3 Review diagnosis; check inhaler use/concordance; eliminate triggers; moni- tor height. If <5yrs: Add 1 evening dose of montelukast 4mg as a mouth- dissolving capsule. If >5yrs: Add inhaled salmeterol 50 g/12h (long-acting \200 -agonist); monitor closely; stop if of no help. If symptomatic \200\200 inhaled steroid and try montelukast 5mg or theophylline, eg Slo-Phyllin 125 \200\223250mg/12h PO if 6 \200\22312yrs. If problems remain, add in step 4. 4 Refer to specialist ( CXR). 470 \200\200Inhaled steroid (Clenil 400 g/12h). 5 Add p rednisolone (if >5yrs) at lowest dose that works; check: growth. Dose examples: \200 -agon ists: Salbutamol 100 g via MDI as needed, with spacer. Admit if an attack is not controlle d by 2 \200\2234 puff s/20 \200\22330min (max 10 puff s). Anti- muscarinics: Ipratropium 20 g/8h by aerosol if 6yrs old; 40 g/8h if older. Treating severe asthma Calmness helps. \200\226Give these treatments if the above life-threatening signs are present, or if not im proving 15 \200\22330min after \200\224 starts. 1 Sit up; high- \202 ow 100% O2 if SpO2 < 92% in air 2 Salbutamol: 5mg O2-nebulized in 4mL saline (2.5mg if <5y) 15 g/kg slow IV (monitor ECG) 3 Prednisolone soluble tabs, 1 \200\2232mg/kg to max 40mg (60mg if already on steroids & <12yr), 50mg >12y 6 Consider 1 IV dose of magnesium sulfate, 40mg/kg over 20min ( \211 2g); intracellular Mg2 + is \200\201 471 7 Peak \202 ow before & after each nebulizer; normal values, see BOX 8 Nebulizers as needed, eg at 30 min, 1h, 2h, 3h & 4h with ipratro- pium 0.25mg mixed in if n eeded 9 Take to ITU if exhausted, confused, coma, or refractory to \200\224 and need- ing IVI salbutamol (2 g/kg/min) 4 Oxygen nebulised ipratropium 250 g if <12y, 500 g if >12y 5 \200\226Aminophylline 5mg/kg IV over 20min (not if al- ready on a xanthine); then IVI am inophylline (BOX) Before discharge ensure: \200 Peak \202 ow >75% of predicted \200 Good inhaler tech- nique \200 Is stable on discharge regimen \200 Taking inhaled steroids+oral predniso- l one \200 Written management plan \200 Follow-up: GP in 1 week; in clinic in 4 weeks. P revention \200\201Triggers. 472 A Mediterranean diet rich in fruit (esp. if eaten by the m other in pregnancy) may help. 473 Homeopathy 474 and \202 u vaccination don \200\231t hel p. 165 Peak \202 ow (litres/min) in normal boys and girls (5 \200\22318 years) Height cm Mean 100 113 120 125 130 135 140 145 3rd centile Height cm Mean 3rd centile 300 320 350 370 400 430 450 470 500 110 160 210 240 260 290 310 350 150 155 160 165 170 175 180 185 190 360 400 420 450 470 500 520 550 570 100 140 160 190 220 240 270 s c i r t a i d e a P Lung function measurements cannot reliably guide management in those <5yrs old. Inhaler and nebulizer questions \200 If <8yrs old, pressurized metered dose inhalers (pMD I)1 with a spacer2 are best for routine use in stable asthma for both steroids and bronchod ilators. Nebulizers are not more effi cacious than a well-used inhaler. \200 Avoid using dry powde r inhalers + pMDIs as techniques get muddled. \200 Is there a better alternative to nebul izers (bulky and need servicing)? Evidence supports valved holding chambers (eg AeroChamber Plus ).2 475 \200 Do combined inhalers off er added value? The SMART study Symbicort mainte- nance & relief therapy shows real bene \201 t from a \201 xed dose of long-actin g \200 -agonist (formoterol) with budesonide (4.5/80 g/day + additional puff s for sympto m relief). Doc- tor dependency was less, and there were fewer exacerbations. 476 Continuous IVI of aminophylline Aminophylline mg/kg/h \200\207Monitor ECG 1.0 0.5 \200\2230.7 After loading dose3 of 5mg/kg IV 1 month \200\22312yrs Children >12yrs \200\207Confer with experts; target serum level: 10 \200\22320mg/L. SE: BP \200\201; arrhythmias; arrest if \200\20625mg/L. Pitfalls in managing asthma \200 Reluctance to diagnose until a serious attack occurs. \200 Faulty inhaler technique. Watch the patient operate the device. \200 Inadequate per ception of, and planning for, the severe attack. \200 Unnoticed, marked diurnal variation in airways obstruction. Always ask about nocturnal waking; it is a sign of dangerous asthma. Being satis \201 ed with less than total symptom control. \200 Forgetting to start proph ylaxis \200\224and not using oral prednisolone early. \200 Too much inhaled steroid (>400 g beclometasone or >800 g of budesonide)/ day if \200\20512yrs old: 477 4 consider adre nal insuf \201 ciency if \200\201consciousness; do blood glucose; IM hydrocortisone may b e needed. Monitoring growth is not a good way to screen for adrenal suppression (cortisol \200\205500nmol/L). 478 1 pMDI=press-and-breathe pressurized meter dose inhaler \200\224as recommended by NICE. 2 S pacers: (eg AeroChamber \200\224a responsive inspiratory valve allows opening on minimal eff ort to aid inhalation; it closes before exhalation disturbs retained aerosol) Static ch arge is a problem. Clean monthly. Wash in detergent. Dry in air. Wipe mouthpiece clean of d etergent before use. Replace yearly. 