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ARDS
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ARDS

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  1. Journal reading: Acute Lung injury and the acute respiratory distress syndrome : a clinical review Lancet 2007; 369: 1553–65 Arthur P Wheeler, Gordon R Bernard <ul><ul><li>96/6/20 Morning meeting </li></ul></ul><ul><ul><li>報告: R1 林軒名 </li></ul></ul><ul><ul><li>指導: VS 徐錦池主任 </li></ul></ul>
  2. Content <ul><li>Definition and diagnosis </li></ul><ul><li>Histopathology </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Treatment </li></ul><ul><ul><li>Supportive care </li></ul></ul><ul><ul><li>Mechanical ventilation, oxygen, and PEEP </li></ul></ul><ul><ul><li>Effects of PEEP </li></ul></ul><ul><ul><li>Prone positioning and recruitment maneuvers </li></ul></ul><ul><ul><li>Corticosteroids </li></ul></ul><ul><ul><li>Extracorporeal support </li></ul></ul><ul><ul><li>Fluid management </li></ul></ul><ul><ul><li>Vasodilators </li></ul></ul><ul><ul><li>Weaning from ventilation and other treatments </li></ul></ul><ul><li>Conclusion </li></ul>
  3. Definition & diagnosis
  4. Simplified consensus definition of acute lung injury <ul><li>Acute onset (less than 7 days) </li></ul><ul><li>Severe hypoxemia (PaO2/FIO2 <300 for acute lung injury, or 200 for acute respiratory distress syndrome) </li></ul><ul><li>Diffuse bilateral pulmonary infiltrates on frontal radiograph consistent with </li></ul><ul><li>pulmonary edema (these can be patchy and asymmetric, and pleural effusions can be present) </li></ul><ul><li>Absence of left atrial hypertension (pulmonary-artery wedge pressure <18 mm Hg if measured) </li></ul>
  5. CXR of ARDS
  6. Causes of acute lung injury : <ul><li>Direct </li></ul><ul><li>Pneumonia </li></ul><ul><li>Gastric aspiration </li></ul><ul><li>Drowning </li></ul><ul><li>Fat and amniotic-fluid embolism </li></ul><ul><li>Pulmonary contusion </li></ul><ul><li>Alveolar hemorrhage </li></ul><ul><li>Smoke and toxic gas inhalation </li></ul><ul><li>Reperfusion (pleural effusion drainage, embolectomy) </li></ul><ul><li>Unilateral lung re-implantation </li></ul><ul><li>Indirect </li></ul><ul><li>Severe sepsis </li></ul><ul><li>Transfusions </li></ul><ul><li>Shock </li></ul><ul><li>Salicylate or narcotic overdose </li></ul><ul><li>Pancreatitis </li></ul>
  7. Differential diagnosis of ARDS <ul><li>Fluid: </li></ul><ul><ul><li>Left ventricular failure </li></ul></ul><ul><ul><li>Intravascular volume overload </li></ul></ul><ul><ul><li>Mitral stenosis </li></ul></ul><ul><ul><li>Veno-occlusive disease </li></ul></ul><ul><ul><li>Lymphangitic carcinoma </li></ul></ul><ul><li>Lung </li></ul><ul><ul><li>Interstitial and airway diseases </li></ul></ul><ul><ul><li>Hypersensitivity pneumonitis </li></ul></ul><ul><ul><li>Acute eosinophilic pneumonia </li></ul></ul><ul><ul><li>Bronchiolitis obliterans with organising pneumonia </li></ul></ul>
  8. Histopathology & Pathophysiology <ul><li>Exaudative phase </li></ul><ul><li>Fibroproliferative phase </li></ul>
  9. Progress and Staging <ul><li>“ Exudative&quot; stage: 0-1 wks, </li></ul><ul><ul><li>Diffuse alveolar damage </li></ul></ul><ul><ul><li>Pulmonary dysfunction : in 24 to 48 hours. </li></ul></ul><ul><ul><li>Tachypnea, dyspnea, and hypoxemia requiring high concentrations of supplemental oxygen ; dry cough and chest pain </li></ul></ul><ul><li>“ Proliferative&quot; stage: 1-3 wks </li></ul><ul><ul><li>Resolution of pulmonary edema </li></ul></ul><ul><ul><li>Oxygenation ↑ after pulmonary edema ↓ </li></ul></ul><ul><ul><li>Most patients remain ventilator-dependent due to continued hypoxemia, high minute ventilation requirements, and poor lung compliance </li></ul></ul>
  10. Progress and Staging <ul><li>“ Fibrotic&quot; stage: </li></ul><ul><ul><li>obliteration of normal lung architecture </li></ul></ul><ul><ul><li>Diffuse fibrosis, and cyst formation. </li></ul></ul><ul><ul><li>Patient may have a large dead space and a high minute ventilation requirement. </li></ul></ul>
  11.  
