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CPC

CPC. Julye Carew, M.D. December 11, 2003. CASE REVIEW. 41 yo AA male No PMH, but allergic rhinitis 2 weeks of dyspnea and fever 3 ER visits-- ABX CT angio of chest-- neg for PE, but with bilateral lower lobe alveolar infiltrates

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CPC

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  1. CPC Julye Carew, M.D. December 11, 2003

  2. CASE REVIEW • 41 yo AA male • No PMH, but allergic rhinitis • 2 weeks of dyspnea and fever • 3 ER visits-- ABX • CT angio of chest-- neg for PE, but with bilateral lower lobe alveolar infiltrates • Progressive course with development of ARDS, hypoxic respiratory failure

  3. CASE REVIEW • MEDS: Zpack, antihistamine, Hydrocodone, nasal steroid • FH: NC • SH: No habits, construction with ceramics, fiberglass and flooring, no significant travel

  4. CASE REVIEW • ROS: • POSITIVE: fever, chills, cough with clear sputum, night sweats, fatigue • NEGATIVE: NO hemoptysis, CP, rash, meningismus, HA, N/V, GU or GI symptoms

  5. CASE REVIEW • PE: • mild respiratory distress • T 103.6, tachycardic, tachypneic • HEENT and Neck-- negative • PULM: Inspiratory rales in bases and dullness on left. • Remainder of exam-- negative • No mention of clubbing?

  6. CASE REVIEW • LABS: • Renal function is normal • TP 6.3, ALB 2.5 • Mild transaminitis, total bilirubin 1.9 • WBC mildly up, left shift and lymphopenia, mildly anemic • U/A minimal protein and no sediment

  7. CASE REVIEW • LABS cont: • Negative serologies for Legionella, Histo, Aspergillus, Blasto, Coccidio, Q-Fever, CMV, CVL cath tip, blood, sputum cultures negative • ABG: 7.42/40/61 on 100%, large A-a gradient ???, shunt • CXR: LL alveolar filling process, LLL air bronchograms

  8. HOSPITAL COURSE • Day 1: Started on broad-spectrum Abx and coverage for Legionella • Days 2-3: Fevers continue, Abx changed and Fluconazole added for thrush • Days 4-6: All cultures- negative. ARDS worsens, on PC. HP panel, IV steroids, becomes hypotensive

  9. HOSPITAL COURSE • Days 7-12: LFTs increase, drug effect? and fevers continue • Days 13-22: Multiple PTX, steroids continued, Legionella, Haanta, CMV-- negative • Days 23-25: Worsening O2, bronch unrevealing, persistent hypotension and bradycardia, PEA.

  10. What’s Missing? • HIV??? • Toxicology screen • Echocardiogram • BAL cell count • Lung biopsy

  11. Approach • Alveolar filling process-- pus, blood, protein, fluid, cells (CA, immunologic) • ARDS • Subacute presentations of lung disease

  12. ARDS • Lung injury from some insult that causes inflammatory cascade • Three stages: Exudative (alveolar edema and hyaline membranes) Proliferative (fibrin ) >24 hr Fibrotic (collagen) >2 wks

  13. Infections • CAP: Pnemococcus, H. flu, Staph aureus, Mycoplasma, Legionella, Chlamydia-- treated with multiple broad-spectrum Abx • Viral: Adenovirus, CMV, Haanta, HSV, influenza, RSV, Varicella-- negative titers for CMV, Haanta, wrong time course for flu, no pustules for varicella

  14. Infections • Fungal: Histo, Blasto, Coccidio, Aspergillus-- negative titers, Crypto usually in immunocompromised hosts • TB: possible, but probably too rapid • Parasites: Toxo, Strongyloides, Filaria, Trichinosis, Echinococcus (cysts), Shistosomiasis-- no peripheral eosinophilia • PCP??

  15. Alveolar Hemorrhage • Caused by bleeding in the small pulmonary vessels, leading to syndrome known as Diffuse Alveolar Hemorrhage • “Pulmonary capillaritis” with PMN infiltration • Presentation: Cough, dyspnea and hemoptysis-- often delayed

  16. Alveolar Hemorrhage • Fever may be present if the patient has an underlying vasculitis (Goodpasture’s- anti-GBM Ab, Wegener’s- cANCA) • Drop in hematocrit • BAL returns bloody fluid

  17. Alveolar Hemorrhage

  18. Etiologies of DAH

  19. Alveolar Hemorrhage • No significant fall in hematocrit • No urine sediment to suggest a glomerulonephritis • No evidence of a CTD or vasculitis

  20. Pulmonary Alveolar Proteinosis • Insoluble, proteinaceous material, rich in phospholipids is deposited in alveoli • Very little inflammatory response, just hypoxemia • Degradation of Type II pneumocytes • BAL reveals PAS-positive fluid • Nocardia is common secondary infection

  21. PAP • “CXR looks much worse than the patient” • Patients can be severely hypoxic • Require serial BAL to remove proteinaceous material “whole lung lavage” • Most patients do quite well

  22. CHF • Multiple cardiac causes for pulmonary edema-- LVSF, valvular disease • No report of cardiomegaly, pleural effusions on CXR