3 If previous theophyllines used but level is subthera peutic, a unique loading dose may be tried; to help calculate this, increasing a dose by 1m g/kg causes an increase in serum theophylline of 2 g/mL. Get help. Erythromycin \200\200 aminophylline \200\231s half-life \200\224also cipro \202 oxacin, propranolol, and the Pil l. Drugs which \200\201t : phenytoin, carbamazepine, barbiturates, and rifampicin. Do pla sma concentrations. 4 Anti-IgE agents may \200\201 need for steroids. Omalizumab is a reco mbinant humanized monoclonal an- tibody directed against IgE and can inhibit the immune sys tem \200\231s response to allergen exposure. It pre- vents IgE from attaching to mast cells , reducing IgE mediated in \202 ammation.479 Infective endocarditis (IE) Signs Fever, splenomegaly, clubbing, splinter hemorrhages, anem ia, rash, heart failure, microscopic haematuria, new murmur (eg with known congeni- tal hea rt lesion or IV line in situ). Typical cause: Streps; staphs. 480 Tests Blood cultures (dif f erent times and diff erent sites), echocardiograms. Blind treatment After 3 blood culture s: benzylpenicillin 25mg/kg/4h IV + gen- tamicin (p175); get microbiological help. Preventi ng endocarditis Prophylactic antibiotics are now generally not rec- ommended. Advise on ora l hygiene. 481 166 OHCM p144 \200 Rheumatic fever This is a systemic febrile illness caused by a cross-sensitivity reaction t o Group A \200 -haemolytic streps, which, in the 2% of the population that is susceptible, may result in permanent damage to heart valves. It is common in developing countries, but is rare in the West, but pockets of resurgence sometimes occur in the USA in overcrowded ar eas (favors streptococcal spread). Some speci \201 c Group A streptococcal serotypes are k nown to be particularly rheumatogen- ic \200\224eg type 5 of the M-protein serotypes. Other ubiquitous serotypes appear to be non-rheumatogenic (eg type 12). 482 Incidence: 500,000/y r (worldwide). 483 Jones diagnostic criteria are said to be over-rigorous (will miss some c ases) 484 \200\224but here they are: elicit 2 major criteria or 1 major and 2 minor plus ev idence of preceding strep infection: scarlet fever, a throat swab with \200 -haemolytic st reptococci or a serum ASO titre >333U/L (reference intervals vary). 485 s c i r t a d e a P i Major criteria: (revised 2001) \200 Carditis (1 of: changed murmur; CCF; car- Minor criteria: \200 Fever \200 ESR >20mm or C-reactive protein \200\200 \200 Arthral gia, ie pain but no swelling \200 ECG: PR interval >0.2sec \200 Previous rheumatic feve r or rheu- diomegaly; friction rub; +ve echo) Polyarthritis (often migratory) \200 Erythema marginatum, OHCM p564 \200 Subcutaneous n odules \200 Sydenham \200\231s chorea (p654). matic heart disease. Don \200\231t count arthralgia if polyarthritis is used as a major criterion; likewise for long P \200\223R if carditis is used. Joints: Knees, ankles, elbows & wrists may be very te nder, but no permanent sequelae. Echo criteria: Mitral regurgitant jet is: >1cm; holosystol ic (throughout systole); visible in 2 planes; mosaic pattern (ie chaotic \202 ow). The MacCallum plaque1 is at the base of the posterior mitral lea \202 et. Aortic, pulmonar y and tricuspid valves are aff ected in descending order of frequency. Treatment of rheumat ic fever Rest/immobilization helps joints and heart. Aspirin (high-dose, p646; but get advi ce re Reye \200\231s, p652). If severe, get help. Prednisolone (below) may help. 486 Penici llin for pharyngitis ( 125mg/6h PO) preceded by one dose of benzylpenicillin (25mg/kg IM or IV). Sydenham \200\231s cho- rea: unless mild, consider prednisolone (2mg/kg/day[5] for 4w ks, then taper; halves time to remission to \200\2058 weeks; emotional and learning diffi culties can take far longer to resolve). 487 Consider haloperidol; valproic acid; carbamaz- epine. 488 Prevention Primary: Where incidence is high, this might be worthwhile, but migh t entail giving IM penicillin for sore throats. 489 Secondary: Symptoms are often worse on recurrence of rheumatic fever \200\224eg seen in 2.6%. 480 Prevent with phenoxymethylpenici llin 125mg/12h <6y; 250mg/12y >6y. 491 1 MacCallum \200\231s plaque is due to subendocardial Aschoff bodies: these are a classic h istological feature of rheumatic fever. They are perivascular with a necrotic core set in a layer of lymphocytes. Nodules are found in joints, tendons, heart, and blood vessels. They heal with extensive myocardial \201 brosis. PANDAS (pediatric autoimmune neuropsychiatric disorders associated with strep infections). Suspect this in those with tics (or Tourette \200\231s syndrome, OHCM p692) and obsessive \200\223compulsive disorder. Anorexia nervosa may also be a fea- ture. Antibiotics and risp eridone have been tried. 