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Ards azocar


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Ards azocar

  1. 1. ARDS ITACCS Key West 2006 Ruben J Azocar, M.D. Assistant Professor of Anesthesiology Boston University School of Medicine
  2. 2. ARDS: Definitions <ul><li>First described in 1967 as Adult Respiratory Distress Syndrome </li></ul><ul><li>American-European Consensus Conference Committee (1994) criteria </li></ul><ul><ul><li>Acute onset </li></ul></ul><ul><ul><li>Bilateral infiltrates in chest radiography </li></ul></ul><ul><ul><li>Pulmonary-artery wedge pressure<18 mmHg </li></ul></ul><ul><ul><li>Acute lung injury PaO2/FiO2<300 </li></ul></ul><ul><ul><li>Acute respiratory distress syndrome PaO2/FiO2<200 </li></ul></ul>
  3. 3. ARDS: Causes
  4. 4. ARDS:Epidemiology <ul><li>Incidence: 80 per 100,000 </li></ul><ul><li>Outcomes: </li></ul><ul><ul><li>Traditionally 40-60% mortality </li></ul></ul><ul><ul><li>Majority of deaths due to MSOF </li></ul></ul><ul><ul><li>Low tidal volume ventilation decreases mortality </li></ul></ul><ul><ul><li>Other critical care improvements may be involved </li></ul></ul><ul><ul><li>Predictive factors for death: CLD, non pulmonary organ dysfunction, sepsis and advance age </li></ul></ul><ul><ul><li>Survivors: Most of them will have normal pulmonary function within a year </li></ul></ul>
  5. 5. ARDS:Pathogenesis <ul><li>ARDS is the manifestation of SIRS in the lungs </li></ul><ul><ul><li>Influx of protein rich edema into the air spaces due to increased permeability of the alveolar-capillary barrier </li></ul></ul><ul><li>Endothelial damage pathophysiology is similar to that of SIRS/SEPSIS </li></ul>
  6. 6. ARDS:Pathogenesis <ul><ul><li>Epithelial damage </li></ul></ul><ul><ul><ul><li>Loss of epithelial integrity which in normal conditions less permeable than endothelium </li></ul></ul></ul><ul><ul><ul><li>Type II cells injury </li></ul></ul></ul><ul><ul><ul><ul><li>disrupts normal epithelial fluid transport </li></ul></ul></ul></ul><ul><ul><ul><ul><li>reduces production of surfactant </li></ul></ul></ul></ul><ul><ul><ul><li>May lead to septic shock in patients with pneumonia </li></ul></ul></ul><ul><ul><ul><li>Severely injured epithelium lead to disorganized repair and fibrosis </li></ul></ul></ul>
  7. 7. ARDS:Pathogenesis <ul><li>Neutrophils </li></ul><ul><li>Cytokines </li></ul><ul><ul><li>Unbalanced production of pro-inflammatory and anti-inflammatory cytokines </li></ul></ul><ul><li>Ventilator induced injury </li></ul><ul><ul><li>High FiO2 </li></ul></ul><ul><ul><li>Overdistention </li></ul></ul><ul><ul><li>Recruitment/De-recruitment </li></ul></ul><ul><ul><li>May exacerbate and perpetuate ARDS/ALI as well as SIRS/Sepsis/MSOF </li></ul></ul>
  8. 8. ARDS: Exudative Phase <ul><li>The definition applies for the acute “exudative” phase </li></ul><ul><ul><ul><li>Rapid onset </li></ul></ul></ul><ul><ul><ul><li>Hypoxemia refractory to supplemental oxygen </li></ul></ul></ul><ul><ul><ul><li>CXR similar to pulmonary edema </li></ul></ul></ul><ul><ul><ul><li>CT Scan: Alveolar filling, consolidation and atelectasis in the dependent lung zones </li></ul></ul></ul><ul><ul><ul><li>Pathologic findings: </li></ul></ul></ul><ul><ul><ul><ul><li>diffuse alveolar damage with capillary injury and disruption of the alveolar epithelium </li></ul></ul></ul></ul><ul><ul><ul><ul><li>hyaline membranes </li></ul></ul></ul></ul><ul><ul><ul><ul><li>protein rich fluid edema with neutrophils and macrophages </li></ul></ul></ul></ul>
