Acute respiratory distress syndrome (ards)
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Acute respiratory distress syndrome (ards)






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Acute respiratory distress syndrome (ards) Presentation Transcript

  • 2. OUTLINE Definition Clinical history Pathophysiology Diagnosis Management
  • 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. 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. 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. ARDS ALI Acute  Acute PaO2/FiO2 < 200  < 300mmHg B/l interstitial /alveolar  Same infiltrates PCWP <18mmHg  Same
  • 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. ARDS CAUSES Direct Lung Injury: a) Pneumonia b) pulmonary contusion c) near drowning d) inhalation injury f) aspiration of gastric contents
  • 10. ARDS CAUSES Indirect lung injury a) sepsis b) severe trauma w/ shock, hypoperfusion c) acute pancreatitis d) transfusion of multp blood products
  • 11. PATHOPHYSIOLOGY Diffuse alveolar damage Lung capillaries damage Inflammatory cells Alveolar edema Severe hypoxemia Decreased lung compliance & atelectasis Pulmonary hypertension
  • 12. NATURAL HISTORY OF ARDS 3 phases - exudative (0-7 d) - proliferative ( 7-21 d) - fibrotic ( > 21 days)
  • 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. CLINICAL HISTORY Acute Critically ill Rapid –tachypnoea,dyspnoea,hypoxia Within in 12-48 hr of precipitating event Initial respiratory alkalosis Respiratory failure
  • 15. LAB INVESTIGATIONS Routine blood counts RFT CXR ABG CT chest BNP 2D Echo BAL PCWP
  • 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. Cardiogenic Non-Cardiogenic Diffuse Bilateral patchy infiltratesBilateral infiltrates predominately in homogenously distributedlung bases. Kerley B’s. throughout the lungs. No KerleyCardiomegaly. B’s.
  • 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. ARDSearly late
  • 20. Cardiogenic Non-Cardiogenic No septal thickening. DiffuseSeptal thickening. More severe in alveolar infiltrates. Atelectasislung bases. of dependent lobes usually seen .
  • 21. THERAPY- GOALS Treatment of underlying cause Cardio-pulmonary support Specific therapy targeted at lung injury Supportive therapy.
  • 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. INDICATION FOR MECHANICAL VENTILATION Inadequate oxygenation ( PaO2- < 60 with FiO2 >=0.6) Rising or elevated PaCO2 ( > 50mmHg) Clinical signs of incipient respiratory failure
  • 24. MECHANICAL VENTILATIONThe Aims are to increase PaO2 whileminimizing the risk of further lung injury(ventilator induced lung injury)
  • 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. 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. 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. 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.  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. OTHER METHODS High flow ventilation ECMO Partial fluid ventilation (PLV)
  • 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. TREATMENT OF SEPSIS Empirical antibiotics Culture sensitivity & change antibiotics Avoid nephrotoxic drug Enteral feeding
  • 35. OTHER TREATMENT MODALITIES NO Ketoconazole Albuterol Pentoxyphylline NSAIDS N-acetyl cysteine
  • 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. REFERENCES Harrison’s text book of medicine-18th edition ARDS Network clinical trials - ARDS Foundation -
  • 38. THANK U….