senior talk- ARDS.ppt


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senior talk- ARDS.ppt

  1. 1. Acute Respiratory Distress syndrome Meron Yimen PGY 3
  2. 2. Historical Background <ul><li>Since WWI physicians have recognized a syndrome of respiratory distress, diffuse lung infiltrates and respiratory failure in pt with various medical conditions including from battle trauma to severe sepsis, pancreatitis, massive transfusions etc </li></ul><ul><li>In 1967, Ashbaugh et al become the first to describe the syndrome which they referred to as adult respiratory distress syndrome in 12 such patients (1) </li></ul>
  3. 3. Historical Background <ul><li>in 1971, Ashbaugh and Petty further defined the syndrome in a form that summarized the clinical features well (but lacked specific criteria to identify pts systematically) (2) </li></ul><ul><li>        -  severe dyspnea         -  cyanosis refractory to O2         - decreased pulm compliance         - diffuse alveolar infiltrates on CXR         - atelectasis, vascular congestion, hemorrhage, pulm edema and hyaline membranes at autopsy </li></ul>
  4. 4. Historical Background <ul><li>in 1988, a more expanded definition was proposed that quantified the physiologic respiratory impairment through the use of 4-point lung injury scoring system (3)         - level of PEEP         - P/F RATIO             - static lung compliance         - degree of infiltration on CXR         - *also included nonpulm organ dysfunction </li></ul><ul><li>This definition still had its shortcomings in that it specific criteria to r/o cardiogenic pulm edema and is not predictive of outcomes </li></ul>
  5. 5. Historical Background <ul><li>1994 American - European Consensus Conference Committee (AECC)  came up with definition that became widely accepted </li></ul><ul><li>also changed the name to acute respiratory distress syndrome from adult respiratory distress </li></ul><ul><li>defined it as a spectrum of ALI         - Acute onset         - bilateral infiltrates on CXR         - PCWP =< 18 mmHg         - P/F ratio =< 200 ( ALI if P/F ratio =< 300 ) </li></ul>
  6. 6. Epidemiology <ul><li>the problem has always been how to identify the cases </li></ul><ul><li>attempts at extrapolating incidences based on the various definitions offered above have resulted in various numbers (1.5-8.3 - 75/100,000) </li></ul><ul><li>the first study using the 1994 AECC definition was done in Scandinavia (reported incidence of 17.6/100,000 for ALI and 13.5/100,000 for ARDS (4) </li></ul><ul><li>More recently the ARDSNet study (done in King County, Washington 4/1999-7/2000) reported much higher numbers for age-adjusted incidence (5)         -  ALI - 86.2/100,000 person-yrs (reaching 306 in ages 75-84)         -  estimated annually cases base on these stats 190,600         -  mortality 74, 500/yr </li></ul>
  7. 7. Morbidity and Mortality <ul><li>prior to ARDSNet study - mortality rate for ARDS has been estimated at 40-70% </li></ul><ul><li>ARDSNet found a much lower overall mortality rate 30-40% (6) </li></ul><ul><li>notable that MR increases with age: 24 % ages 15-19 and 60 % in > 85 yrs </li></ul><ul><li>2/2 co-morbid conditions </li></ul><ul><li>Mortality is attributable to sepsis or multiorgan dysfunction </li></ul>
  8. 8. Morbidity and Mortality <ul><li>Morbidity </li></ul><ul><li>- prolonged hospital course- nosocomial infections especially VAP </li></ul><ul><li>- wt loss </li></ul><ul><li>- muscle weakness </li></ul><ul><li>- functional impairment in months following </li></ul>