  9. 9. ARDS:Pathogenesis
  10. 10. ARDS: Exudative Phase <ul><li>CT Scan During Acute Phase </li></ul>
  11. 11. ARDS: Fibroproliferative phase <ul><li>Some patients progress to fibrosing alveolitis with persistent hypoxemia, increase alveolar dead space and further decrease in pulmonary compliance </li></ul><ul><li>The process may start as early as 5-7 days </li></ul><ul><li>The alveolar space becomes filled with mesenchymal cells and their products as well as new blood vessels </li></ul>
  12. 12. ARDS: Fibroproliferative phase <ul><li>Pulmonary HTN due to obliteration of pulmonary bed may lead or worsen RV dysfunction </li></ul><ul><li>CXR shows linear opacities. </li></ul><ul><li>PTX and bullae are common </li></ul><ul><li>Histologically, there is fibrosis and partial resolution of the pulmonary edema </li></ul><ul><li>Mortality is 80% if this phase persists </li></ul>
  13. 13. ARDS: Fibroproliferative phase <ul><li>CT Scan during fibroproliferative phase. </li></ul><ul><ul><li>Diffuse interstitial opacities and bullae </li></ul></ul>
  14. 14. ARDS:Pathogenesis
  15. 15. ARDS:Treatment <ul><li>Recent decrease of mortality </li></ul><ul><ul><li>Treatment of underlying cause </li></ul></ul><ul><ul><li>Better supportive ICU Care </li></ul></ul><ul><ul><ul><li>Prevention of infections </li></ul></ul></ul><ul><ul><ul><li>Appropriate nutrition </li></ul></ul></ul><ul><ul><ul><li>GI prophylaxis </li></ul></ul></ul><ul><ul><ul><li>Thromboembolism prophylaxis </li></ul></ul></ul>
  16. 16. ARDS Treatment <ul><li>Mechanical ventilation </li></ul><ul><ul><li>Buys time for the lungs to heal and solve the inciting cause </li></ul></ul><ul><ul><li>“ New” ventilator strategies </li></ul></ul><ul><ul><ul><li>Recognition of ventilator induced injury (VILI) </li></ul></ul></ul><ul><ul><ul><ul><li>Overdistention </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Recruitment/de-recruitment </li></ul></ul></ul></ul><ul><ul><ul><li>Mechanical ventilation induces cytokine response which is worse with alveoli overdistention and recruitment/ de-recruitment of the lung (Ranieri et al JAMA 1999;282: 54-61) </li></ul></ul></ul>
  17. 17. ARDS: Treatment
  18. 18. ARDS: Treatment <ul><ul><ul><li>Protective ventilation </li></ul></ul></ul><ul><ul><ul><ul><li>Smaller tidal volumes </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Avoid overdistention </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Tolerate “permissive hypercarbia” </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>“ Open lung” ventilation </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Avoid alveolar collapse and reopening </li></ul></ul></ul></ul></ul>
  19. 19. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome The Acute Respiratory Distress Syndrome Network N Engl J Med 2000;342:1301-8 <ul><ul><ul><li>Study stopped after 2nd interim analysis </li></ul></ul></ul><ul><ul><ul><li>Reduction of mortality by 22% </li></ul></ul></ul>
  20. 20. NIH/ARDS Network <ul><li>VARIABLES </li></ul><ul><ul><li>Ventilator mode </li></ul></ul><ul><ul><li>Tidal Volume </li></ul></ul><ul><ul><li>Plateau Pressure </li></ul></ul><ul><ul><li>Ventilation rate/pH goal </li></ul></ul><ul><ul><li>Inspiration flow, I:E </li></ul></ul><ul><ul><li>Oxygenation goal </li></ul></ul><ul><ul><li>FIO2/PEEP </li></ul></ul><ul><ul><li>Weaning </li></ul></ul><ul><li>PROTOCOL </li></ul><ul><ul><li>Volume assist control </li></ul></ul><ul><ul><li>< 6mL/Kg body weight </li></ul></ul><ul><ul><li><30 cm H2O </li></ul></ul><ul><ul><li>6-35/min adjusted for pH of 7.30 if possible </li></ul></ul><ul><ul><li>Adjust to 1:1-1:3 </li></ul></ul><ul><ul><li>PaO2>55 and or SpO2>88% </li></ul></ul><ul><ul><li>Combinations </li></ul></ul><ul><ul><li>PS wean when FiO2/PEEP<.40/8 </li></ul></ul>
