Acute respiratory distress syndrome


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Acute respiratory distress syndrome

  1. 1. Ahad Aftab Khan Lodhi, MD
  2. 2.  Adult RespiratoryDistress Syndrome Da Nang Lung Transfusion Lung Post Perfusion Lung
  3. 3. Acute respiratory distressCyanosis refractory to oxygen therapyDecreased lung complianceDiffuse infiltrates on chest radiographDifficulties:  lacks specific criteria  controversy over incidence and mortality
  4. 4. 1988: four-point lung injury score  Level of PEEP  PaO2 / FiO2 ratio  Static lung compliance  Degree of chest infiltrates1994: consensus conference simplified the definition
  5. 5. Acute onset  may follow catastrophic eventBilateral infiltrates on chest radiographPAWP < 18 mm HgTwo categories:  Acute Lung Injury - PaO2/FiO2 ratio < 300  ARDS - PaO2/FiO2 ratio < 200
  6. 6. ALIAcute AcutePaO2/FiO2 < 200 < 300mmHgB/l interstitial /alveolar Same infiltratesPCWP <18mmHg Same
  7. 7. The 1994 NAECC Definition LimitationsDescriptive definition - Permits inclusion of a multiplicity of clinical entities ranging from autoimmune disorders to direct and indirect Pulmonary injury Does not address the cause of lung injury Does not provide guidelines on how to define acute The radiological criteria are not sufficiently specific Does not account for the level of PEEP used, which affects the Pao2/Fio2 ratio Does not specify the presence of nonpulmonary organ system dysfunction at the time of diagnosis Does not include the different specific mechanistic pathways involved in producing lung injury
  8. 8. The 1998 NAECC Updated Recommendations The collection of epidemiologic data should be based on the 1994 NAECC definitions.The severity of ALI/ARDS should be assessed by the Lung Injury Score (LIS) or by the APACHE III or SAPS II scoring systems.The factors that affect prognosis should be taken into account.The most important of these are incorporated into the GOCA stratification system. It will be also useful to record: Information relating to etiology (at a minimum, direct or indirect cause) Mortality,including cause of death,and whether death was associated with withdrawal of care Presence of failure of other organs and other time-dependent covariates Follow-up information, including recovery of lung function and quality of life
  9. 9. 3 phases - exudative (0-7 d) - proliferative ( 7-21 d) - fibrotic ( > 21 days)
  10. 10. Acute, exudative phase  rapid onset of respiratory failure after trigger  diffuse alveolar damage with inflammatory cell infiltration  hyaline membrane formation  capillary injury  protein-rich edema fluid in alveoli  disruption of alveolar epithelium
  11. 11. Subacute, Proliferative phase:  persistent hypoxemia  development of hypercarbia  fibrosing alveolitis  further decrease in pulmonary compliance  pulmonary hypertension
  12. 12. Chronic phase  obliteration of alveolar and bronchiolar spaces and pulmonary capillariesRecovery phase  gradual resolution of hypoxemia  improved lung compliance  resolution of radiographic abnormalities
  13. 13. Inciting eventInflammatory mediators  Damage to microvascular endothelium  Damage to alveolar epithelium  Increased alveolar permeability results in alveolar edema fluid accumulation
  14. 14. Type I cell Alveolar macrophageEndothelialCell RBC’s Type II cell Capillary
  15. 15. Type I cell Alveolar macrophageEndothelialCell RBC’s Type II cell Capillary Neutrophils
  16. 16.  Target organ injury from host’s inflammatory response and uncontrolled liberation of inflammatory mediators Localized manifestation of SIRS Neutrophils and macrophages play major roles Complement activation Cytokines: TNF-α, IL-1β, IL-6 Platelet activation factor Eicosanoids: prostacyclin, leukotrienes, thromboxane Free radicals Nitric oxide
  17. 17. Abnormalities of gas exchangeOxygen delivery and consumptionCardiopulmonary interactionsMultiple organ involvement
  18. 18. Hypoxemia: HALLMARK of ARDS  Increased capillary permeability  Interstitial and alveolar exudate  Surfactant damage  Decreased FRC  Diffusion defect and right to left shunt
  19. 19. Pathologic flow dependency  Uncoupling of oxidative dependency  Oxygen utilization by non-ATP producing oxidase systems  Increased diffusion distance for O2 between capillary and alveolus
  20. 20. A = Pulmonary hypertension resulting in increased RV afterloadB = Application of high PEEP resulting in decreased preloadA+B = Decreased cardiac output
  21. 21. Routine blood countsRFTCXRABGCT chestBNP2D EchoBALPCWP
  22. 22. Can be difficult to do. Should always try to make the diagnosis in light of the clinical picture.Need to determine Cardiogenic vs. Non- cardiogenic edema.
