \202 ammatory, e.g. ulcerative colitis. Sec retory diarrhea (rare), e.g. vasoactive intestinal peptide producing tumor. \200 \200 \200 Causes Age 0 \200\22324mths \200 b p.334), e.g. post-infective gastroenteritis Malabsorption (see syndrome, lactose intolerance, cystic \201 brosis, coeliac disease. Fo od hypersensitivity, e.g. to cow \200\231s milk protein. Chronic non-speci \201 c diarrhea (toddler diarrhea); child is usually thriving (b p.305). Excessive \202 uid intake. Prot racted infectious gastroenteritis. Immuno-de \201 ciencies, including HIV. b p.870). Hirsc hsprung \200\231s disease ( Rarer causes (intractable diarrhea) include congenital mucosal transportation defects and autoimmune enteropathy. Tumors (secretory diarrhea). Fabricated induced illness. \200 \200 \200 \200 \200 \200 Older children \200 \200 \200 \200 \200 In \202 ammatory bowel disease (IBD). Constipation (spurious diarrhea). Malabsorption \200 \224see Causes. Irritable bowel syndrome (IBS). Chronic infections, including giardiasis, b acterial overgrowth, and pseudomembranous colitis. Laxative abuse. Excessive \202 uid int ake. Fabricated induced illness. \200 \200 History Nature and frequency of stool, presence of undigested food, relationship to diet ch anges (e.g. weaning) or travel, stool blood, or mucus, weight loss. Examination Features of malnutrition or other illness, e.g. peri-anal disease in in \202 a mma- tory bowel disease, or \201 nger clubbing in cystic \201 brosis. 10_McClure_10.indd 304 11/14/2012 11:28:46 PM CHRONIC diarrhea 305 Investigations \200 Stool: fat globules (pancreatic diseases), fatty acid crystals (diffuse mucosal defects); c ulture; pH (<5.5 = carbohydrate malabsorption); reducing substances (>0.5% = carbohydrate m alabsorption); fecal occult blood (colitis); electrolytes (i Na+ and K+ = secretory diarrhe a; i Cl \200\223 = congenital chloridorrhoea). U&E; FBC (d Hb = haematinic de \201 ciency or blood loss; Blood: i eosinophil = food hypersensitivity or parasites); i CRP/ESR (in \202 ammatory); blood gas; radioallergosorbent test (RAST) (food allergy); hormone level (v anillylmandelic acid (VMA), catecholamines, vasoactive intestinal polypeptide (VIP)) for se cretory tumors. Radiology: Other: overgrowth); GI endoscopy biopsy (e.g. upper for coeliac disease, upper and lower for suspected IBD); sweat test/genetic testing (CF); rectal biopsy (Hirschsprung \200\231s disease). inspection; microscopy for bacteria or parasites, leucocytes, \200 AXR, ultrasound, barium meal and follow through. breath hydrogen test (lactose malabsorptio n or bacterial Treatment \200 \200 \200 Treat underlying cause. Nutritional intervention if de \201 ciencies are present. Antibiot ics are only useful if systemic illness or prolonged infection is present, e.g. Salmonella, Campylobacter, giardiasis, or amoebiasis. Rarely, other drug treatment may be useful, e.g. loperamide or cholestyramine. Chronic non-speci \201 c diarrhea (toddler diarrhea) \200 \200 Occurs from 6mths to 5yrs. Presents with colicky intestinal pain, loose stools with undiges ted food ( \200\230peas and carrots \200\231 stools). Child is otherwise well and thriving. Examination and investigations are normal. i \202 atus, abdominal distension, \200 Treatment Reassurance; dietary (i fat intake; normalize \201 bre intake; d milk, f ruit juice, and sugary drink intake); loperamide occasionally may be necessary. Encopresis \200 Voluntary defaecation in unacceptable places, including the child \200\231s pants in older children. No organic abnormality is present; it is a symptom of an emotional disorder. It i s three times more common in boys. Once organic disease or spurious diarrhea secondary to c onstipation with loading are excluded (see b pp.306 \200\223307), consider behavioral probl ems and referral to a child and adolescent psychiatrist. \200 10_McClure_10.indd 305 11/14/2012 11:28:46 PM CHAPTER 10 Gastroenterology and nutrition 306 Constipation De \201 ned as infrequent passage of stool associated with pain and dif \201 culty, or delay in defaecation. \200 \200 \200 \200 95% of infants pass (cid:1)1 stool/day. 95% of school children pass (cid:1)3 stools/wk. Con stipation is common