Pediatrics March 2009

Vol. 8, Issue 2 Jan - March 20091

Vol. 8 Issue 2 Jan - March 2009

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EDITOR SPEAKS

Editor-in-Chief Dr. Vinay Aggarwal

SectionalEditor Dr. S. K. Mittal

EditorialBoard

Dr. Vijay Agarwal Dr. Ashok GroverAtul Gandotra Dr. Madhumita Puri Dr. Sharda Jain Dr. Parkash Gera Dr. Rajiv Gupta Dr. S. Arul RhajDr. Deepak Pande Dr. Yogesh Jhamb Dr. Vineet Jain Dr. Neeraj JainDr. B.K. Gupta Dr. Hariharan Dr. Atul Jain Mr. S.K. Singhal

DesignandLayout Tabassum

Photographer Mukesh Kapoor

CONTENTS

1. Obesity-AMoribundEpidemic 3inChildren

2. PneumococcalVaccinationinIndia: 5ScienceandCommerce

3. DiagnosticApproachtoAcute 9 PyrexiainYoungChildren4. CeliacDiseaseRevisited 135. ImprovingCureRatesandreducing 19 side-effectsbymodernRadiotherapy Techniques6. OfficeManagementofAsthma 217. CommonDrugsActingon 24 CardiovascularSystemandOptimal DosingTime6.TheRoleofSpiritualityinMedicine 297. ClinicalChallenge:Acute 31 AppendicitiswithPregnancy (Threecasereports,oneineach trimester)8. NocturnalEnuresis 339. IsSunlightanEffectiveTreatment 37 forJaundiceinTermInfants?10.RotavirusVaccine 3911.RecentAdvancesinManagement 43 ofChildhoodTuberculosis12. PushpanjaliHealthcareEvents47 andInitiatiaves13. Guidelinesforsubmissionof 51 Manuscripts

Dear ColleagueIt gives me great pleasure in presenting to you the latest issue of Medi-Focus, a scientific periodical being published by the Pushpanjali group to update the knowledge and skills of physicians in various fields of Medicine. This issue is entirely devoted to the problems related to child health. I am sure you will find the issue very informative and helpful in your

day-to-day practice. You will be glad to know that the Department of Pediatrics and Adolescent Medicine at Pushpanjali Crosslay Hospital is now geared to provide comprehensive services in various areas of child health under the supervision of an expert team of specialists and super specialists. The following facilities are available: i. Round-the-clock emergency facilities with qualified

consultants.ii. Outpatient consultations by Senior specialist from 9:00 am to

8:00 pm on all working days.iii. Specialized clinics in the afternoon (2:00 pm to 4:00 pm) Monday: Pediatric Gastroenterology Tuesday: Pediatric Respiratory Thursday: Pediatric Endocrinology Saturday: Pediatric Cardiology and ECHO iv. Special diagnostic facilities like Pediatric GI endoscopy,

ECHO cardiography, PFT, Bronchoscopy, Hormonal assays for endocrinal problems.

v. Special diagnostic facilities in allied fields like BERA, OAE (For hearing assessment) Detailed retinoscopy (For retinopathy of prematurity) etc.

vi. Neonatal Intensive Care with facilities for all levels of neonatal care including monitoring, Ventilation, CPAP, Parenteral alimentation under the supervision of a qualified neonatologist.

vii. Pediatric Intensive Care with all Level III facilities under the supervision of pediatric intensivists.

viii. Pediatric Surgery by a fully qualified and dedicated Pediatric surgeon.

All efforts are being made to continuously upgrade the facilities available in the department .and very soon we will be in a position to provide additional services like:i. Child Guidance and Development services with dedicated

Clinical Psychologist, Speech therapist and Occupational therapist.ii. Diagnostic and rehabilitative services for children with Autism,

Learning disabilities, Attention Deficit and Hyperactivity Disorders.

iii. Special Clinic and Diagnostic facilities in Pediatric Neurology, hemato-oncology, nephrology.

The department also conducts weekly clinical meetings with all consultants on Friday afternoons. Further, the department also provides Continuing Medical Education through monthly clinical meetings for neighborhood pediatricians.We invite you to participate in all the academic activities of the Department and also to spare some of your valuable time to visit the hospital and witness first hand the world class facilities being developed in the department. We will be happy to look after all your problem cases with an assurance of developing a long term - partnership for the continued care of your pediatric patients.

Dr S K MIttalChairmanDepartment of Pediatrics, Neonatologyand Adolescent Medicine

Department of Pediatrics

Chairman Dr S K Mittal9818372811

Consultants Mon-ThursDr Ravi Malik9811078350Dr Dinesh Aggarwal9811078283Dr Rajiv Singh9810346080Tues-FridayDr Deepak Pandey9810366571Dr Alok Gupta9312248808Dr Anuradha9899646715Wed –Sat Dr P D Garg9811109048Dr. Vineet Jain9810121098Dr K K Pandey9810184791Dr Manpreet9811121285NeonatologyDr Vivek Jain9999444303Dr. Sudershan Kumari (Ex. LHMC)Tues-10.00am to 1.00pm

Intensive careDr Praveen Khilnani9810159466Dr Deepika Singhal9811702443EndocrinologyDr I P S Kocher9910240919GastroenterologyDr S K MittalDr ManpreetRespiratory Dr Deepak PandeyDr Tilak Raj DangwalPediatric SurgeryDr Rajeev Aggarwal9810032906Development PediatricsMr. Sudershan KumariClinical PsychologistDr Sanjeeta Kundu9811271220Speech TherapistDr Mani Bansal9873880510


IPS KocharConsultant Pediatrician

& Adolescent Endocrinologist

Fellow, Pediatric Endocrinology

London

Obesity - A Moribund Epidemic in Children

IPS Kochar

Obesity is defined as a condition of abnormalorexcessivefataccumulationinadiposetissueto the extent that health may be impaired.Childhoodobesityisaglobalepidemicandisacomplexmultifactorchallengingandfrustratingproblem that is escalating at an alarming ratein the western world and paradoxically ina developing country like India. Along withthe prevalence of under malnutrition thereis a paradox of increase obesity. Though thepredictionofobesityhasbeenlargelyinlowersocial economic group inwesternworld, it istheurbaneffluentpopulationeffectedinIndia.

Obesity in childhood factors for obesity inadulthood.About80%oftheobeseadolescentsareexpectedtoremainobeseasadults.Severalpathologies develop concomitantly withobesityduringchildhood.These include type-2 diabetes, a range of respiratory problems,metabolic syndrome, liver, steaaotosis, andpseudo-tumor cerebrei. Childhood obesity isessentially an exogenous disorder, preventingintervention should focus onmodifying theseetiologiesimprovenatureofchildhoodnutritionanditssocialandlucidbehaviour.

Epidemology: According to the AmericanObesityAssociation,15.5%ofadolescents(age12 to 19 years) and 15.3% of children (age 6to 11 years) are obese. There has been a 45%increase in prevalence in overweight childrenasreportedfromestimatesof11%and16%fromthe NHANES 3 survey. Several studies fromIndiatoohaveconfirmedtherisingprevalenceofchildhoodobesityandoverweightinpediatricand adolescent population. Prevalence ofobesity is from 5-14% and overweight 9-16%inuppersocialeconomicgroup.Obesityislesscommon in lower social economic group andinruralchildrenvaryingfromlessthan1%to3.6%insomeofthestudies.

Measurement of Obesity: Obesity ismeasuredusing the Body Mass Index (BMI). BMI iscalculated easily from weight and height tocorrelatewithothermeasuresofbodyfatmassinchildrenandadolescents.TheBMIchangesphysiologically with age and sex. At birthmedian BMI is low as 13kg/M2 increasing to17kg/m2atage1year,decreasingto15.5kg/m2atage6years,andthenincreasingfurtherto21kg/m2atage20.

AgeandgenderspecificBMIcutoffpointsfordefining overweight and obesity in childrenhave been derived by identifying percentilesin children analogous to adult BMI are nowrecommended as standards for internationalcomparison of data by the InternationalObesityTaskForce(IOTF).Othermeasureslikeskin fold thickness, waist hip ratio andwaist

circumference are also used for measuringobesity. Body fat measurements technique,DEXA,CT,MRI,andultrasoundareadditionaltoolsforquantificationofbodyfat.

Risk Factors

Non-Pathological

Genetic Obesity in both parents

Environmental Socioeconomicdeprivation,singlechild,singleparent

Dietrelated Bottlefedininfancy,highfatfood,sugarsnacksdisorganizedeatinghabits

Activityrelated Increaseinactivity,IncreaseTVwatching

Pathological SyndromesLawrenceMoonBiedlSyndromeDownSyndrome,PraderWilliSyndromeBeckwith-WiedemanSyndromeAlstromSyndromeCohenSyndromePseudohypoparathyroidism

Hypothalamic DamageTraumaTumorsCraniopharyngiomaPostEncephalitis

DrugsInsulinSteroidsAntiThyroidDrugSodiumValporateThiazoldineRisperidone

Single Gene MutationMelancortin4Receptor(Mc4r)Propiomelancortin(POMC)Leptin,LeptinReceptorDefect

Endocrine AbnormalityGhDeficiencyHypothyroidismCushingSyndromeHyperinsulismInsulinResistanceKlinefelterSyndromeTurnerSyndromeInsulinomaPCOS

ImmobilitySpinaBiifidaCerebralPalsy

Impaired Skeletal GrowthAchondroplasia

Clinical ManifestationsObesitymayoccuratanyage,butismostcommoninthefirstyear, around 5-6 years andduring adolescence.Childrenwithobesity due to excessive caloric intake are also taller for theirmid-parent height and often this characteristic association ofaccelerated linear growth is one of the singlemost importantclinicalparametersinevaluationofchildrenwithobesity.Thosewith exogenous or nutritional obesity are tall and maintainsignificant accelerated linear growth, whereas those withendogenous pathological causes are usually short below the25thpercentileforageandsexormayhaveagrowthrateandgrowthcurvefallingofftheirpreviouspercentileonthegrowthcurve.Overgrowth in children in childrenwith obesity seemsrelatedtoelevatedinsulinlevelsduetoobesity-inducedinsulinresistance.

Increased aromatization of adrenal androgens by fat tissuecauses advancement of bone maturation, which ultimatelyresults in normal adult height. Increased aromatization dueto excess fat leading to excess production of estrogen maycontributetogynecomastiainassociationwithlipomastia.Thesechildren have adiposity around the breast (whichmaymimicgynecomastia)withpendulousabdomenand fattyacidsat thesides. Striaemay be present if excessive or rapidweight gainoccurs.Inboys,externalgenitiliamayappeardisproportionatelysmallwithpenisusuallyembeddedinthefat.Thisisoftenthemajorreasonforpresentationinobeseboysratherthanconcernabouttheexcessbodyweight.Pubertymayoccurearlyaffectingtheirultimateheight.Thereisgenuvalgumandmorefatintheupperarmandthighcomparedtotherestoftheextremities,withsmalltaperingfingers.

Investigations

Fasting sugar, total cholesterol, liver function, fastingtriglycerides, low and high density lipoproteins, insulin levelandglycostylatedhemoglobinlevels,thyroidfunctiontest,urineanalysis (specific density), thyroid function test in a growingobeseadolescentfemale.Ifmenstrualirregularitiesarereportedpossibly combined with sign of hirsutism and/or acanthosisnigricans,investigationforPCOSmayberequired.

Special Hormonal profile for GHD, thyroid, Parathyroidgland, IGF1,karyotype, insulinlevel, imagingofpituitaryandadrenalarea,ifrequired.

Complications The long term sequelae of childhood obesity include obesityin adulthood hypertension, insulin resistance, type 2 diabetescholelithiasis, hyperurcemia, cardiovascular disease,dyslipidemia, early pubertal changes, menstrual irregularitiesorthopedic problems, sleep apnea, reparatory infections andcytologicaldisturbances.

Metabolic and Endocrine Hypernsulinemia (impaired glucose syndrome), advanced pubertal development, polycystic ovarian disease, steatohepatitis

Cardiovascular Hypertension

Respiratory Breathlessonexertion,obstructivesleepapnea,Pickwickiansyndrome

Skeletal Knockkneeorbowlegs,slippedcapitalfemoralepiphysis

Psychological Poorselfimage,bullying,behavioralproblem

Management Strategies ChildhoodobesityisagreatchallengetoPediatricEndocrinologists.Recognizing the problem, setting goals, initiating treatmentstrategies,properimplementationandmonitoringofthetherapyaretheessentialstepsofmanagement.Dietexerciseandbehaviormodificationare the corner stonesof therapy.Anorecticdrugsand bariatric surgery are to be avoided in themanagement ofchildhoodobesityexceptinrarelifethreateningorveryspecialsituations.

DietEducationofparentsandchildrenregardingtheneedforproperandadequatenutritionfornormalgrowthandtheneedtoavoidexcessofemptycalories,andothercaloricadviceisimportant.Energy-dense, high-fat, high calorie snacks and fast food andnonnutritivesweeteneddrinksaretheusualculprits.Inclusionof fruits vegetables, lentils andmulti-grain breads in the dietimprovesthenutritivevalueinthefiber.

ExerciseLack of exercise and sedentary lifestyles contributes more toweightgain inchildrenthaninadults.Activities likewalking,cycling, tennis, aerobics, cricket, volleyball, basketball, andbadminton are some of the activities that children enjoyand should be encouraged as there is greater chance of therecommendationbeingfollowed.Calisthenicsandmonotonousactivities are found to annoy and frustrate children, leadingto a negative impact on outcome. Swimming helps in weightmaintenanceandtoningofmusclebutisoftenassociatedwithanincreaseinappetiteaftertheswim,socareandcautionmustbe exercised to circumvent this. School academic activitiesshouldbebalancedwithphysicalactivities,playtimeandfamilytime.Healthcampsthateducateandencouragechildrentoleadamoreactivelifehavebeenfoundtobesuccessful.

Appetite suppressantsPharmacotherapyisnotrecommendedforappetitesuppressionin children and adolescents, and the uses of these agentsare strongly discouraged. New modality of leptin therapy iscurrentlyundergoinghumantrialandhasbeensuccessfulwithleptindeficiency.GrowthhormoneisbeingusedinpatientswithPrader-Willisyndrome.

Batriatic surgeryThis is traditionally reserved for obese adults with very highBMI(>40kg/m3)orwithcomorbiditiesthatarelifethreatening.Generally such procedures (gastric stapling/gastric/jejunoilealbypassprocedures)aretobeconsideredonlyinmorbidobesitywithcomplications.Thismodalityof treatmenthasbeenusedintheadolescentpopulationwhereindicated,withconsiderablesuccess.

Prevention Childhood is a critical period for the initiation of obesity andtherefore the ideal time forbeginningpreventionprogrammes.Television progammes, articles and newspapers, lecture byhealthcareprofessional,healthcampandhealthfairsaresomeof the ways of spreading the messages of good nutrition andactivelifestyleagainsttheproblemsofobesity.


Joseph L. MathewAdvanced Pediatrics Centre

PGIMER

Chandigarh

Pneumococcal Vaccination in India: Science and Commerce

Joseph L. Mathew

IntroductionMuch has been written and spoken aboutPneumococcalvaccineforroutineimmunizationin India. This article attempts to explore thefactswithparticularreference to thescientificand commercial issues behind it. As Indiaaccounts for 120 out of 478 million (25%)under-five children, developments here arecloselywatchedallovertheworld.

A. ScienceI. Burden of diseaseThe exact number of Invasive Pneumococcaldisease (IPD) is not known; even a reliableestimateisunavailable.Currentlyquotedfiguresare summarised in Table 1, from which it isclearthatthecalculationsareneitherbasedonrobustdata,norashighasprojected.However,thisdoesnotnecessarilymean that IPDcouldnotbeasignificantproblem;afactpointedoutearlier1.Theissuecanonlyberesolvedthroughmulti-centric population-based surveillancestudies,thatarecumbersome,timeconsumingandexpensive,butinevitable.

II. Significance of Pneumococcal diseasePneumococcal disease is significant fordevelopedcountriesbasedonknowledgeof(i)diseaseburden, (ii) serotypescausing invasivedisease,(iii)controlofothercausesofpneumoniaespecially Hib and measles, (iv) increasingantibioticresistanceamongS pneumoniae,(vi)pre-existing high level of hygiene, sanitation,health-care delivery etc; which cannot besignificantly improved further to reducepneumoniamorbidityandmortality.Therefore,these countries have included Pneumococcalvaccine in routine immunizationprogrammes.In developing countries, (i) burden of diseaseisnotclear,(ii)knowledgeofserotypescausinginvasive disease is limited, (iii) even if IPD isa significant cause of pneumonia morbidityandmortality,itisnotlikelytosupersedeothercauses including H influenzae and measlesowing to poor immunization coverage, (iv)antibioticresistanceisnotasignificantproblemyet, and (vi) there is scope for improvementinqualityof lifeandthusmorbidity/mortality.Therefore,developedcountryargumentscannotbeextrapolatedtodevelopingcountries.

If the figures presented in theUNICEF reportof 20062 are correct, the case fatality rate ofpneumonia is 0.93% (410,000 deaths among44 million cases). This relatively low case-fatalitysuggestseithermilddiseaseorexcellentresponse to therapy. However, the samedocumentstatesthatonlytwo-thirdsofIndianchildren are taken to an appropriate health-

careprovider2,againsuggestingmilddisease.Ifthisisthecase,itwouldnotmeritalarge-scaleexpensivevaccinationprogramme.However,thedocumentclaimsthatpneumoniaisresponsiblefor20%ofunder-fivemortality,whichmakesitaveryseriousproblem.Thisapparentparadoxstemsfromthelargedenominatorof44millionthatisusedtodemonstratehighdiseaseburden.Asthisfigureappearstobeobviouslyincorrect,all thecalculationsbasedonthispremisealsobecomesuspect.

III. Role of Pneumococcal vaccinesSinceyounginfantsareatgreatestriskofIPD,vaccinationshouldbeefficaciousandeffectiveinthisage-group.The23-valentPneumococcalpolysaccharidevaccineisnotrecommendedforyounginfants,hencecannotbeusedforroutineimmunization. The 7-valent Pneumococcalconjugatevaccine(PCV-7)coversonlyalimitedproportion of serotypes causing IPD in mostdeveloping countries, hence at best wouldbe “something better than nothing”. This isbecausePCV-7wasdesignedtoprotectchildrenin developed countries; and hence serotypecoverageis90%forUSAandCanada,78%forAustraliaand75%forEurope.Itismuchlowerfor Africa (67%) and Latin America (63%),though this is still much better than for Asia(43%)andIndia(53%orlower)3,4.

IV. Administration and logisticsThevaccinationscheduleofPCVcanbelinkedwith that of DPT in routine immunizationprogrammes, making it an attractive optionlogistically. However, it cannot be mixed inthe same syringewith other vaccines and theWHO estimates the need for a “substantiallyincreased capa 300%5. Administration wouldnecessitateuseofseparatesyringesandinjectionsites. Therefore, safety data comparing bothvaccinationsagainstDPTalonewouldneedtobegeneratedpriortousage.Thesefactorsmakevaccination less attractive than one is led tobelieve.