  12. Acute stage :exudative phase <ul><li>Diffuse neutrophilic alveolar infiltrate, with hemorrhage, and the accumulation of a protein-rich pulmonary edema . </li></ul><ul><li>Cytokines (eg, TNF, IL-1, IL-8) incites and perpetuates inflammation </li></ul><ul><li>Reduces surfactant production , and inactivates remaining surfactant, thereby promoting widespread atelectasis </li></ul><ul><li>Elastases damage the structural framework of the lung, and both alveolar capillary and epithelial-cell injury . </li></ul>
  13. Acute stage :exudative phase <ul><li>Damage of the epithelial barrier exacerbates the tendency for alveolar flooding, and delays recovery by impairing fluid clearance . </li></ul><ul><li>A procoagulant tendency is seen in the lung as concentrations of anticoagulant proteins (protein C, protein S) fall and expression of procoagulant proteins (tissue factor) and anti-fibrinolytic proteins ( plasminogen activator inhibitor 1) increases. </li></ul>
  14. Acute stage :exudative phase <ul><li>Leakage of edema fluid into the lung and inflammatory cellular infiltrates cause diffusion abnormalities and ventilation perfusion mismatch </li></ul><ul><li>Cellular infiltration, diffuse atelectasis, and edema fluid reduce thoracic compliance . </li></ul><ul><li>Regional alveolar over-distention and small-vessel thrombosis increases dead space . </li></ul><ul><li>Hypoxemic vasoconstriction and capillary obliteration raise pulmonary-artery pressures </li></ul>
  15. Chronic stage: Fibroproliferative phase <ul><li>Chronic inflammation, fibrosis, and neovascularisation. </li></ul><ul><li>We do not know why most survivors rapidly resolve the acute inflammation but some progress to the chronic phase. </li></ul>
  16.  
  17. Treatment <ul><li>Supportive care </li></ul><ul><li>Mechanical ventilation, oxygen, and PEEP </li></ul><ul><li>Effects of PEEP </li></ul><ul><li>Prone positioning and recruitment maneuvers </li></ul><ul><li>Corticosteroids </li></ul><ul><li>Extracorporeal support </li></ul><ul><li>Fluid management </li></ul><ul><li>Vasodilators </li></ul><ul><li>Weaning from ventilation and other treatment </li></ul>
  18. Supportive care <ul><li>Treat underline disease </li></ul><ul><li>Prevent complication </li></ul><ul><ul><li>DVT </li></ul></ul><ul><ul><li>GI bleeding </li></ul></ul><ul><ul><li>Pressure ulcer </li></ul></ul><ul><ul><li>Aspiration pneumonia </li></ul></ul><ul><li>Nutrition support </li></ul><ul><li>Sedation </li></ul><ul><ul><li>Decreased ICU course and MV course </li></ul></ul><ul><li>Aggressive control blood sugar </li></ul>
  19. Mechanical ventilation: high Tv <ul><li>Traditional ventilation: </li></ul><ul><ul><li>10-15 ml/kg </li></ul></ul><ul><ul><li>To keep PaO2/FiO2 </li></ul></ul><ul><li>Evidence of side effect: </li></ul><ul><ul><li>Lung CT scans of patients with acute lung injury showed the heterogeneous nature of alveolar effects. </li></ul></ul><ul><ul><li>High-volume ventilation led to local and systemic inflammation , sometimes referred to as biotrauma . </li></ul></ul>
  20. Mechanical ventilation: low Tv <ul><li>Low Tidal volume ventilation </li></ul><ul><ul><li>Tv: 5-7ml/kg </li></ul></ul><ul><ul><li>Add PEEP to keep PaO2/FiO2 </li></ul></ul><ul><li>Benefits </li></ul><ul><ul><li>Avoid barotraumas </li></ul></ul><ul><ul><li>Decreased hospital days and days under ventilator . </li></ul></ul><ul><ul><li>Smaller tidal volumes were associated with reduced edema formation. </li></ul></ul>
