Acute eosinophilic pneumonia

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Acute eosinophilic pneumonia

  1. 1. Eosinophilic PneumoniaAbdalmohsen AbabtainSenior ResidentSaudi Board for Emergency MedicineMarch 31st 2013Supervised by :Dr Ghassan Alghamdi
  2. 2. Case 19 Years old Presented to ER with SOB and Sore throat and fever for 2 Days after coming Back from Makkah Has a Hx of atopy (SOB from Dust) with positive Family history too He Started to smoke cigarettes a week ago (a cigarette/day)
  3. 3. Exam T 36.8 P:122 BP 120/65 RR 30 SpO2 79% RA Patient looks in Respiratory Distress In Tripod Position Equal Bilatral Airentry No Wheeze, No Stridor nor drooling
  4. 4. Labs WBC 25.6 (mostly Nuetrophilic) Lactate 12.3 Urine Tox Negative BG : PH 7.27 Co2 30 Po2 85 Hco3 14
  5. 5. In ER Asthma Management Started In ER Patient continue to Deteriorate Tubed ! HIGH Peak and Airway Pressure !
  6. 6. In ICU H1N1 & Influenza & Parainfluenza and AFB Negative Lactate started to Normalized BAL Done and ShowedEos 14% Acute Eosinophilic Pneumonia !!!
  7. 7. What’s the Fastest Legal StreetCar on Earth ?
  8. 8. Bugatti Veyron Super Sport Max Speed 430km/hr 0-100 km in 2.4 Seconds !! 1200 hp !! Base Price $2,400,000
  9. 9. Eosinophilic Lung Diseases Group of Disorders with high eosinophils in Lung Parenchyma The Defining Characteristics include either:1. Peripheral Blood Eosinophilia with Radiological Pulmonary Abnormality2. Lung tissue eosinophilia in Biopsy3. High eosinophils in BAL
  10. 10. Eosinophilic Lung Diseases Acute Eosinophilic Pneumonia (AEP) Chronic Eosinophilic Pneumonia (CEP) Helminthic Infections (Löfflers syndrome) Non-Helminthic Infection (Coccidioidal infection) Medications (NSAID) Toxins Churg-Strauss Syndrome Allergic Bronchopulmonary Aspergellousis (ABPA)
  11. 11. Toxins Scorpion stings Inhalation of heroin or crack cocaine Inhalation of organic chemicals during rubber manufacture Inhalation of dust or smoke Abuse of 1,1,1-trichloroethane (Scotchguard)
  12. 12. Acute eosinophilic pneumonia Acute febrile illness with  Severe hypoxaemia,  Diffuse pulmonary infiltrates  Increase in bronchoalveolar lavage (BAL) eosinophils  No evidence of infection or Drug ingesion
  13. 13.  Less than 100 cases of AEP have been reported to date The largest series including only 33 patients An epidemiologic study of this disease identified 18 patients with AEP among183,000 US military personnel deployed in Iraq, all of them were smokers, with 78% of them recently beginning to smoke Chest 2008; 133: 1174–1180 JAMA 2004; 292:2997–3005
  14. 14. Inhalational exposuresassociated with AEP Smoke (Most common specially first time) Passive smoking* !! World Trade Center demolition dust Firework Tear gas bomb explosion Gasoline tank cleaning Cave exploration Woodpile moving Chest 2000;117:277–279 *Allergology International. 2010;59:421-423
  15. 15. ApproachHistory :  Chief complain and Associated symptoms  Medication  Chemical and occupational Exposure (NSAID, Dust, Smoke)  Travel Hx (Fungal inf.)  Respiratory Hx (Asthma)  Extrapulmonary Involvment
  16. 16. Physical Exam Fever Tachypnea Bibasilar inspiratory crackles or could be clear in 20% of Patients Hypoxemic respiratory insufficiency is frequently identified at presentation and often requires mechanical ventilation Semin Respir Crit Care Med. 2006 Apr;27(2):142-7.
  17. 17. Labs Patients generally present with an initial neutrophilic leukocytosis Blood eosinophilia, However, the absence of it does not exclude these conditions. Any concomitant glucocorticoid therapy will suppress blood eosinophilia The magnitude of blood eosinophilia is not a reliable means to distinguish the possible etiologies of pulmonary eosinophilia. High ESR !
  18. 18. Imaging At the Start, Subtle reticular or ground glass opacities, often with Kerley B lines Small pleural effusions are common
  19. 19. Imaging High resolution CT ground-glass attenuation, airspace consolidation, poorly defined nodules. The triad of • Interlobular septal thickening, • Bronchovascular bundle thickening, and • Pleural effusionsare most suggestive AEP
  20. 20. Eur Respir J 2013; 41: 402–409
  21. 21. BAL
  22. 22. Biopsy If BAL is not Revealing Biopsy, via a transbronchial or open lung biopsy or VATS approach depending upon the clinical and radiographic findings
  23. 23. Cultures If there have been appropriate geographic exposures for coccidioidomycosis or clinical and radiographic findings suggestive of ABPA, fungal cultures should be obtained
  24. 24. AEP is a diagnosis of exclusionand Requires : An acute febrile illness of short duration (usually less than one week) Hypoxemic respiratory failure Diffuse pulmonary opacities on chest radiograph BAL eosinophilia >25 percent Lung biopsy evidence of eosinophilic infiltrates (acute and/or organizing diffuse alveolar damage with prominent eosinophilia is the most characteristic finding) Absence of known causes of eosinophilic pneumonia, including drugs, infections.
  25. 25. Treatment1. Glucocorticoid administration (preferably after blood extraction) is medically indicated if: Hypoxemia and in respiratory distress If the etiology is either AEP or a medication or toxin-elicited AEPRegimens :  In the absence of respiratory failure, initial treatment is with oral prednisone (40 to 60 mg daily).  In the presence of respiratory failure, methylprednisolone (60 to 125 mg every 6 hours)  Optimal Duration is not yet clear (2-4 wks no diff)* *Eur Respir J 2013; 41: 402–409
  26. 26. After ImprovmentContinue oral prednisone in a dose of 40-60 mg per day for 2-4 weeks2. Supportive Therapy3. Smoking Cessation
  27. 27. Recurrence Relapse is uncommon and is usually associated with resumption of cigarette smoking after initial cessation
  28. 28. Refrences Up to date Eur Respir J 2013; 41: 402–409 Chest 2008; 133: 1174–1180 JAMA 2004; 292:2997–3005 Chest 2000;117:277–279 Semin Respir Crit Care Med. 2006 Apr;27(2):142-7.
  29. 29. Thank You

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