  9. 9. Causes <ul><li>DIRECT LUNG INJURY </li></ul><ul><li>COMMON </li></ul><ul><li>PNA </li></ul><ul><li>Aspiration </li></ul><ul><li>LESS COMMON </li></ul><ul><li>Pulm contusion </li></ul><ul><li>Fat emboli </li></ul><ul><li>Near-drowning </li></ul><ul><li>Inhalation injury </li></ul><ul><li>Reperfusion injury (transplant etc) </li></ul><ul><li>INDIRECT LUNG INJURY </li></ul><ul><li>COMMON </li></ul><ul><li>Sepsis* </li></ul><ul><li>Severe trauma with shock and multiple transfusions </li></ul><ul><li>LESS COMMON </li></ul><ul><li>Cardiopulm bypass </li></ul><ul><li>Acute pancreatitis </li></ul><ul><li>Transfusions </li></ul><ul><li>Drug overdose </li></ul>
  10. 10. Pathophysiology <ul><li>Diffuse alveolar damage </li></ul><ul><li>Lung capillary damage </li></ul><ul><li>Inflammation/pulm edema* </li></ul><ul><li>Resulting severe hypoxemia and decreased lung compliance </li></ul>
  11. 11. Pathophysiology <ul><li>Occurs in stages </li></ul><ul><li>Exudative ( Acute Phase) </li></ul><ul><li>Proliferative </li></ul><ul><li>Fibrotic </li></ul><ul><li>Recovery </li></ul>
  12. 12. Exudative phase (Acute Phase) <ul><li>Alveolar-capillary barrier is formed by microvascular endothelium and alveolar epithelium </li></ul><ul><li>Under normal conditions epithelial barrier is much less permeable than endothelium </li></ul><ul><li>Epithelium is made up of type I and II cells </li></ul><ul><li>Type I cells are injured easily and Type II cells are more resistant </li></ul>
  13. 13. Exudative Phase <ul><li>In ALI/ARDS – damage to either one occurs resulting in increased permeability of the barrier </li></ul><ul><li>influx of protein-rich edema fluid into the alveolar space </li></ul><ul><li>Injury of Type I cells results loss of epithelial integrity and fluid extravasation (edema) </li></ul><ul><li>Injury of Type II cells then impairs the removal of the edema fluid </li></ul>
  14. 14. Exudative Phase <ul><li>Dysfunction of Type II cells also leads to reduced production and turnover of surfactant which leads to alveolar collapse </li></ul><ul><li>If severe injury to epithelium occurs – disorganized/insufficient epithelial repair occurs resulting in fibrosis </li></ul><ul><li>In addition to inflammatory process, there is evidence that the coagulation system is also involved </li></ul>
  15. 15. Exudative Phase
  16. 16. Fibrotic Phase <ul><li>After acute phase, some pt will have uncomplicated course and rapid resolution </li></ul><ul><li>Some pts will progress to fibrotic lung injury </li></ul><ul><li>Such injury occurs histologically as early as 5-7 days </li></ul>
  17. 17. Fibrotic Phase <ul><li>Intense inflammation leads to obliteration of the normal lung architecture </li></ul><ul><li>Alveolar space is filled with mesenchymal cells and their products </li></ul><ul><li>Reepithelialization and new blood vessel formation occurs in disorganized manner </li></ul><ul><li>Fibroblasts also proliferate, collagen is deposited resulting in thickening of interstitium </li></ul><ul><li>Fibrosing alveolitis and cyst formation </li></ul>
  18. 18. Proliferative Phase <ul><li>With intervention (mechanical ventilation) there is clearance of alveolar fluid </li></ul><ul><li>Soluble proteins are removed by diffusion between alveolar epithelial cells </li></ul><ul><li>Insoluble proteins are removed by endocytosis and transcytosis through epithelial cells and phagocytosis through macrophages </li></ul>
  19. 19. Proliferative Phase <ul><li>Type II cells begin to differentiate into Type I cells and reepithelialize denuded alveolar epithelium </li></ul><ul><li>Further epithelialization leads to increased alveolar clearance </li></ul>