492 \200\223494 See p654. 167 s c i r t a i d e a P Deaths/yr=1.5 \211\210106 children worldwide495 Diarrhea Diarrhea may be an early sign of a ny septic illness. Feces are sometimes so liquid they are mistaken for urine. NB: it is nor mal for breastfed babies to have liquid stools. Gastroenteritis Rotavirus is the most commo n cause of gastroenteritis in in- fants and children. It causes 600,000 childhood deaths/y r (a vaccine is availa- ble). 496 Other enteric viruses: Norovirus (most common cause in ad ults), astro- virus; adenovirus. Treatment: 497 \200\207If dehydrated, see p234. Weigh, to monitor progress and quantify dehydration, if a recent previous weight is known. Start ora l rehydration therapy (ORT), eg Dioralyte , at 50mL/kg over 4h ( \211\2101mL/kg every 5min s). Continue breastfeeding. If child refuses ORT, off er other \202 uids (eg bottle milk/ water \200\224not fruit juice) or consider ORT via a nasogastric tube. IV therapy is reserv ed for those who deteriorate or are in shock. Reintroduce milk after 4h of rehydration with ORT (even if <6 months), or sooner if he re- covers and is hungry (starving harms). 498 Us e of antiemetics (ondansetron 0.1 \200\2230.15mg/kg) has been shown to decrease vomiting 49 9 and reduce need for IV \202 uids, hospital admission 450 and overall costs, 451 but isn \200\231t offi cially recommend- ed. Complications: Dehydration; malnutrition; temporary s ugar intolerance after D&V with explosive watery acid stools. (Rare; manage with a lactose- free diet.) Post-enteritis enteropathy resolves spontaneously after 7wks. Tests: Stool: lo ok for bacteria, ova, cysts, parasites. Prevention: Hygiene, good water & food, education, \202 y control. Classi \201 cation diarrhea by mechanism Secretory ( \200\201absorption or \200\200secretion) Stool is watery even if fasting, eg: cholera, C. dif \201 cile, E. coli, carcinoid. Osmotic: ( \200\200osmotic load in gut lumen). Stool is watery, acidic, an d +ve for reducing substances; to detect mix 5 drops of stool + 10 drops H2O + 1 Clinitest tablet, eg: galactose, glucose, sorbitol, or lactose intoler- ance, laxative abuse. Motil ity disorders: Increased: Thyrotoxicosis, irritable bowel syndrome dumping syndrome. Decrea sed: Pseudo-obstruction, intus- susception (eg <4yrs old). In \202 ammatory: (eg bloody di arrhea), salmonella, shigella, campylobacter, rotavirus, amoebiasis, NEC (p120), Crohn \200 \231s/UC (look for weight \200\201; anemia; WBC \200\200; platelets \200\200; ESR \200\200) , coeliac disease, haemolytic uraemic syndrome (p176). 168 \200 s c i r t a d e a P i \201\201Rising food prices + global warming + political corruption \211\210 malnutrition + war Malnutrition \200\207Being a major cause of death and misery, this is a global issue for u s all. Kwashiorkor is due to \200\201intake of protein & essential amino acids. Signs: Poo r growth; diarrhea; apathy; anorexia; oedema; skin/hair depigmentation; distended abdomen; glucose \200\201; K+ \200\201; Mg2+ \200\201; Hb \200\201; cholesterol \200\201; albumin \200\201. \201\227: Re-educate child, family, and politicians. Off er a gradually increasi ng, high-protein diet + vitamins. Marasmus is lack of calories + discrepancy between height and weight. It is HIV-associated. 502 Signs: distended abdomen, diarrhea, constipation, in fec- tion; albumin \200\201. Mid-arm circumference <9.9cm (any age) predicts severe mal- nu trition better than being <60% of median weight for age, or 85% of median height for age an d 70% of median weight for height. Most can be treated at home with forti \201 ed ready-to -use foods if >6 months. 503 Parenteral feeding may be needed to restore hydration and rena l function. Next off er a balanced diet with vitamins. Despite this, stature and head circu mference may remain poor. Kwashiorkor and marasmus may coexist (protein-energy malnutrition ). 504 Prevention: \200\207Stop man-made activity contributing to climate instability. \200\207Stop biofuels supplanting food crops. \200\207Give to charity www.oxfam.org (to pa y for fertilizers, high-yield seeds, and simple irrigation schemes). Medically, we often ta rget the malnourished (Z score \200\2232, p227) at aged \200\2235yrs, found by screenin g, but better results are got by giving universal help at \200\2232yrs in at- risk place s. 505 169 How does poverty impinge on childhood mortality & morbidity? Worldwide, poor mothers are at \200\200 risk of death: there is no worse start to life than the death of one \200\231s m other (100% fatal to her babies in some places). Poverty-associated short stature, BMI <18.5 (p530) and iron de \201 ciency in \200\235 g n i h g u a l mothers accounts for 20% of maternal mortality. Malnutrition causing stunting causes 2.2 million deaths/yr and 21% of disability-adjusted life years (DALYs) in children <5yrs old. 506 e l p o e p De \201 ciencies in vitamin A and zinc cause 1 million deaths/yr. Zinc supple- mentation1 cannot always be relied on to \200\201morbidity in children recovering from diarrhea and r espiratory illness in developing countries. 