  21. 21. Ventilation with Lower Tidal Volumes <ul><li>The goal of providing small tidal volumes is to maintain the patient on the steep, more compliant portion of the curve without exceeding the upper inflection point </li></ul>
  22. 22. ARDS:Permissive Hypercapnia <ul><li>Hypercarbic acidosis </li></ul><ul><ul><li>Hypoxemia </li></ul></ul><ul><ul><li>Respiratory failure and arrest </li></ul></ul><ul><ul><li>Decrease myocardial contractility </li></ul></ul><ul><ul><li>Cerebral vasodilatation </li></ul></ul><ul><ul><li>Decrease seizure threshold </li></ul></ul><ul><ul><li>Hyperkalemia </li></ul></ul><ul><li>Permissive hypercapnia </li></ul><ul><ul><li>Supplemental oxygen overcomes CO2 induced hypoxia </li></ul></ul><ul><ul><li>No evolution to respiratory arrest </li></ul></ul><ul><ul><li>Lack of significant deleterious effects </li></ul></ul><ul><ul><li>Is hypercarbia beneficial? </li></ul></ul>
  23. 23. Kregenov et al: Hypercapnic acidosis and mortality in ALI CCM 2006;34:1-7 <ul><li>Patients from the low tidal volume trial </li></ul><ul><li>Hypercapnic acidosis was associated with reduced 28-day mortality in the 12 mL/kg VT group after controlling for comorbidities and severity of lung injury. </li></ul><ul><li>These results are consistent with a protective effect of hypercapnic acidosis against ventilator-associated lung injury that was not found when the further ongoing injury was reduced by 6 mL/kg predicted body weight tidal volumes. </li></ul>
  24. 24. Effect of a protective ventilation strategy on mortality in ARDS Amato M et al NEJM 1998;338:347-354 <ul><li>End-expiratory pressure above the lower inflection point </li></ul><ul><li>VT less 6ml/kg </li></ul><ul><li>Driving pressures less than 20 cm H2O above PEEP </li></ul><ul><li>Permissive hypercarbia </li></ul><ul><li>38% Mortality in protective group vs. 71% in control group </li></ul><ul><li>66% of patient in “protective” group wean off ventilation vs. 29% control group </li></ul><ul><li>No difference in survival at 28 days </li></ul>
  25. 25. Optimal “PEEP” <ul><li>Positive end-expiratory pressure should be high enough to shift the end-expiratory pressure above the lower inflection point by 2-3 cm H 2 O (usually 12-15 cm H 2 O) </li></ul><ul><ul><li>Allows maximal alveolar recruitment </li></ul></ul><ul><ul><li>Decreases injury by repeated opening and closing of small airways </li></ul></ul>
  26. 26. Slutsky, A. S. et al. N Engl J Med 2006;354:1839-1841 Ventilation of an ex Vivo Rat Lung
  27. 27. Higher Vs. Lower PEEP in Patients With ARDS, NEJM 2004 <ul><li>NIH/ARDS Trail Network </li></ul><ul><li>549 patients </li></ul><ul><li>Lower PEEP 8.3+/- 3.2 </li></ul><ul><li>Higher PEEP 13.2+/-3.5 </li></ul><ul><li>All on low tidal volume ventilation </li></ul><ul><li>No differences on clinical outcome </li></ul><ul><li>Trial stop due to rule of futility </li></ul>
  28. 28. BUT….. <ul><li>In the first 171 patients: “the difference in mean PEEP levels between study groups on days 1 to 7 was less that the difference in the previous study that tested the effects of higher PEEP levels and smaller tidal volumes” </li></ul><ul><li>Should have these patients not been included, would have the trial been stopped early? </li></ul>
