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Tuberculosis in children

Tuberculosis in children. dr . Ery Olivianto, SpA Dr. dr . Wisnu Barlianto, SpA (K) Prof . D r . d r. HMS. Chandra K usuma , SpA (K) Child Health Department Faculty of Medicine Brawijaya University Saiful Anwar General Hospital. Back Ground. WHO :

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Tuberculosis in children

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  1. Tuberculosis in children dr. Ery Olivianto, SpA Dr. dr. Wisnu Barlianto, SpA(K) Prof. Dr. dr. HMS. Chandra Kusuma, SpA(K) Child Health Department Faculty of Medicine Brawijaya University Saiful Anwar General Hospital

  2. Back Ground WHO : • 1990 – 1999 30 millions died • 1/3 world population infected • Per year  8 milionsnew cases  3 milions die • 5 – 10% infected active TB • Eradication is difficult : • MDR  • HIVPandemi • BCG : various protection rate

  3. Mycobacterium tuberculosis colony

  4. M.Tb cell wall stucture

  5. Pathogenesis of TB

  6. Mechanism of T cell activationKilling of M.Tb bacteria

  7. Granuloma formation

  8. Granuloma (Tubercle)  Central for protection •  replication of bacteria • The process is confined • Characteristic feature of TB: • Caseating centre • Extracellular bacteria • Cells : • macrophage • Epiteloid cells • T cells • Giant cells of Langhans

  9. Pathogenesis of TB infection

  10. Primary focus: Structural and cellular changes due to response tomultiplication of M.Tb in tissues first to be implantedusually lungs Primary adenitis = regionallymphadenitis Changes in lymphnode secondary todrainage from primary focus Primarynodes : Anatomic reflection of primary focus Primary complex: Primary focus +regional lymphadenitis

  11. primary complex pleural effusion bronchial erosion Milliary TB Meningitis Skeletal TB Renal TB infection 3-9 mos 3-24 mos 3-6 mos within 12 mos within 3 ys within 5 ys Hypersensitivity Acquired immunity Positive TST 1 year 2 year 2-12 wks (6-8 wks) greatest risk of locals and disseminated lesion diminishing risk

  12. Primary focus undergo caseation  Focus enlarged disrupted to bronchus cavity persisted Round/coin lesions (>>) calsification 1 years • Caseation depends on: • Host immunity • Nutrition • Amount of bacteria and its virulence

  13. AGE-SPECIFIC RISK TO PROGRESS TO DISEASEAFTER PRIMARY INFECTION WITH Mycobacterium tuberculosis IN IMMUNOCOMPETENT CHILDREN

  14. Time table • primary focus • regional lymphadenitis • hematogenic spread

  15. Usually single • One /both lung(s) • near pleura Primary focus: • Sensitization : • 4 – 8 wksafter infection • depends on : • age • nutrition • Phenomena of sensitization : • Febrile illness lasting  2-3 wks • Phlyctenularis conjuctivitis • Erythema nodosum

  16. Pleural Effusion • Essential sensitivity reaction • Massive effusionis rare for < 5 years • 75% 6 monthsafter infection • 25% 3 monthsafter infection • Usuallyserous (empyema )

  17. Hematogenic spread • Miliarydan meningitis TB • Within 1st year after infection • More common in younger age • Decreased immunity: • Malnutrition • HIV infection • Measles • Pertussis • Streptococcus infection

  18. Hematogenic spread • Bone and joint • 3 years after infection •  younger age • Renal, skin • 5 years after infection • first 5 years: rare • 10 years: often

  19. Regional Lymphnodes • Complications are more common (than primary focus) • Compliactions occur within first 9 months after infection: • Disrupted  abscess • Endobronchitis with : • a. Incomplete bronchial obstruction • b. Complete bronchial obstruction

  20. Segmental lesions : • d. permanentchanges (common): • Bronchial stricture • Bronchiectasis • Lung fibrosis • e. Bronchopneumonia : • Immunity  • Bacteria 

  21. Diagnosis TBC in children • History • Contact /sources • TuberculinTest(Mantoux) • Physic Diagnostic • X – ray • AFB /Hystopathology