507 Prevention of the poverty which caused the diarrhea is more important. y n a m d r a e h s c i r t a i d e a P Not breastfeeding for the 1st 6 months of life (especially non-exclusive breastfeeding) cau ses 1.4 million deaths/yr in children <5yrs old. 508 NB: the position is further complicate d by the fact that proteins, fat concentrations and caloric value in breast milk from under nourished mothers are lower than in breast milk from well-nourished mothers. i e v r a t s n o s r e p 1 \200\2234 above account for 35% of child deaths and total global disease burden. In many other conditions (eg diarrhoeal diseases, HIV, asthma, obesity) pov- erty plays a leading r ole. But the main health issue is that it \200\231s harder to edu- cate yourself if you liv e in a slum. \200\207No power \211\210 no light \211\210 no homework \211\210 no learni ng \211\210 an early death. e n o d r a e h I \200\234 Southern diarrhea is only an excuse for northern amnesia As you read this page two events u nfold: in the northern hemisphere a child is born with a silver spoon in his mouth, his fut ure assured thanks to incubators, ventilators, wealth, and family planning. Diametrically o pposed to this birth another occurs in the southern hemisphere where the silver was mined f or that lovely spoon. This child, according to our stereotype, must \200\234Wait for his f uture like a horse that \200\231s gone lame To lie in the gutter and die with no name \200 \235. 509 We assume that this death is from diarrhoeal diseases that we are all working, mo re or less effi ciently, towards control- ling \200\224and we are pleased to blame non-huma n agencies for these deaths. . g n i n i l r e v l i s o n d n a s s e r g o r p o n This model of our imperfect world does not stand up to scrutiny for two reasons: one is eas y to understand (the diarrhea was the mode of dying not the cause of death, which was pover ty) and the other is impossible to understand \200\224we didn \200\231t just let him die. W e wanted him to die: in fact we killed him: in some cases, literally. Follow this well-docu mented thought sequence: There are too many homeless children living in my back yard \200 \203This threat- ens health and hygiene \200\203How do we deal with this? \200\203Other thr eats to health and hygiene are vermin \200\203Street children are a sort of vermin \200\203 Vermin need eradicating \200\203Let \200\231s shoot the vermin \200\203Extrajudicial shooti ng of children \200\224as occurred in Rio de Janeiro in 1994 and Sao Paulo in 2004. 510 In the former, most \200\230ordinary decent folk \200\231 approved of the killings when they phoned a local radio station, as the events unfolded \200 \200\234I killed you because yo u had no future. \200\235 511 \201\201The point of all this is to illustrate that if we wa nt to do something for children it is no good just doing something about the big killers, s uch as diarrhea, and it \200\231s no good simply attacking poverty, for there is something dark in our human heart which needs addressing before merely statisti- cal or biological in terventions have any chance of success. There is only one way of in \202 uencing human nat ure for the better, and that is through dialog. So, in this sense, the treatment of diarrhe a is dialog. Without such dialog the rich wring their hands while poverty wrings necks. s i e r e h t : s n i w s y a w l a d n a , m s i u r t l a h t i w r a w t a s i m s i l a i r e t a M 1 Strategies for supplementing vit A (in neonates & late infancy), Zn & Fe for children and universal pro- motion of iodized salt can improve nutrition and prevent related diseases, and may reduce stunting at 36 months by 36% and mortality between birth and 36 months by ab out 25%.512 Abdominal pain Acute abdominal pain Children \200\2058yrs old often have diffi culty in lo calizing pain, and other factors in the history may be more important. 