  29. 29. ARDS: Treatment <ul><li>Recruiting maneuvers </li></ul><ul><li>Prone positioning </li></ul><ul><li>Steroids </li></ul><ul><li>APRV </li></ul><ul><li>Volume cycle vs. pressure cycle </li></ul><ul><li>Inverse-Ratio Ventilation </li></ul><ul><li>Non invasive Positive Pressure Ventilation </li></ul><ul><li>High-Frequency Ventilation </li></ul><ul><li>Tracheal Gas Insufflation </li></ul><ul><li>Extracorporeal gas exchange </li></ul><ul><li>Fluorocarbon Liquid Gas Exchange </li></ul>
  30. 30. Recruitment maneuvers <ul><li>Lung recruitment in patients with ARDS Gattinoni NEJM 2006;354:1175-86 </li></ul><ul><ul><li>Sixty eigt patients with ALI/ARDS underwent whole lung CT Scan during breath holding session at airway pressures of 5, 15 and 45 cm of water </li></ul></ul><ul><ul><li>The percentage of potentially recruitable lung was defined as the proportion of lung tissue in which aeration was restored (Recruited) </li></ul></ul>
  31. 31. Recruitment <ul><li>The potentially recruitable lung was significantly variable but highly correlated with the percentage of lung tissue in which aeration was maintained with PEEP </li></ul><ul><li>Patients with more recruitable lung were sicker </li></ul><ul><ul><li>Greater lung weight </li></ul></ul><ul><ul><li>Poorer oxygenation </li></ul></ul><ul><ul><li>Poorer compliance </li></ul></ul><ul><ul><li>Higher levels of death space </li></ul></ul><ul><ul><li>Higher mortality </li></ul></ul>
  32. 32. Recruitment <ul><li>Knowing the % of recruitable lung might be the key to the effects of PEEP </li></ul><ul><li>PEEP in patients with limited recruitable areas might be of little benefit or harmful </li></ul><ul><ul><li>Overdistention </li></ul></ul><ul><ul><li>Worsening of Shunt </li></ul></ul><ul><ul><li>Authors suggest PEEP of 15 for those recruitables and 10 for those who are not </li></ul></ul>
  33. 33. ARDS Treatment <ul><li>Prone positioning </li></ul><ul><ul><li>In about 70% of ARDS patients, prone positioning improves the PaO 2 by > 20% </li></ul></ul><ul><ul><li>Consider a lung recruitment strategy, since allows a decrease in FiO 2 and PEEP </li></ul></ul><ul><ul><li>A more uniform distribution of pleural pressure gradients, result in greater ventilation of dependent lung than in supine positioning </li></ul></ul>
  34. 34. ARDS Treatment <ul><li>Gattinoni et al, NEJM 2001;345:568-573 </li></ul><ul><ul><li>304 patients with ARDS </li></ul></ul><ul><ul><li>Prone group: at least six hours/day for ten days </li></ul></ul><ul><ul><li>Better oxygenation in the prone patients </li></ul></ul><ul><ul><li>Similar incidence of complications </li></ul></ul><ul><ul><li>No improvement in survival </li></ul></ul><ul><ul><li>However patient only prone for 7 hours a day and up to 10 days </li></ul></ul>
  35. 35. ARDS Treatment <ul><li>Fluid and hemodynamic management </li></ul><ul><ul><li>Optimal fluid management is controversial </li></ul></ul><ul><ul><ul><li>There is data supporting fluid restriction as a mean to minimize lung edema </li></ul></ul></ul><ul><ul><ul><li>However maintenance and preservation of oxygen delivery may require fluid administration </li></ul></ul></ul><ul><ul><li>Euvolemia, judicious use of vasopressors </li></ul></ul><ul><ul><li>Effects of ventilation in circulation </li></ul></ul><ul><ul><li>To Swan or not to Swan </li></ul></ul>