in childhood. Approximately 5% of school children suffer signi \201 ca nt constipation, usually functional. Organic cause more likely if: delayed passage of mecon ium beyond 24hr of age; onset in infancy; severe; associated with faltering growth or abnor mal physical signs (include per anal examination). Causes Idiopathic Commonest due to a combination of: \200 \200 \200 Low \201 bre diet. Lack of mobility and exercise. Poor colonic motility (55% have a posit ive family history). Gastrointestinal \200 \200 \200 \200 \200 Hirschsprung \200\231s disease. Anal disease (infection, stenosis, ectopic, \201 ssure, h ypertonic sphincter). Partial intestinal obstruction. Food hypersensitivity. Coeliac diseas e. Non-gastrointestinal \200 Hypothyroidism. \200 Hypercalcaemia. \200 Neurological dise ase, e.g. spinal disease. \200 Chronic dehydration, e.g. diabetes insipidus. \200 Drugs , e.g. opiates and anticholinergics. \200 Sexual abuse. Presentation \200 \200 \200 \200 \200 \200 Straining and/or infrequent stools. Anal pain on defaecation. Fresh rectal bleeding (anal \201 ssure). Abdominal pain. Anorexia. Involuntary soiling or spurious diarrhea (liquid fe ces passes around solid impaction). Flatulence. Growth. d \200 \200 \200 \200 \200 Abdominal distension. Palpable abdominal or rectal fecal masses, usually indentible. Anal \201 ssure. Abnormal anal tone. A rectal examination is normally unnecessary unless child fails to responds to initiation of simple treatment, except in infancy when anal stenosis s hould be considered. 10_McClure_10.indd 306 11/14/2012 11:28:46 PM CONSTIPATION 307 Management (See Box 10.2) Investigations are usually not necessary. If an organic cause is suspected consider: FBC; coeliac antibody screen; thyroid function tests; serum Ca2+; RAST testing; AXR; bowel transit studies (older child); rectal biopsy (for Hirschsprung \200\231 s disease); anal manometry; spinal imaging (neurological cause). Box 10.2 Treat in a stepwise manner \200 \200 \200 Treat any underlying organic cause Dietary: Behavioral measures: meals; star charts and rew ards for child passing stool; reassure parents and encourage them not to show concern to th e child i oral \202 uid and \201 bre intake, natural laxatives, e.g. fruit juice toilet footres ts; regular 5min toilet time after The aim of medication maintainance. \200 \200 is to achieve disimpaction and then Emphasize the need for consistency and adherence Poor adherence and failure to evacuate fec al masses preclude improvement Treat for at least 3mths. It is important not to wean therap y too soon Regular oral fecal softeners, e.g. Movicol docusate, will aid disimpaction Oral stimulant laxatives, e.g. senna, sodium picosulphate, may be required Consider treatment of any anal \201 ssure with topical anesthetic (2% lidocaine ointment) to reduce pain and r emove voluntary inhibition to defaecate Oral magnesium citrate, magnesium phosphate or larg e volume polyethylene glycol (PEG) electrolyte solution bowel clean out (may require nasoga stric administration for rapid infusion) Enemas, e.g. Micralax intensive treatment with abo ve Hospital admission may be required for the most severe for either manual evacuation unde r sedation or general anesthesia, or oral PEG , lactulose, or sodium or phosphate enemas, only if no response to Prognosis The vast majority of children can be \200\230cured \200\231 by an enthusiastic a nd sympa- thetic pediatrician with complete evacuation of any stool masses, main- taining s oft stools, and defaecation training. Many children need long term therapy. Do not underest imate the misery that this condition can in \202 ict on both the child and family. 