B. CommerceI. Role of industryThecurrentheightenedinterestinPneumococcaldisease in India is not related to increase inscientific knowledge of the epidemiology ofPneumococcal disease or vaccine/vaccination,but the thrustby industry to increase sales ofPCV-7.This is through the ‘academicchannel’(organization of countless sponsored lectureson theproductby ‘experts’;manyof these fora fee)andthe ‘commercialchannel’ (extensivemarketing, advertising and providing thevaccinetophysiciansatabout20%lessthanthe


References 1. Invasive bacterial Infection Surveillance (IBIS) Group,

International Clinical Epidemiology Network (INCLEN).ProspectivemulticentrehospitalsurveillanceofStreptococcuspneumoniaediseaseinIndia.Lancet1999;353:1216-1221

2. KanungoR,RajalakshmiB.Serotypedistribution&antimicrobialresistance in Streptococcus pneumoniae causing invasive &other infections inSouth India. Indian JMedRes2001; 114:127-132.

3. Mathew JL. Universal Pneumococcal faccination for India.IndianPediatr2008;45:160-161.

4. Noauthorscited.Pneumococcalconjugatevaccineforchildhoodimmunization – WHO position paper. Wkly Epidemiol Rec2007;82:93–104.

5. Pneumonia:theforgottenkillerofchildren.TheUnitedNationsChildren’sFund(UNICEF)/WorldHealthOrganization(WHO),2006.

retailprice).Thesepracticesencouragephysicianstobeorientedinfavourofavaccinewhoseeffectivenessislimitedinthelocalsetting.

II. Role of the WHOThe WHO issued a position paper5 recommending PCV-7 indeveloping countries, temporally coinciding with aggressivemarketing of the same. This has given a substantial boost tosalesofPCV-7.The“WHOconsidersthatitshouldbeapriorityto includethisvaccine innational immunizationprogrammes,particularly incountrieswheremortalityamongchildrenaged<5 years is >50/1000 live births or where >50,000 childrendieannually”5.However,noexplanationisofferedforchoosingthese particular cut-off criteria. The option of using eithercriterion (rather thanboth)permits theadditional inclusionofsevencountriesthatwouldotherwisenothavebeenconsidered.Thesesevencountries togetheraccount for161millionunder-fivechildren,ofwhichBrazilandChinaaloneaccountsfor104million.Ascurrently there isonlyonebrandofPCVavailableintheworld,itisobviouswhowillbenefitthemostfromthesestatements.

III. Role of the Indian Academy of Pediatrics (IAP)The recent IAP guidelines6 recommend PCV-7 in routineimmunizationafterone-to-onediscussion;thismeansthatthosewhoarewillingtopayforavaccinewithlimitedeffectivenessshould be vaccinated. The IAP further recommends thatGovernment of India should seriously consider PCV-7 forroutine immunization. Since this is impossible owing to thehugeexpenseinvolved,IAPrecommendsthatGovernmentcouldoffsetthecostbyavailingtheGAVIofferofsubsidizedvaccinetill20156.ItisnotclearwhattheGovernmentisexpectedtodowhen/ifGAVIpullstherugfromunderitafter2015.

IV. Role of the Government of IndiaThe Government of India has shown unusual promptness inadvocatingPCV.Anexpertcommitteeunder thechairmanshipof the DG, DBT recommended PCV for routine immunizationprogrammewithina record timeof twoweeksafter itwas setup. This is very impressive considering that a rational policyoverHib,hepatitisBandmeaslesvaccineshasnotemergedoverseveralyears.Althoughtheexpertcommitteealsorecommendeda vaccine covering at least 70% serotypes; since this is notavailableitisunclearhowtherecommendationwillbefulfilled.Meanwhile, these actions have boosted sales of currentlyavailablePCV-7.

C. What is the solution?Thedecisiononusingavaccine(orotherwise)shouldbebasedonactualorexpectedburdenofdisease,likelyeffectivenessofavailablevaccinesandexistinghealth-carepriorities;itmustnotbe based solely on efficacy, safety, availability or affordability.Accordingly, it is possible that India needs a pneumococcalvaccine foryoung infants,but thecurrentlyavailablevaccinesare not suitable. Knowledge of locally relevant serotypes andindigenous manufacture of tailor-made vaccine should beencouraged.Thiswillmakevaccinationeffective,affordableandsustainableinthelongterm.

ConclusionThe current hype over Pneumococcal vaccines is largelycommercialinorigin,boosteddirectlyandindirectlythroughtheloud and/or quiet acquiescence of professionals in individual,institutional and organizational capacities. The relegation ofscientificconsiderationstotheback-seatisthemostunfortunateoutcomeofthesestrategies.Sucheventsarelikelytobewitnessedwithincreasinglyregularityinthefutureaswell.

Table 1: Scientific claims on burden of Pneumococcal disease in India

Published scientific claim

Comments

Thereare43-44millionannualchildhoodpneumoniacasesinIndia2

•The basis for arriving at this‘estimate’hasnotbeenpresented.Thedocumentquotes apersonalcommunicationofanunpublishedpaper.•Thesubsequentlypublishedpaperalsodoesnotexplainthefigureof43million ‘predicted’ new casesamongunderfivechildren.•If this estimate and ‘prediction’are correct, it means that everythirdIndianchildhaspneumonia.This suggests gross inflation ofnumbers.

S pneumoniaeisresponsiblefor15-50%casesofchildhoodpneumonia6.

•Thisisadirectquotefromanotherpaper published in a developedcountry.•As H influenzae is difficult toisolatethroughculturetechniques,itisoftennotdetected.•TheroleofS aureus,Gramnegativeorganisms, M. tuberculosis andmeasles virus in causation ofchildhoodpneumoniaisnotevenmentioned.

S pneumoniaeisresponsiblefor50%childhoodpneumoniamortality6.

•This is lifted from Reference2whichactuallystates“InAfrica,S pneumoniae may be responsibleforover50%ofseverepneumoniacases, and probably a higherproportionoffatalcases”.Thereisnocross-referenceforthisclaim.

S pneumoniaecauses6.6to22millionepisodesofpneumoniainIndiaannually6.

•Thisrangehasbeenarrivedatbyapplying the 15-50% calculation(unproven)to44million2annualepisodes(doubtful).

S pneumoniaeisresponsiblefor200,000under-fivedeathsyearly6.

•This has been calculated bymultiplying 410,000 estimateddeathsinReference2by50%.Thebasis for both these numbers isnotclear.


Diagnostic Approach to Acute Pyrexia in Young Children

Vineet Jain

Acute febrile illness in infants and childrenis very common in day-to-day practice and isprobably the foremost reason for taking thechild to a doctor. It is usually a self-limitingviral illness. Approximately 10% of children<36 months without evident source of feverhave occult bacteremia and serious bacterialinfection(SBI).However,therearetimeswhenitposesadiagnosticdilemma.Thechallengeinthe evaluation of a febrile young child lies inbalancingtheminimizationofrisktothepatientwiththecostoftestingandtreatment.

Definition of fever and detection techniques The most commonly accepted definition offeverisrectal temp>380C(100.40F)(PCNA).For previously healthy children 3-36 monthofage, rectal temp>390C (102.20F)warrantsfurther evaluation. This cut off is >380 C incasesofneonatesandyounginfants0-3months.Anumberof studieshaveshown thataxillaryand tympanic temperatures are unreliable inyoungchildren.

Achildwithhistoryofrectaltemphigherthan380C(100.40F)whoisafebrileatthetimeofpresentationshouldbegiventhesamelevelofattentionasonewhohasfeveratpresentation.Parental perception of fever with the back ofthehandshouldbeconsideredvalidandtakenseriously.

Risks and benefits of fever:Risks •Fatigue•Bodyaches•Delirium•Anorexia•Tachycardia•FebrileconvulsionBenefits•Enhancedimmunologicalfunctions•Someorganismsdieathightemperatureeg-Viruses-Polioandrhinovirus-Bacteria–pneumococcal• Children with chicken pox have prolongedcrusting if treated with Paracetamol vsplacebo.

Antipyretics should be used judiciously forsymptomatic relief, not merely to decreasetemperature in an otherwise well but febrilechild.

Approach to a young febrile childManagementoffebrileyoungchildrencontinuestoevolve.Contributingtothisconfusionisthe

changing epidemiology of bacterial infectionsinyoungchildrenafter theadventofHibandPCV7vaccinesinthewest.

Although the differential diagnosis of fever isquite broad and includes both infectious andnon infectious causes, the majority of febrilechildren have underlying infectious causes offever.Forthepurposeofthisarticle,patientsarepresumedtobefebrilefrominfectioussources.Additionally, diagnostic strategies emphasizethe detection of bacterial diseases, as thesearemorelikelytobeassociatedwiththeworstoutcomes.

Viral infections can also be associated withsignificantmorbidity andmortality, especiallyin young children. Finally most studies offebrile young children exclude patients whohave potentially complicating risk factors– immunocompromised, HIV, patients withindwellingmedical devices, on Antibiotics orhavingprolongedfevers(>5days).

History and physical examinationHistoryandphysicalexaminationareinvaluablein the assessment of febrile children. Theduration and intensity of fever at the time ofpresentation does not predictwhether a childhas occult bacteremia. Use of antipyreticsshould be noted. A response (or lack thereof)to antipyretics does not predict whetherunderlyingcauseisbacterialorviral.

Anassessmentofthechild’soverallappearanceiscritical.Ifthechildappearstobetoxic,thismandatesanaggressiveworkup,antibioticsandhospitalizationregardlessofageorriskfactors.Physical examination may reveal an obvioussourceofinfectionandidentificationofafocalinfectionmaydecreasetheneedforadditionaltesting.

a) Identify potentially serious illnessAll febrilechildrenshouldbeassessed for thepresenceorabsenceofsymptomsandsignsthatpredicttheriskofseriousillness.(Table1)

b) Look for symptoms and signs of specific illness (localization) (Table 2)

c) Look for clinically recognizable viral illnessFebrile patients with recognizable viralconditions (eg, croup, chickenpox, measles,stomatitis)havelowerratesofbacteremiathanpatients with no obvious source of infection,thusdecreasingtheneedforelaboratediagnosticworkup.

Vineet JainConsultant Pediatrician

PushpanjaliMedicalCentre,

Delhi

PushpanjaliCrosslayHospital,

Ghaziabad,NCR


Table 1. Is it a potentially serious bacterial illness (SBI)

Parameter Green (low risk) Red (high risk)

Colour Normalskin/mucousmembrane

Pale/mottledskin

Activityappearsill

•respondsnormallytosocialcues•smiles/playful•staysawakeorawakensquickly•strongnormalcry/notcrying

•Noresponsetosocialcues

•Appearsill•Unarousable/ifarouseddoesnotstayawake

•Weak/highpitchedorcontinuouscry

Respiratory •Normalbreathing •Gruntingtachypoea•RR>60/minchestindrawing

Hydration •Normalskin/mucousmembranes

•Normaleyes

•Reducedskinturgor•Sunkeneyes

Others Noneoftheredalertsigns

•Nonblanchingrash•Bulgingfontanelle/neckstiffness•Statusepilepticus•Focalneurologicalsigns/focalSz

Age Others •Age0-3mo,temp>38°C•Age3-6mo,temp>39°C

Fever without source (FWS)Most children0-36months of agewhohave feverwithout anobvioussourcehaveviralinfections,butcertainfebrilechildrenareathigherriskformoreSBI(7-13%cases).

DiagnosticapproachinFWSdependsuponClinical look - Well- ToxicCharacterizedby •lethargy(absenteyecontactwithparentsand surroundings)

•poorperfusion •hypo/hyperventilation

AgeThreedistinctgroups:-0-28days-1-3months-3-36months

Neonates (0- 28 day) • Neonates are at particularly high risk for SBI. Althoughmajority of neonates are diagnosed ultimately as having anonspecificviralillness,10-12%ofallfebrileneonateshaveSBI.Theyareinfectedtypicallybymorevirulentbacteria(eg,streptococcigpB,Ecoli,L.monocytogenesandstaph.

Table 2. Look for localization signs

Sx and signs in conjunction with fever

Possible diagnosis

Nonblanchingrashwith>ofthefollowing-•Illlookingchild•Capillaryrefilltime>3sec•Neckstiffness

Meningococcaldisease

•NeckstiffnessbulgingAF•Delirium/seizures

Meningitis

•Focalneurologicalsigns•FocalSeizures•Decreasedconsciousness

Herpessimplexencephalitis/TBM

•Tachypnoea-(0-6mo>60/min-6-12mo>50/min->12mo>40/min•Nasalflaring/chestindrawing/rales/rhonchi

Pneumonia/bronchitis

•Vomiting/poorfeeding•Lethargy/irritability•Dysuria/frequency•Offensiveurine/hematuria

UTI

•Swellingoflimborjoint•Notusinganextremity•Nonweightbearing

Septicarthritis

Fever >5 d with at least 4 of the following :• B/L conjuctival injection• Changes in mucous membranes• Changes in extremities• Polymorphous rash• Cervical LN

Kawasaki disease

aureus)withhigh rates ofmeningitis, nonmeningeal focalinfections(UTIbeingcommonest)andoccultsepsis.

• Studies have shown that clinical evaluation alone fails toidentifyneonatesatriskofSBI,hencediagnosticworkupisrecommendediftemperature>380Cirrespectiveofclinicalwellbeingorsignsofviralinfection.

Diagnosticworkupincludes:• BloodC/S–inallcasesasCBCaloneisnotreliableinthisagegroup

• Urineanalysis>10WBC/HPFinanuncentrifugedsampleissignificantbutalonecannotdetectallcasesofUTI

• UrineC/S–mustinallcases.Catheterorsuprapubicsamplesarepreferabletoavoidcontamination)

• LP–mustinallcases• CBC–isof limitedvalueas itcannotdifferentiatebetweenSBIandnonbacterialinfections.WBC>15000or<5000or/andAbsolutebandcells>1500/mm3maybeassociatedwithhigherrisk

• CXR–onlyifpulmonarysymptomsareobserved.Hospitalization and IV Antibiotics are strongly recommendedregardless of lab results or general condition. Outpatientmanagementoccursfrequentlywhenpatientspresenttopediatricclinics, but there are no prospective studies that address thisapproach.


Young infants (1-3 months)Toxicpatients in this agegroup require the sameapproachasforallfebrileneonates;however,patientswhoappearclinicallywellarealsoathighriskforSBI.ClinicalevaluationalonemaymissasubstantialnumberofSBI,hencebasicdiagnosticworkupisessentialandpatientsaredividedinto twogroupsbasedonreports:

Table 3. Clinically well Young infants (1-3 months)

Basic diagnostic tests

Low risk (mostly viral)

High risk (UTI and SBI)

WBC 5000-15000 <5000or>15000

BandneutroratioAbsolutebandcount

<0.2<1500

>0.2<1500

Urineanalysis <10WBC/HPFNoorganismsongramstain

>10WBC/HPForganismson

gramstain+

Recommended OPDMx/reviewin24h/lookforredflagsignsorlocalizationNoantibioticsNoLP/Nobloodc/s

Admit/completediagnosticworkupincludingLP/IVantibiotics

SomestudiesdonotmandateLPinviewofrarityofmeningitisin clinically well young infants with normal CBC and urineanalysis.However,sincetheprevalenceofbacterialmeningitisininfant<3montholdis4per1000patients,andsinceclinicalexaminationnorCBCisreliableindiagnosingmeningitisinthisagegroup;LPshouldbestronglyconsidered.

Older infants and toddlers (3-36 months)Physical examination is more informative in this age group,thoughsomeoccult infectionsmaystillbemissed.Diagnosticworkupisinitiatedattemp>39oC(cfinfants<3monthswhereworkupisinitiatedat>38oC).Clinicallywellbabies3-36monthsmayhaveoccultSBIin1.5%cases.ThreemainoccultSBI:•Occultbacteremia•OccultUTI•Occultpneumonia

Occult bacteremia: With widespread immunization againstH influenza, streptococcus pneumoniae has become thepredominant cause of SBI in infants and toddlers.(92% of alloccultbacteremiasinthisagegroup),butmostchildreninthisage group clear spontaneously without antibiotics. However~10% children with S Pneumoniae bacteremia progress toSBIandapproximately1caseper1000to2500ofthesefebrilechildren progress to meningitis. (out of 100 children with Spneumoniaebacteremia-10willhaveSBIand0.5maygoontomeningitis).

• Riskofbacteremiaincreasesasthetemperaturerises,

• Riskofpneumococcalbacterermiaincreaseswithage

• Prevalenceofbacteremiainwellappearingolderinfantsand

youngchildrenincreaseswithincreaseofWBCcount.

Atcount<15000risk0.5%

>30,000risk18%

• Absolute neutrophil count >10,000/mm3 is a stronger

predictorofbacteremiathanelevatedTLCof>15000/mm3

Most pediatricians use empirical antibiotics in children with

highTLC.Thequestionthatneedstobeaddressedwhiledoing

sois-Whatisbeingtreated?Ifitispossibleoccultbacteremia

thatisbeingtreatedinordertopreventSBIespeciallymeningitis,

thenmetaanalysisreportsarestillunclearwhetherantibiotics

reduceriskofmeningitisintheseolderinfantsortoddlers.

• Evidencesupportsthatclinicallywellinfants(3-36months)

withrectaltemp<390C(102.20F)andwithoutanevident

sourcesofinfectioncanbedischargedwithouttestingandno

antibiotics.They shouldhave followupvisits if symptoms

worsen.

• Wellappearingchildren3-36monthswithfever>390Cbutwithout any obvious source may have a basic diagnosticworkupincludingCBC,andurineanalysis.IfTLC>15000orANC>10,000,thenbloodc/sshouldbeobtained.

Occult UTI: It is a common source of fever and may causepermanent renal damage. Symptoms are nonspecific. Identifyhighriskgroup:•Female<2years•Male<6month/uncircumcised<12months,•Temperature>390CwithnoothersourceoffeverUrineC/Sisthegoldstandard,butresultstake48hours,hencerapidurineanalysisshowing>10WBC/HPForbacteriaongramstaininanuncentrifugedsampleistakenassignificant.

Occult pneumonia: Most common pathogens in childhoodpneumoniaarevirusesandS pneumoniae. Thepresenceofanypulmonary findingonexamination increases the likelihoodofpneumoniaandconverselytheabsenceofthesefindingsdecreases

thelikelihoodofpneumonia.Althoughchestradiographisoften

believed to be gold standard, it cannot reliably differentiate

betweenbacterialandnon-bacterialcauses.

