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WHAT IS THE DIAGNOSIS

WHAT IS THE DIAGNOSIS. Prof. Dr. İnci GÜLMEZ Erciyes University Medical Faculty Department of Pulmonology, Kayseri. Case. 36 years old, woman with two children housewife, hometown Pınarbası, lives in Kayseri. 2004. Cough , exercitional dyspnea

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WHAT IS THE DIAGNOSIS

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  1. WHAT IS THE DIAGNOSIS Prof. Dr. İnci GÜLMEZ Erciyes University Medical Faculty Department of Pulmonology, Kayseri

  2. Case 36 years old, woman with two children housewife, hometown Pınarbası, lives in Kayseri

  3. 2004 • Cough , exercitional dyspnea • Diagnosed with asthma five years ago • Four years history of joint pains, finger swelling and elevated RF, diagnosed wtih rheumatoid arthiritis • Medications: NSAIDs, Leflunomide (Arava) • Her mother is affected with asthma • Chest X-ray: bilateral reticulonodular infiltration and apical consolidation

  4. CT

  5. 2004 • Physical examination: has a BCG scar Long expiratory time , bilateral ronchus and ralles • Laboratory: Hb:11,8gr/dl WBC:5300/mm3 Sedimentation: 52mm/h RF:276Ü/mL( 0-20) CRP:215 mg/L(0-200)

  6. What is the differantial diagnosis? • Tuberculosis • Rheumatoid lung • Drug induced pulmonary disease • Caplan’s syndrome

  7. 2004 • Spirometry: FVC %70 FEV1 %48 FEV1/FVC: %60 • DLCo:%82 • ADA:15Ü/ml( cut of point 25 U/ml) • ANA(+) • Sputum EZN: Three times (-) • Bactec and L-J culture: negative • PPD: 7 mm/ 72 h Watts RA et al Semin Arthritis Rheum.1995;25:28–34

  8. 2004 • Bronchoscopy : BAL EZN(-) • BAL Bactec and L-J: negative • BAL cytology: Clas II • Bronchoscopic Bx: no lung tissue, normal bronchial tissue • ECG: normal • ECHO: EF: %68, PAP: 25 mmHg

  9. What is the diagnosis? • Tuberculosis • Rheumatoid lung • Drug induced pulmonary disorders

  10. What is the diagnosis? • Tuberculosis • Rheumatoid lung • Drug induced pulmonary disorders

  11. THERAPY • Oral steroid (for one year) • ICS+LABA • NSAIDs

  12. June 2006 • Had been taking NSAID, ICS +LABA for eight months • Joint pain • Physical examination: additional sign: small joints of the hands are inflamed • Laboratory: Hb: 11,9gr/dl Sd: 32mm/h RF:606 and 1070 U/mL • ANA:+ CRP:79,3 mg/L

  13. June 2006 • Spirometry : Baseline: FVC%87 FEV1:%63 FEV1/FVC: %63 Post bronchodilatör: FVC:%88 FEV1:%66 FEV1/FVC:65 • DLCo: %74

  14. Chest CT

  15. Therapy • Oral steroid • ICS+ LABA • NSAİDs

  16. June 2007 • 10 mg florokortolon, ICS+LABA, NSAID • Exercitional dyspnea and chest pain • Exercitional palpitation • ECG: Right axis, right ventricular hypertrophy

  17. What test would you choose at first at this step? • HRCT • RF • DLCo • ECHO • Spirometry • 6 MWT

  18. What test would you choose at first at this step? • HRCT • RF • DLCo • ECHO • Spirometry • 6 MWT

  19. June 2007 • ECHO: 2nd degree T sufficiency, • PAP: 60-65 mmHg, • Left ventricular function is normal

  20. June 2007 • RF: 69 U/mL • DLCo: %72 • Spirometry: postbronchodilatory FVC: %66 FEV1.%46 FEV1/FVC: 60 • 6 MWT: 310 M, heart rate at the end of the test :145/min

  21. What is the additional suggestion in therapy? • Teophylin • Spironolactone • Bosentan • İlomedin • Calcium canal blocker • Sildenafil

  22. What is the additional suggestion in therapy? • Teophylin • Spironolactone • Bosentan • İlomedin • Calcium canal blocker • Sildenafil

  23. One month later • Complaint of dyspnea • ABG ( room air):PH: 7,52 PaCO2:29mmHg PaO2:79 mmHg • DLCo: %52 • Spirometry: FVC:%51 FEV1: %40 FEV1/FVC: %68 • 6MWT: 270 M

  24. One moth later

  25. Therapy • Prednizolon 60mg+ cyclophospamide 100mg • Diltiazem 3x60 mg • ICS+ LABA • Anticoagulant

  26. October 2007 • Oral lesions • Elevation in dyspnea symtoms • Palpitations • Sweating • Chest pain • Lab: WC: 25300/mm3 sed:96 mm/h • Hospitalisation