  21. Effects of PEEP <ul><li>By recruiting atelectatic alveolar and increasing functional residual capacity of supine patients, PEEP reduces intrapulmonary shunting and improves oxygenation in many lung diseases. </li></ul><ul><li>PEEP can decrease venous return and increase right-ventricular impedance , thereby causing hypotension </li></ul>
  22. Higher & lower PEEP in patients with ARDS <ul><li>All patients were ventilated with 6 mL/kg predicted bodyweight of tidal volume but were randomly assigned to receive treatment using the PEEP-FIO2 scale. </li></ul><ul><li>In the first 4 days of the trial </li></ul><ul><ul><li>the higher PEEP group had higher pressure (14 mm Hg) than in the lower PEEP group (8 mm Hg), and oxygenation and lung compliance were better in the higher PEEP group. </li></ul></ul><ul><ul><li>no benefit on survival, time on ventilator, or non-pulmonary organ function. </li></ul></ul><ul><li>ventilated with 6 mL/kg predicted body weight, both groups had mortality rates of about 25%, the same with past report </li></ul>ARDS Network. Higher versus lower positive end expiratory pressures in patients with acute respiratory distress syndrome. N Engl J Med 2004; 351: 327–36.
  23. Effects of PEEP <ul><li>NO Evidence of high PEEP is harmful in ARDS patient. </li></ul><ul><li>We do not advocate routine use of recruitment manouevres; however, recruitment manouevres are not unreasonable in patients with refractory hypoxemia in an attempt to improve oxygenation. </li></ul>
  24. Prone positioning <ul><li>Most lung infiltrates in dependent lung regions. </li></ul><ul><li>prone positioning of patients </li></ul><ul><ul><li>Redistributes blood flow and ventilation to the least affected areas of the lung </li></ul></ul><ul><ul><li>Promotes secretion clearance </li></ul></ul><ul><ul><li>Shifts the weight of the mediastinal contents anteriorly. </li></ul></ul>
  25. Prone positioning <ul><li>Measurable improvement in oxygenation (PaO2/FIO2 ratio) shortly after prone positioning </li></ul><ul><li>No study has shown that prone positioning improves important clinical outcomes such as survival, time on ventilation, or time in the ICU . </li></ul><ul><li>no recommendations can be offered on the optimum timing or duration of prone positioning until large randomised trials provide more information. </li></ul>
  26. Corticosteroids <ul><li>Treatment of patients at risk of acute lung injury with high doses of glucocorticoids does not decrease the frequency of the disease </li></ul><ul><li>We do not recommend corticosteroids to prevent or treat early acute lung injury. </li></ul><ul><li>Corticosteroids could offer some benefit with respect to gas exchange and homodynamic stability . </li></ul>
  27. Efficacy and Safety of Corticosteroids for Persistent ARDS <ul><li>Randomly assigned 180 patients with ARDS of at least seven days’ duration to receive either methylprednisolone or placebo in a double-blind fashion. </li></ul><ul><li>The primary end point was mortality at 60 days </li></ul><ul><li>Secondary end points included the number of ventilator-free days and organ-failure–free days , biochemical markers of inflammation and fibroproliferation, and infectious complication </li></ul>N Engl J Med 2006;354:1671-84.