Some cases of pneumonia bacteria are likely to be clinically

occult. Various studies have recommended that children <5

years having temp>39°C,WBC count>20,000 and no other

sourceoffever,shouldhavechestX-rayevenwithoutpulmonary

symptoms.(Table4)

Summary

Most febrile illnesses (<7 days) in children 0-36 months of

age turn out to be non-specific viral.However, certain febrile

childrenareathigherriskformoreseriousbacterialinfection.

Meticulous clinical evaluation can pickup life threatening

illnesses; identify potentially serious illnesses and pickup

localizingsignsinordertochannelizeinvestigativeworkupthus

minimizingmortalityandmorbidity.However,inneonatesand

youngchildrenclinicalevaluationalonemaymissSBIin~10%

cases,hencetheneedforadiagnosticapproach.


Table 4: Guidelines for evaluations

Age Clinically well Clinically Toxic

0- 1 months High risk for SBI at >38° C

• Comprehensive workup if >38°C

• LP • Admit • IV Antibiotics

ADMIT

Comprehensive Diagnostic Workup - TLC - ANC - Bandcells - Urine analysis - Bactec c/s - Urine culture - LP

IV ANTIBIOTICS

1-3 monthsHigh risk for SBI at >39°C

• Basic diagnostic work-up if >38°C (TLC, Band cells, ANC/urine analysis)

if positive high risk if negative low risk • Observe • Review • Look for localization

3-36 months Low risk for SBI at > 39°C

• Observe/review if < 39°C • If >39°C but well No diagnostic workup• Look for red signs/lo-

calizing signs• No antibiotics• If sick/ >39°C Basic diagnostic

workup• if positive – look for

occult SBI - UTI urine c/s - Pneumonia chest X - ray - Bacteremia Bactec c/s

Practical recommendations• AllneonatesandyoungchildrenwhoappeartoxicregardlessofageneedcomprehensiveworkupincludingLP,hospitalizationandparentralantiboiticsinviewofseriousriskofSBI.

• Febrilechildren1-3monthswhoareclinicallywellarealsoatriskofSBI,hencebasicworkupisrecommended(TLC,ANC,Bandcellsandurineanalysis).

o Ifpositive(highrisk)acompletediagnosticevaluationistobecarriedout,beadmittedandtreatedwithIVantibiotics.

o Ifbasicdiagnosticworkupisnegative(lowrisk)theyshouldbe followed up fromOPDwithout antibiotics, reviewed in24hoursfordevelopingsignsoftoxemiaorlocalizationandtreatedaccordingly.

• Febrile older infants and toddlers (3-36months) should betreatedmore selectively, observed and reviewed repeatedlyfor red flag signs or localization and basicworkup neededif temp >39°C or child appears sick to identify high riskgroup for occult infections especiallyUTI, Pneumonia andbacteremia.

Finally,nosingleexamination,nosingletestorcombinationofexaminationsandtestscanidentifyallpatientsofSBIatthetimeofinitialassessment,sotheneedforrepeatedevaluationcannotbeoveremphasized.Anydiagnosticprotocolcanonlyserveasadjunctandnotasareplacementforclinicaljudgment.

References 1. Alpern ER, Alessandrini EA, Bell LM, et al. Occult

bacteremia from as pediatric emergency department:current prevalence. Time to Detection and outcome,Pediatrics2000;106(3):505-11.

2. Backur R, Perry H, Harper MB, Occult pneumoniasempirics chest radiographs in febrile children withleucocytosis.AnnEmergencyMed1999;33(2):166-73.

3. Baker MD, Bell lM, Avner JR. Outpatient managementwithout antibioticsof fever in selected infantsNEngl JMed1993,329(20):1437-41.

4. BaraffLJ.Managementoffeverwithoutsourceininfantsandchildren.Anm.EmergMed2000,36,602-14.

5. BisgardKM,KaoA,LeakJ,etal.Haemophilusinfluenzaeinvasive disease in the United States. 1994-1995: neardisappearanceofavaccinepreventablechildhooddisease.EmergInfectDis1998:4(2):229-37.

6. KuppermannN,HersherG, JaffaD.Predictorsofoccultbactermia in young febrile children. Ann Emerg Med1998;31(6):679-87.

7. Mackowiak PA. Concepts of fever. Arch Intern Med1998,58(17):1870-81.

8. SteereM, Sharieff GQ, Stenklyft PH. Fever in childrenless than36monthsofage:questionsandstrategies formanagementintheemergencydepartment.JEmergMed2003:25(2):149-57.

9. ShawKN,GorelickM,McGowanKL. et al.PrevalenceofurinarytractinfectioninfebrileyoungchildrenintheemergencydepartmentPediatrics1998;102(2):E16.

10.Torrey SB, Henretig F, Fleisher G, et al. Temperature,responsetoantipyretictherapyinfebrilechildren.PediatrEmerCare1987:3(4):223-7.

11.Wenger JD. Epidemiology of haemophilus influenzaetypeb disease and impact of haemophilus influenzaetypebconjugatevaccinesintheUnitedStates&Canada.PediatrInfectDisJ1998:17(9Suppl):S132-6.

invites case studies, original, and review articles on different specialties

Please sumit your contributions by email at [email protected], [email protected]

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Pushpanjali Medical Publications Pvt. Ltd. A-14, Pushpanjali, Vikas Marg Extn., Delhi-110092

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Fax no. 011-22372851


Celiac Disease Revisited

Manpreet SethiConsultant Pediatrics


Ghaziabad,NCR

Manpreet Sethi

Celiac disease (CD) is an immune-mediatedenteropathy that occurs in geneticallysusceptibleindividualsfollowingtheingestionofgluten-containingstorageproteinsofwheat,barley and rye. Grains and genes are the twobasic elements in the pathogenesis of CD.Originally considered a rare malabsorptionsyndromeofchildhood,CDisnowrecognizedasacommonconditionthatmaybediagnosedatanyageandthataffectsmanyorgansystems.

Prevalence: Worldwide, the incidence isapproximately 1% reported from many largepopulation-based epidemiological studies.Few population studies have looked at theprevalenceofCDinourcountry.InIndia,Laletalhavereportedanincidenceof0.5-1%.Soodet al1 screened 4347 children aged 3-17 yearsattending different schools in the Ludhianadistrict of Punjab, and found an incidence of0.32%.Most reports of CD are from northernIndia(Punjab,Delhi,Haryana,Rajasthan,UttarPradesh) where wheat is the staple cereal inthediet.ItisnotsurprisingthatCDinIndiaisunder-reported. It canbe attributed tovariousfactorsincludinglowawarenesslevels,lackoffacilities forendoscopiesandbiopsiesandthepoor availability and high costs of serologicaltests.Moreover,thereispoorclinicalsuspicioninatypicalcasesandinterpretationofhistologyisvaried.

Prevalence of CD among siblings of an indexpatientinourcountryisashighas22%-23%.2,3

In the West, the risk of CD in first degreerelativesis13%.

Pathogenesis:Glutenisdigestedbyluminalandbrush-border enzymes into amino acids andpeptides.Thegliadinpeptidesinducechangesin the epithelium through the innate immunesystemand,inthelaminapropria,throughtheadaptive immune system. In the epithelium,gliadin damages epithelial cells, resulting inincreased expression of interleukin-15, whichin turn activates intraepithelial lymphocytes.These lymphocytes become cytotoxic and killenterocytesthatexpressMIC-A(astressprotein)on their surface. During infections or as theresult of permeability changes, gliadin entersthe laminapropria,where it isdeamidatedbytissue transglutaminase, allowing interactionwithHLADQ2(orHLA-DQ8)onthesurfaceofantigenpresenting cells. Gliadin is presentedto gliadinreactive CD4+ T cells through a T-cell receptor, resulting in the production ofcytokinesthatcausetissuedamage.Thisleadstovillousatrophyandcrypthyperplasia,aswellastheactivationandexpansionofBcellsthatproduceantibodies.

Clinical Manifestations:ComparedtotheWest,CDinIndiaischaracterizedbyalateronsetof

Whaet Flour Pathogenesis

Gluton

Glutonine Prolaminoz (Gliadin) Albumins, Glebulins Resistent to digestion Transported to Lamina Propria

Deamidated gliadin

Recognized by HLADQ2 / DQS Aetivation of T Cells

Cytokines Interferon a Interulukin 4 TNF

Intestinal Mucosal Injury


disease.Themean age of onset of symptoms is 2.4 to 3 yearsandageatdiagnosisis6.3to8.6(range2.5to14)years,whichindicatesadelayindiagnosisby3.4to5.9years.[4],[5],[6],[7]Ontheotherhand,childrenwithCDintheWestclassicallypresentbetween9-18monthsofageandthemajorityarediagnosedbytwo years of age.[8],[9] Prolonged breast-feeding and delayedintroductionofgluteninthedietcouldberesponsibleforlateronsetofCDinIndianchildren.DelayeddiagnosiscouldbeduetolackofCDawarenessandpresenceofrecurrentgastrointestinalinfections causing diarrhea, protein-calorie malnutrition andnutritionalanemia.

Overtheyears,theclinicalpictureofCDischanging.Previously,the classical form (ie, CD presenting with diarrhea andmalabsorptionsyndrome)usedtobethecommonestpresentationamong children. However, nowadays, CD is diagnosed earlierinthesilentorasymptomaticstageandalsoinatypical forms.As a result of this, the proportion of classicalCD in theWesthasdecreased.Diarrhea,asapresenting featureofCD, isnowseeninonly25-50%ofcases9,10,11comparedto>80%ofcasesinthe1970’sand1980’s.8HoweverthesceneinIndiaisdifferent.Diarrhea(80-94%)isthemostcommonpresentationofchildhoodCD;4,5,6,7anemia, failure to thrive,andstuntedgrowtharemorefrequent in India than in the West, reflecting more severedisease thatprobablycorrelateswithdelayeddiagnosis.ThesedifferencesinclinicalpresentationalsosuggestthatatypicalCDinchildreninIndiaremainsundiagnosed.

Clinical ManifestationsGIT related Non GITChronicdiarrhea BiochemicalAbdominalpain ElevatedSGOT/SGPTFailuretothrive ElevatedpancreaticenzymesAnorxia EndocrineApathy ShortstatureIrritability HypogonadismVomiting AmenorrheaAbdominaldistension NeurologicalMusclewasting Seizures,peripheralneuropathyPallor BrainwhitematterlesionsonMRIConstipation MiscellaneousNonGIT DermatitisherpetiformisHematological CryptogenichepatitisIrondeficiencyanemia DentalenameldefectsFolatedeficiency RecurrentaphthousstomatitisVit.B12deficiency Osteopenia

Diagnosis Histology: AtpresentthegoldstandardofdiagnosingCDisthemodifiedEuropeanSocietyofPediatricGastroenterology,HepatologyandNutrition(ESPGHAN)criteria.12

Diagnostic criteriaESPGHAN 1969• 3biopsycriteriawithclinicalresponse/relapseESPGHAN 1989• 1biopsycriteriawithclinicalresponse• Positiveserologyhelps• Repeatbiopsymayberequiredin<2years

DetailedhistologicalevaluationshouldbebasedonMarsh

criteria13whicharelistedinthetablebelow.

Histology revisited

MODIFIED MARSH SCORE

0IEL<40/100EC&atleast4villiseen(<40/100ECIEL,normalvilli)

1>40/100ECIEL,normalvillus&cryptht

2>40/100ECIEL,hyperplasticcrypts,normalvilli

3a>40/100ECIEL,mildvillusflattening,↑cryptht

3b>40/100ECIEL,modvillusflattening, ↑cryptht

3c>40/100ECIEL,totalvillusflattening,↑cryptht

4hypoplasia

ThespectrumofhistologicalchangesofCDiswellrecognizedinthewesternpopulation.Indevelopingcountrysettings,itisnotroutinelyconsideredasalikelydiagnosisinchildrenpresentingwithchronicdiarrheaandamildtomoderate(modifiedMarsh1-3b)bluntingofintestinalvilli.Morelikely,itisassumedthatsuchalesionmaybecausedbytropicalsprue,persistententericinfectionorinfestation,postinfectiouscomplications,orproteinenergy malnutrition with associated small bowel bacterialovergrowth.RecentdatahaveshownthatamongIndianchildrenwithchronicdiarrheaconfirmedtohaveCD,classicalflatmucosawithcrypthyperplasiawaspresentonlyinonethirdofchildrenwhileasimilarproportionhadcrypthyperplasiawithmoderate

villous blunting.14 Interestingly among children in whom the

mucosal changeswere limited tomild blunting of villi (equal

cryptdepthandvillusheight),at leasta thirdwereconfirmed

to have CD by the presence of serological antibodies, clinical

responsetoglutenfreedietandapositiveglutenchallenge.On

theotherhand,evenseverevillousatrophymaynotalwaysmean

CD in the Indian context because such lesions are commonly

seen with primary protein energy malnutrition, recurrent

gastrointestinal infections including parasitic infestations and

thesechildrendevelopanemia,diarrhea,growthfailure,vitamin

deficiencies;allofwhichadverselyaffectsmallbowelhistology.

Therefore,inIndia,itissuggestedtodoCDserologyatdiagnosis.

Inagivenclinicalsetting,antibodypositivityalongwithtypical

smallintestinalmucosalchangesandresponsetoGFDishelpful

toestablishthediagnosis.

Serological Tests:Thefirstimmunologicalassaytobetestedwere

theanti-gliadinantibodies(AGA)whicharepredominantlyofthe

IgGandIgAclassanddonebysolidphaseELISA.However,post

infectionmalabsorption,Crohn’sdiseaseandcow’smilkprotein

intolerancecangivefalsepositivetestsforAGA.Thevariability

andgenerallyloweraccuracyassociatedwiththeAGAtestsmake

themunsuitablefordiagnosticorscreeningpurposes.

Anti-EMA (anti-endomysial antibodies) primarily belongs to

theIgAclassandisdirectedagainsttheintermyofibrilsubstance

of the smooth muscle. Anti-EMA is identified using indirect

immunofluorescence on frozen sections ofmonkey esophagus

or human umbilical cord sections. Positive serum samples

reactwith the connective tissuewhich surrounds the smooth

musclebundlesinthelaminapropria,andgiveacharacteristic

laceworkpatternaroundtheunstainedsmoothmusclescells.15


Thediscoveryofanti-tissuetrans-glutaminaseantibodies(anti-tTG)astheautoantigenrecognizedbytheendomysialantibodiesisseenasamajorbreakthrough[16].ThistestiscarriedoutusingtheELISAtechniqueandsubstratesusedincludetheguineapigantigenandnoweventhehumanrecombinanttTGantigen.

What antibodies are most reliable?17

SENSITIVITY SPECIFICITY

India West India West

Antigliadin

IgG 75 69-85 78 73-90

IgA 80-94 75-90 84-92 82-90

AEA 90 85-98 95 94-100

tTG(g.pig) 76 85-98 94 94-95

tTG(human) 93 99

Whiletheperformanceoftheanti-EMAissuperiortoanti-tTGA,[18] interpretationof immunofluorescenceassay(IFA)foranti-EMA tests is operator-dependent andmore liable to errors inlessexperiencedhands.ELISAbaseddetectionofanti-tTGAisa simplerandmoreaccessiblediagnostic tool andanti-humanrecombinanttransglutaminaseantibodiesisreportedtoperformbettertotheantiguineapigtransglutaminaseantibodies.19

The disadvantage of the anti EMA and anti-tTGA is that theyare unreliable in less than 2 years.20,21 Further they are IgAdependentantibodiesandwillbenegativeinthosewithselectiveIgA deficiency, as is seen in 3% of individuals with CD.22 Inchildrenwith ahigh clinical andhistological suspicionofCDbut a negative IgA based serology, IgA deficiency needs to beexcluded.TheIgGAGAorthemorerecentlyevaluatedIgGEMAortheIgGtTGAwouldbeusefulinthesesituations.Sincethepositivecut-offshavebeendesignedtooptimizethesensitivityof the test, it is recommended thatusinghighercut-offvalueswhileusingthesetestsforscreeningasymptomaticindividualsat riskwill improve the specificity and thepositivepredictivevalue.Barkeretalhaveshownthatthesensitivityandspecificitywasashighas98%and97%respectivelywhencutoffvaluesof>100Uand<20Uwereused.23Certaincautionisrequiredwhileinterpreting theanti tTGAELISAassays for routinediagnosticpurposes.ThedifferentsourceoftTGantigen,variedtechniquesof production i.e. genetically engineered or tissue extraction,and theuseof arbitraryunitsbydifferent commercial kits fordefiningapositivecutcaninfluencethediagnosticaccuracyoftheassay.Thefalsepositivityrateshaverangedfrom28%toashighas80%usingtheassaycut-offoffourdifferenttTGassays.24Thisvariationintheassaysemphasizestheneedforglobalandnationalstandardizationamongdifferentlaboratories.Highfalsepositivityhasalsobeenreportedfrompatientswithliverdisease,inflammatoryboweldiseaseandconnectivetissuedisorder.24

Newantibodies in thepipeline (to assessdisease severity andresponsetotreatment):1. IgAanti-actinantibodies(IgAAAA)2. SolubleCD163

3. Matrixmettaloprotienases(MMPs)4. PlasmaNitricoxideproductsHLA: ThereisastronggeneticassociationofCDwithHLA–DR3-DQ2 inherited as an extendedhaplotype. Patientsnegative forDQ2arepositive forDQ8and therefore90-95%of individualswithCDhaveanassociationwithDQ2orDQ8.DQ2andDQ8moleculesbindgliadin-derivedpeptides,someafterdeamidationbytissuetransglutaminase,andpresentthemtotheintestinalTlymphocytes.TheactivatedTh1Tcellssecreteproinflammatorycytokineswhich produce the intestinal lesions of CD.25 ThesefindingscouldexplaintheroleofHLAandtTGinthepathogenesisof thedisease.HoweverDQ2 is alsopresent in 20-25%of thenormalpopulationasreportedfromthewesternpopulationandNorthIndia.26WhileHLADQ2typing isnotrecommendedforroutinediagnosisasitiscumbersomeandexpensive,itcanbeusedforrulingoutCDwherethediagnosisisequivocalasithasanegativepredictivevalueofgreaterthan95%.26

Is Gluten Challenge Necessary?Glutenchallengeisnotmandatory,butmaybeindicatedwhenthere is doubt about thediagnosis. Since cow’smilk sensitiveenteropathy and post enteritis syndrome occur in the firsttwoyears of life, gluten challenge is usually recommended inchildrendiagnosedwithin the first twoyearsof life. It shouldbe considered in patients with equivocal clinical response toGFDandinthosewhowereasymptomaticatfirstpresentationdiagnosedthrough‘atrisk’screeningprograms.Whereverglutenchallengeisrequireditshouldbeavoidedbefore6yearsofagetominimizerisksfordentalenameldefectsandduringperiodsofrapidgrowthlikepuberty.