  22. Algorithm for Early Detection and Referral for Childhood Tuberculosis in Indonesia Next page If > 3 positive Suspected TB: Close contact with adult with AFB sputum (+) Early reaction of BCG (in 3-7 days) Weight loss with no apparent cause, or underweight with no improvement in 1 month with adequate nutritional support (failure to thrive) Prolonged/recurrent fever with no apparent cause Cough more than 3 weeks Specific enlargement of superficial lymph node Scrofuloderma Phlychten conjunctivitis Tuberculin test positive (> 10 mm) Radiological findings suggestive TB

  23. Considered TB Give anti-TB therapy Observation in 2 months No clinical response/worsening Clinical response (+) Not TB MDR TB TB Continue anti-TB therapy Refer to hospital • ATTENTION • Presence of any dangerous signs: • Seizure • Decreased level of consciousness • Neck stiffness • Or signs such as: • Spinal tumor/lump • Limping • Dam board phenomenon •  Refer to hospital • Reevaluation in Referral Hospital: • Clinical signs • Tuberculin test • Radiological findings • Microbiology and serology examination • Histopatology examination • Diagnostic procedure and therapy according to each hospital’s protocol UKK Pulmonologi –IDAI. Jakarta;2002.

  24. History : Chronic Fever Chronic cough Body Weight Malaise Activity • Source of infection: • Difficult • Important: • Diagnosis • Therapy

  25. Physic Diagnostic Primary TB: asymptomatic Respiratory symptoms /Rö ~ other infection search extrathoracal TB Scrofuloderma Cold absces Bone /joint TB Lymphnode enlargement Conjunctivitis phlyctenularis Serous meningitis

  26. TUBERCULIN TEST • Important role in diagnostic • Agents : • OT 0,9 mg • PPD RT-23 2 TU/ PPD S 5 TU • Intra-cutaneusly, antebrachii volar area • Intepretation: 48-72 h after injection • Transversal diameter of induration, ≠ erythema

  27. TST interpretation > 10 mm POSITIVE 0-4 mm NEGATIVE 5-9 mm DOUBTFUL Current / past clinical infection No clinical infection • Technical error • Clinical infection • Cross reaction to BCG vaccine Active, if: No need to repeat the test, unless strong suspicion of TB < 6 ys Tx (-) BCG(-) Conversion: (-)  (+) 1 year Tx (-) , BCG(-) Repeated with same dose > 10 mm Same result Same result + other signs Clinical infection Cross reaction toBCG vacc probableTB

  28. False Positive: • Post BCG vaccination • Mycobacteriumatypis • Morbus Hansen Negative: • Incubation: 2 – 10 mgg • Severe TB: miliary/meningitis • Severe Malnutrition • Dehydration • Diseases with high fever • Tx. Corticosteroid / immunosupresive • Certain infections : • Morbili (or its vaccination): 10 ds– 6 wks • Rubella : 1 – 3 wks • Pertussis • HIV

  29. Notifications: • Tuberculin Test (Mantoux) • Should be routinally started at 6 – 8 mos every year • if contact (+) and TST (-) repeat after 10 wks • still in close TST each 3 mos • Interpretation of TSTpost BCG • difficult • Induration varies: 0 – 20 mm • Kendig 1972 : susp. active infection if  15 mm • Lotte 1971 : active infection if:pre /post BCG 18 mm

  30. Notifications: • II. BCG Scar (+) • not exclude the disease active infection • when BCGvaccination: • Within incubation period • Active TB already • Infected during incubation of BCG • Not effective vaccine

  31. CHEST X RAY • Not specific • Normal chest X ray : not excluding the process • DIAGNOSISCAN NOT BE ACHIEVED BASE ON CHEST X RAY • Strongly suggestive TB: • miliary • paratracheal lymphnode enlargement

  32. Diagnostic scoring TB in children

  33. Note : • Diagnosis using scoring system performend by a doctor • If scrofuloderma is present  diagnose Tuberculosis • Body weight assessed at the time of admission (moment opname) • Fever /cough which not respond tostandard therapy • Chest x ray is not main diagnostic tool in childhood TB • Children with rapid BCG reaction shoud be evaluated using scoring system • diagnosis TB when the score > 6, (max 14)

  34. Diagnosis of TB in children Anthony Harries & Dermot Maher, 1997 If you find the diagnosis of TB in children easy, you probably overdiagnosing TB If you find the diagnosis of TB in children difficult, you are not alone It is easy to over-diagnose TB in children It is also easy to miss TB in children Carefully assess all the evidence, before making the diagnosis

