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Acute respiratory distress syndrome (ards)


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Acute respiratory distress syndrome (ards)

  2. 2. OUTLINE Definition Clinical history Pathophysiology Diagnosis Management
  3. 3. CASE 35 yr old male met with an RTA was admitted in surgery icu developed severe tachpnoea,dyspnoea within 24hrs admission o/e- pulse- 110/mt,bp- 80/50mmHg pallor+ cyanosis + no jvp S1/S2- NL Chest b/l rales present in mid/lower area p/a- soft ,no HSM Abg analysis- O2 sat 50%,pao2-40%,pco2-45% ph – 7.3
  5. 5. ARDS -DEFINITION ARDS is a clinical syndrome of dyspnea of rapid onset,hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. Inflammatory cells and proteinaceous fluid accumulate in the alveolar spaces leading to a decrease in diffusing capacity and hypoxemia.
  6. 6. ALI V/S ARDS ALI is the term used for patients with significant hypoxemia (PaO2/FiO2 ratio of ≤ 300) ARDS is the term used for a subset of ALI patients with severe hypoxemia (PaO2/FiO2 ratio of ≤ 200)
  7. 7. ARDS ALI Acute  Acute PaO2/FiO2 < 200  < 300mmHg B/l interstitial /alveolar  Same infiltrates PCWP <18mmHg  Same
  8. 8. ARDS DIAGNOSTIC CRITERIAAcute OnsetPredisposing ConditionBilateral InfiltratesPaO2/FiO2 ≤ 200 mm HgPulmonary capillary Wedge Pressure ≤ 18 mm Hg or no clinical evidence increase in LA pressure.
  9. 9. ARDS CAUSES Direct Lung Injury: a) Pneumonia b) pulmonary contusion c) near drowning d) inhalation injury f) aspiration of gastric contents
  10. 10. ARDS CAUSES Indirect lung injury a) sepsis b) severe trauma w/ shock, hypoperfusion c) acute pancreatitis d) transfusion of multp blood products
  11. 11. PATHOPHYSIOLOGY Diffuse alveolar damage Lung capillaries damage Inflammatory cells Alveolar edema Severe hypoxemia Decreased lung compliance & atelectasis Pulmonary hypertension
  12. 12. NATURAL HISTORY OF ARDS 3 phases - exudative (0-7 d) - proliferative ( 7-21 d) - fibrotic ( > 21 days)
  13. 13. HISTOLOGIC FINDINGS Hyaline Protein in air spaces Cellular Congestion  Typical histological findings in  alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume ←Normal Lung Histology—large alveolar volumes, septal spaces very thin, no cellular congestion.
  14. 14. CLINICAL HISTORY Acute Critically ill Rapid –tachypnoea,dyspnoea,hypoxia Within in 12-48 hr of precipitating event Initial respiratory alkalosis Respiratory failure
  15. 15. LAB INVESTIGATIONS Routine blood counts RFT CXR ABG CT chest BNP 2D Echo BAL PCWP
  16. 16. HOW TO DETERMINE ARDS BY CXR 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.
  17. 17. Cardiogenic Non-Cardiogenic Diffuse Bilateral patchy infiltratesBilateral infiltrates predominately in homogenously distributedlung bases. Kerley B’s. throughout the lungs. No KerleyCardiomegaly. B’s.
  18. 18. CARDIOGENIC V/S NON CARDIOGENIC EDEMA cardiogenic Non-cardiogenic Patchy infiltrates in bases  Homogenous pluffy Effusions + shadows Kerley B lines +  Effusions – Cardiomegaly +  Kerley B lines – Pulmonary vascular  Cardiomegaly – redistribuition  No pulm.vascular Excess fluid in alveoli redistribuition  Protein,inflammatory cells,fluid
  19. 19. ARDSearly late
  20. 20. Cardiogenic Non-Cardiogenic No septal thickening. DiffuseSeptal thickening. More severe in alveolar infiltrates. Atelectasislung bases. of dependent lobes usually seen .
  21. 21. THERAPY- GOALS Treatment of underlying cause Cardio-pulmonary support Specific therapy targeted at lung injury Supportive therapy.
  22. 22. SPONTANEOUSLY BREATHING PATIENT  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
  23. 23. INDICATION FOR MECHANICAL VENTILATION Inadequate oxygenation ( PaO2- < 60 with FiO2 >=0.6) Rising or elevated PaCO2 ( > 50mmHg) Clinical signs of incipient respiratory failure
  24. 24. MECHANICAL VENTILATIONThe Aims are to increase PaO2 whileminimizing the risk of further lung injury(ventilator induced lung injury)
  26. 26. ARDS NET PROTOCOL -WEANING Spontaneous breathing trial daily PaO2/FiO2-<8/<.4 or <5/ <.5 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
  27. 27. EVIDENCE BASED RECOMMENDATIONS FORARDS THERAPYTREATMENT RECOMMENDATIONS MECHANICAL VENTILATIONLow tidal volume AMinimize LAFP BHigh PEEP CProne positionRecruitment maneuvers CHigh frequency ventilation C Glucocorticoids D Sufactant D replacement,inhaled D NO,others
  28. 28. MANAGEMENT: REDUCING VENTILATOR-INDUCED LUNG INJURY 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
  29. 29. ARDS NETWORK CLINICAL TRIALS 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
  30. 30.  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
  31. 31. OTHER METHODS High flow ventilation ECMO Partial fluid ventilation (PLV)
  33. 33. MANAGEMENT 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
  34. 34. TREATMENT OF SEPSIS Empirical antibiotics Culture sensitivity & change antibiotics Avoid nephrotoxic drug Enteral feeding
  35. 35. OTHER TREATMENT MODALITIES NO Ketoconazole Albuterol Pentoxyphylline NSAIDS N-acetyl cysteine
  36. 36. PROGNOSIS Mortality ranges-26 %-44% Risk factors- - advanced age - CKD,CLD - Chronic immunosuppression - chronic alcohol abuse ARDS from direct lung injury has double mortality
  37. 37. REFERENCES Harrison’s text book of medicine-18th edition ARDS Network clinical trials - ARDS Foundation -
  38. 38. THANK U….