  20. 20. Proliferative Phase
  21. 21. Consequences <ul><li>Impaired gas exhange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic deadspace </li></ul><ul><li>Decreased lung compliance – due to the stiffness of poorly or nonaerated lung </li></ul><ul><li>Pulm HTN – 25% of pts, due to hypoxic vasoconstriction, Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction </li></ul>
  22. 22. Clinical Features <ul><li>Pts are critically ill </li></ul><ul><li>develop rapidly worsening tachypnea, dyspnea, hypoxia requiring high conc of O2 </li></ul><ul><li>Occurs within hours to days ( usually12-48 hours) of inciting event </li></ul><ul><li>Early clinical features reflects precipitants of ARDS </li></ul><ul><li>Physical exam shows cyanosis, tachycardia, tachypnea and diffuse rales and other signs of inciting event </li></ul>
  23. 23. Work Up <ul><li>ARDS is a clinical diagnosis </li></ul><ul><li>No specific lab abnormality beyond disturbance in gas exchange is evident </li></ul><ul><li>Radiologic findings may be consistent but not diagnostic </li></ul><ul><li>w/u therefore is useful in identifying inciting event or excluding other causes of lung injury </li></ul>
  24. 24. Work Up Useful diagnostic workup may include <ul><li>- CBC, Renal panel, Coags, LFTs, pancreatitic enzymes, UA </li></ul><ul><li>Blood cx, urine cx </li></ul><ul><li>Tox screen </li></ul><ul><li>BNP (low BNP may point to ARDS) (8) </li></ul><ul><li>TTE </li></ul><ul><li>CXR </li></ul><ul><li>CT </li></ul><ul><li>Bronchoscopy/BAL </li></ul><ul><li>CVP, PCWP </li></ul>
  25. 25. CXR findings diffuse, fluffy alveolar infiltrates with prominent air bronchograms
  26. 26. CT findings
  27. 27. Treatment <ul><li>No specific therapy for ARDS exists </li></ul><ul><li>Mainstay of treatment is supportive care </li></ul><ul><li>Treat underlying/inciting conditions </li></ul>
  28. 28. Treatment – Fluids <ul><li>ARDSNet study comparing a conservative and a liberal fluid stategies (9) </li></ul><ul><li>Rationale behind this study is decreasing pulm edema by restricting fluids </li></ul><ul><li>Randomized, using explicit protocols applied for 7 days in 1000 pts in ALI </li></ul><ul><li>Randomization was into fluid liberal vs fluid conservative </li></ul><ul><li>Primary end point was death at 60 days </li></ul><ul><li>Secondary end points included vent-free days, organ failure free days </li></ul>
  29. 29. Treatment – Fluids <ul><li>Study did not show any significant difference in 60 day mortality </li></ul><ul><li>However pts treated with fluid conservative strategy had an improved oxygenation index and lung injury score </li></ul><ul><li>In addition, there was an increased in vent-free days without increase in nonpulm organ failures </li></ul><ul><li>Also noted in this study is that in fluid conservative group the fluid balance was more even than negative which may indicate the observed benefit may be underestimated </li></ul>
  30. 30. Treatment - Ventilation <ul><li>Goals of ventilation in ARDS are to: </li></ul><ul><li>Maintain oxygenation by keeping O2 sats at 85-90% </li></ul><ul><li>Avoiding oxygen toxicity and complication of mechanical ventilation – decreasing FiO2 to less than 65% within the 1 st 24-48 hours </li></ul>
  31. 31. Treatment - Ventilation <ul><li>Known – TV in normal persons at rest is 6-7ml/kg </li></ul><ul><li>But historically TV of 12-15ml/kg was recommended in ALI/ARDS </li></ul><ul><li>It was also recognized this strategy of high TV causes Vent-associated lung injury as early as 1970s </li></ul><ul><li>Then came the land mark ARDSNet study which compared traditional TV to lower TV </li></ul>