  35. Hospitalization • Ascertain diagnosis: repeated AFB, biopsy • Initial treatment in: severeTB /life threatening /infants • Corticosteroid /surgical treatment • Severe adverse reaction to TB regiment • Treatment for concomitant disease • Initial treatment for children whose parents /environments are not adequate

  36. TB bacilli population

  37. TB drugs & pharmaceutical formulation Isoniazid (H) monosubstance Rifampicin (R) combi-packs Pyrazinamide (Z) Ethambutol (E) fixed dose comb

  38. FDC (Fixed Dose Combination) tablet formulation WHO H : 30 mg R : 60 mg Z : 150 mg IDAI H : 50 mg R : 75 mg Z : 150 mg

  39. Dosage of antituberculosis drug Drugs Daily dose (mg/Kg/day) 2 Time/week dose (mg/Kg/dose)) Adverse reactions Isoniazid (INH) 5-15 (300 mg)) 15-40 (900 mg)) Hepatitis, peripheral neuritis, hypersensitivity Rifampicin (RIF) 10-15 (600 mg)) 10-20 (600 mg) Gastrointestinal upset,skin reaction, hepatitis, thrombocytopenia, hepatic enzymes, including orange discolouraution of secretions Pyrazinamide (PZA) 15 - 40 (2 g) 50-70 (4 g) Hepatotoxicity, hyperuricamia, arthralgia, gastrointestinal upset Ethambutol (EMB) 15-25 (2,5 g) 50 (2,5 g) Optic neuritis, decreased visual acuity, decreased red-green colour discrimination, hypersensitivity, gastrointestinal upset Streptomycin (SM) 15 - 40 (1 g) 25-40 (1,5 g) Ototoxicity nephrotoxicity When INH and RIF are used concurrently, the daily doses of the drugs are reduced National consensus of tuberculosis in children, 2001

  40. TB therapy regimen 2 mo 6 mo 9 mo 12mo INH RIF PZA ETB SM PRED DOT.S !

  41. Therapy problem solutions DOTS : Directly Observe Treatment Short-course FDC : Fixed Dose Combination i.e. >2 drugs in one tablet / capsule in a fixed dose formulation

  42. Corticosteroid • Meningitis • Serositis (pleura, pericard,peritoneal) • Endotracheal • Miliary

  43. STOP therapy • Regular treatment : 6 bln – 1 ½ th • improvement, BW, fever (-) • Chest x ray  improvement • ESR, if previous ESR • Source of infection (-) • If source (+) : continue with IPT (INHprophylaxis • treatment)

  44. Side Effects • Streptomycin : 20 mg/kgBW/day • Nefrotoxic: rare • N. VIII disturbance (mainly vestibular nerve) • Ataxia • Vertigo • rare: deafness • Pyrazinamide : 30 – 40 mg/kgBW/day • Hepatotoxic

  45. INH : 10 – 20 mg/kgBW/day– 1 dd • Periferal neuritis : rare • due to B6 defisiensi • Hepatotoxic: previous liver disorder • other hepatotoxic drug: rifampicin • Other : GI irritability • hypersensitive reaction • neurology: • psichosis • seizure • confusion

  46. ETB : 15 – 20 mg/kgBW/day– 1 DD • Reversible occular complications • Blurred • Color blindness • Narrowed visual field

  47. Rifampicin: 15 – 20 mg/kgBW/day– 1dd • Orange discoloration : saliva, tear, conjunctiva • GI. Symptom • Hepatotoxic • Trombocytopenia– leukopenia • “Influenza syndrome” • Fever • headache • Malaise • “Respiratory syndrome” • Tightness • Wheezing

  48. INH Prophylaxis Single treatment : 5-10 mg/kgBW/day • Infection prophylaxis Healthy child Exposed to adult with AFB (+) TST (-) 3 mos TST (+) 1 y

  49. Disease prophylaxis prevent the disease (current /past TB infection): • 2.1. latent TB: • TST (+), BCG (-), Tx (-), < 6y, healthy • conversion (+), BCG (-), Tx (-) • duration: 1 year • 2.2. prevent exacerbation: • healedmorbili, pertussis • Narcose • Tx. Corticosteroid • duration: 6 wks

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