10_McClure_10.indd 307 11/14/2012 11:28:46 PM CHAPTER 10 Gastroenterology and nutrition 308 Faltering growth (failure to thrive) Faltering growth, also known as failure to thrive (FTT ), is when there is a failure to grow at the expected rate (i.e. growth \200\230falls away \200\231 from stan- dardized weight or height centile). Weight is the most sensitive indic ator in infants and young children, whilst height is a better in the older child. Under str ess, head circumference growth is more preserved than linear growth, which in turn, is more than weight gain. In infancy, birth weight re \202 ects the intrauterine environment. It is a poor guide to the child \200\231s correct \200\230genetic potential \200\231 and weight may naturally fa ll until the correct \200\230level \200\231 is attained. In a well, happy child consider c onstitu- tional small stature (characterized by normal growth velocity in a healthy child o f small stature parents). Causes 95% of true FTT is due to not enough food being offered or taken. In developing coun tries poverty is the main cause. In the UK, causes include socioeconomic dif \201 culties, emotional deprivation, unskilled feeding, or a particular belief system regarding appropri ate nutrition. Organic causes include: Decreased appetite, e.g. psychological or secondary to chronic illn ess. Inability to ingest, e.g. GI structural or neurological problems. Excessive food loss, e.g. severe vomiting (gastro-oesophageal re \202 ux disease (GORD), pyloric stenosis, dys motility), diabetes mellitus (urine). Malabsorption (see Increased energy requirements, e.g . congenital heart disease, cystic \201 brosis, malignancy, sepsis. Impaired utilization, e.g. various syndromes, IEM, endocrinopathies. \200 \200 \200 b p.334). Causes may overlap, e.g. in cystic \201 brosis there is simultanous malabsorp- tion, incr eased energy requirements, anorexia, and chronic infection. Management \200 Detailed history: Consider asking pediatric dietitian to perform detailed dietary history. Full examination: If organic disease possible: \200 including age of onset of FTT, and timing of weaning. \200 including accurate measurement of growth. basic investigations should include: 2+, FBC, ESR/CRP, U&E, creatinine, total protein and albumin, Ca PO4 immunoglobulins; coeliac a ntibody screen; urinalysis, including M, C&S. 3 \200\223 , LFT; \200 \200 are indicated if there are suggestive symptoms Further investigations: or the faltering growth is severe, and include: IEM screen; karyotype; serum lead (pica); sweat t est; upper endoscopy and small intestinal biopsy; CXR; bone age, skeletal survey (NAI); abd ominal US; head CT/ MRI; oesophageal pH monitoring; ECG; fecal occult blood. If non-organic disease: pediatric dietitian: is likely, seek dietary advice, preferably by a 10_McClure_10.indd 308 11/14/2012 11:28:47 PM FALTERING GROWTH (FAILURE TO THRIVE) 309 If FTT resolves in the next few weeks, give positive reinforcement and supervise subsequent growth as an outpatient. If FTT persists, admit to hospital for basic investigations and o bserve the response to supervised adequate dietary input. Adequate growth in hospital sugge sts a non-organic cause; explore and support family dynamics. Should FTT occur again at hom e after improvement in hospital, and then refer to social services for family assessment an d appropriate intervention. If FTT continues in hospital despite adequate dietary input, oc cult organic disease is most likely and requires extensive investigation as above. Provide dietetic input, whatever the cause, to support nutritional correction and education . Identify and correct associated comorbidities, e.g. developmental delay or early presenta tion of neurological disorder such as cerebral palsy; fall off in head growth is suggestive . Prognosis The prognosis depends on the severity of FTT. It is good if mild. Severe FTT, wha tever the cause, may be associated with later developmental and behavioral impairment. 10_McClure_10.indd 309 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 310 Recurrent abdominal pain \200 De \201 ned as more than two discrete episodes in a 3mth period interfering with school an d/or usual activities. Incidence: 10 \200\22315% in school age children. Causes No organic cause is found in 90%. Organic causes include: constipation; dietary indi scretion; food intolerance (lactose or fructose); irritable bow- el syndrome; psychogenic p ain; peptic ulcer (H. pylori); coeliac disease; abdominal migraine (cyclic vomiting syndrom e); gallbladder disease; renal colic; dysmenorrhoea; UTI; mittleschmerz; and physical or se xual abuse. Presentation Non-organic disease This form occurs in a thriving, generally well