  23. 23. Cardiogenic Non-Cardiogenic Diffuse Bilateral patchyBilateral infiltrates infiltrates homogenouslypredominately in lung bases. distributed throughout theKerley B’s. Cardiomegaly. lungs. No Kerley B’s.
  24. 24. Non-cardiogenicPatchy infiltrates in Homogenous pluffy bases shadowsEffusions + Effusions –Kerley B lines + Kerley B lines –Cardiomegaly + Cardiomegaly –Pulmonary vascular No pulm.vascular redistribuition redistribuitionExcess fluid in alveoli Protein,inflammatory cells,fluid
  25. 25. late
  26. 26. Cardiogenic Non-Cardiogenic No septal thickening. DiffuseSeptal thickening. More severe in alveolar infiltrates.lung bases. Atelectasis of dependent lobes usually seen .
  27. 27. RESPIRATORY SUPPORTConventional mechanical ventilationNewer modalities: High frequency ventilation  ECMOInnovative strategies  Nitric oxide  Liquid ventilation  Exogenous surfactant
  28. 28. Monitoring:  Respiratory  Hemodynamic  Metabolic  Infections  Fluids/electrolytes
  29. 29. Treatment of underlying causeCardio-pulmonary supportSpecific therapy targeted at lung injurySupportive therapy.
  30. 30. In the early stages of ARDS the hypoxia may be corrected by 40 to 60% inspired oxygen .If the patient is well oxygenated on <= 60 % inspired oxygen and apparently stable without CO2 retention then ward monitoring may be feasible but close observation( 15 to 30 Min), continuous oximetry, and regular blood gases are required
  31. 31. Inadequate oxygenation ( PaO2- < 60 with FiO2 >=0.6)Rising or elevated PaCO2 ( > 50mmHg) Clinical signs of incipient respiratory failure
  32. 32. The Aims are to increase PaO2 whileminimizing the risk of further lung injury(ventilator induced lung injury)
  33. 33. Spontaneous breathing trial dailyPaO2/FiO2 less than previous daySystolic BP > 90 without vasopressorsNo neuromuscular blockade2 hr trial- with T piece with 1-5cm water CPAP.ABG,RR,SPO2 monitoringIf tolerated for 30 mt,consider extubation
  34. 34. RECOMMENDATION S MECHANICAL VENTILATIONLow tidal volume AMinimize LAFP BHigh PEEP CProne position CRecruitment maneuvers CHigh frequency ventilation D Glucocorticoids D Sufactant D replacement,inhaled NO,others
  35. 35. Low tidal volume mechanical ventilation  In ARDS there is a large amount of poorly compliant (i.e. non-ventilating) lung and a small amount of healthy, compliant lung tissue. Large tidal volume ventilation can lead to over-inflation of the healthy lung tissue resulting in ventilator-induced lung injury of that healthy tissue.PEEP  Setting a PEEP prevents further lung injury due to shear forces by keeping airways patent during expiration
  36. 36. High TV vs low TV (12ml/kg vs 6ml/kg) - 861 pts - mortality rate 39.2 % vs 31%High PEEP vs low PEEP 13cm H20 vs 8 cm H20 –NO differenceAmato etal- optimal PEEP- 15cm H20
  37. 37. Inverse ratio ventilation - reduce peak airway pressure - I: E – 1:1 & 4:1 - severe hypoxemic resp.failurePermissive hypercapnea - controlled hypoventilation - PaCO2 upto 55mmhg - pH upto 7.25 Proning
  38. 38. High flow ventilationECMOPartial fluid ventilation (PLV)
  39. 39.  Fluids – - conservative management - normal or low LAFP - reduce icu stay,duration of ventilation Steroids - Meduri et al study - methyprednisolone-2mg/kg & taper to .5-1mg/kg in 1-2wk
  40. 40. Empirical antibioticsCulture sensitivity & change antibioticsAvoid nephrotoxic drugEnteral feeding
  41. 41. NOKetoconazoleAlbuterolPentoxyphyllineNSAIDSN-acetyl cysteine
  42. 42. Mortality ranges-26 %-44%Risk factors- - advanced age - CKD,CLD - Chronic immunosuppression - chronic alcohol abuseARDS from direct lung injury has double mortality