  27. Loss of volume on the right hemithorax • Increase in the pulmonary artery diameter • Increase of parietal pleural nodules on right hemithorax • Mass in the anterior mediastinum • Increase of ascendan aorta diameter

  28. Loss of volume on the right hemithorax • Increase in the pulmonary artery diameter • Increase of parietal pleural nodules on right hemithorax • Mass in the anterior mediastinum • Increase of ascendan aorta diameter

  29. October 2007 • Kandidomannan: positive • freeT3-freeT4- TSH: normal • Sputum gram stain: PK(+), no microorganism is seen • Galaktomannan: 0,27 (-) • CRP: 184mg/L

  30. What do you think about differential diagnosis? • Tuberculosis • Candida pneumonia • İnvazive aspergillosis • Cyclophospamide toxicity • Thymoma • Actinomycosis • Nocardiosis

  31. Additional Therapy • Liposomal Amphotericin B 1mg/kg • Moxifloxasin 400mg/day

  32. Oral culture : (-) • Blood culture: (-) • Suputum microscopy: no fungus is found • Sputum culture: candida albicans • Suputum EZN: negative • Bronchoscopy: enflamation , BAL is taken from upper left lobe, and TBBx is taken from apicoanterior upper left lobe

  33. Third day • Reduced general contidition • Tachycardia unresponsive to medical treatment • Hypoxaemia despite Oxygen therapy mask use • Control X-ray

  34. Control Chest X-Ray Intralesionar punction: pus

  35. Third day • Pus material EZN stain: negative Gram stain: PK(+), suspicious gram pozitive microorganism • Lavage culture: No reproduction • Patient’s Hypoxaemia went deeper, respiratory failure, mechanic ventilation support, exitus!

  36. What is the diagnosis? • Tuberculosis • Necrotizing pnomonia (resistant microorganism) • İnvasive aspergillosis • Actinomycosis • Nocardiosis

  37. Pus material : Nocardia spc Specification is not done

  38. Nocardiosis • Nocardiosis is an acute, subacute, or chronic suppurative infection caused by Nocardia • Weakly gram-positive, filamentous bacteria found worldwide in soils • A total of approximately 30 strains of Nocardia have been associated with human disease • Infections are localized or dissemineted

  39. Nocardiosis • Disseminated and fulminant disease mainly occurs in immunocompromised host with underlying illnesses, such as HIV, cytotoxic chemotherapy, bone marrow transplantation, or prolonged glucocorticoid treatment

  40. NocardiosisClinical manifestations • Bronchopneumonia • Lobar pneumonia • Necrotizing pneumonia • Mediastinitis • Mediastinal abscesses • Cerebral abscesses • Intra-abdominal abscesses • Peritonitis

  41. Nocardiosis • The primary disease occurs in the pulmonary system and may mimic tuberculosis, staphylococcal, or mycotic infections • Hematogenous dissemination may occur to all organs of the body • The brain, kidneys, and liver are the most common metastatic sites

  42. Nocardiosis • Mortality is increased in patients with acute infection and in those with disseminated disease involving two or more contiguous organs or the CNS • Mortality is also increased in patients taking corticosteroids or antineoplastic agents

  43. NocardiosisPhysical examinations • Subacute abscesses are palpabl at the site of trauma and generally fell firmer than fluctuant • A lung examination may reveal diffuse or localized abnormal breath sounds • Mild-to-severe respiratory distress that progresses to respiratory failure may occur

  44. Nocardiosisİmaging studies • Generalized infections - chest radiographic findings vary and include fluffy infiltrates, scattered nodules, and confluent lobar infiltrates progressing to complete consolidation and cavitation - Chest CT scanning may be necessary to visualize the extent of disease and to rule out empyema

  45. NocardiosisDiagnosis • Gram-stain -Directly examine clinical materials (eg, sputum, bronchoalveolar lavage, cerebral spinal fluid, pus) by gram stains and acid-fast stains -Use methamine-silver stains for demonstrating the organisms in tissue specimens • Serological diagnosis is not readily available • Cultures typically grow within 3-5 days on blood or chocolate agar

  46. NocardiosisTreatment • Sulfa-based therapy is recomended. TM-SM, given intravenously in high doses, is the treatment of cohoice • Linezolid has a growing literature in support of its use in combination and monotherapy • Additional concurrent therapy with an aminoglycoside plus ceftriaxone benefits patients with fulminant disease

  47. NocardiosisTreatment • Patients who are immunocompetent with lymphocutaneous disease are usually treated for 6-12 weeks • Therapy includes incisions and drainage of abscesses • Patients with immunocompromising conditions are treated for at least three months after clinical cure( usually up to one year of threapy)

  48. THANK YOU

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