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PULMONARY GRAND ROUNDS

PULMONARY GRAND ROUNDS. Eduardo Santiago March 08,2012. HPI. 65 year old woman, no PMH. Subjective fever, chills, malaise and mild cough 1 month ago. Progressive shortness of breath. Dry cough. . HPI. Seen by her PCP: Diagnosis of CAP. Azithromycin for 1 week. Started on oxygen.

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PULMONARY GRAND ROUNDS

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  1. PULMONARY GRAND ROUNDS Eduardo Santiago March 08,2012

  2. HPI • 65 year old woman, no PMH. • Subjective fever, chills, malaise and mild cough 1 month ago. • Progressive shortness of breath. • Dry cough.

  3. HPI • Seen by her PCP: Diagnosis of CAP. • Azithromycin for 1 week. • Started on oxygen.

  4. PMH: Unremarkable. • SH: ½ pack per day for 20 years. • Denies any occupational or recreational exposure. • Denies any prior use of medications. • ROS: Unremarkable.

  5. PE • HR 70, BP 126/80, RR 14, T 100, O2 SAT 90% on 2 LPM Weight:172.92 • CHEST EXAM: Decreased breath sound at both bases. Diffuse inspiratory crackles at both lower lungs. • CARDIAC EXAM: RRR, S1 and S2 within normal limits. No S3 or S4. • EXTREMITIES: No edema. No clubbing or cyanosis. • SKIN: No skin rash.

  6. FVC: 1.36L (46%) • FEV1: 0.91 (40%) • FEV1/FVC: 87% • DLCO:5.89 (25%)

  7. BAL • Macrophages :46% • Lymphocytes:7% • Neutrophils:43% • Bronchial lining cells:4%

  8. Pathology • Patchy organizing pneumonia, fibroblastic intra alveolar infiltrate, scattered lymphocytes within the interstitium. • No significant acute inflammation. • No granulation tissue. • No evidence of vasculitis.

  9. COP

  10. COP • J.M Charcot 1877–1878. • Milne: Type of pneumonia where the usual process of resolution has failed and organization of the inflammatory exudate in the air alveoli of the lung by fibrous tissue has resulted.

  11. COP • Organizing pneumonia: Endobronchial connective tissue masses composed of myxoid fibroblastic tissue resembling granulation tissue. • Central cluster of mononuclear inflammatory cells. • Chronic inflammation in the walls of the surrounding alveoli. • Preserve lung architecture.

  12. COP • Organizing pneumonia pathologic pattern is a nonspecific reaction that results from alveolar damage with intra-alveolar leakage of plasma protein with alveolar organization.

  13. COP • Clinical, radiological and pathological diagnosis. • Pattern of organizing pneumonia must be prominent.

  14. Pathogenesis • The intra alveolar fibrosis is its usual dramatic reversibility with corticosteroids and not associated with progressive irreversible fibrosis .

  15. Pathogenesis/ First Stage • Alveolar epithelial injury with necrosis and sloughing of pneumocytesresulting in the denudation of the epithelial basal lamina. • The endothelial cells are only mildly damaged. • Infiltration of the alveolar interstitium by inflammatory cells: lymphocytes, neutrophils and eosinophils.

  16. Pathogenesis/ Second Satge • Intra alveolar stage: formation of fibrinoid inflammatory cell clusters with prominent bands of fibrin and inflammatory cells. • Formation of fibro inflammatory buds, fibrin is fragmented and reduction of inflammatory cells. • Migration of fibroblast from the interstitium and proliferation.

  17. Pathogenesis/Second Stage • Myofibroblast. • Proliferation of the alveolar cells and re epithelialization of the basal lamina.

  18. Pathogenesis/Third stage • Inflammatory cells have disappeared. • There is no fibrin within the alveolar lumen. • Concentric rings of fibroblasts alternate with layers of connective tissue.

  19. Connective Matrix • Loose connective matrix with high type III collagen content which is more susceptible to degradation and reversal of fibrosis.

  20. Angiogenesis • Prominent capillarization of the intra alveolar buds. • Vascular endothelial growth factor and basic fibroblast growth factor. • Angiogenesis could contribute to the reversal of buds in OP.

  21. Pathogenesis • The opposing mechanisms of reversibility of fibrosis in COP and ongoing fibrosis in UIP are not yet established.

  22. Radiology

  23. Radiology • Multiple alveolar opacities: typical COP. • Solitary opacity: focal COP. • Infiltrative opacities: infiltrative COP.

  24. Diagnosis • Diagnosis of organizing pneumonia. • Exclusion of any possible cause. • Histopathology: Buds of granulation tissue consisting of fibroblasts myofibroblastsembedded in connective tissue.

  25. Diagnosis • Definite: compatible clinicoradiologic manifestations and typical pathologic pattern on a pulmonary biopsy of sufficient size. • Probable: findings of organizing pneumonia on transbronchialbiopsy and a typical clinicoradiologic presentation without pathologic confirmation. • Possible: typical clinicoradiologic presentation without biopsy confirmation.

  26. Treatment • Rapid clinical improvement and clearing of the opacities. • The precise dose and duration of treatment have not been established. • Prednisone 0.75–1.5 mg/kg/day. • 0.75 mg/kg/day during 4 weeks, followed by 0.5 mg/kg for 4 weeks, then 20 mg for 4 weeks, 10 mg for 6 weeks, and then 5mg for 6 weeks.

  27. Treatment • Complete clinical and physiologic recovery in 65 % of patients. Gary Epler. Bronchiolitis Obliterans Organizing Pneumonia. NEJM; 1985:152-8

  28. Treatment • Predictors of relapse: delayed treatment and mildly increased gammaglutamyltransferase and alkaline phosphatase levels.

  29. Treatment • Severe cases: prednisolone 2mg/kg/day for the first 3-5 days.

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