  23. Malignancies • Bronchoalveolar cell carcinoma subtype of adenocarcinoma which fills alveoli viral etiology is postulated (retrovirus) role of tobacco is controversial • Primary Pulmonary Lymphoma occurs in immunocompromised hosts

  24. Bronchoalveolar Cell CA

  25. Drug Toxicities • Multiple drugs which cause acute lung injury and ARDS • Predominantly drugs of abuse, chemotherapeutics

  26. Drug Toxicity

  27. Drug Toxicity • “No habits” • No exposure to chemotherapy • Overdose-- not acute

  28. Subacute Interstitial Diseases • Bronchiolitis Obliterans with Organizing Pneumonia • Hypersensitivity Pneumonitis • Acute Eosinophilic Pneumonia • Pneumoconioses • Sarcoidosis • Acute Interstitial Pneumonia

  29. BOOP • Clinicopathologic diagnosis characterized by “pneumonia-like” illness with proliferation of granulation tissue within small airways with chronic inflammation in the surrounding alveoli • Mean age at presentation is 58, M=F • Flu-like illness with cough, fever, malaise, fatigue and weight loss

  30. BOOP • Subacute presentation <2 months duration • Inspiratory crackles • Finger clubbing is rare • Labs are not helpful, with elevation of WBC and eosinophilia in about 50%, elevated ESR

  31. BOOP • CXR shows peripheral, bilateral, alveolar filling with normal lung volumes • CT reveals patchy air-space consolidation with bronchial wall thickening and dilatation • PFTs show restrictive defect, with significant hypoxemia. DLCO is often reduced

  32. BOOP

  33. BOOP • PATH: Intraluminal fibrotic buds (Masson bodies) in respiratory bronchioles and alveoli, foamy cells in alveolar spaces, Type II cell hyperplasia, and fibrinous exudates • Corticosteroid therapy results in complete resolution in >2/3 of patients and is rapid • Relapses can occur when steroids are withdrawn

  34. BOOP • Presentation is consistent • Steroid dose? • Most patients who develop a progressive fatal form of the disease have the diagnosis delayed or missed

  35. Hypersensitivity Pneumonitis • “Extrinsic allergic alveolitis” • Granulomatous, interstitial, bronchiolar, and alveolar-filling lung disease resulting from repeated inhalation of sensitization to a wide variety of organic aerosols and low-molecular weight chemical antigens • Improvement or reversal if antigen exposure ceases, continued exposure leads to progressive fibrosis

  36. HP • List of specific agents is lengthy • Three major categories of antigens: Microbes Animal Proteins LMW Chemicals • Antigen is deposited in alveoli, triggering T-lymphocyte inflammation • Antigen is not digested and acts to fix complement and increase inflammatory response

  37. HP • Presbyterian has 3 HP Panels • “Extended” includes “farmer’s lung” and “bird fancier’s”: Aspergillus fumigatus and flavus, Aureobasidium Actinomyces, Microsporidium Pigeon feather antigen DOES not include any other animal or chemical Ag

  38. HP • Microbes • Animal: Avian antigens most common, also laboratory animal handlers (pelts, serum and excreta), miller’s lung (grain), silk producers (larval secretions and cocoons) and mollusk shell dust • Chemicals: Isocyanates in adhesive, foams and surface coatings and Ag in paints, plastics and resins

  39. HP • Development of disease is dependent upon the antigen, degree of exposure, host factors • Repeated antigen exposure • Immunologic sensitization of host to antigen • Immune-mediated damage to the lung • Exertional dyspnea, cough with sputum production, malaise, fever. Often misdiagnosed as infection, but patients improve b/c of removal from Ag

  40. HP • Chronic presentation leads to crackles on exam, clubbing and cor pulmonale • Unfortunately precipitating Ab tests are non-specific because of huge numbers of Ag MOST IMPORTANT IS HISTORY • CXR and CT reveal GG opacities and micronodules • BAL reveals lymphocyotosis with CD8 predominance

  41. HP

  42. HP • Symptoms usually respond to removal of antigen in acute cases • Chronic forms with repeat exposures have decline in lung function and fibrosis • ?? Role for steroids • This patient has no known exposure, and worsened despite “removal of Ag”

  43. Eosinophilic Pneumonias Acute Eosinophilic Pneumonia • thought to represent a hypersensitivity reaction to an inhaled Ag • Symptoms of fever, myalgias, hypoxemia (severe) for a few hours to days • WBCs elevated, eosinophilia in 1/3 • Diffuse infiltrates • BAL with eosinophils (>25%)

  44. Eosinophilic Pneumonias • May require mechanical ventilation • Respond to Solumedrol at high doses (60-125 mg q 6 hours) • Must document an absence of infection • Do not develop relapses after steroids are tapered

  45. Eosinophilic Pneumonias Chronic Eosinophilic Pneumonia • Subacute presentation with cough, dyspnea, fever and night sweats • Mild hypoxemia • Diffuse, peripheral infiltrates “-- CHF” • Serum and BAL eosinophilia • Response to steroids, but relapses occur

  46. Eosinophilic Pneumonia

  47. Eosinophilic Pneumonias • CXR is not consistent • No response to steroids • No eosinophilia • Presentation too late for AEP and too short for CEP

  48. Sarcoid • Alveolar pattern which is coalescence of reticulonodular disease • Wrong time frame for presentation in our patient

  49. Sarcoid

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