513 Pointers: \200 Hard feces suggest that constipation is the cause (p210). \200 In those of African or Me diterranean origin, suspect sickle-cell disease. \200 Do tuberculin test (OHCM p398) if t ravel or other factors suggest TB risk. \200 In children with pica (p210), do a blood lea d level (and ferritin). \200 Abdominal migraine is suggested by periodic abdominal pain w ith vomiting 170 \200 especially if there is a positive family history. If any past UTI, suspect GU disease (eg renal colic or hydronephrosis). Common physical cau ses Gastroenteritis, UTI, viral illnesses (eg tonsillitis as- sociated with mesenteric aden itis), and appendicitis. Rarer causes Mumps pancreatitis; diabetes; volvulus; intussuscepti on; Meck- el \200\231s diverticulum; peptic ulcer; Crohn \200\231s/ulcerative colitis, Hirs chsprung \200\231s dis- ease; Henoch \200\223Sch nlein purpura and hydronephrosis. Conside r menstruation or salpingitis in older girls. \200\207In boys always check for a torted te stis. Tests \200\207Always microscope and culture the urine. Others: consider plain ab- do minal x-ray; ultrasound; FBC; ESR; renal imaging, barium studies. Appendicitis (OHCM p610) is rare if <5yrs, but perforation rates are high in this group (nearing 90%). Think: how ca n I tell this from other causes of abdominal pain? \200 Clues in the history: increasing pain in right lower quadrant, no previ- ous episodes, anorexia, slight vomiting, absence of cough and polyuria. \200 Ex- amination hint: fever and pulse \200\200 are likely; if the child appears well and can sit forward unsupported, and hop, appendicitis is unlikely. \200 Tests have very low positive and negative predictive values. Gastro-oesophageal re \202 ux/oesophagitis Presents with regurgitation, dis- tress after feeds, apnoea, pneumonia , failure to thrive, and anemia. Tests: En- doscopy + evaluation with an oesophageal pH pro be is more reliable than bar- ium studies. Ultrasound is not much help. Treatment: Reassura nce; avoid over feeding (a common cause). Drugs may be needed, eg an antacid + sodium/mag- nesium alginate, eg for term infants, Infant Gaviscon dual dose sachets, 1 dose mixed wit h 15mL boiled (cooled) water. This paste is given by spoon after each breast feed. If bottl e fed, give each half of a dual sachet dose dissolved in 4oz of feeds. Carobel thickens t he feeds. If this fails, some experts use domperidone omeprazole (or similar). Most reso lve by 6 \200\2239 months; if not, consider fundoplica- tion, eg if there is failure to thr ive, severe oesophagitis, apnoea, or bleeding. s c i r t a d e a P i Abdominal distension Always remember acute GI obstruction as a cause; also consider: Cysts: Air: Fecal impaction Nephrosis Air swallowing Malabsorption Solid masses: Wilms \200\231 tumor Polycystic kidney Hypoproteinaemia Neuroblastoma Hepatic ; dermoid Cirrhosis; CCF Ascites: Adrenal tumor Pancreatic Hepatomegaly Infections: many, eg infectious mononucleosis, CMV. M alignancy: leukemia, lymphoma, neuroblastoma (see below). Metabolic: Gaucher \200\231s and Hurler \200\231s diseases, cystinosis; galactosaemia. Others: sickle-cell disease and other haemolytic anaemias, porphyria. Splenomegaly All the above causes of hepatomegaly (not neu roblastoma). Neuroblastoma This may be thought of as an embryonal neoplasm, derived from sy mpathetic neuroblasts. presenting with decreasing frequency from birth to 5yrs of age. Some forms regress, while others present after 18 months old (eg with metastases DVT) are hi ghly malignant (outlook is poor and has not improved over the last 25yrs). Prevalence: 1 : 6000 \200\2231 : 10,000 \200\224the most common solid tumor in the under-5s. Signs: Abdomin al swelling. Metastatic sites: Lymph nodes, scalp, bone (causing pancytopenia osteolytic lesions). In 92%, urina ry excretion of catecholamines (vanillylmandelic & homovanillic acids) are raised. Treatmen t: Refer to special center. Excision (if possible) and chemotherapy (eg cyclophosphamide + doxorubicin). Prognosis: Worse if cer- tain genotypes (pseudodiploid karyotypes, chromosome 1p deletions, N-myc gene ampli \201 cations), less mature catecholamine synthesis, and if >12 months old. Those <1yr do best. Prevention: Pre-morbid screening by looking for ex- cr etion of catecholamines in the urine detects disease early, but may not to save lives. 514 Uncertainty is added by a 2008 study which appeared to record lower mortality in a screened group, (although it was a very large study, it is dubious, being retrospective). 515 Recur rent abdominal pain \211 10% of children >5yrs suff er recurrent abdominal pains interferi ng with normal activity. Is there organic disease? No cause is found in most, but don \200 \231t let this encourage complacency (you may delay di- agnosis of Crohn \200\231s or pepti c ulcer) or lead to zealous diagnosis of underlying psychological problems (now thought to be less important, but do consider it: who is present when the pain starts; what, or who, m akes the pain better?). NB: long-term follow-up indicates a 4-fold \200\200risk of psychol ogical problems manifesting in adult life. Consider: gastro-oesophageal re \202 ux, small bowel dysmotility, gastritis, duodenitis, carbohydrate malabsorption (eg lactose, sorbitol) , abdominal migraine. Who to investigate: There are no rules. Do an MSU. Be suspicious if p ain is unusual in terms of site, character, frequency, or severity. Whenever symptoms are p resent for more than a few months re- check for associated features, eg in in \202 ammator y bowel disease (Crohn \200\231s) there may be no diarrhea in 50%, according to one careful study, 516 but poor growth is often the clue that prompts further tests. 