  32. 32. Treatment – Ventilation ARDSNet ( low vs traditional TV) <ul><li>861 pts with ALI/ARDS at 10 centers </li></ul><ul><li>Patients randomized to tidal volumes of 12 mL /kg or 6 ml/kg (volume control, assist control) </li></ul><ul><li>In group receiving lower TV, plateau pressure cannot exceed 30 cm H2O </li></ul><ul><li>22% reduction in mortality in patients receiving smaller tidal volume </li></ul><ul><li>Number-needed to treat: 12 patients </li></ul>
  33. 33. ARDSNet <ul><li>6ml/kg 12m/kg </li></ul><ul><li>PaCO2 43 ± 12 36 ±9 </li></ul><ul><li>Respiratory rate 30 ± 7 17 ± 7 </li></ul><ul><li>PaO2/F /FIO2 160 ± 68 177 ± 81 </li></ul><ul><li>Plateau pressure 26 ± 7 34 ± 9 </li></ul><ul><li>PEEP 9.2 ± 3.6 8.6 ± 4.2 </li></ul>
  34. 34. ARDSNet low vs traditional TV protocol <ul><li>* Calculated predicted body weight(pbw) </li></ul><ul><li>male: 50+2.3[height(inches)-60] </li></ul><ul><li>female: 45.5+2.3[height(inches)-60] </li></ul><ul><li>Mode: Volume assist-control </li></ul><ul><li>Change rate to adjust minute ventilation (not>35/min) </li></ul><ul><li>PH goal 7.30-7.45 </li></ul><ul><li>Plateau press<30cmh20 </li></ul><ul><li>PaO 2 goal: 55-80mmhg or SpO 2 88-95% </li></ul><ul><li>FiO 2 /PEEP combination to achieve oxygenation goal. </li></ul>
  35. 35. Treatment - Ventilation What about PEEP? <ul><li>Another ARDS net study compared higher vs lower PEEP in ARDS </li></ul><ul><li>This study was conducted because of the observation that low tidal volume pt required high PEEP and this may have contributed improved survival </li></ul><ul><li>In the same token, there has always been a concern that high levels of PEEP may contribute to vent-associated lung injury </li></ul>
  36. 36. Treatment - Ventilation What about PEEP? <ul><li>Another multicentered, randomized study involved 549 pts </li></ul><ul><li>Low Tidal volume strategy - calculated predicted body weight (pbw) </li></ul><ul><li>male: 50+2.3[height(inches)-60] </li></ul><ul><li>female: 45.5+2.3[height(inches)-60] </li></ul><ul><li>Mode: Volume assist-control </li></ul><ul><li>Change rate to adjust minute ventilation(not>35/min) </li></ul><ul><li>PH goal 7.30-7.45 </li></ul><ul><li>Plateau press<30cmh20 </li></ul><ul><li>PaO 2 goal: 55-80mmhg or SpO 2 88-95% </li></ul><ul><li>FiO 2 /PEEP combination to achieve oxygenation goal </li></ul>
  37. 37. Treatment - Ventilation What about PEEP? <ul><li>Result of the study showed no benefit from higher levels of PEEP in either mortality or secondary outcomes ( vent- free days, icu-free stays or organ failure) </li></ul><ul><li>No significant increase in lung injury was noted either </li></ul><ul><li>So PEEP really does not matter! </li></ul>
  38. 38. How to select vent settings <ul><li>PEEP/FiO 2 relationship to maintain adequate PaO 2 /SpO 2 </li></ul><ul><li>PaO 2 goal: 55-80mmHg or SpO2 88-95% use FiO2/PEEP combination to achieve oxygenation goal </li></ul>
  39. 39. How to select vent settings
  40. 40. other ventilation strategies <ul><li>Recruitment maneuvers </li></ul><ul><li>Prone </li></ul><ul><li>Inhaled nitric oxide </li></ul><ul><li>High frequency oscillation </li></ul>
