acute respiratory distress sysndrome and magt

ards

1. Acute Respiratory Distress Syndrome:- Presentator – Dr. Jatin Sharma 04 January 2025

2. 2 Include: Introduction Etiology Pathophysiology Diagnosis Classification Management TRIALS

3. 3 Introduction:- ARDS defines as acute onset <7 days of a known clinical insult, Bilateral chest X-ray opacities that are not fully explained by effusions, lobar/lung collapse, or nodules, Respiratory failure that is not fully explained by cardiac failure or fluid overload, Presence of hypoxemia and severity of ARDS.

4. 4 Introduction: Acute respiratory distress syndrome (ARDS) is a life threatening condition characterized by acute onset of noncardiogenic pulmonary edema associated with hypoxemia and decreased lung compliance. None of the single clinical features or diagnostic test defines ARDS. It is a syndrome rather than a specific pathology currently represented by clinical criteria.

5. 5 Introduction:- The stages of mild, moderate, and severe ARDS are associated with mortality risk and with the duration of mechanical ventilation in survivors. The annual incidence of ARDS is estimated to be as high as 60 cases/100,000 population. Approximately 10% of all intensive care unit (ICU) admissions involve patients with ARDS.

6. 6 Etiology:- ARDS develops in the setting of various risk factors which can cause direct and indirect injury to the lung. These risk factors can broadly be categorized into:- Direct :- Pneumonia Gastric content aspiration Lung contusion Inhalational injury Drowning

7. 7 Etiology:- Indirect :- sepsis polytrauma acute pancreatitis burns blood transfusions reperfusion injury

8. 8 Pathophysiology:- Increased endothelial permeability, epithelial dysfunction, and dysregulated lung inflammation are critical features of ARDS pathophysiology.

9. 9

10. 10 Pathophysiology:- The clinical course of ARDS can be divided into three phases: 1 Exudative Phase 2 Proliferative Phase 3 Fibrotic Phase

11. 11 Exudative Phase:- It represents an initial acute phase of the illness, usually lasting for 7 days. This phase occurs due to the injury of the alveolar epithelium and capillary endothelium. It manifests as acute onset of radiographic infiltrates (pulmonary edema), hypoxemia and increased work of breathing. This phase is characterized by capillary congestion and intra-alveolar edema

12. 12

13. 13

14. 14 Proliferative Phase:- After resolution of the acute phase, ARDS progresses to a proliferative phase marked by an intense cellular proliferation. The proliferative phase usually starts after 7–10 days of acute onset to 21 days. This leads to repair of damaged epithelium, endothelium, restoration of barrier function, and proliferation of fibroblast. This phase can result in normal tissue formation or disease progression leading to fibrosis if lung injury is persistent.

15. 15 Fibrotic Phase:- While many patients with ARDS recover lung function 3–4 weeks after the initial pulmonary injury, some enter a fibrotic phase that may require long-term support on mechanical ventilators and/or supplemental oxygen. In some cases, ARDS syndrome progresses to fibrosing alveolitis. A severe fibroproliferative process fills the airspaces with granulation tissue that contains an extracellular matrix rich in collagen and fibrin.

16. 16 Diagnosis: Arterial blood gas analysis is necessary to confirm the diagnosis and to assess the severity of ARDS. The chest X-ray is essential to make the diagnosis, and serial X-ray helps in treatment follow-up. Echocardiography should be done to rule out the possibility of a cardiovascular cause of respiratory failure. Bedside point-of-care ultrasound may rule out other causes of pulmonary edema such as heart failure and consolidation.

17. 17 Diagnosis High-resolution CT (HRCT) of thorax may help to know the extent of lung involvement. Leukocytosis or leukopenia on complete blood count points toward an infectious etiology. Evaluation of renal and liver function may be helpful to assess the presence of multiorgan dysfunction. Other commonly used investigations are serum electrolyte, serum lactate level, plasma NTproBNP levels and sepsis markers such as C-reactive protein and procalcitonin. If infectious etiology is suspected, blood, urine, and bronchial lavage are evaluated for culture and sensitivity.

18. 18 Baby Lung: The “baby lung” is a functional concept. In ARDS, the fraction of lung parenchyma that maintains normal inflation is known as the “baby lung.” The “baby lung” is a small lung with normal elasticity. The size of the baby lung depends upon the severity of ARDS and relates to the compliance of the respiratory system. In the ARDS lung, the gaseous exchange of oxygen and CO2 primarily occurs in the baby lung. To prevent ventilator-induced injury to the baby lung, low tidal volume should be used.

19. 19 Classification: The “Berlin definition” is the most commonly used clinical criterion for diagnosing ARDS which is proposed by the European Society of Intensive Care Medicine (ESICM) in 2012.