TreatmentThemainstayofmanagement inCDis life longGFD;andironandfolicsupplementationforthefirst3monthsafterdiagnosis.The patient should be reassessed between 8-12 weeks afterstartingGFDtolookforresponsetotreatmentie,improvementof symptoms and growth parameters. This is the stage whenthe diagnosis is finally confirmed (as permodified ESPGHANcriteria). CD in India occurs mainly in regions where wheatisastaplediet.Familiesat thefirstcontactareworriedduetoprolonged illness of their child despite several consultationsfromdoctors. Parents and older children should be counseledfollowing confirmation of diagnosis. Dietary advice of glutenavoidanceanddrugsupplementationisreadilyaccepted.SincewedonothavemarketedglutenfreeproductsavailableinIndia,each center has to devise GFD charts in local languages. AvisibleresponseisthekeyfactorthatgivesparentsconfidencetostrictlyadheretoGFDdespitedifficultiesinimplementationparticularlyinfamilieswhereothermembersconsumewheatasastaplediet.

ThemajorhardshipfacedbyparentsistofulfillthespecialneedsoftheirCDchildrenlikebirthdaycakes,chocolates,icecreams,biscuits etc, and social participation on different occasions.Nonavailabilityofready-madegluten-freefoods(bakeryproductsand gluten-free flour) and unlabelled food packs in India arebottlenecks in the dietarymanagement of CD. In our country,thoughvegetarian symbolhasbeen implemented, the “gluten-free”symbolonpackedfoodsisnotyetintroduced.Thereason


for this isa limitednumberofCDcasesandnon-feasibilityatthecommerciallevel.InIndia,itiscommonpracticeforfamiliestopurchasewholegrainandhavetheflourprocessedatasmallneighborhoodflourmill,whereothercereals likecornandricearegroundseparatelyatadifferenttimeslotaftercleaningthegrinding machine. These measures are inadequate, and somequantity of wheat gets mixed with other cereals27 and maybe a factor of non-response in a strictly compliant patient.Thereforepatientsshouldbetaughttousehomegrindingsolelyforgluten-freeflour.Patientsmostlyadheretofollow-upvisits.Noncomplianceisobservedbyconsumingtoffees,sharingfoodwith other schoolmates, or in large joint families’ ingestion ofglutencontainingdomesticfooditems.Oneachfollow-upvisitadherencetodietmustbeemphasized,andgrowthparametersandsexualmaturitymonitoredwhereverapplicableaswellasasearchforcomplicationsifany.

Diet chart for CD patientsFood Items Drinks•Rice •FreshJuice•Sabudana •FreshMilk•Arrowroot •FreshCurd•Bajra •FreshLassi•Makka •FizzyDrinks•Jowar •Soda•Singharaatta •FreshSoup•Idly Desserts•Dosa •RiceKheer•Vada •PaneerSandesh•Mumura •CaramelCustard•RiceNoodles •CarrotHalwa•FreshMeat •Jaggery•FreshMutton/Chicken•Egg/Fish

Diet chart for CD patientsFood Items Drinks•Atta/Maida •HotChocolate•Suji •Complan•Rye •Horlicks•Barley •Boost•Noodles •BottledMilkShake•Pasta/Sphagetti •SoupPowder•Bread/Bun Desserts•SoupStick •Cake•Sevian •Pastry•Dalia •IceCream•Patty/Pizza •Éclair•Burger •Chocolate•Kulcha •Jalebi•Bhujia •GulabJamun•UpmaSevian Tinned and Canned Preparations•Biscuits •Preparationcontainingbakingpowder •ProcessedmeatslikeSausagesand •Kebab

Complications of Untreated CDThereisacontinuedinterestinthelongtermconsequencesofCD,whichofcoursehasparticularsignificanceinthegroupofsilentCDindividualsdetectedonscreening,

andthosethatarepoorlycompliantwiththegluten-freediet.IthasbeenproposedthatevenabriefperiodofaGFDmayconferrelativeprotection to the sequelaeofCD.Listedbeloware themajorconsequencesandcomplicationsassociatedwithuntreatedCD.Apart from these,delayeddiagnosis and failure to adheretoaGFDhasalsobeenassociatedwithincreasedprevalenceofotherautoimmuneconditions,mortalityandmalignancies.

Consequences of untreated CDGrowth abnormalitiesAnemiaNutritionaldeficiencies Fe Folicacid B12 Zn FatsolublevitaminsHormonaldisturbances Delayedsexualmaturity Infertility/recurrentabortions/low birthweight HypothyroidismGastrointestinalrelated Malignancies(smallbowel lymphomas) Delayedguttransit (constipation/reflux)

Refractory Celiac DiseaseApproximately5%ofpatientsmayhaverefractoryCD,definedaspersistentsymptomsandvillousatrophydespitescrupulousadherence to a gluten-free diet28. The symptoms that usuallydevelop in these patients include diarrhea, weight loss,recurrence of malabsorption, abdominal pain, bleeding, andanemia,andulcerativejejunitisoftenarisesaswell.This syndrome is also known as Refractory sprue. RefractoryCD may be classified as type 1, in which there is a normalintraepitheliallymphocytephenotype,ortype2,inwhichthereisaclonalexpansionofanaberrantintraepitheliallymphocytepopulation and a high risk of developing intestinal T celllymphoma. Treatment of refractory CD involves nutritionalsupportandrepletionofvitaminsandminerals,togetherwithastrictgluten-freediet.Inmostcases,corticosteroidsinduceclinicalimprovement29. Immunosuppressive drugsmay be beneficial30but shouldbeusedwithcaution, since theymaypromote theprogressiontolymphoma31.Otherproposedmodalitiesincludeanti-TNFalpha,andstemcell transplantationbut their role inmanagementofrefractoryCDneedstobeevaluatedfurther.

SummaryCDoccurs in nearly 1%of the population inmany countries.Thediagnosis,whichisstraightforwardinmostcases,isusuallyestablished on the basis of serologic testing, duodenal biopsy,andobservationoftheresponsetoagluten-freediet.Increasingawareness of the epidemiology and diverse manifestations ofthedisease,aswellastheavailabilityofsensitiveandspecificserologic tests, especiallyamongprimarycarephysicians,willleadtomorewidespreadscreeninganddiagnosis,whichinturnwill lead togreateravailabilityof gluten-free foodsandeffortstodevelopdrugtherapiesthatrelievepatientsoftheburdenofa gluten-free diet. In addition, earlier diagnosismay lead to areductioninthecomplicationsofthedisease.


Key Messages• PrevalenceofCDishighinIndia.• It may present with protean manifestations; atypically

presentingdiseasemustbepickedupmoreoften.• Serologyishelpfulinscreening;Confirmatorydiagnosisis

stillbyhistopathology.• Correctinterpretationofhistologyisofprimeimportance.• Managementisbasedonstrictlifelongglutenfreedietand

continuous supervision andmonitoringunder apediatricgastroenterologistandnutritionist.

• All casesmaynot respond toGluten freediet (RefractoryCeliac).

References 1. SoodA,MidhaV,SoodN,AvasthiG,SehgalA.Prevalence

ofCeliacDiseaseamongschoolchildreninPunjab,northIndia.JGastroenterolHepatol2006;21:1622-5.

2. GautamA,JainBK,MidhaV,SoodA,SoodN.PrevalenceofCeliacDiseaseamongsiblingsofCeliacDiseasepatients.IndianJGastroenterol2006;25:233-5.

3. Goel GK, Pokharna RK, Khatri PC, Senger GS, Joshi A,KhatriM,etal.PrevalenceofCeliacDiseaseinfirst-degreesiblingsofCeliacDiseasepatients.IndianJGastroenterol2007;26:46.

4. Mohindra S, Yachha SK, Srivastava A, Krishnani N,AggarwalR,GhoshalUC,etal.CeliacDiseaseinIndianchildren:assessmentofclinical,nutritionalandpathologiccharacteristics.JHealthPopulNutr2001;19:204-8.

5. PoddarU,ThapaBR,NainCK,PrasadA,SinghK.CeliacDisease in India: are they true cases of CD? J PediatrGastroenterolNutr2002;35:508-12.

6. PatwariAK,AnandVK,KapurG,NarayanS.ClinicalandnutritionalprofileofchildrenwithCeliacDisease.IndianPediatr2003;40:337-42.

7. PoddarU,ThapaBR,SinghK.ClinicalfeaturesofCeliacDisease in Indian children: are they different from theWest?JPediatrGastroenterolNutr2006;43:313-7.

8. WalkerSmithJA.CeliacDisease.In:Diseaseofthesmallintestine in childhood, 3rd edn. Butterworths, London1988;p.88-143.

9. BottaroG,FaillaP,RotoloN,SanfilippoG,AzzaroF,SpinaM et al. Changes in Celiac Disease behaviour over theyears.ActaPediatr1993;82:566-8.

10.George EK, Mearin ML, Franken HCM, Houwen RH,HirasingRA,VandenbrouckeJP.TwentyyearsofchildhoodCeliac Disease in the Netherlands: a rapidly increasingincidence?Gut1997;40:61-6.

11.Ascher H, Holm K, Kristiansson B, Maki M. DifferentfeaturesofCeliacDisease in twoneighboring countries.ArchDisChild1993;69:374-80.

12.Walker-Smith JA, Guandalini S, Schmitz J, SchmerlingDH,VisakorpiJK.RevisedcriteriafordiagnosisofCeliacDisease.ArchDischild1990;65:909-11.

13.OberhuberG,GranditschG,VogelsangH.HistopathologyofCeliacDisease:timeforstandardizedreportschemeforpathologist.EurJGastroenterol1999;11:1185-94.

14.Bhatnagar S,Gupta SD,MathurM, PhillipsAD,KumarR, Knutton S, Unsworth DJ, Lock RJ, Natchu UC,Mukhopadhyaya S, Saini S, Bhan MK. Celiac Diseasewithmild tomoderate histologic changes is a commoncause of chronic diarrhea in Indian children. J PediatrGastroenterolNutr2005Aug;41(2):204-209.

15.Bhatnagar S, Bhan MK Serological diagnosis of CeliacDisease.IndianJPediatr1999;66(1Suppl):S26-31.

16.DieterichW,EhnisT,BauerM,DonnerP,VoltaU,RieckenEO,SchuppanD.Identificationoftissuetransglutaminaseas the autoantigen of Celiac Disease. Nat Med 1997Jul;3(7):797801.

17.BhatnagarSandTandonN.DiagnosisofCeliacDisease.IndianJofPediatr,Volume73August,2006.

18.RostomA,DubeC,CranneyA,SaloojeeN,SyR,GarrittyC, SampsonM, Zhang L, Yazdi F,Mamaladze V, Pan I,MacNeil J, Mack D, Patel D, Moher D. The diagnosticaccuracyofserologictestsforCeliacDisease:asystematicreview.Gastroenterology2005Apr;128(4Suppl1):S38-S46.

19.Sblattero D, Berti I, Trevisiol C, Marzari R, TommasiniA, Bradbury A, Fasano A, Ventura A, Not T. HumanrecombinanttissuetransglutaminaseELISA:aninnovativediagnostic assay for CD. Am J Gastroenterol 2000May;95(5):12531257.

20.Agardh D, Borulf S, Lernmark A, Ivarsson SA. TissueGarcia-MasdevallMD.Antibodiestogliadin,endomysium,transglutaminase immunoglobulin isotypes in childrenwith and tissue transglutaminase for the diagnosis ofCeliac Disease. untreated and treated Celiac Disease. JPediatr Gastroenterol Nutr J Pediatr Gastroenterol Nutr1999Nov;29(5):571-574.2003Jan;36(1):77-82.

21.Burgin-Wolff A, Gaze H, Hadziselimovic F, Huber H,Lentze MJ, Nussle D, Reymond-Berthet C. Antigliadinand antiendomysium antibody determination for Celiacdisease.ArchDisChild1991Aug;66(8):941-947.

22.Bhatnagar S, Natchu MU. Celiac Disease in Indianchildren.NatlMedJIndia2004May-Jun;17(3):124-127.

23.PicarelliA,SabbatellaL,DiTolaM,VetranoS,CasaleC,AnaniaMC,PorowskaB,VergariM,SchiaffiniR,GargiuloP.Antiendomysial antibody of IgG1 isotype detectionstrongly increases the prevalence of celiac disease inpatients affected by type I diabetes mellitus. Clin ExpImmunol2005Oct;142(1):111-115.

24.LiuE, LiM,Bao F,MiaoD,RewersMJ, EisenbarthGS,Hoffenberg EJ. Need for quantitative assessment oftransglutaminase autoantibodies for Celiac Disease inscreening-identified children.JPediatr 2005Apr;146(4) :494499.

25.Molberg O, Mcadam SN, Korner R, Quarsten H,Kristiansen C, Madsen L, Fugger L, Scott H, Noren O,Roepstorff P, LundinKE, SjostromH, Sollid LM.Tissuetransglutaminase selectively modifies gliadin peptidesthatarerecognizedbygut-derivedTcellsinCD.NatMed1998Jun;4(6):713-717.

26.Kaur G, Sarkar N, Bhatnagar S, Kumar S, Rapthap CC,BhanMK,Mehra NK. Pediatric Celiac Disease in Indiais associated with multiple DR3-DQ2 haplotypes. HumImmunol2002Aug;63(8):677-682.

27.Walker Smith JA.CD. In:Disease of the small intestineinchildhood,3rdedn.Butterworths,London1988;p.88-143.

28.TrierJS.Celiacsprue.NEnglJMed1991;325:1709-1719.29.Cellier C, Delabesse E, Helmer C, et al. Refractory

sprue, celiac disease, and enteropathy-associated T-celllymphoma.Lancet2000;356:203-208.

30.Peter H.R. Green, and Christophe C. Celiac Disease. NEnglJMed2007;357:1731-1743.


Dinesh Singh Director, Department of

Radiation Oncology

Galaxy Cancer Institute

PushpanjaliCrosslayHospital

Ghaziabad,NCR

Improving Cure Rates and reducing side-effects by modern Radiotherapy Techniques

Dinesh Singh

Radiotherapyisoneofthethreemaintreatmentmodalities of cancer treatment. The other twobeingCancersurgeryandChemotherapy.

Radiotherapy utilizes ionizing radiation toinactive DNA of cancer cells. Most commonequipmentusedforthispurposeinthewesternworldisLinearAccelerator,butinIndiaitistheCobalt Machine because of cost of equipmentandthatofrunningandmaintainingit.

Linear AcceleratordeliversfocusedandselectableenergiesthathelpreductionofsideeffectsandallfurtherdevelopmentshavehappenedinthetechnologyofLinearAccelerator.Devices suchas Multi leaf Collimator for giving irregularshapes are present like Digital Portal ImagingDevice for portal verification, ComputerizedTreatmentPlanningSystemforfastandaccuratecalculationofcomplexplans.

Thesehelpgenerate3DConformalplansforbet-terdeliverytotargettissues.

IMRT or intensity Modulated Radiotherapygivesirregularplanswhichcantreattumortis-suesaccuratelyandsparenormaltissues.Tech-nologygoesastepfurtherwhereinaCTscannerismountedontotheLinearAccelerator.

Givenbelowisaplangeneratedfor3DConformalandIMRTTTechnology goes a step further where ina CT scanner is mounted on to the LinearAccelerator.

Intensity Modulated RT (IMRT)

(a) 3DCRT (b) IMRT (c) IMRT (0.5 cm cord margin)

Cobalt Machine


G alaxy C anc er Ins titute @ P us hpanjali C ros s lay Hos pitalW 3, S ec tor 1, Vais hali (Near G azipur B order)

Galaxy Cancer Institute,

Pushpanjali Crosslay Hospital

This allows us to perform Image Guided Radiotherapy, whenwehaveaCTscanmountedontheLinearAccelerator,wecanactuallyseewhatwearetreating.

Because of this confidence, a reduction in the margins forradiation given especially when the treatment area cannot bevisualized.Thisfeaturepermitsselectiveradiationtothetargetonly,thussavenormaltissuesfromhigherradiation.Thistranslatesin High cure rates and lower side effects.

Anothercomplimentarytechnologyisoneinwhichradioactivesourcesareinsertedintothetumorornearvicinityofthis.ThistechnologyiscalledBrachytherapy.

Brachytherapy,likeexternalradiationhasevolvedtremendously.Inthecurrentupdation,HighDoseRate,radiationisdeliveredinminutes,whereasintheearliermodelsittookdaystodeliveranequivalentdose.Brachytherapy,helpsdeliververyhighdosespreciselytothetumorsite.

Inmanycases,acombinationofthesetwomodalitiesisusedtogiveveryhighdoseofradiation,leadingto1)HighCureRates2)Lowsideeffectsofradiation.AlltheabovetechniquesareavailableatGalaxyCancerInstitute,PushpanjaliCrosslayHospital.


Deepak PandeConsultant Pediatrician

PushpanjaliMedicalCentre,

Delhi


Ghaziabad,NCR

Office Management of Asthma

Deepak Pande

Asthma and wheezing disorders account fora large number of children coming to clinics.Whileacuteasthmaisattendedtobyvirtueoftheseverityofsymptoms,persistentasthmaremainsa grossly underreported, underdiagnosed andundertreated disease resulting in considerablemorbidity in children. Recent developmentshavegreatlyimprovedthemanagementofthesedisorderstoagoodextent.

DiagnosisHistory of recurrent episodes of cough,breathlessness, wheezing, tightness of chestshould alert the clinician. Exam may revealrhonci, prolonged expiration, a silent chest ormayevenbenormal.Someotherfeaturesmayalso be suggestive of asthma. These includepersonal or family history of skin allergy,absence of fever in above episodes, nightsymptoms, symptoms induced by exercise oron exposure to specific allergens eg, pollens,housedust,foodetc.Responseafterinhalationof bronchodilator is also a good indicator ofdiagnosis.

Some other diseases (especially in youngchildren)maypresentwith featuresofasthmain addition to other features, which helpsin exclude them. Some of these are GER,bronchiolitis,cong.defects,immunodeficiency,mucociliary defects, cystic fibrosis, adenoids,tuberculosis,foreignbody,allergiestofoods.

Childrenlessthan5yearsageoftenhaveviralLRTI,whichmaybeassociatedwithwheezingandisrecurrent.Althoughmostchildrenrecoverwithinaperiodof timesomemaycontinuetohaverecurrentwheezinginadolescence.

Investigations1. Investigations are not a must in treating

asthma.2. HemogramandX-raychestmaybedoneto

serveasbaseline.3. Respirometryandpeakflowmeasurements

maybeusedasdiagnosticandmonitoringtools but they have many limitations

and are not usually used in day-to-daypractice.

4. Testsforallergyeg,IgE,specificIgE,RAST,skin testing for allergies have a limitedrole.

Assessing ControlDegreeofcontrolachievedisusedtoguidethetherapy.