  36. 36. Swan and ARDS <ul><li>PAC versus CVP to guide treatment of ALI NEJM 2006; 354: 2213-2224 </li></ul><ul><ul><li>1000 patients </li></ul></ul><ul><ul><li>Mortality at 60 days was similar between groups, as well as the ventilator free days and days not spent in the ICU </li></ul></ul><ul><ul><li>Fluid balances were similar among the groups </li></ul></ul><ul><ul><li>PAC had double complications mainly arrhythmias </li></ul></ul>
  37. 37. APRV <ul><li>It uses a release of airway pressure from an elevated baseline to simulate expiration. </li></ul><ul><li>The elevated baseline facilitates oxygenation avoids collapsing of alveoli and the timed releases aid in carbon dioxide removal. </li></ul><ul><li>Potential advantages of APRV include lower airway pressures, lower minute ventilation, minimal adverse effects on cardio-circulatory function. </li></ul><ul><li>Airway pressure release ventilation is consistent with lung protection strategies that strive to limit lung injury associated with mechanical ventilation, particularly recruitment/derecruitment </li></ul><ul><li>More (larger) studies are needed to define its role in ALI/ARDS </li></ul>
  38. 38. ARDS:Treatment <ul><li>Inhaled nitric oxide and other vasodilators </li></ul><ul><ul><li>Most ARDS/ALI patient may have mild to moderate pulmonary HTN </li></ul></ul><ul><ul><li>Improvement in oxygenation was small and not sustained </li></ul></ul><ul><ul><li>No change on mortality or duration of mechanical ventilation </li></ul></ul><ul><ul><li>May be used as “rescue” therapy </li></ul></ul><ul><li>Surfactant </li></ul><ul><ul><li>Successful in neonatal respiratory distress syndrome </li></ul></ul>
  39. 39. ARDS: Treatment <ul><li>Glucocorticoid s </li></ul><ul><ul><li>No benefits in acute phase </li></ul></ul><ul><ul><li>Some evidence of improvement during proliferative phase (Meduri et al JAMA 1998;280:159-165) </li></ul></ul><ul><ul><ul><li>Methylprednisolone 2mg/kg initially for 32 days </li></ul></ul></ul><ul><ul><ul><li>Improvement in Lung injury scores, MOSD scores and mortality </li></ul></ul></ul><ul><ul><ul><li>Benefits may be noticed by day 3 </li></ul></ul></ul><ul><ul><li>High risk of infection </li></ul></ul><ul><ul><li>? May consider a short course of high dose as rescue therapy </li></ul></ul>
  40. 40. ARDS: Steroids <ul><li>Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome NEJM 2006.354: 1671-84 </li></ul><ul><ul><li>180 patients </li></ul></ul><ul><ul><li>Mortality at 60 days </li></ul></ul><ul><ul><ul><li>28.9% mortality in the placebo group and 29.2% in the methylprednisolone group </li></ul></ul></ul><ul><ul><ul><li>Methylprednisolone increased the number of ventilator free and shock free days during the first 28 days in association with an improvement in oxygenation, respiratory system compliance and blood pressure with fewer vasopressor days </li></ul></ul></ul><ul><ul><ul><li>But methylprednisolone was associated with a significant increase 60-180 days mortality in patients enrolled at least 14 days after the onset of ARDS </li></ul></ul></ul>
  41. 41. ARDS: Treatment <ul><li>Anti-inflammatory Strategies </li></ul><ul><ul><li>Prostaglandin agonist/inhibitors </li></ul></ul><ul><ul><li>Lisofylline and pentoxifylline </li></ul></ul><ul><ul><li>Anti IL-8 </li></ul></ul><ul><li>Antioxidant therapy </li></ul><ul><li>Enhanced resolution of pulmonary edema </li></ul><ul><li>Enhanced repair of alveolar epithelial barrier </li></ul>
  42. 42. ARDS: Questions