171 s c i r t a i d e a P Coeliac disease: an example of malabsorption Malabsorption typically presents with diarrhea , failure to thrive anemia (folate \200\201; ferritin \200\201), possibly with abdominal protrusion, everted umbilicus and wasted buttocks (if late-present- ing). As subclinical/l atent forms exist, investigate any unexplained anemia, fatigue, \200\230irritable bowel \200\231 symp- toms, diarrhea, weight \200\201, arthralgia, eczema, and short stature. Pati ents may present at any age. Coeliac dis- ease may cause short stature without overt gastro intes- tinal signs or symptoms. There may be a deceleration on the growth chart after intro duction to gluten at wean- ing (4 \200\2236 months). See \201 g 1. Cause: Enteropathy ind uced by gluten (in wheat, barley, and rye). \202\202 : Serological tests show raised IgA a nti-tissue transglutaminase (IgA- tTG), anti-gliadin (IgA-AGA), and endomysial antibodies ( EMA). Also measure total IgA \200\224if de \201 cient measure IgG anti-gliadin antibodies. 517 Serology is less reliable if <18mths \200\224IgA-AGA may be most useful in this age gr oup. 518 Con \201 rm by \201 nd- ing villous atrophy on small bowel biopsy (endoscopic u nder GA is better than Crosby capsule). Villi return to normal on the special diet; avoid a gluten chal- lenge test unless diagnosis is in doubt. 519 \201\227: Gluten-free diet: no wheat, barley, rye (no bread, cake, pasta, pizza, pies). Rice, maize, soya, potato, and jam are OK (also \200\20525g/day of pure oats). 520 Canadian Celiac Assoc. 2007 Gluten-free b iscuits, \202 our, bread, and pasta are prescribable. Minor dietary lapses may matter. Ot her causes of malabsorption: Cystic \201 brosis; post-enteritis enteropathy; giardia; rot avi- ruses; bacterial overgrowth; milk sensitivity; worms; short bowel syndrome. Coeliac as sociations: Diabetes mellitus (type I). Fig 1. Coeliac disease Some acute surgical problems Infantile hypertrophic pyloric stenosis Presents at 3 \200\223 8 weeks ( \200 : \200 \211\210 4 : 1) with vomiting which occurs after feeds, and becomes projectile (eg vomit- ing over far end of cot). Pyloric stenosis is distinguished from oth er causes of vomiting by the following: \200 The vomit does not contain bile, as the obst ruction is so high. \200 No diarrhea: constipation is likely (occasionally \200\230starv ation stools \200\231). \200 Even though the patient is ill, he is rarely obtunded: he is alert, anxious, and 172 \200 always hungry \200\224and possibly malnourished, dehydrated. The vomiting is extremely large volume and within minutes of a feed. Observe left-to-right LUQ (left upper quadrant) peristalsis during a feed (seen in late-presenting babies). Try t o palpate the olive-sized pyloric mass: stand on the baby \200\231s left side, palpating wi th the left hand at the lateral border of the right rectus in the RUQ, during a feed from a bottle or the left breast. There may be severe water & NaCl de \201 cit, making urine out put & plasma Cl \200\223 (also K+ & pH) vital tests to guide resuscitation and determine wh en surgery is safe (Cl \200\223 should be >90mmol/L). The picture is of hypochloraemic, hyp okalaemic metabolic alkalosis. NB: don \200\231t rush to theater. 521n=84 Imaging: Ultrasou nd detects early, hard-to-feel pyloric tumors, but is only needed if examination is \200 \223ve. 522 Barium studies are \200\230never \200\231 needed. Management: Correct electrol yte distur- bances. Before surgery (Ramstedt \200\231s pyloromyotomy/ endoscopic surgery) p ass a wide-bore nasogastric tube. Intussusception The most common cause of intestinal obstr uction in chil- dren.The small bowel telescopes, as if it were swallowing itself by invagin a- tion. Patients may be any age (typically 5 \200\22312 months; \200 : \200 \211\210 3 : 1) presenting with episodic intermittent inconsolable crying, with drawing the legs up (c olic) vomiting blood PR (like red-currant jam or merely \202 ecks \200\224a late si gn). A sausage-shaped abdominal mass may be felt. He may be shocked and moribund. In betwee n pains there may be no signs. Tests/Management: The least invasive approach is ultrasound with reduction by air enema (preferred to barium). CT may be problematic, and is less avail able. There may be a right lower quadrant opacity perforation on plain abdominal \201 lm. Doppler studies to show bowel viability have been used but are non-standard. If reducti on by enema fails, reduction at laparoscopy or laparotomy is needed. Any necrotic bowel sho uld be resected. Pre-op care: \200 