Long Term ManagementThegoalistoreachthelevelofcontrolwherethere arenodaytime symptoms,no limitationofactivity,nonightsymptoms,andnoneedforreliever medicines. Additionally, pulmonaryfunctions are normal, and there are noexacerbations.At this time,maintenancewithminimum medications should be attempted.There are five components essential tomanagementofasthma.1. Developing a patient/Caregivers/ Parent/

Doctor partnership: Since asthmais a chronic disease with long-termmanagement, developing a strategy ofa ‘guided self management plan’ bringsthe best results. The goals of treatmentare arrived after discussion with parentsand a written plan is prepared. Patientis taught self-monitoring techniques (bysymptomsorbypeak flowmeter), tohelpadjusttherapywithintheparametersoftheplan,recognizeanexacerbation,andthenfollowed-upevery4-8weeksformonitoringandeducation. Duringthesevisits,someofthekeyissuestobediscussedinclude:• chronicandepisodicnatureofdisease,ie,nocure,butcontrol;

• need for compliance as drugs taketime;

• merits and correct use of inhalationtherapy

2. Prevention of asthma or its symptoms: Avoidance of smoking in pregnancy andensuring smoke free environment forthe newborn may reduce developmentor occurrence of symptoms. Exclusive

Feature Green (low risk) Red (high risk) Uncontrolled

DaytimeSymptoms*LimitationofactivityNightsymptomsRelievermed.reqd.PFT(ifdone)

Nil(<2/wk)NilNilNil(<2/wk)normal

Upto2featuresderangedinaweek

>2featuresderangedinaweek

AcuteExacerbations* Nil Any/yr. Any/wk.

*Progressive in symptoms makes it exacerbated.


breastfeedinginearlyinfancymayprotectagainstepisodesof wheezing later. Any food, drug, additive known toprecipitatesymptomsshouldbeavoided.

Takingreasonableprecautions,helpsavoidindoorandoutdoorallergens.Theseinvolvewashingbedlinenevery10days with hot water, use of plastic covered pillows andmattresses,removingdampnessfromwalls,avoidingcarpetsand upholstery, vacuum cleaning, removing furred petsfromhome.Outdoor allergens can be avoided by stayingindoorswithwindowanddoorsclosedduringseasons,andavoidingtheoutdoorsindry,coldweather.Exercisingafterproperwarmingupisencouraged.

3. Assess, Treat and Monitor: Inhalation therapy is mosteffective form of treatment and pressurized Meter DoseInhalers (pMDI) aremostversatiledevices,whichcanbeusedacrossallages.Itispreferredasitreduceslocalandsystemicsideeffectsandmakesiteasiertouse.Afacemaskis required for children less than 4 years. Nebulizers,dry powder inhalers, breath actuated inhalers are otheralternatives. The technique of inhalation should bedemonstratedandcheckedateveryvisit.a) Ages 5 years and above: Drugoptionsarearrangedinto

fivesteps(Table2)ofincreasingefficacy.Everypatientfitsintooneofthe‘steps’andtreatmentissteppedup

Level of control Treatment action

Controlled Maintain and find lowest controlling step

Partly controlled Consider stepping up to gain control

Uncontrolled Step up until controlled

Exacerbation Treat a exacerbation

Step 1 Step 2 Step 3 Step 4 Step 5

As needed rapid acting β2-agonist

Asthma educationEnvironmental control

Controller options****

Select one Select one Add one or more Add one or both

Low-dose inhaled ICS*

Low-dose ICS pluslong-acting β2-agonist

Medium-or high-doseICS plus long-actingβ2-agonist

Oral glucocortico-steroid(lowest dose)

leukotriene modifier**

Medium-orhigh-dose ICS

Leukotriene modifier

Anti-IgETreatment

Low-dose ICS plusLeukotriene modifier

Sustained releasetheophylline

Low-dose ICS plussustained releasetheophylline

Management Approach Based On ControlFor Children Older Than 5 Years, Adolescents and Adults

Reduce Treatment Steps Increase

* ICS=inhaled glucocorticosteroids**=Receptor antagonist or synthesis inhibitors***Preferred controller options are shown in shaded boxes

Alternative reliever treatments include inhaled anticholinergics, short-acting oral _2-agonists, some long-acting _2-agonists, and short-acting theoph-ylline. Regular dosing with short and long-acting _2-agonist is not advised unless accompanied by regular use of an inhaled glucocorticosteroid.

Incr

ease

Red

uce

Table 2: Management based on control


or down according to the level of control, which isassessedeachtimethepatientreportsforfollow-up.Anexacerbationshouldbeactivelyconsideredforsteppingupcontroltherapy,iftheprecedingperiodshowsalossofcontrol.

Everystepuprequires3monthsofobservationbeforefurther step up. If the patient is controlled for 3months,considersteppingdownastepatatimeuntiltheminimumrequireddoseformaintainingcontrolisreached.When the patient has been controlled for 1yearandisonminimumdosesfor3months,considerstoppingbutcontinuefollow-up.

Every patient should continuously receive asthmaeducation,environmentcontrolandarapidactingB2Agonistasrequired.

b) Ages <5 years: ICS in low-meddosesisthebestoptionforcontrol.Leukotrinemodifiersmaybeused>2years.In viewof good spontaneous recovery inmost youngchildren, stepping down may be considered just ascontrolisachievedandneedfortherapyreviewedat6monthsofcontrol.

4. Manage Exacerbations: Whenever acute increase insymptomsisreported,patientisadvisedtotake2-4puffs

ofRapidActingB2Agonist(salbutamol)every20minutesupto3 times. If relief isnotsustainedfor4-6hoursor ifriskfactors (Table4)arepresent, firstdoseoforalsteroid(prednisolone1mg/day)isstartedandanearlyappointmentisscheduled.Incaseofsevereexacerbationsorifriskfactorsarenotedanytimefurthertreatmentshouldbecarriedoutinanacutecarefacility.

Table 4: Red flag signs (Risk factors)

Alteredsensorium,Bradycardia,lowvolpulse,cyanosis,exhaustion, diaphoresis, silent chest, abnormal ABG,SpO2<92

5. Special Situations: Special considerations are requiredin managing surgery, rhinitis, sinusitis, nasal polyps,respiratoryinfections,GER,anaphylaxisinasthmatics.

Drug MOA Avail as Age Side Effects Remark

ICS:Beclometh,Budesonide,Fluticasone

Antiinflammatory InhalationLowdose<200Meddose200-400/500Highdose>400/500

All OralthrushGrowth,pubdelay(Highdoses)

Usedatalllevels

Leukotrinemodifiers,Montelucast

Antileukotrines Oral4,5,10mg >2yrs Nil Atalllevels,ExerciseInducedAsthma,Inferioralternatives

LABASalmeterol,Formeterol

Longactingbrdil Inhalation >4-5yrs NilincombwithICS

Add-onafterlowdoseICS

SRtheophylline,CromonesSRSABA(SRsalbutamol,terb,bam)

Anti-inflammatoryLongactingbrdil

OralOralOral

><5yrs>5yrs

SerumLevels(if>10mg/kg/day)++

Monotherapy,Add-on,AllareInferioralternatives

Table 3: Controller drugs

Referencs 1. GINA - the Global Initiative For Asthma - http://www.

ginasthma.com


Drugs Optimal dosing time Patients

Calcium channel blockers

Isradipinesustainedreleaseformulation Evening Hypertensivepatientswithchronicrenalfailure

Isradipinesustainedreleaseformulation Regardlessoftime Patientswithuncomplicatedessentialhypertension

NifedipineGITS Bedtime Patientswhoarenon-responderstotheinitial30mg/day

NifedipineGITS Regardlessoftime Hypertensivepatientsreceiving30mg/daynifedipineGITS

Amlodipine Morning Patientswithmild-to-moderateessentialhypertension

Nisoldipineextendedrelease Morning Patientswithmild-to-moderateessentialhypertension

Cilnidipine Bedtime Patientswithuncontrollablemorninghypertension

Verapamilextended-release(marketedasCovera-HS®)

Bedtime Anginaorhypertensivepatients

Diltiazemextendedrelease(marketedasCardizemLA®)

Bedtime Anginaorhypertensivepatients

Angiotensin II receptor blockers

Losartan Uncertain

Ibesartan Regardlessoftime Patientswithuncomplicated,mild-to-moderateessential

Olmesartanmedoxomil Regardlessoftime Patientswithuncomplicated,mild-to-moderateessential

Valsartan Bedtime Non-dipperhypertensivepatients

Telmisartan Bedtime Non-dipperhypertensivepatients

Telmisartan Morning Youngmenwithmildormoderateessentialhypertension

Candesartancilexetil Awakening Patientswithmild-to-moderateessentialhypertension

Angiotensin-converting enzyme inhibitors

Benazepril Morning Patientswithprimarymild-to-moderatehypertension

Perindopril Morning Patientswithprimarymild-to-moderatehypertension

Quinapril Evening Patientswithprimarymild-to-moderatehypertension

Ramipril Bedtime Patientswithprimarymild-to-moderatehypertension

Trandolapril Bedtime Patientswithprimarymild-to-moderatehypertension

Lisinopril Bedtime Patientswithprimarymild-to-moderatehypertension

Enalapril Bedtime Patientswithprimarymild-to-moderatehypertension

Beta-blocker

Metoprololsuccinatesustainedrelease Morning Patientswithhypertension,anginapectorisorheartfailure

Carvedilol Evening Patientswhohavebeentreatedwithfirst-lineantihyperten

Carvedilolphosphateextendedrelease Morning Patientswithheartfailure,leftventriculardysfunctionfol

Propranololextendedrelease Bedtime Patientswithhypertension

Antihyperlipidaemicdrugs

Statinswithashorterhalf-life(ie,lovastatin,simvastatinandfluvastatin)

Evening Patientswithhypercholesterolaemia

Common Drugs Acting on Cardiovascular System and Optimal Dosing Time


Statinswithlongerhalf-lives(ie,fluvastatinextendedrelease,rosuvastatinandatorvastatin)

Regardlessoftime Patientswithhypercholesterolaemia

Pravastatin Evening Patientswithhypercholesterolaemia

Atorvastatin Evening PatientsundergoingPCI

Ezetimibe Morning Patientswithprimaryhypercholesterolaemia

Ezetimibe/simvastatintablet Evening Patientswithprimaryhypercholesterolaemia

Fenofibrateretard Regardlessoftime Patientswithhypertriglyceridaemia

Bezafibrateretard Morning Patientswithhypertriglyceridaemia

DoxazosinGITS Morning Patientswithgrade1–2essentialhypertension

Regardlessoftime Patientswithbenignprostatichyperplasia

Low-doseaspirin Bedtime Patientswhoareatriskforacardiovascularand/orcerebrovas-cularevent

Isosorbidemononitratesustained-releaseformulation(eg,ElantanLA®,IMDUR®)

Awakening Patientswithanginapectoris

Diuretics

Indapamide,hydrochlorothiazide Morning Patientswithessentialhypertension

Torasemide Bedtime Patientswithessentialhypertension

Once-dailyhydrochlorothiazidebasedfixed-dosecombination

Before6pmandpreferablyinthemorning

Patientswithessentialhypertension

Cited in: ZhuL-L,ZhouQ,YanX-F,ZengS.CME-OptimalTimetoTakeOnce-DailyOralMedicationsinClinicalPractice.JClinPract62(10):1560-1571,2008.


Amit GuptaConsultant & Head

Emergency & Critical Care

PushpanjaliCrosslayHospital

Ghaziabad,NCR

The Role of Spirituality in Medicine

Amit Gupta

The focus of spirituality in the practice ofmedicine has increased to historic levels inrecentyears.VictorFrankl,1apsychiatristwhowroteofhisexperiencesinaGermanNazicamp,stated:“Manisnotdestroyedbysuffering;heisdestroyedbysufferingwithoutmeaning”.

Spirituality is “a personal search formeaningandpurposeinlife,whichmayormaynotberelated toreligion.” In1992,onlyonemedicalschool had a formal course in spiritualityand medicine, which was an elective course.Today, more than 70 medical schools in theUnitedStatesoffercoursesonspiritualityandmedicine.2 Spirituality is at the heart of thepatient-centered rather than disease-centeredmedicine.The goal of goodmedical care is toact in thebest interestof thepatient.Religionandspiritualpracticesareamongtheresourcesusedbythepatientstocopewithchronicpain.

Dr. SarahMWhitman3 said that religion andspiritualityareoftenimportanttopatients.Shedescribes the way the Hindu traditions dealwithpainandsuffering including theconceptofacceptanceandshefindsthattheseconceptswillbehelpfulwhentreatingnotonlyfollowersofHinduismbutallpatients.

The results of fMRI (functional MRI) studysupport thenotionof increasedactivity in theregions of amygdala and hippocampus duringmeditation.4

Activityofparasympatheticsystemwouldalsocauseareductioninheartrateandrespiratoryrate.Allof thesephysiological responseshavebeenobservedduringmeditation.5Intercessoryprayersandcolloquialprayerswereassociatedwith higher levels of well being and lifesatisfaction.

Meditation may decrease anxiety, depression,irritability andmoodiness as well as improvelearning ability, memory, self-actualization,feelings of vitality and rejuvenation, andemotionalstability.6

Experiments have shown that blood lactatelevels drop four times faster when subjectsmeditate than when subjects simply lie on

theirbacks.7Yogahasshownbenefitinpatientswithasthma,hypertension,heartfailure,mooddisorders,anddiabetes.8

To conclude, the prevalence of spiritual andreligious activities makes it important for allpainmanagement professionals to understandandtobepreparedtodiscusstheseissues.

References 1. Frankl VE. Man’s Search for Meaning.

NewYork:SimonandSchuster;1984;18-22.

2. Miriam SW, Eisenberg DM, KaptchukTJ. Courses Involving ComplementaryandAlternativeMedicineatUSMedicalSchools.JAMA.1998;280:784-787.

3. Whitman SM. Pain and Suffering asviewed by the Hindu Religion. TheJournalofPain,1998;8(8):A12-A16.

4. Lazar, Sara W. Bush G, Gollub et al.Functionalbrainmappingoftherelaxationresponse and meditation. NeuroReport:2000;11(7):1581-1585.

5. TeresaES,DubinLF,SeemanM.Religiosity/SpiritualityandHealth:ACriticalReviewof theEvidence forBiologicalPathways.AmericanPsychologist2003:53

6. Harinath K, Malhotra AS, Pal K etal. Effects of Hatha Yoga and OmkarMeditation on CardiorespiratoryPerformance, Psychologic Profile, andMelatoninSecretion

The Journal of Alternative and Complementary Medicine. 2004,10(2):261-268.

7. Delmonte MM. Meditation and anxietyreduction: A literature review. ClinicalPsychologyReview1985;5(2):91-102.

8. Ramesh LB, Rama PM, Yadav RK et al.A Brief but Comprehensive LifestyleEducation Program Based on YogaReducesRisk Factors forCardiovascularDisease and Diabetes Mellitus. TheJournalofAlternativeandComplementaryMedicine.2005,11(2):267-274.


AK MittalHead of General SurgeryLaproscopy and GI SurgeryPushpanjali Crosslay HospitalGhaziabad, NCR

Clinical challenge: Acute appendicitis with pregnancy

(Three case reports, one in each trimester)

AK Mittal

Introduction

Acute appendicitis is most common extra

uterinesurgicalemergencywhichneedsurgical

intervention.Itisachallengefortheobstetrician

as well as for the surgeon. The challenge

is to diagnose accurately and to intervene

appropriately especially since the natural

historyof acute appendicitisdoesnot change.

Mostpregnantwomenvisittheirobstetricianfor

anytypeofabdominalproblemandsubsequent

treatment. In the event of acute appendicitis

it is of utmost importance that the surgeon is

consultedforearlydiagnosisandmanagement

forbetterprognosisofbothmotherandbaby.

It is reported that one out of 1500 pregnant

mothershaveanincidentofacuteappendicitis.

Pregnancy obscures the accurate diagnosis

of acute appendicitis due to gestational

physiological changes. This diagnostic delay

increases the incidence of complications like

perforation, peritonitis, lump formation and

septicemia leading to high morbidity and

mortalityformotherandchild.

Case History

Presented here are three cases of acute

appendicitis during pregnancy. The cases are

fromeachtrimester.

Case 1:Thepatientwasthewifeofaphysician

whoreporteddirectlytothesurgicalOPDwith

a history of periumlical pain with vomiting

and low grade fever with leucocytosis. The

ultrasound showed right iliac fosse probe

tenderness with 12 week size normal fetus.

Thediagnosisof acuteappendicitiswasmade

clinicallyandthedecisionofsurgerywastaken.

Theobstetricianwasconsultedandsheadvised

theuseofsometocolyticagentpostoperatively.

Thepatientwasoperateduponsuccessfullyand

shedeliveredanormalbabyatfullterm.

Case 2: The second patient, five months

pregnant presented to the gynaecologist with

pain in lower abdomen andhistory of nausea

without any fever. The gynecologist managed

herfor24hourspriortoreferringtothesurgeon.

Clinically the symptoms were that of acute

appendicitiswithlocalizedtendernessinright

iliac fossa.Shewas investigated for the same.

Theultrasonologistsuspectedanappendicular

lump and the decision for surgery was taken

as the patient was not responding tomedical

treatment and the appendix was acutely

inflamed. Postoperative recovery was good,

though no lumpwas found during surgery. A

normalbabyatfulltermwasdelivered.

Case 3: The third patient was seven months

pregnant with a history of two previous

cesareanswithonelivechild,andhencethiswas

apreciouspregnancy.Shepresentedwithacute

pain in abdomenwith loosemotion and high

gradefevertohergynecologistandthentothe

surgeon.Oninvestigation,hertotalleucocytosis

washigh,andtemperaturebetween101-102°F.

On clinical examination, the right iliac fossa

andrightlumberregionwereverytender.Based

ontheclinicalandlabfindings,thepatientwas

advisedsurgeryforacuteappendicitis.However,

herrelativeswerereluctantduetotheprecious

nature of this pregnancy. She was placed

on a good coverage of antibiotics with other

supportivetreatments.Sherespondedpartially

with total leukocytecountand fever receding.

Eventhoughthepatientrespondedtomedical

treatment in the initial stages, on the 5th day

shedevelopeduterinecontractionswithsevere

paininabdomen.Theultrasoundindicatedthin

scarandthepatientdidnotrespondtomedical

treatment of premature contraction. After a

period of 24 hours, a sessarian section was

performed.Aonekgfemalechildwasdelivered

andimmediatelyshiftedtothenursery.During

thesessariantheuteruswasobservedtobevery

red,congestedwithpusflakesinrightiliacfosse

(RIF).Thiswasexploredfurtherandanabscess

with many pus flakes was found behind the

uterus.Theappendixwasedematousandwas

adheredtothecaecum.Anappendicectomywas

carriedoutwithdrainageofabscess.Peritoneal

toilet was done. Post operative recovery was

uneventfulbutthepatientstayedinthehospital

forelevendays.Thebabywasshiftedtothein

nursery, she developed septicemia and could

notbesaved.