  41. 41. Treatment <ul><li>Treatment strategy is one of low volume and high frequency ventilation (ARDSNet protocol) </li></ul><ul><li>- Low Vt (6ml/kg) to prevent over-distention </li></ul><ul><li>- increase respiratory rate to avoid very high level of hypercapnia </li></ul><ul><li>- PaCO 2 allowed to rise, usually well tolerated </li></ul><ul><li>- May be beneficial </li></ul><ul><li>- low CVPs </li></ul><ul><li>Search for and treat the underlying cause; surgery if needed </li></ul><ul><li>Ensure adequate nutrition and place on GI/DVT prophylaxis </li></ul><ul><li>Prevent and treat nosocomial infx </li></ul><ul><li>Consider short course of high dose steroids in pts w/ severe dz that is not resolving . </li></ul>
  42. 42. ARDSnet and Long-term outcome <ul><li>120pts randomized to low Vt or high Vt </li></ul><ul><li>a) 25%mortality w/ low tidal volume </li></ul><ul><li>b) 45% mortality w/ high tidal volume </li></ul><ul><li>20% had restricitve defect and 20% had obstructive defect 1 yr after recovery </li></ul><ul><li>About 80% had DLCO reduction 1 yr after recovery </li></ul><ul><li>Standardized tested showed health-related quality of life lower than normal </li></ul><ul><li>No difference in long-term outcomes between tidal volume group </li></ul>
  43. 43. References <ul><li>1. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute Respiratory distress in Adults. Lancet 1967; 2: 319-23 </li></ul><ul><li>2. Petty TL, Ashbaugh DG. The adult respiratory distress syndrome: clinical features, factors influencing prognosis and principles of management. Chest 1971; 60:233-9 </li></ul><ul><li>3. Murray JF, Matthay MA, Luce JM, Flick MR. An expanded definition of adult respiratory distress syndrome . Am Rev Respir Dis 1988; 138:720-3 </li></ul><ul><li>4. Luhr OR, Antonsen K, Karlsson M. Incidence and mortality after acute respiratory failure and acute respiratory distress syndrome in Sweden, Denmark, and Iceland. The ARF Study Group. Am J Respir Crit Care Med. Jun 1999;159(6):1849-61. </li></ul><ul><li>5. Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M.Incidence and outcomes of acute lung injury. N Engl J Med. Oct 20 2005;353(16):1685-93. </li></ul><ul><li>Davidson TA, Caldwell ES, Curtis JR. Reduced quality of life in survivors of acute respiratory distress syndrome compared withcritically ill control patients. JAMA. Jan 27 1999;281(4):354-60 </li></ul><ul><li>Ware LB, Matthay MA. The acute respiratory distress syndrome.  N Engl J Med . May 4 2000;342(18):1334-49. </li></ul><ul><li>8. Levitt JE, Vinayak AG, Gehlbach BK, et al. Diagnostic utility of BNP in critically ill patients with pulmonary edema: a prospective cohort study. Crit Care 2008; 12: R3 </li></ul>
  44. 44. References <ul><li>The NHLBI ARDS Clinical Trials Network. Comparison of two fluid-management strategies inacute lung injury.  N Engl J Med . Jun 15 2006;354(24):2564-75 </li></ul><ul><li>The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distres syndrome.  N Engl J Med . May 4 2000;342(18):1301-8 </li></ul><ul><li>Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome.  N Engl J Med . Jul 22 2004;351(4):327-36 </li></ul><ul><li>Esteban A, Alia I, Gordo F. Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS. For the Spanish Lung Failure Collaborative Group.  Chest . Jun 2000;117(6):1690-6 </li></ul><ul><li>Griffiths MJ, Evans TW. Inhaled nitric oxide therapy in adults.  N Engl J Med . Dec 22 2005;353(25):2683-95. </li></ul><ul><li>Albert RK. The prone position in acute respiratory distress syndrome: where we are, and where do we go from here.  Crit Care Med . Sep 1997;25(9):1453-4 </li></ul><ul><li>Herridge MS, Cheung AM, Tansey CM. One-year outcomes in survivors of the acute respiratory distress syndrome.  N Engl J Med . Feb 20 2003;348(8):683-93 </li></ul>