Resuscitate, crossmatch blood, pass nasogastric tube. N B: children over 4 years old present diff erently: rectal bleed- ing is less common, and th ey have a long history (eg >3 weeks) contributing pathology (cystic \201 brosis, Henoc h \200\223Sch nlein or Peutz \200\223Jeghers \200\231 syndromes; ascariasis, nephrosis or tumors such as lymphomas \200\224in the latter obstruc- tive symptoms caused by intussuscep tion are the most frequent mode of pres- entation). Recurrence rate: 5 \200\22315% in infa nts. 523 Post-op pain relief Morphine IVI: child \200\231s loading dose: 100 g/kg in 30min , then 20 \200\22330 g/kg/h (prem neonates 50 g/kg, then 5 \200\22320 g/kg/h) or diclof enac 0.3 \200\223 1mg/kg/12h (max 75mg/12h for \211 2 days) if over 2yr (eg a 12.5mg suppo sitory every 12h if 1yr old). Ibuprofen dose: 7.5mg/kg/6h PO (syrup is 100mg/5mL). Pre-op (pre-emptive) tramadol also has a few advocates ( 0.5 \200\2231mg/kg[6]). 524 N=45 Phimosis The foreskin is too tight, eg due to circumferential scarring; retrac- tion over the glans is impossible, eg with foreskin ballooning on voiding bal- anitis. It is normal to have a simple non-retractile foreskin up to the age of 4yrs. By 11yrs or older, prevalence is < 8%. 525 Time or a wait-and-see policy will usually obviate the need for circumcision. Force d retraction may be causative, not therapeutic. 0.05% betamethasone cream also helps (esp. before 8yrs. Use twice-daily with stretching exercises for 15 days, then daily for 15 days. 526 Other surgical problems: appendicitis, hernias, volvulus, torsion of the tes- tis, acu te abdomen: p170, p130, OHCM p654; OHCM p608. s c i r t a d e a P i This page intentionally left blank Childhood urinary tract infection (UTI) NICE 2007 Presentation \200\207Often the child may be non-speci \201 cally ill. Infants may pre- sent with collapse and septicaemia, and tod dlers as vomiting, \200\230gastroenteritis \200\231, failure to thrive, colic, or PUO. Man y with dysuria and frequency have no identi- \201 able UTI, and often have vulvitis. The urinary tract is normal in most with UTI, but 35% have vesico-ureteric re \202 ux (VUR), 14% have renal scars (most have re \202 ux too), 5% have stones, 3% develop hypertensio n. Each year in the UK, 10 \200\22320 children enter endstage renal failure programs becaus e of re \202 ux and chronic pyelonephritis complications. UTI is a common source of morbid ity.1 De \201 nitions Bacteriuria: Bacteria in urine uncontaminated by urethral \202 ora . It may be covert ( \200\230no \200\231 symptoms), and can lead to renal scarring, BP \200 \200, and, rare- ly, chronic renal failure. UTI denotes symptomatic bacteriuria that may in volve diff erent GU sites ( \200\230 loin/suprapubic tenderness; fever; dysuria). Chronic p y- elonephritis is a histological/radiological diagnosis. Juxtaposition of a cortex scar an d a dilated calyx is the key feature. It is a big cause of hypertension and can result in r enal failure, eg if the kidneys are congenitally dysplastic. Dur- ing micturition, urine ma y re \202 ux up ureters, seen on a micturating cystogram (requires catheterization) or MAG 3 scan (catheterization not needed) \200\224grades: I Incomplete \201 lling of upper urin ary tract, without dilatation. II Complete \201 lling slight dilatation. III Ballooned calyces. IV Megaureter. V Megaureter + hydronephrosis. UTI incidence Boys: \211 0.23%/yr; girls: 0.31 \200\2231%; ratios are reversed in neonates. Recurrence: 35% if >2yrs old. Pre valence of covert bacteriuria in schoolgirls: 3%. Prevalence of associated GU anomalies: 4 0% ( have re \202 ux; others: malpositions, duplications, megaureter, hydronephrosis). R enal scars and age: We used to concentrate on treating babies early, thinking new scars wer e rare after 4yrs old, but prospective 99mTc dimercaptosuccinate (DMSA) scintig- raphy (the best test) shows new scars appearing on repeat scans in 43% of those <1yr old, 84% of thos e aged 1 \200\2235, and 80% of those >5yrs old. Tests Dipstick all ward urines. If nitrites or WCC +ve, get a clean catch (or a suprapubic aspirate or catheter sample; bag urines hav e many false posi- tives from vulvitis or balanitis). Wash the genitals gently with water, and tap repeatedly in cycles of 1min with 2 \201 ngers just above the pubis, 1h after a f eed, and wait for a clean voided urine (CVU) sample, avoiding the stream \200\231s 1st part . Do prompt microscopy2 & culture. >108 organisms/L of a pure growth signi \201 es UTI. Fo r suprapubic aspiration, ward ultrasound helps identify a full bladder. Method: clean skin over the bladder; insert a 21G needle in the midline 1cm above symphysis pubis. Aspirate on advancing (any organisms found are signi \201 cant). Ultrasound (us): US is cheap, non-in vasive, getting more accurate, and is worthwhile in 1st UTIs (a good prenatal scan may suff i ce); 527 sensitivity, speci \201 city, positive predictive value, and negative predictiv e value for de- tecting re \202 ux are 18%, 88%, 23%, and 83%, respectively. 