Discussion

There are some conditions like acute

cholecystitis,pancreatitis,acutegastroenteritis,


ureteric colic, salpingitis, threatened abortion and premature

contraction,whichcanbeconsideredasdifferentialdiagnosisof

acuteappendicitis.Insuchsituations,theroleoftheobstetrician

isimportantasallpregnantwomenwithpaininabdomenconsult

onlythem.Ifthetreatingdoctorisunabletoreachaconclusive

diagnosis, then cross consultation with a surgeon should be

initiatedtoavoidanydelayasitcouldworsentheprognosisof

motherand/orchildaswastheoutcomeinCase3.

Acuteappendicitisshouldbedealtwithpregnantwomenasif

thepregnancyitselfwerenotpresent.Ifsurgeryisperformedin

timeduringpregnancy,thentheoutcomeisusuallyuneventful.

However,theobstetricianmustbeassociatedduringsurgeryaswell

aspostoperatively.Operatingearlyisalwaysadvisablewhenever

the diagnosis is confirmed. An aggressive surgical approach

mustbeadoptedeven though the resultof appendicectomy is

usuallypositive,butperforationandsepticemiaaredangerous

complications.Morbidityishighbecauseofadelayindiagnosis

andasaresultoftheinitialapproachoftreatmentforpremature

contractionofuterus.

Conclusion

Toconclude,acuteabdomenwithpregnancyisalwaysadilemma.

Earlydiagnosis,earlycross referenceandearly intervention is

themainstayofasuccessfuloutcome.Surgeryisthetreatmentof

choice,irrespectiveofthestageofpregnancy.Currentmodalities

likeMRIanddiagnosticlaparoscopyserviceasexcellentaids.

References

1. HorowitzMD,GomejGA,SantiestebanR,BurkettG.Acuteappendicitisduringpregnancy.ArchSurg1985;120:1362-8

2. Robert A, DeSantis, Ernest G. Appendectomy duringpregnancy.Asurveyoftwoarmymedicalactivities.MilitaryMedicine.1999;164:671-4

3. Mazze RI, Kallen B. Appendectomy during pregnancy.A Swedish Registry Study of 778 cases.Obstet Gynaecol1991;77:835-40.

4. LimHK,BaeSH,SeoGS.Diagnosisofacuteappendicitisinpregnantwomen:Valueofsonography.AmJRoentogenol1992;159:539-24.

5. Manmoodian S. Appendicitis complicating pregnancy.SouthMedJ1992;177:371-6.

6. 6. Sharp HT. Gastrointestinal surgical conditions duringpregnancy.ClinObstetGynaecol.1994;37:306-15.

7. AL-MulhimAA.Acuteappendicitisinpregnancy.Intsurg1996;81:295-302.

8. Tamir IL, Bongard FS, Klein SR. Acute appendicitis in apregnantpatient.AmJsurg1990;81:295-302.


Dinesh AgarwalAssociate ConsultantDepartment of PediatricsPushpanjali Crosslay HospitalGhaziabad, NCR

Nocturnal Enuresis

Dinesh Agarwal

Nocturnal enuresis or bedwetting is one of

the most common developmental problems

encounteredintheday-to-daypracticeofboth

thePediatricianandtheGeneralpractitioner.It

isdistressing forchildrenandtheirparents. If

leftuntreated,itcanleadtosocialisolation,loss

ofselfesteemandparentalintolerance.

Nocturnal enuresis is defined as involuntary

passageofurineduringsleepafterfiveyearsof

age.Itisoftwotypes:

• Primary(persistent):Childneverachieves

dryness at night. Commonest with an

incidenceof75-90%

• Secondary (regressive): Child achieves

drynessatnightbutafter6monthsstarts

bedwettingagain.Itsincidenceis10-25%.

Theprevalenceofnocturnalenuresishasbeen

difficult toestimatebecauseofvariation in its

definition and in social standards. It is now

accepted that 15-20% of children will have

somedegreeofnighttimewettingat fiveyears

of age with a spontaneous resolution rate of

approximately 15 per year. Therefore, at 15

years of age only 1-2% continue to wet their

bedsatnight.

Boys wet their beds more frequently than do

girls. A family history of nocturnal enuresis

is found in most children. If both parents

had enuresis in their childhood, 77% of their

children will also have enuresis. Further, if

onlyoneparenthadenuresis,then44%oftheir

childrenwillhaveenuresis.

Etiology: This remains elusive. The condition

appears to be multi-factorial involving a

combination of physiological, genetic and

psychological causes. Possible etiologies of

primarynocturnalenuresisaresummarizedin

Table1.

Evaluation of Primary Nocturnal Enuresis

The most important factors in the evaluation

includethefollowing:

• Ageandsex,

• Severityoftheproblem,

• Perceiveddisturbancewithinthefamily,

• Spontaneousresolutionrate,and

• Patient’sresponsetotherapy.

To achieve best results, a goal oriented and

consistentapproach is required.This includes

a consistent method of treatment with follow

up, cooperative attitude of parents and child,

support and care for the child in the family

socialstructureandhomeenvironment.

A careful medical history and physical

examination including urine analysis will

usuallyprovidesufficientinformationtoarrive

at a diagnosis. The history should include

an assessment of the child’s voiding pattern.

Psychologicalandfamilyhistoriesareimportant

as the attitudes of the child and their parents

are significant in selecting proper therapy.

The physical examination should include

abdominal,genitalandneurologicalassessment

toobtainevidenceofchronicdistendedbladder,

epispadias and spinal lesions. Investigations

Factors Pathophysiology Evidence

Developmentaldelay DelayinfunctionalmaturationofCNS

Spontaneouscurerateaschildrengrowolder

Antidiuretichormonelevel LowlevelofnighttimeADHsecretion

Hormonalstudies

Genetics Unclear Familyhistory,Geneidentificationatchromosome5,12,13,22

Sleepdisorder Deepsleep Sleepstudies

BehavioralandPsychologicaldisorder

Unclear Resultsratherthancause

Anatomy Nonefound Normalphysicalexamination

Table 1: Etiology of primary nocturnal enuresis


includeurineanalysis forspecificgravityanddipsticktests to

ruleoutthepresenceofdiabetesinsipidusandmellitus.Urine

culture is recommended only if the patient has symptoms

suggestiveofurinarytractinfectionoriftheurineanalysisresults

arepositiveforthepresenceofredandwhitebloodcells.

Treatment

Table 2: Treatment choice by Age

Age <5 5-7y >7

Educate + + +

Reassure + + +

DDAVP occasionally + +

Alarm

devices

+ +

Oxybutinn +

Imipramine +

Treatmentcanbedividedintotwobroadcategories:

• Non Pharmacological treatment: Include motivational

therapy, behavior modification (conditional therapy),

bladdertrainingexercises,psychotherapy,diettherapyand

hypnotherapy.

• Pharmacologicaltreatment:Evolvedsignificantlyoverthe

past15years,andsafer,moreeffectivemedicationsarenow

available.

Non Pharmacological treatment

Motivational therapy:This involvesboth theparentsandthe

childandworksbyremovingtheguiltassociatedwithenuresis,

providingemotionalsupporttothechild,avoidingpunishment

and humiliation, encouraging the child to make bedtime

resolutions,maintainingachartordiaryforwetanddrynights,

andasystemofrewardsfordrynights.

The cure or resolution rate is only 25%. About 70% show

marked improvement, with a relapse rate of approximately

5%.Motivational therapyisa first lineapproachfor treatment

especiallyinyoungerchildren.Ifthetherapyisnotsuccessful

within three to six months, a different treatment should be

offered.

Behavioral treatment

• Waking the child 2-3 hours after sleep will induce a

conditional response ofwakingwhen the bladder is full.

The success rate is unknown. The child’s cooperation is

difficulttoobtain.

• Alarm device: Analarmisplacednearthegenitals.When

thechildvoidsinbed,amoisturesensingdeviceactivates

andtriggersanalarm.Thisevolvesaconditionalresponse

of waking and inhibiting urination. Alarms are sound

and vibratory type. Vibratory alarms have found to be

moreeffective thansoundalarminwakingchildren. It is

recommended in children older than seven years of age.

It requires a cooperative andmotivated child and family.

Longtermsuccesshasbeenreportedinapproximately70%.

Childrenshouldcontinue tousedeviceafter threeweeks

ofcompletedryness.Relapseoccursin20-30%ofpatients.

Alarmdevicesaregenerallysafe.

• Bladder Training Exercises:Insomechildrenwithasmall

bladder capacity, urine retention training during the day

mayhelp increasebladdercapacityatnight.Thechild is

askedtoholdtheirurineforincreasingperiodsoftime.Six

monthsofbladdertrainingexercisesresultsinabout19%

achieving complete resolution of symptoms, while 66%

showsomeimprovement.

Table 3: Comparative choices

Modality Cure (%) Relapse at 6

months (%)

Relapse at 1

year (%)

Alarm 70-80 3 56

Alarmclock 77 24 -

DDAVP 25 Very high

if stopped

abruptly

10

Imipramine 25 10

Pharmacological treatment

Thisformoftherapyisusuallyreservedforchildrenolderthan

sevenyearsofage.Twoapproachesareused:

• Increasebladdercapacity

• Reducetheamountofurineproducedbythekidneys

Several medications are available; however, none of these

medications cure enuresis. They provide a stop gap measure

untilthechilddevelopstheirownwakinghabitsduringthenight

tovoid.Parentsshouldnotexpectimmediateresults.Drugshave

potentialsideeffects.

• Reservefor>7yrs• Secondlineoftreatment• First line of treatment (Family circumstances or quick

symptomaticrelief)

• Noneofthesemedicationcure• Provideastop-gapmeasure• Donotexpectimmediateresults• Potentialsideeffect

Drugtherapyshouldbeinitiatedonlyafterthefirstlivetherapy

has failed or quick systematic relief needed. Three groups of

drugsareused:

• Tricyclic Antidepressant: Imipramine has been used

extensively during the past 25 years. Suggestive

mechanismsalterthesleepandarousalmechanisms;alter

secretion of anti-diuretic hormone,weak peripheral anti-

cholinergiceffectandeffectonthesympatheticnerves in

the bladder. The initial dosage is 25mg taken one hour

beforebedtime.Evaluate responseafter twoweeks. If the

responseisnotsatisfactory,thedosagecanbeincreasedto

50mginchildren7-10yearsofageandupto75mginolder

children.Treatmentshouldcontinueforthreetosixmonths

andweaningby reducing thedosage in incrementsof25


overthreetofourweeks. Itsusedecreasesbecauseof thesideeffects,drymouth,nausea,tiredness,sleepdisorders,anxiety,nervousnessandpersonalitychanges.Imipraminehasalsobeenassociatedwithsevereaccidentaloverdoseinbothpatientsandtheirsiblings.Curerateisabout25%withthisformoftherapy

• Anti-cholinergic Therapy: Drugs eg, hyosyamine andoxybutyninhaveadirecteffectonsmoothmusclerelaxation.It results in decreasing the bladder’s ability to contract.Experiencewithanti-cholinergicislimited.Oxybutyninisadministeredinthedosageof5mgatbedtime.Thedosagecan be increased to 10 mg in older children. Commonside effects are dry mouth, constipation, facial flushing,dizziness, tremulousness, drowsiness, anthyperpyrexiaduringsummer

• Desmopressin Acetate (DDAVP): A synthetic analogue ofargininevasopressin(anti-diuretichormone),hasahighlyspecific anti-diuretic effect, a relatively longhalf life andextended duration of action. The biological half life isfour to six hours. It can be administered by oral and/ornasal route.The initialdoseofnasalspray is20mg (onespray in eachnostril) at bedtime.Evaluate response aftertwoweeksoftherapyandifnoresponseseem,thedosagecan be increased to 40mg at bedtime. In childrenmorethantwelveyearsofagecanbeadministeredupto60mgintranasally. Nasal spray should be avoided in childrensufferingformRhinorrhea.Thetabletscanbeadministeredinthedosageof200microgram(0.2mg)halfanhourbeforeortwohoursaftermealcanincreaseupto600microgram

(0.6 mg) for desired response. Tablets are preferred overnasalsprayasnasalspraycanbeadministeredinoverdose.Therapyshouldbegivenforatleastthreetosixmonthsforadesireresponse.Thedosageshouldbetaperedslowlyby10microgrampermonthbecauseabruptdiscontinuationoftherapycanresultinhighreplacerate.

Medication Combined modalities Combination therapy Response Cure / Resolution

•Adjustdoseeverytwoweeks

•Continuetherapyfor3-6monthsofdrynights

•Weanoverthreetofourweeks

•Restartifrelapseoccursonstopping

•Considerbehavioralmodi-ficationinconjunction

•Structuredwithdrawaloftherapyratherthantaper-ingthedosesofmedica-tionsseemstoimprovetheoutcome*

• Motivationanddrybedtrainingbetter(DBT)thannotreatment

• AnalarmbetterthanDBTonitsown

• AlarmwithDBTbetterthanalarmalone

• Directcontactwithathera-pistmightenhancetheeffectsofanintervention

•Refractoryprimarynocturnalenuresis

•AlarmtherapywithDesmopressin

•OxybutyrinandDesmopressin

•DesmopressinandImipramine(notcombined)

•Partial/com-pleteresponseTreatfor3-6monthandta-pergradually

•RecurrenceRestartsametherapy

•PoorresponseInterchangeorcombinetwomodalities

•RefractorytotherapyReas-sess

Onlyoneortwowetnightoverthreemonthperiod

References 1. Howe AC, Walker CE. Behavioral management of

toilettraining,enuresisandencopresis.PediatrClinNorthAm1992;39(3):413-32.

2. Rittig S, Knudsen UB, Norgaard JP, Peterson EB,Djurhuus JC. Abnormal diurnal rhythm of plasmavasopressin and urinary output in patients withenuresis.AmJPhysiol1989;256(4Pt2):664-71.

3. Marshall S, Marshall HH, Lyon RP. Enuresis:an analysis of various therapeutic approaches.Paediatrics1973;52:813-7.

4. Rushton HG. Nocturnal enuresis: epidemiology,evaluationandcurrentlyavailabletreatmentoptions.JPaediatr1989;114(4pt2):691-6.

5. Schmitt BD. Nocturanal enuresis. An update ontreatment.PediatrClinNorthAm1982;29:21-36.

6. BamfordMF, CruickshankG. Dangers of intranasaldesmopressinfornocturnalenuresis[Letter].JRCollGenPract1989;39:345-6.

7. TerhoP.Desmopressininnocturnalenuresis.JUrol1991;145(4):818-20.

A Happy and Successful First

ThedepartmentofAestheticandPlasticsurgerycommenceditsinternationalserviceswithMs.Wendy,aresidentofNewYorkState,USA.

Dr.DineshBhargava,headofdepartmentanddirectorof‘ANewImage’CenterforAestheticSurgeryandMedicineperformedtheUltrasonicAssistedLiposuctiontechniqueonMsWendy.TheprocedurewasdoneasadaysurgeryandthepatienthassincereturnedtoherhomeinUS.Thefeedbackispositive;andMs.WendyhasalreadyscheduledanotherprocedureonhernextvisittoIndia.

Congratulationstoallwhowereinvolvedinhercare.Thepatientalsoconveysherappreciationtothehospitalstaff,nursesandotherswhomadeherexperienceapleasantone.

Table 4: Summary


Rajiv Singh Consultant Pediatrician


Ghaziabad,NCR

Is Sunlight An Effective Treatment For Jaundice in Term Infants?

Rajiv Singh

History: Serum sample color change observed in icteric blood samples left in daylight. Babies lying on the side of nursery that received natural sunlight were observed to have less incidence of jaundice.

Theoretically: it can be effective as it has thespectrumof425-475nm,knowntobeeffectiveindissolvingbilirubin.

Review of LiteratureExtensive screening of published scientificevidence,viz,CochraneLibrary,BestEvidence,MEDLINE, CINAHL (Cumulative Index toNursingandAlliedHealthLiterature),CurrentContents andBiologicalAbstractswas carriedout.

Our extensive search identified only a singleoriginal study reporting the effect of sunlightinjaundicedpreterm,ratherthanterm,infants.This widely cited and historically importantarticlethatprovidedthefirstEnglish-languagereport of an association between light and areduction in neonatal jaundicewas publishedin 1958. The same authors then reporteda case series of artificial light therapy forjaundiced preterm infants, which stimulatedthe subsequent volumeof researcharticles onthe effectiveness of phototherapy for neonataljaundiceinbothtermandpreterminfants.

Information analysisWe found no controlled trials comparingsunlightagainsteithernotreatmentorartificiallighttreatmentforjaundice.Theuseofsunlightappearstohaveresultedfromanecdotalreportsof its effectiveness rather than from rigorousmedical evidence. In fact, most of the time,exposure to sunlight is grossly inadequatebecause of fear of cold exposure. Moreover,if the effectiveness of sunlight exposure forjaundice is unknown, so too is the incidenceof potential risks to the neonate, for example,undueexposureto(cold)weather(possibilityofhypothermia)sunburn,photosensitivityorevenskinmalignancyinfuture.

Discussion• There is insufficient evidence to support

exposure to sunlight for the treatment of

jaundice.Thepersistence of thispractice50yearsafterpublicationofareportonasingle case series raises questions abouttheinfluenceofevidenceonthebeliefsofprofessionalhealthcareworkers.

• AnAustralianstudyreportedthat36%ofmothersbelievethatsunlightishelpfulinJaundiceandthebeliefwascommunicatedmostly by health workers. The studytherefore identified the need to educatethe Health professionals regarding theinefficacy inadvisability and potentialharmofSuntherapyinNNH.

AAP Recommendation“Putting your baby in sunlight is notrecommendedasasafewayoftreatingjaundice.Exposingyourbabytosunlightmighthelplowerthe bilirubin level, but this will only work ifthebabyiscompletelyundressed.Thiscannotbedonesafelyinsideyourhomebecauseyourbabywillgetcold,andnewbornsshouldneverbeput indirect sunlightoutsidebecause theymightgetsunburned.”

ConclusionSunlight is not effective in NNH and it canexposethenewborntopotentialhazards.

Additionally, hyperbilirubinemia may bemissedandthiscouldprovetobedetrimentalforthebaby.

Therefore it is strongly recommended that allphysicians andpediatricians shouldavoid theadvice of sunlight for jaundice. Instead, theparentsand familymemberscouldbeadvisedto follow up with the pediatrician for properevaluationoftheseverityofjaundice.

Thisarticleshasbeencopiedfromhttp://www.mja.com.au/public/issues/178_08_210403/joh10652_fm.pdf

References 1. American Academy of Pediatrics.

