Acute respiratory distress syndrome (ards)

1. Acute respiratory distress syndrome ( ards ) GUIDE - DR.SHIV.S.SHARMA - DR.Y. JAMRA CANDIDATE-DR.SARATH MENON.R Intensive care unit,Dept.Internal Medicine MGM MEDICAL COLLEGE & M Y HOSPITAL,INDORE

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

4. Cxr – what’s diagnosis ?

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. Acute PaO2/FiO2 < 200 B/l interstitial /alveolar infiltrates PCWP <18mmHg Acute < 300mmHg Same Same ARDS ALI

8. ARDS Diagnostic Criteria Acute Onset Predisposing Condition Bilateral Infiltrates PaO2/FiO2 ≤ 200 mm Hg Pulmonary 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 Typical histological findings in ARDS alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume www.burnsurgery.com/.../pulmonary/part3/sec4.htm ← Normal Lung Histology—l arge alveolar volumes, septal spaces very thin, no cellular congestion. Hyaline Protein in air spaces 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 Bilateral infiltrates predominately in lung bases. Kerley B’s. Cardiomegaly . Diffuse Bilateral patchy infiltrates homogenously distributed throughout the lungs. No Kerley B’s.

18. Cardiogenic v/s non cardiogenic edema Patchy infiltrates in bases Effusions + Kerley B lines + Cardiomegaly + Pulmonary vascular redistribuition Excess fluid in alveoli Homogenous pluffy shadows Effusions – Kerley B lines – Cardiomegaly – No pulm.vascular redistribuition Protein,inflammatory cells,fluid cardiogenic Non- cardiogenic

19. ards early late

20. Cardiogenic Non- Cardiogenic No septal thickening. Diffuse alveolar infiltrates. Atelectasis of dependent lobes usually seen . Septal thickening. More severe in lung bases.

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 CO 2 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 Ventilation The Aims are to increase PaO2 while minimizing the risk of further lung injury (ventilator induced lung injury)

25. ARDSNet Ventilator protocol

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 FOR ARDS THERAPY TREATMENT MECHANICAL VENTILATION Low tidal volume Minimize LAFP High PEEP Prone position Recruitment maneuvers High frequency ventilation Glucocorticoids Sufactant replacement,inhaled NO,others RECOMMENDATIONS A B C C C D D D

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)

32. Extra corporeal membrane oxygenation ( ecmo )

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-18 th edition ARDS Network clinical trials - www.ardsnet.org ARDS Foundation - www.ardsusa.org

38. thank u ….