528 A right k idney long- er than the left by 10 mm is a good predictor of an abnormal DMSA scan. 529 Re serve renography for: infants Recurrent UTI and +ve family history of GU abnormality. If th ese are present and US is normal, proceed to 99Technetium renography \200\224static for sca rring (99mTc DMSA scan, dynamic for obstructive uropathy) isotope cystography. Micturati ng cystourethrography (MCU) is still the best way of excluding re \202 ux \200\224but it i s said that if DMSA is negative, MCU \200\230never \200\231 shows signi \201 cant re \202 ux. 530 In general, it is not needed in over 1yr olds if initial tests are normal, pye lonephritis is unlikely, there is no family his- tory of re \202 ux, and there are no recu rrent UTIs; it is invasive and unpleasant, but careful preparation with play therapy (p377) mitigates this. If it is done ill-advisedly on an uncomprehending and angry toddler, it ma y constitute as- sault. NB: operating on re \202 ux is unlikely to improve renal function. 531 174 \200 s c i r t a d e a P i 1 Prevalence unknown as under-reported. See Urol Clin North Am 2008 35 47 2 Microscopy is m ore reliable than stix tests for nitrites & leucocytes: Effective Health Care 2004 8.6 175 Treatment and prevention of urinary infections Antibiotic treatment Age <3 months: IV amoxi cillin + gentamicin (below) or IV cephalosporin alone (p106). Child >3 months with uncompli cated low- er UTI: 3-day course of trimethoprim1 50mg/5mL, 4mg/kg/12h (max 200mg) PO pro phylaxis (see below), nitrofurantoin, or amoxicillin/co-amoxiclav \200 Avoid constipation \200 \200\200Oral \202 uids \200 Encourage full voiding \200 Repeat MSU. \200 \207Resistance to trimethoprim and ampicillin renders monotherapy insuffi - cient in some p laces. 532 If the child or infant is ill (pyelonephritis + septicaemia) and blind parenteral therapy i s needed, \200 gentamicin (5 \200\2237mg/kg/day) may be given in a once-a- day regimen (IM if IV access fails). In one study, children and infants were randomly assigned to once-dai ly gentamicin 5mg/kg/day2 or 2.5mg/kg/8h slowly IV, where kg = lean body weight if obese.2 There was no diff erence in effi cacy, nephrotoxicity, ototoxicity, or renal scarring. 533 If neonate >35 weeks postmenstrual age, 2.5mg/kg/12h IV, slowly: consider a longer course i f pre- mature (gestation <34 weeks). 534 Do levels.3 IV cefotaxime and co-amoxiclav are alt ernatives. Treating ureteric re \202 ux If prophylactic antibiotics fail, ureteric reimpla nta- tion can reduce re \202 ux, but scarring remains. Keep on antibiotic prophylaxis. Pre vention Just one episode of re \202 ux of infected urine may initiate renal scarring, so s creening for bacteriuria is useless: damage is too quick. But once a UTI is suggested (eg b y stix) treat it at once, before you know culture sensitivities, as renal damage may be abo ut to happen. Obtain 2 high-quality urine samples for analysis. Consider prophylaxis if rec urrent UTI, signi \201 cant GU anomaly/renal damage. Example: trimethoprim prophylaxis (2m g/kg at night, max 100mg), eg while awaiting imaging \200\224and sometimes inde \201 nitel y (optimum duration is unknown, but may be after 2 negative cystograms, if the indication i s re \202 ux). Consider screening siblings for re \202 ux. Prophylaxis can be stopped aft er re \202 ux has been ruled out if there is no scarring. s c i r t a i d e a P Surgical correction of moderate re \202 ux is \200\230unlikely to be bene \201 cial \200 \231, and in minor re \202 ux is \200\230likely to be harmful \200\231 (carefully made EBM phrases!) 1 Trimethoprim every 12h, eg if aged 6 weeks \200\2236 months 25mg; 6 months \200\2236yrs 5 0mg, 6 \200\22312yrs 100mg. 2 Assumes normal renal function; give lower dose if the patient is obese, based on lean body weight estimated by the 50th centile on weight-for-age charts . See OHCM p738. 3 Levels may not be needed if gentamicin is given for <72h (usually the ca se). One-hour post-dose (peak) serum gentamicin concentration should be 5 \200\22310mg/L (3 \200\2235mg/L for streptococcal or enterococcal endocarditis); pre-dose ( \200\230trough \200\231) concentration should be <2mg/L in neonates and <1mg/L in others on a once-daily r egimen (<1mg/L for streptococcal or enterococcal endocarditis \200\224BNF advice). In neona tes phlebotomy is diffi cult and causes anemia \200\224so an example of monitoring advice f rom one NICU is: No levels before 48h of therapy unless proven infection requiring gentamic in and one of: \200 Perinatal asphyxia \200 Congenital renal defects \200 Renal insuffi ciency (creatinine >133 mol/L, ie >1.5mg/dL). www.cop.u \202 .edu/ wppd/research/sample7. pdf