QuestionandAnswers:JaundiceandYourNewborn. Accessed: http://www.aap.org/family/Jaundicefaq.htm

2. Cremer RJ, Perryman PW, Richards DH.Influence of light on the hyperbiliru-binaemiaofinfants.Lancet1958;i:1094-1097


IntroductionRolavirus is the leading cause of diarrheahospitalizationamongchildrenworldwide.1It is thesinglemost importantcauseofseveredehydratingdiarrhea.Developmentofasafeandeffectiverotavirusvaccineisveryimportant.Globally every year, rotavirus is associatedwithnearly25millionclinicalvisits,2millionhospitalizationandmorethan6,00,000deathsworldwideamongchildrenyoungerthan5yearsofage.2,3

It is important to study local distribution ofrotavirusstrainsandconductactivesurveillanceprogramsforemergingreassortantstrainspriortoandaftertheintroductionofvaccines

EpidemiologyFirstdescribedin1973rotavirusdiarrheaoccursmostcommonlyinwintermonthsintemperateclimates.Their clinical relevance, structural complexityanduniquemodeoftransmissionhaveinvitedextensiveresearchonthereviruses.

Structure and ClassificationItisadoublestrandedRNAvirus.itisgroupedintogroups(A-G),subgroupsI&IIannonIandnon II -basedon innercapsidprotein - VP6(madeofVP7andVP4)furthertypingschemesto describe rotavirus sprains are based on theproteins to elicitneutralizingantibodies –VP-7 (G serotypes) andVP4 (P serotype)G andPserotypes are defined based on reactivity tospecificmonoclonalantibodies(MABS).

Rotavirus detection and strain characteristics ELISAisthemethodofchoiceforscreening.

Epidemiology in IndiaRotavirus epidemiology is complex due tocontinuous modes of transmission and straindiversity of the virus in different setting. Thenewhopepresumptionofmortalityduetothisagent is the use of oral vaccines which haveproved to be effective in developed countriesbutweneedevidencefromdevelopingcountrieswith the highest disease burden.Beforeacceptingtheirefficacyinoursetting,wemustunderstandtheepidemiologyinIndia .Studiesdone in India through1982-1999 and2001 to2004prove that the incidenceof rotavirusGErequiring hospitalization ranges from 6-45%(median20.8%).In the community the disease varies from4%-29% (median 12.3%) most of which issymptomatic.G1&G2aremostprevalentstrains.CommonestPtypewasP[8]-(27%)followedbyP[6]-(22%)andP[4]-(20%)In India newer strains have been discoverede.g.,G-6fromPune5,G(8)VelloreandKolkata

G 38 (8) from Western India and G12 fromDelhi. In neonates, rotavirus causes mostlyasymptomatic infection. Neonatal Rotavirusstrains(attenuated)arepossiblecandidatevirusfor vaccine.These include G9P[11] in Delhi4andG10P[11]inBangaloreandMysore5.Bothsymptomatic and asymptomatic infections byG10P[11]strainhavebeenreportedinVellore6.Both neonatal strains appear to be bovine-humanreassortants.G9P[11]isahumanstrainwithabovineVP4whileG10P[11]iscomposedmainlyofbovinegenesandhasgenesegments5and7,encodingNSP1and3,ofhumanorigin7.

Vaccine PreparationsRota shield (a tetravalent rhesus- humanreassortant rotavirus vaccine – discovered in1998 but was withdrawn frommarket due toincreasedincidenceofintussusceptionsamongvaccinerecipients.Theestimatedriskwas1in10,000.Theriskwasgreatestduring3-4dayperiodafter1stdoseand3-7dayperiodafter2nddose.Itwasalso associatedwith fever, vomiting, diarrhea,abdominalpainandbloodystools.

Rotaeq: Oral,Live,Pentavalnt(G1,G2,G3,G4,and P(8)) human bovine (WC3) reasortantrotavirusvaccinesodiumcitrateandphosphatebufferatanaggregateviraltypeofapproximately6.7X107to12.4X107infectiousunitperdose.Pentavalent rotavirus vaccine was highlyefficacious against severe rotavirusgastroenteritis and provided substantialprotection against rotavirus gastroenteritis ofany severity. Its efficacy persisted through asecondrotavirusseason.The immunologic mechanism by whichrotavirusprotectagainstrotavirusgastroenteritisisunclear.

EfficacyThe efficacy of the vaccine against G1-G4gastroenteritisofanyseveritywas74.0percent.Efficacy against hospitalization for G1-G4rotavirus gastroenteritiswas 95.8percent..Theefficacyofthevaccineagainstallgastroenteritis-relatedhospitalizationsafterthefirstdosewasshowntobe58.9percent.R2

Adverse effects: Studies done have notdemonstratedanyincreasedriskof• Intussusceptions(1.6)• duringa42-dayperiodafteranydose• fever,vomiting,hematochezia,weresimilar

among vaccine and placebo recipients instudy.

RecommendationsThree-2ml doses starting 6wk of age 1.0 hastobecompleted2,4,6monthsofagebefore6months.

Study Report

Rotavirus Vaccine

AnuradhaConsultant Pediatrician


Ghaziabad,NCR

Anuradha


Rotarix (GSK)AliveattenuatedhumanrotavirusvaccinecontainingtheR1X4414strainofG1P(8)specificityhasbeendeveloped2,4,6,16,22fromtheparentvaccinestrain89-12.Twodosesarewelltoleratedandimmunogenic.

EfficacyTheefficacyofthevaccineagainstsevererotavirusgastroenteritisand against rotavirus associated hospitalization was 85percent(P<0.001) in the large multicentric trial.,and reached100 percent against more severe rotavirus gastroenteritis.Hospitalisation for diarrhea of any cause was reduced by 42percent(95 confidence interval,29 to 53 percent;P<0.001).Thevaccineefficacywasshowntopersistthroughasecondrotavirusseason.91.0 percent efficacy was demonstrated against G1P[8]rotavirusesand45.4percentforG2p[4].Thevaccinewasnotassociatedwithanincreasedriskof

Adverse effects 1. Intussusceptions.Observedriskestimateof–0.32per10,000

infantsbelowtheinitialriskincreaseof4per10,000.2. Diarrhea,vomiting,dehydrationandhypovolaemicshock.

SummaryThe Cochrane Evidence Database analyses data from 64 trialswith three kinds of vaccine, bovine, rhesus and human, andresults indicate protection from rotavirus diarrhoea of anyseverity9.However, the importantcaveat to thisupdate is thatthemajorityofthetrialswerecarriedoutindevelopedcountrieswhere the age of first rotavirus infection is later in childhoodandwherethedegreeofdiversityofcirculatingstrainsislimitedin comparison to developing countries. Rotavirus vaccinesgenerallyhaveyieldedpoorefficacywhentestedindevelopingcountrieshasledtoconcernsaboutthepotentialeffectivenessofanyfuturelive,oralrotavirusvaccineinthesesettings64Althoughrotavirusinfectionisuniversalearlyinchildhood,theepidemiologyofthediseaseisquitedifferentindevelopedanddevelopingcountries.Differencesinageoffirstinfection,strain

distribution, occurrence of mixed infections, seasonality andriskofmortalitycanaffectdecisionsaboutvaccinecompositionanddelivery.Higherdosesofvaccineoradditionaldosesmayberequiredtoovercometheinhibitoryeffectsofcompetingintestinalflora, concomitantuseoforalpoliovaccineandhigh levelsofhumorally transferred maternal antibodies against rotavirus.DespitearecommendationbytheWorldHealthOrganizationthatallrotavirusvaccinesbetestedearlyindevelopingcountries,nodata from the current vaccines are available inAfrica or poorAsiancountries.Thesedatawillbecritical todetermining theprobability of success of the current rotavirus vaccines and toestablish requirements for vaccines inpre-clinical andclinicaldevelopment.In summary, rotavirus epidemiology is complex as would beexpected for a virus with multiple modes of transmission,and this complexity is amply illustrated in studies from Indiademonstratingthediversityofthevirusindifferentsettings.Thenewhopeforpreventionofmorbidityandmortalityduetothisagentistheuseoforalvaccines,whichareeffectiveindevelopedcountries,butweneedevidencefromdevelopingcountrieswiththehighestdiseaseburdenandvirusdiversitybeforeaccepting

theirefficacyinallsettings.

Type of Gastroentritis HRV Pentavalent

Severe,asClinicaldefinition

NoofIn-fantswith>1episode

Noofinfants>1episode

RotavirusGE Vaccine Placebo VACCINEEFFICACY

Vaccine Placebo VaccineEfficacy

Severe 12 77 84.7 98.0-100%

Hospitalisation 9 1.5 85

Gastroenteritisofanycause

Severe 183 300 40

Hospitalisation 145 246 42 58.9

Severe,as Clinical definition

No of Infants with>1 episode

No of infants>1 episode

Serotypespecificgastro-enteritis

Efficacy Efficacy

G1P[8] 90.8 G1 72/286 74.9

G3P[8],G4P[8],G9P[8]

86.9 G2 6/17 63.4

G2P[4] 45.4 G3 1/6 82.7

G4 3/6 48.1

G9 1/3 65.4

NENGJMED354:1JAN5,20068

References 1. Parashar UD, Hummelman EG, BreseeJS, Miller MA, Glass RI.Global illness anddeaths caused by rotavirus disease inchildren.EmergInfectDis2003;9:565-72.

2.ParasharUD,GibsonGJ,BreseeJS,GlassRI.Rotavirusandseverechildhooddiarrhea.EmergInfectDis.2006;12:304–6.[PubMed].

3.Bresee JS, Glass RI, Ivanoff B, Gentsc JR. Current status andfutureprioritiesforrotavirusvaccinedevelopment,evaluationandimplementationindevelopingcountries.Vaccine1999;17:2207-22.

The Journal of Alternative and Complementary Medicine. 2004,10(2):261-268.


Tilak Dangwal Consultant Pediatrician


Ghaziabad,NCR

Recent Advances in Management of Childhood Tuberculosis

Tilak Dangwal

Tuberculosis (TB) is a major public health

problem worldwide. The advent of HIV

infection pandemic and AIDS has resulted in

the significant increase in the global burden

of tuberculosis. In the developing countries,

tuberculosis is a disease of the young.

Childhood TB is a reflection of the ongoing

transmissionoftheMycobacteriumtuberculosis

inthecommunityandistheresultofrecently

acquired infection. Thus, the extent of the

problemofchildhood tuberculosis reflects the

tuberculosis control in the given geographical

area.Since there is little advance in thebasic

knowledge of microbiology, immunology and

thepathophysiologyofMycobacterium,newer

diagnosticmodalities, newerdrugs andnewer

treatmentregimensneedtobediscussed

Epidemiology

Tuberculosis is leading cause of death

worldwide from a single infectious disease

agent. WHO estimates that up to half of the

world’s population is infected .The registered

numberofnewcasesofTBworldwideroughly

correlates with economic conditions. The

highest incidence is seen inAfrica, Asia, and

Latin America ie, countries with the lowest

gross national products. Around eightmillion

peoplegetTBeveryyear,ofwhom95%livein

developing countries and around two million

peoplediefromTBeveryyear.

InIndia,estimatedincidence/yearis1.8million

new cases out of which 0.8 million are new

smearpositivecases.Theestimatedprevalence

ofTBdisease(in2000)was3.8millionbacillary

casesand1.7millionnewsmearpositivecases

and the estimatedmortality is 370,000 deaths

duetoTBeachyearie,over1000deathsaday.

ChildhoodTB is a neglected aspect of theTB

epidemic.Despiteconstituting20%ormoreof

theTBcase-load inmanycountrieswithhigh

TBincidencethis“orphandisease”existsinthe

shadow of adult TB and is a significant child

health problem. It is neglected because it is

usually smear-negativeand thus is considered

tomakea relativelyminorcontribution to the

spread. To redress this neglect and integrate

childhood TB into the mainstream of TB

control activities, it is important that research

prioritiesbeidentifiedtoassistinimprovingthe

preventionandmanagementofchildhoodTB.

Approach to diagnosis

Diagnosis of pulmonary tuberculosis (PTB) is

difficult in children aged less than 6-8 years.

Contact with a smear-positive PTB case and

respiratorysymptomsformorethan2-3weeks,

not responding to broad-spectrum antibiotics

usually raises the suspicion of the disease.

Clinical signs suchas erythemanodosumand

phlyctenularkeratoconjunctivitis,weightlossor

failuretothrivemaybepresent.Thediagnosis

of PTB in children is often presumptive.

Various scoring systems have been produced

forscreeninganddiagnosisbuttheirevaluation

isdifficult in theabsenceofa“goldstandard”

diagnosis.

Laboratory investigations

Detection of Mycobacterium: All possible

effortsmustbemade todetect and isolate the

bacteria from appropriate specimens. Gastric

aspirates are used in lieu of sputum in very

youngchildren (<6yearsof age)whousually

do not have a coughdeep enough to produce

sputum for analysis. Bronchoalveolar lavage

mayalsobeusedtoprovidebronchialsecretions

for detection of bacilli. Other body fluids (eg,

CSF,pleuralfluid,peritonealfluid)canalsobe

centrifugedso thesedimentscanbeevaluated

forthepresenceofAFB.Conventionalmethod

is Ziehl Neelsen staining and staining of the

AFBprovides preliminary confirmation of the

diagnosis.Sinceittakes6¬-8weeksforbacilli

tobeisolatedfromconventionalculturemedium

(Lowenstein-Jensen), automated radiometric

culturemethod(BACTEC)isincreasinglybeing

usedfortherapidgrowthofthebacteria

Imaging studies: Chest X-ray is a classic


diagnostic tool when evaluating patient for pulmonary

tuberculosis. CT scan (HRCT) and MRI are not routinely

indicatedwhenCxRfindingsareunremarkablebut incaseof

high suspicion these imaging studies can demonstrate hilar

lymph node, endobronchial lesions, pericardial evasion and

earlycavitationsandbronchiectasis.

Mantoux test: Positive test to thestandarddoseof tuberculin

is still themost reliable investigation of choice especially in

youngchildrenbutitmustberememberedthatwithsevereTB

and/or advanced immunosuppression, tuberculin testmay be

negative.

ELISA: It detects different antibodies (IgA, IgM) to different

tubercularproteins.Asnoantigenisstandardized,sensitivity,

specificity,andreliabilityofElisaarealwaysdoubtful.Asthis

testisexpensive,itisappropriatetosaythatitalleviatesparent

anxietyandgenerates funds for the laboratoryperforming the

test.

PCR: Polymerase Chain Reaction (PCR) test detects the DNA

oftheMycobacteriumtuberculosiscomplexfrombodyfluids

samples It is a highly sophisticated technology with high

sensitivity (0.98) and specificity (0.7). Therefore, if PCR is

negative,MTBinfectionisextremelyunlikely,butpositivePCR

doesnotnotnecessarilyreflectactiveMTBinfection.

QuantiFERON®-TBGold(QFT-G):DetectionofIFN-gammaby

ELISAisusedtoidentifyinvitroresponsestoESAT-6andCFP-

10thatareassociatedwithM tuberculosisinfection(substituteof

TST).ItdetectsbothTBdiseaseandLTBI(LatentTBInfection)

butcannotdifferentiatebetweenthem.Bloodmustbeincubated

withthetestantigens<12hoursaftercollection.Collectingthe

required5-mLbloodsamplefromyoungerchildrenmightnot

bepossibleoracceptable.SensitivityofQFT-GfordetectingM.

tuberculosisinfectioninpersonswithuntreatedinfectionis80%

(Nodataisavailableforchildren<17yrs,immunocompromised

andfrompopulationofendemicareaslikeIndia).

Treatment

Thebasicprinciplesofcare

• Diagnosisshouldbeestablishedpromptlyandaccurately

• Standardizedtreatmentregimensofprovenefficacyshould

beused

• Appropriatetreatmentsupportandsupervision

• Responsetotreatmentshouldbemonitored

• Essential public health responsibilities must be carried

out.

Armamentarium

1st line drugs 2nd line drugs

Isoniazid Cycloserine

Rifampin Ethionamide

Pyrazinamide Streptomycin

Ethambutol Amikacin

kanamycin

Capreomycin

p-Aminosalicylicacid(PAS)

Levofloxacin

Moxifloxacin

Gatifloxacin

To achieve 95-99%cure rates “short-course” chemotherapy is

recommended.

INHandPAS=24months

INHandEMB=18months

INHandRIF=9months

INH,RIF&PZA=6months

AsMycobacteriagrowslowly, their generation timebeing12-

24hours.RevisedNationalTuberculosisControlProgrammeis

becauseAntiTubercularTherapy (ATT) canbeprescribedon

intermittentbasiswithincreaseddosagesandundersupervision

toimprovethecompliancewiththerapy.

Essential Drug

Recommended dosage (Dose range in mg/kg)

Daily 3 times weekly

H 5(4-6) 10(8-12)

R 10(8-12) 10(8-12)

Z 25(20-30) 35(30-40)

S 15(12-18) 15(12-18)

E 15(15-20) 30(20-35)

T 2.5 N/A

Eachpatientisassignedacategoryaccordingtotheclinicaland

laboratoryfeaturesandtreatedaspertherecommendations.The

parentscanoptfordailyregimenaspertheirchoiceandtreating

physician should ensure regular monitoring and compliance

withthetreatment

Category I:

2(HRZE)3

4(HR)3

• NewsmearpositivePTB

• New smear negative PTB with extensive parenchymal

involvement

• NewcasesofsevereformsofextrapulmonaryTB.

Pulmonary tuberculosis (PTB) refers to disease involving

the lung parenchyma. Therefore, tuberculous intrathoracic

lymphadenopathy (mediastinal and/or hilar) or tuberculous

pleural effusion, without radiographic abnormalities in the

lungs,constitutesacaseofextrapulmonaryTB.Apatientwith

bothpulmonaryandextrapulmonaryTBshouldbeclassifiedas

acaseofpulmonaryTB.Extrapulmonary tuberculosis (EPTB)

referstotuberculosisoforgansotherthanthelungs,eg,pleura,

lymph nodes, abdomen, genitourinary tract, skin, joints and

bones, meninges. Diagnosis should be based on one culture-

positive specimen, or histological or strong clinical evidence

consistentwithactiveEPTB,followedbyadecisionbyaclinician

to treat with a full course of tuberculosis chemotherapy. The

casedefinitionofanextrapulmonaryTBcasewithseveralsites

affecteddependsonthesiterepresentingthemostsevereform

ofdisease.

Category II:

2(SHRZE)3/1(HRZE)3

5(HRE)3

Sputumsmearpositive:

• Relapse

• Treatmentfailure

• Treatmentafterinterruption

Thefollowingdefinitionsareused:

• New:ApatientwhohasneverhadtreatmentforTBorwho

hastakenantituberculosisdrugsforlessthan1month.

• Relapse: A patient previously treated for TB who has

been declared cured or treatment completed, and is

diagnosedwithbacteriologicallypositive(smearorculture)

tuberculosis.

• Treatment after failure:A patientwho is started on a re-

treatmentregimenafterhavingfailedprevioustreatment.

• Treatmentafterdefault:Apatientwhoreturnstotreatment,

positive bacteriologically, following interruption of

treatmentfor2monthsormore.

• Transfer in: A patient who has been transferred from

anotherTBregistertocontinuetreatment.

• Other:Allcasesthatdonotfittheabovedefinitions.This

group includes chronic case, a patient who is sputum-

positiveattheendofare-treatmentregimen.