  28. Results <ul><li>At 60 days, the hospital mortality rate was 28.6 percent in the placebo group (95 percent confidence interval, 20.3 to 38.6 percent) and 29.2 percent in the methylprednisolone group (95 percent confidence interval, 20.8 to 39.4 percent; P = 1.0 ); </li></ul><ul><li>At 180 days, the rates were 31.9 percent (95 percent confidence interval, 23.2 to 42.0 percent) and 31.5 percent (95 percent confidence interval, 22.8 to 41.7 percent; P = 1.0 ), respectively. </li></ul>
  29. Results <ul><li>Methylprednisolone was associated with significantly increased 60- and 180-day mortality rates among patients enrolled at least 14 days after the onset of ARDS. </li></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 days of vasopressor therapy. </li></ul><ul><li>As compared with placebo, methylprednisolone did not increase the rate of infectious complications but was associated with a higher rate of neuromuscular weakness. </li></ul>
  30. Conclusion <ul><li>These results do not support the routine use of methylprednisolone for persistent ARDS despite the improvement in cardiopulmonary physiology. </li></ul><ul><li>In addition, starting methylprednisolone therapy more than two weeks after the onset of ARDS may increase the risk of death. </li></ul>
  31. Extracorporeal support <ul><li>Extracorporeal support has not conclusively shown outcome benefits and has been associated with substantial risks (eg, infection, bleeding) and costs, therefore, it cannot be recommended. </li></ul>
  32. Fluid management <ul><li>Lung capillary permeability increases, lung water accumulates to a greater degree than usual at lower pressures of pulmonary-artery occlusion. </li></ul><ul><li>Reduction of lung water improves oxygenation, and lung compliance. </li></ul><ul><li>prompt resuscitation of hemodynamically unstable patients improves outcome, whereas the same resuscitative efforts given later might not be helpful and could be harmful. </li></ul>
  33. Comparison of Two Fluid-Management Strategies in Acute Lung Injury <ul><li>A conservative and a liberal strategy of fluid management using explicit protocols applied for seven days in 1000 patients with acute lung injury. </li></ul><ul><li>The primary end point was death at 60 days. </li></ul><ul><li>Secondary end points included the number of ventilator-free days and organ-failure–free days and measures of lung physiology. </li></ul>(NEJM 354;24 June 15, 2006)
  34. (NEJM 354;24 June 15, 2006)
  35. (NEJM 354;24 June 15, 2006)
  36. Results <ul><li>Although there was no significant difference in the primary outcome of 60-day mortality, the conservative strategy of fluid management improved lung function and shortened the duration of mechanical ventilation and intensive care without increasing nonpulmonary-organ failures. </li></ul><ul><li>These results support the use of a conservative strategy of fluid management in patients with acute lung injury. </li></ul>(NEJM 354;24 June 15, 2006)
  37. Vasodilators <ul><li>Non-selective (nitroprusside, hydralazine) and semiselective (nitric oxide, prostaglandin E1, prostacyclin) vasodilators </li></ul><ul><li>NO: </li></ul><ul><ul><li>oxygenation and pulmonary vascular resistance are improved </li></ul></ul><ul><ul><li>do not translate into better clinical outcomes . </li></ul></ul>
  38. Unproven treatments for acute respiratory distress syndrome <ul><li>Ketoconazole </li></ul><ul><li>Pentoxyfi lline and lisofylline </li></ul><ul><li>Nutritional modification </li></ul><ul><li>Antioxidants </li></ul><ul><li>Neutrophil elastase inhibition </li></ul><ul><li>Surfactant </li></ul><ul><li>Liquid ventilation </li></ul><ul><li>β-adrenergic agonists </li></ul><ul><li>Nitric oxide </li></ul>
  39. Conclusion <ul><li>treatment of the underlying cause </li></ul><ul><li>Prevention of nosocomial complications </li></ul><ul><li>Reduction of tidal volume to 6 mL/kg predicted bodyweight (or lower if needed), to achieve a plateau pressure of less than 30 cm H2O. </li></ul><ul><li>This reduced tidal volume is coupled with use of the minimum FIO2-PEEP combination that is sufficient to achieve a saturation of 88–95. </li></ul><ul><li>Conservative strategy of fluid management: to keep dry lung. </li></ul>

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