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Ards atef

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Ards atef

  1. 1. ARDSAtef Kamel
  2. 2. Outline Define ARDS and describe the pathological process Know causes of ARDS, and differential diagnosis Understand specific challenges in mechanical ventilation of patients with ARDS Understand treatment strategies and evidence behind
  3. 3. ARDSSevere lung injury characterized by non- cardiogenic pulmonary edema, decreased lung compliance, refractory hypoxemiaDefinition  Acute onset (<2 weeks)  Bilateral infiltrates on chest x ray  PCWP ≤18mmHg  Acute lung injury if PaO2/FiO2 ≤300  ARDS if PaO2/FiO2 ≤200
  4. 4. Most common causes ARDSPneumonia (34%)Sepsis (27%)Aspiration (15%)Trauma (11%)  Pulmonary contusion  Multiple fractures
  5. 5. Causes cont.
  6. 6. Risk factors for ARDS Preexisting lung disease Chronic alcohol use Low serum pH Sepsis 40% of patients with sepsis develop ARDS
  7. 7. Differential diagnosisPulmonary edema from left heart failureDiffuse alveolar hemorrhageLupus pneumonitisDrug-induced pulmonary edema and pneumonitisAcute major pulmonary embolusSarcoidosisInterstitial pulmonary fibrosis
  8. 8. Excluding other diagnoses Echo Central venous catheter Bronchoscopy with bronchoalveolar lavage (to evaluate for hemorrhage, etc) Chest CT
  9. 9. Pathogenesis
  10. 10. Pathophysiology Diffuse alveolar damage Lung capillary damage Inflammation/pulm edema Resulting severe hypoxemia and decreased lung compliance
  11. 11. Phases of ARDS Acute - exudative, inflammatory (0 - 3 days) Subacute - proliferative (4 - 10 days) Chronic - fibrosing alveolitis ( > 10 days)
  12. 12. Phases of ARDS
  13. 13. Exudative phase (Acute Phase) Alveolar-capillary barrier is formed by microvascular endothelium and alveolar epithelium Under normal conditions epithelial barrier is much less permeable than endothelium Epithelium is made up of type I and II cells Type I cells are injured easily and Type II cells are more resistant
  14. 14. Exudative PhaseIn ALI/ARDS – damage to either one occurs resulting in increased permeability of the barrierinflux of protein-rich edema fluid into the alveolar spaceInjury of Type I cells results loss of epithelial integrity and fluid extravasation (edema)Injury of Type II cells then impairs the removal of the edema fluid (loss of surfactant)
  15. 15. Exudative Phase
  16. 16. Proliferative Phase With intervention (mechanical ventilation) there is clearance of alveolar fluid Soluble proteins are removed by diffusion between alveolar epithelial cells Insoluble proteins are removed by endocytosis and transcytosis through epithelial cells and phagocytosis through macrophages
  17. 17. Proliferative Phase Type II cells begin to differentiate into Type I cells and reepithelialize denuded alveolar epithelium Further epithelialization leads to increased alveolar clearance
  18. 18. Proliferative phase
  19. 19. ARDS - OutcomesMost studies - mortality 40% to 60%; similar for children/adultsDeath is usually due to sepsis/MODS rather than primary respiratory
  20. 20. Management of ARDSTreat underlying illness  Sepsis, etcNutritionSupportive careDVT prophylaxisGI prophylaxisMedications
  21. 21. Fluid management“Dry lungs are happy lungs”Conservative fluids:  Improved oxygenation  More ventilator-free days  More days outside ICU  No increase in shock or dialysis  No mortality effects
  22. 22. Pulmonary supportKEYS  Low tidal volumes – 6-8mL/kg ideal body weight  Maintain plateau (end-inspiratory) pressures <30cm H20  Permissive hypercapnia and acidosisDecreased mortality by 22%
  23. 23. Positive End-Expiratory Pressure(PEEP)Titrate PEEP to decrease FiO2  Goal sat 88% with FiO2 <60% Minimize oxygen toxicity  PEEP can improve lung recruitment and decrease end-expiratory alveolar collapse (and therefore right-to-left shunt)  Can also decrease venous return, cause hemodynamic compromise, worsen pulmonary edema
  24. 24. Other Ideas in VentilatorManagement Prone positioning  May be beneficial in certain subgroup, but complications including pressure sores  RCT of 304 patients showed no mortality benefit High-frequency oscillatory ventilation  In RCT, improved oxygenation initially, but results not sustained after 24 hours, no mortality benefit ECMO  RCT of 40 adults showed no benefit
  25. 25. Complications of mechanicalventilationMechanical ventilation causes:  Overdistention of lungs (volutrauma)  Further damaging epithelium  Increased fluid leak, indistinguishable from ARDS damage  Barotrauma  Rupture alveolar membranes  Pneuomothorax, pneumomediastinum  Sheer stress  Opening/closing alveoli  Inflammatory reaction, cytokine releaseOxygen toxicity  Free radical formation
  26. 26. Drug therapy Agents studied:  Corticosteroids  Ketoconazole  Inhaled nitric oxide  Surfactant No benefit demonstrated

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