Category III

2(HRZ)3

4(HR)3

• NewsmearnegativePTB(otherthanincategoryI)

• NewlesssevereformsofextrapulmonaryTB

Category IV

• TreatmentFailure

To be treated at Specialist Center with specially designed

individualizedregimen

Actions in interruption of TB treatment

Interruptionforlessthan1month

• Tracepatient

• Solvethecauseofinterruption

Continue treatment and prolong it to compensate for missed

doses

Interruptionfor1–2months

Action1

•Tracepatient

•Solvethecauseofinterruption

•Do3sputumsmears.

Continuetreatmentwhilewaitingforresults.

Action2

IfsmearsContinuetreatmentandprolongitto

negativeorcompensateformisseddoses

EPTB

Ifoneor TreatmentContinueRxand

moresmears received: prolongittocompensate

positive <5months formisseddoses

>5monthsCategoryI:startCategor

CategoryII:refer(may

evolvetochronic)

Interruptionfor2monthsormore(defaulter)

•Do3sputumNegative Clinicaldecision

smears smearsorEP onindividualbasis

whethertorestart

•Solvethe orcontinue

causeof treatment,orno

interruption, furthertreatment

ifpossible OneormoreCategoryI StartCategoryII

•Notreatmentsmears CategoryIImaywhile

results positive evolvetowaitingfor

thechronic

Management of children contacts of infectious adults

• Screening-thoroughhistory,clinicalexamination,Mxtest,

CXR

• DiagnosisofTB-Treat

• Symptomfree&<5yearsshouldreceiveprophylaxis(INH

5mg/kg)

• Breastfeedingchildrenofasputumsmear-positivemothers,

amust

• Prophylaxis shouldbe for at least 6months and requires

regular(eg,every2months)follow-up

• Symptomfree&>5yearsdonotrequireprophylaxis

• Childrenmayalsobeinfectedbysmear-negativePTBcases

butbecausetransmissionislesscommon,routinecontact

tracingisnotrecommendedinthiscircumstance

Key Messages

• Anaccurateandpromptdiagnosisshouldbeestablished

• Alleffortsshouldbemadetoisolatethebacteria

• Detailed clinical history, thorough physical examination

and positiveMantoux test are suggestive of diagnosis of

ChildhoodTB

• Intheabsenceofbacteriologicalconfirmationthediagnosis

ispresumptiveinmanyofthepatients

• Thenewerdiagnostictestsmustbeinterpretedwithgreat

caution

• Standardized treatment regimens will treat most of the

patients

• Regular monitoring, assessment of response to treatment

and side effects and compliance must be ensured while

prescribingthetreatment.


Pushpanjali Health Care Events and Initiatives

September 14, 2008Workshop: Level I - Infertility and Recurrent Loss of Pregnancy

DrShardaJainconductedthefirstofaseriesofworkshopsonInfertility and Recurrent Loss of Pregnancy at the ConferenceHall of Pushpanjali Crosslay Hospital. The conference wasattended by over 100Gynecologists fromDelhi and adjoining

NCR region. The day longconference comprised sessionsby eminent speakers ondifferentaspects of the theme. Speakingon the occasion Dr Sharda Jaininformed the participants abouttheIVFcentrebeingsetupatPCHfor the benefit of young couplesrequiringspecializedIVFservicesto fulfill their dream of havingchildrenoftheirown.

September 28, 20081st Basic Airways Workshop

DepartmentofAnesthesiaandDepartmentofOtorhinolaryngologyundertheguidanceofDrSwarajGargandDrAtulJainorganizeda1-dayworkshop.About125delegatesattendedthelectureand40 delegateswere trained in the hands-on sessions.DelegateshadcomefromplaceslikeLudhiana,Muzzfarnagar,Agra,Jaipur,HapurandDehradun.ChiefGuestShriNSeshadri,GM,CanaraBank and Guest of Honor, Dr AK Dhaon, CMO, Ghaziabadinaugurated the workshop. Speaking on the occasion, ShriSeshadriappreciatedtheeffortsofPCHinitsregulareffortsinconductingCMEs.HestatedthattheCanaraBankwasproudtobeaPCHpartner.

DrAKDhaon, inhis address, thankedDrVinayAggarwal forhis quick response in providing a dedicated space for storageofvaccinesatPCHpremisesandlaudedthemanyservicesDrVinayAggarwal andDr VijayAgarwal had undertaken in theareaofcommunityhealth.

October 12, 2008Pediatric Digest

PediatricDigest-organizedjointlybyPCH,IMA-EDBandIAP-EDB,oncommonlyoccurringchildhooddiseaseswasconceivedandplannedbyDrSKMittal,Director,Dept.ofPediatricsandsupportedbyDrPDGarg,DrRaviMalik,DrTilakDangwal.Theconferencehadsixsessionscomprising3-4lecturesineach.

Over 165 delegates attended the conference. ChiefGuest ShriAshokPradhan,MemberofParliament, spokeon theoccasionandreminiscedabouthisschooldayswithDrVinayAggarwaland added thatDrVinay’s zeal for PCHwas very special.MrPradhanspokeoftheimportanceoftheDoctor’sroleinsociety,citing in the process of his own experience when his owndaughterwas ill and the exemplary gentleness and carewithwhichDrVijayAgarwaltreatedthechildandthefamily.

Several pharmaceutical and companies from allied industriesparticipatedintheconference.

November 5, 2008Guest Lecture on Rheumatology

Dept.ofMedicineundertheleadershipofDrParkashGeraorgan-izedaGuestLectureon“RecentAdvancesintheManagementofRheumaticDisorders”byDrManveen Saluja, a leadingconsultantinRheumatologyandProf.WyaneUniversity,USA.

The sessionwasby chairedby Dr YP Munjal, DirectorDiabetology and LifeStyle diseases, BanarsidasChandiwala Institute ofMedicalSciences.

Speaking on the occasion,DrManveenemphasizedtheneed to pay equal attention

Dr Basu, Dr Dhall and Dr Swaraj Garg

Dr Sharda Jain welcomesthe delegates

Mr Ashok Pradhan, MP lighting the lamp

Dr Manveen makingher presentation


to life style management and regular counseling of patientsin association with administering prescribed medications.According to Dr Saluja, the rheumatologist’s role was vitalin the counseling process. He said that contrary to popularbelief the incidence of Rheumatic Arthritis also occurs verycommonlyintheyoungandthusshouldnotbeviewedonlyasaconsequenceofoldage.Hepointedoutthatasaresultitwasextremelyimportantthatcounselingandlifestylemanagementbepaidattentiontointhisagegroupaswell.DrMunjalsharedwith audience his professional experience and endorsed theguidelinesstatedbyDrManveen.ThesessionwasattendedbyPhysicians,OrthopedicsurgeonsandGeneralPractitionersfromNCR.

November 13, 2008Seminar on “Female Feticide: Social Evil or Medical Vice”Aseminarentitled“FemaleFeticide:SocialEvilorMedicalVice”wasorganizedjointlybyNationalMedicosOrganization(NMO),DelhiState,MaulanaAzadMedicalCollege(MAMC)Departmentof Social and Preventive Medicine, National Commission forProtection of Child Rights, Delhi Gynecologist Forum andPushpanjaliCrosslayHospitalatMaulanaAzadMedicalCollegeAuditorium.

Theseminarwasattendedbyover500personsincludingdoctorsandgeneralpublic.

Speakingon theoccasionDr.VinayAggarwal,PresidentNMOandCMDPushpanjaliCrosslayHospital,expressedhisconcernsondecliningfemalepopulationandtheeffectsthereof.

DrArunAggarwal,DeanMAMC,duringhisinauguraladdresssaid that themedical fraternity and paramedics were equallyresponsiblefortherisingincidenceoffemalefeticide,whichwasshameful.Hesaidthattheseunscrupulouspersonswouldneedto be identified and weeded out before the situation reachedalarmingproportions.

Addressing the gathering, Ms Suman Nalwa, ACP, In-chargeCrimeagainstWomenwasoftheopinionthatthefemalefeticidewasaheinouscrimeandthattheculprit/sshouldbedealtwithsternly.

Ms.SandhyaBajaj,Member,NationalCommissionforProtectionofChildRightinheraddressstatedthatnohumanbeinghadtherighttotakenature’slawintotheirownhandsandthatallsuchactionsshouldbestronglycondemned.

Religious leader and activist, Didi Maa Sadhvi Ritambharareiterated the sentiments of the previous speakers who had

expressed the fact that nature’s law of equality must not betemperedwith. She said that lifewas God’s gift and that thefemaleofthespecieswasthemotheroflife,thereforetheactoffemalefeticidewasagainstthisbalanceofnature.Sheexpressedtheviewthattheneedofhourwastoeducatepeopleabouttheadvantageofmaintaining themale-female equilibriumdespitethestrongpublicfavorforamalechild.

Sheurgedallpresenttobecomeavitalpartofthecrusadeagainstfemale feticide which was both a social devil and a medicalvice.

Dr. Jugal Kishore, Professor, Community Medicine, MAMCthanked the speakers for their thought provoking and highlyenlighteningwordson suchaburning issueandextendedhisservicestocurbtheevilbyeducatingthemasses.

LeadingmedicalactivistsagainstfemalefeticideDrShardaJainandDrSuneelaGargmoderatedtheseminar.

November 28, 2008 Sensitizing GPs on DiabetesA lecture session on “The Right time to start insulin in atype-II Diabetes Patients” by Dr VipinMishra, MD, PhD, DM(Endocrinology), Commonwealth Medical Fellow (UK), SrConsultant & Head, Department of Diabetes & Endocrinologywasorganizedattheconferencehall.Thelecturemeetingwasattended by over 50 doctors, andwas appreciated and by thedelegatesonaccountofthequalityofinformationanditsuseinclinicalpractice.

December 5, 2008 Spirometery in Clinical PracticeDr Tilak Raj Dangwal, Consultant, Department of PediatricsaddressedpediatriciansfromEastDelhi,GhaziabadandNOIDAon “Spirometery inClinical Practice”.The sessionwashighlyinteractive,andasexpressedbyparticipantsofgreatbenefitforall.

December 20, 2008 Guest LectureAGuestLectureontheChangingscenarioofHealthcarewasde-livered byDrRavinderMamtani,Diplomate of TheAmericanBoardofPreventiveMedicine.ThelecturewasattendedbyPCHConsultantsanddoctorsfromtheNCRregion.

January 11, 2009Workshop on Uterine Balloon TherapyThe Dept. of Gynecology in association with the DelhiGynecologistForumorganizedaworkshoponDUB-MadeEasyat conference hall of PCH from9.30 am to 1.30 pm. EminentdoctorslikeDrGopinathfromChennaiandDrSushmaChawlafromJallandherconductedsessions.Didi Maa releasing the book

Dr. Mamtani making a point


January 18-19, 20092nd International Temporal Bone Dissection and Live Ear Surgery CoursePCH in association with Claros Foundation, Barcelona, Spainorganized the2nd InternationalTemporalbonedissectionandLiveEarsurgerycourseforENTsurgeonsatthehospitalpremisesonJanuary18and19,2009.

Surgeries, including cochlear implant, were performed byinternationally renowned ear surgeon, Prof. Pedro Claros,Chairman of the Claros Foundation in Barcelona, Spain. ProfClaroshasperformedover800successfulcochlearimplants.

TheworkshopcomprisedofacourseonTemporalbonedissectionfor ENT surgeons. About 60 ENT surgeons from North IndiaattendedthecourseandlearnedthedetailsofearsurgeryfromDrPedroClaroshimself.ClarosFoundationdonatedacochlearimplantworthRs10lakhtoaneedyyoungchild

February 4, 2009 Symposium on World Cancer Day Cancer is a leading cause of death around the world. WHOestimatesthatifnointerventionmeasuresaretakenthenabout84millionpeoplewilldieofcancerbetweentheyears2005and2015.

OntheoccasionofWorldCancerDay,4February,GalaxyCancerInstitute,PushpanjaliCrosslayHospitalorganizedasymposiumon“Cancer:DonotFearit,Fightit”.ChiefGuest,ShielaDikshit,Hon’bleChiefMinister ofDelhiwaswarmlywelcomedbyDr.VinayAggarwal,ChairmanandManagingDirectorofPushpanjaliCrosslay Hospital. Dr. Vinay Aggarwal spoke of the ongoingbattlebeingfoughtbythemedicalcommunityandhighlightedthe world class healthcare facilities being developed at thePushpanjaliCrosslayHospital.

Smt. Sheila Dikshit, Hon’ble Chief Minister of Delhi thankedthe organizers and reiterated that everyone - government andprivatesectors-neededtoworkconjointlytoensurethatcancertreatmentbemadeaffordableforall.However,theHon’bleCMalsosaidthatthefirstlineprioritywouldhavetobeprevention.

Dr VB Bhatnagar, former Head of the Department of Surgery,LLRMMedicalCollege&SubhartiMedicalCollegeandGuestofHonouremphasizedtheappropriatenessofsuchaseminarandhoped thatmanymorewould follow toestablishconclusivelythatcancercanandshouldbefought.

Dr Mahesh Verma, Director Principal, Maulana Azad DentalCollegesaidthatthenumberofcasesofcancersofheadandneckwere on the rise becauseof the increased use ofGutka and Khaini. Heemphasized the need forregular oral examinationssothatanywhite/redpatchcouldbedetectedbeforeitturnedcancerous.

Padmashri Sh AlokMehta, Chief Editor, NaiDunia highlighted therole of media in the waragainst cancer. He saidthat print media becauseof its circulation was ina better position to reachthe masses for cancerawareness.Healsoemphasizedthatotherformsofmediashouldalsobeusedforcancerawarenesscampaign.

Dr Dharam Prakash, Secretary General, Indian MedicalAssociation, highlighted the role of doctors in early diagnosisofcancer.Hesaidthatthealldoctorsshouldbetrainedinearlydiagnosisofcancer.DrArunGoel,DirectorOncologyatGalaxyCancer Institute briefed the gathering about the Institute andspokeofthemodernequipmentandprotocolsavailableforthetreatmentandmanagementofalltypesofcancers.ThehighlightofthecenterwastheLinearAccelerator,whichwascapableofdeliveringImage-guidedRadiotherapyandIntensityModulatedRadiotherapy.Inaddition,thebrachytherapyfacilitiesavailableat the centre with its 30 channels HDR Remote afterloadingdevicecouldtreatlargetumors,werealsoappreciated.

The seminar concludedwith a vote of thanksbyDr.SandeepAgarwal, Senior Consultant at Galaxy Cancer Institute,PushpanjaliCrosslayHospital.

Workshop Captured in Camera

Honorable Chief Minister lighting the lamp

Dr. Mahesh Verma addressing the audience

(L to R) Shri Alok Mehta, Dr. Vinany Aggarwal, Smt. Sheila Dikshit, Dr. Vijay Agarwal, Dr. Dharam Parkash on dias


February 7, 2009 Recent Advances in Prostate Surgery DrB Sunder, an eminentUrologist fromChicago addressed agathering of clinicians including Physicians and Surgeonson Recent Advances in Prostate Surgery. Dr Ajit Saxena, SrConsultant,Urologychairedthesession.

March 1, 2009CME on TimGalekop,Director,Ahlstrom,Belgium,anexpertinGlobalTechnicalsupportforhospitalsdiscussedInfectionPrevention-AwaytoearlyrecoveryandincreasedPatientturnover.MrMayankPremi,Director,ProgressiveHealthcareSolutionsdeliberatedonCollectiveBargainingforincreasingEffectivity,ProductivityandProfitabilityinhealthcare.TheCMEwassponsoredbyDispoline,Bangalore.SpeakingontheoccasionMrSumitMarwaha,CEOandMD,committedtoprovidingcontinuedsupporttoPCH.

March 15, 2009 Health CampContinuingwithcorporatesocialresponsibility,ahealthcampwas organized in association with the RajasthanMaheshwariSewaSamitiatLionsBhawan,VivekVihar.SeniorconsultantsDrParkashGera,DrVipinMishra,DrLDSota,DrNeeraj Jain,DrBK.Gupta,DrDhirendraSinghaniaandDrKPSinghofferedfreeconsultation to thevisitors. Campparticipantswerealsoprovided free investigations including Blood Sugar, BloodPressureCheckupandECGbythedepartmentofLabMedicine.Yogacharya Sheshpal ji demonstrated Yogasanas. Over 250personsbenefitedfromtheservicesofferedatthecamp.March 17, 2009

Guest lecture on Sleep Medicine Aguest lectureonSleepMedicinewasdeliveredbyDr.TilakKiran Verma, Director, Sleep Medicine, Rhode islands, USA.

The lecture wasattended by over70 medical pro-fessionals fromvarious special-ties. Dr. ParkashGera,chairedthesession.

March 22, 2009 Hearing Screening CampAdaylonghearingscreeningcampontheinitiativeofMrRajSharma, Head, Audiology and Speech therapy, department ofENTandunder the leadershipofDrAtul Jain,wasorganized.Thehighlightofthecampwasanawardoftendigitalhearingaidstothosediagnosedatthecamp.ThehearingaidscostingRs.1lacwerearrangedbyMr.RajSharma.Atotalof57patientswerescreenedfortheirhearingofwhich10wererecommendedhearingaids.Sincetherewere10prizes,eachdiagnosedpatientemergedawinner.

Training Programs ConductedACommunityCPRprogramwasconducted toprovidepeoplewiththeknowledgeandskillnecessaryinanemergencytocallforhelp,tokeeppeoplealive,toreducepainandminimizetheconsequencesofinjuryorsuddenillnessuntilprofessionalmed-icalhelparrives.

BLS Training and Resuscitation Programme“BLStrainingandresuscitationprogramme”,isconductedeveryWednesdayofthemonth,from10amto1pmbyDrAmitGup-ta,ConsultantandHead,EmergencyMedicalServices,TraumaCareandMedicalIntensiveCareUnit.Themainobjectiveofthisprogram is to guide people about CPR, first aid and commonmedicalemergencies.

Honors ReceivedDr Narendra Sainiafter been desig-nated as PresidentElect, DMA wasselected as the In-dia Representativefor “World HygieneCouncil”ataglitter-ingfunctionatLon-don,U.K.

Yogacharya Sheshpal ji demonstrating Yoga

Sumit Marwah, Tim Galekop, Dr. Vijay Agarwal and Mayank on the dies (L to R)

Dr. Tilak Kiran talking to the Delegates

Mr. Raj Sharma addressing patients on hearing

Dr Narinder Saini with others from


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1. Mehta MN, Mehta JN. Serum lipids and ABO bloodgroups in cord blood of neonates. Indian J Pediatr 1984;51 :30-43.

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3. Malhotra KC. Medicogenetic problems of Indian tribes.In Verma IC, ed. Medical Genetics in India. Vol. 2.,Pondicherry;AuromaEnterprises,1978;51-55.

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Documents

Pediatrics March 2009