child; with short episodes of peri-umbilical pain, good appetite, no other GI symptoms, no family his- tory of migraine or coeliac disease, and normal examination. Co-existent symptoms such as headache and fatigue are common and this is often referred to as recurrent abdominal pain s yndrome. Organic cause Likely if presentation is different to above or child <2yrs. \200\230Red \202 ag \200\231 symp- toms include weight loss, diarrhea, blood per rectum, joint symptoms , skin rashes, family history of in \202 ammatory bowel disease, or coeliac di- sease. Management History Ethnic origin (lactase de \201 ciency occurs in dark skinned races), at opy, rela- tionship to eating, precipitating events (e.g. cow \200\231s milk introduction i n milk protein enteropathy), social history (e.g. start of school, parental separa- tion), and family history. Full examination Investigation \200 If non-organic disease is likely: no or very little investigation is needed, e.g. FBC, ESR/ CRP, U&E, LFT, coeliac antibody screen, urine M, C&S, fecal M, C&S (if there is a recent hi story of foreign travel). If organic disease is likely: investigate as above, plus consider hydrogen breath test (lactose intolerance); C13 breath test (Helicobactor pylori); US; bar ium radiology; upper and lower GI endoscopy. Treatment Non-organic disease Con \201 dent reassurance; education that condition is commo n and pain is genuine (just like headaches); personal support; avoidance of associated stre ssful events (e.g. bullying); acknowledgement of symptom, whilst at same time down playing pain; minimize secondary gains from abdominal pain, e.g. school avoidance; increased dietar y \201 bre intake may be bene \201 cial; 10_McClure_10.indd 310 11/14/2012 11:28:47 PM RECURRENT ABDOMINAL PAIN 311 formal psychotherapy in complex and resistant cases. Multidisciplinary support and engageme nt of the family is essential. Organic disease: Treat the underlying cause. Prognosis Approximately 25% of children with functional recurrent abdominal pain continue t o have pain or headaches in adulthood. Functional sequelae are common. Abdominal migraine Abdominal pain is associated with pallor, headaches, anorexia, nausea, + / \200\223 vomiting. The condition overlaps with periodic syndrome and cyclic vom- iting sy ndrome. There is usually a strong family history of migraine. Treatment \200 Dietary cola), solid cheeses. Pharmacological: may be helpful. : avoid citrus fruits, chocolate, caffeine-containing drinks (e.g. pizotifen, sumatriptan, gabapentin, or amitriptyline 10_McClure_10.indd 311 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 312 Gastrointestinal hemorrhage This condition is relatively rare in childhood. Upper GI tract bleeding may present as haematemesis (vomiting of frank blood or \200\230coffee grounds \200\231) or melaena (black, tarry, foul-smelling stools). Haematochezia (bright or dark re d blood PR) indicates lower GI tract bleeding. Beware of spurious hemorrhage, e.g. black stools after bismuth/iron ingestion, red vomit af ter beetroot, urate crystals in nappies, or normal pseudomenstruation in newborns. Use Dips tix test or laboratory testing to con \201 rm blood you are if unsure. Causes Neonates \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Swallowed maternal blood, i.e. not GI hemorrhage. NEC. Dietary protein intolerance. Coagulo pathy. Stress ulcers. Gastritis, vascular. Malformations. Duplication cyst. Infectious coli tis, including pseudomembranous colitis. In \202 ammatory colitis. Infants Most of the above plus: \200 \200 \200 \200 \200 Oesophagitis. Swallowed blood from upper airway, e.g. epistaxis. Anal \201 ssure. Intussu sception ( Meckel \200\231s diverticulum (often presents as a massive painless rectal bleed ; b p.865). b p.860). Older children Most of the above plus: \200 Peptic ulcer disease. \200 Mallory \200\223 Weiss tear. \200 Oesophageal varices. \200 Nonsteroidal anti-in \202 ammatory drugs (N SAIDs). \200 Intestinal polyps. \200 b p.332). IBD ( \200 GI infection, e.g. dysenter y. \200 HSP ( \200 HUS ( b p.788). b p.376). 10_McClure_10.indd 312 11/14/2012 11:28:47 PM GASTROINTESTINAL hemorrhage 313 Management See Box 10.3 \200 \200 