20. 20 Berlin definition: Acute onset <7 days of a known clinical insult Bilateral chest X-ray opacities that are not fully explained by effusions, lobar/lung collapse, or nodules Respiratory failure that is not fully explained by cardiac failure or fluid overload Presence of hypoxemia and severity of ARDS: – Mild (200 mm Hg < PaO2/FiO2 ≤ 300 mm Hg) and CPAP/PEEP ≥ 5 cmH2O – Moderate (100 mm Hg < PaO2/FiO2 ≤ 200 mm Hg) and PEEP ≥ 5 cmH2O – Severe (PaO2/FiO2 ≤ 100 mm Hg) and PEEP ≥ 5 cmH2O

21. 21

22. 22 Management:

23. 23 Management strategy: 1. Identify and treat underlying cause 2. Ventilator support –Lung protective ventilatory support strategy - Application of PEEP 3. Restore and maintain hemodynamic function - Conservative fluid replacement strategy - Vasopressors and inotropic support 4. Prevent complication of critical illness 5. Ensure adequate nutrition 6. Avoid oversedation 7. Using Weaning protocol with spontaneous breathing trials

24. 24 Role of NIV NIV may be used with great caution in case of mild ARDS and that too only in ICU ( Level 3 ) Reserved for hemodynamically stable patient who can be closely monitored in an ICU where facilities for invasive ventilation are present Failure rate ranges from 50% to 80% Risk factors for NIV Failure - Severe hypoxemia - Shock - Metabolic acidosis

25. 25 Use of High-Flow Nasal Cannula High-flow nasal cannula (HFNC) oxygen consists of the delivery of high (50–60 L/min), heated, and humidified oxygen flow at a chosen FIO2 via a wide-bore nasal cannula. This high oxygen flow allows inspiratory flow increases in hypoxemic patients. Oxygen dilution is therefore minimized, and the delivered FiO2 is close to the set FiO2.

26. 26 Lung Protective ventilation: GOALS: 1. VT- 6ml/kg 2. Ppl < 30 cm H2O 3. PH = 7.30- 7.45

27. 27 FIRST STAGE A) Calculate patients Predicted body weight (PBW) Male PBW (kg) = 50 + 2.3 [(height in inches) - 60 ] Female PBW (kg) = 45.5 + 2.3 [(height in inches) - 60 ] B) Set initial tidal volume (TV ) to 8 ml / kg PBW C) Add positive end- expiratory pressure (PEEP ) at = 5-7 cmH2O D) Reduce TV by 1 ml /kg every 2 hours until TV = 6 ml / kg PBW

28. 28 SECOND STAGE A) When TV down to 6 ml/kg , measure plateau pressure (Ppl). B) Target Ppl < 30 cm H2O C) If Ppl > 30 cm H2O , decrease TV in 1 ml /kg steps until Ppl drops below 30 cm H2O or TV down to 4 ml/kg.

29. 29 THIRD STAGE: Monitor Arterial blood gases for Respiratory acidosis A. Target PH =7.30-7.45 B. If PH 7.15-7.30 , Increase respiratory rate ( RR ) until PH > 7,3 or RR = 35 bpm C. If PH < 7.15 , Increase RR to 35 bpm , if PH still < 7.15 increase TV at 1 ml / kg increments until PH > 7.15

30. 30

31. 31 Concept Of Permissive Hypercapnia: Paco2- 60 to 70 mmHg and PH – 7.2 to 7.25 are safe for most patients . Troublesome side effects brainstem hyper stimulation, which often requires neuromuscular blockade to asynchrony . The risk of hypercapnic acidosis is determined by the benefit of maintaining low- volume ventilation to protect the lungs from volutrauma. Contraindication: Pregnancy ACS Raised ICP

32. 32 RECRUITMENT MANEUVER: Rational – Improving arterial oxygenation with short lasting increase in intrathoracic pressure. Current evidence suggest that the Recruitment maneuvers should not be routinely used in all ARDS patients unless 1. Severe hypoxemia persists 2. As a rescue maneuver to overcome severe hypoxemia 3. To open the lung when setting PEEP 4. Following evedence of acute lung derecruitment such as ventilator circuit dissconnect

33. 33 Study found that most of the alveolar recruitment occurred during the first 10 sec of the maneuver . This was followed by a decrease in the blood pressure which recovered within 30 seconds after the Recruitment maneuvers.

34. 34 WHEN TO CONSIDER FOR RESCUE STRATEGIES: Ventilator- based criteria If SPO2 remains < 88-90 % despite….. FiO2 > 0.6 and / or PEEP > 12-15 cmH2O and / or Pplat > 24-28 cmH2O and / or Paralytic drugs needed

35. 35 CPAP recruitment Maneuver: 40 cmH20 for 30 seconds (Arnal et al, 2011) Use pressure controlled ventilation Set respiratory rate to zero and turn off apnoea alarm Increase PEEP to 40 cmH20 for 40 seconds Most recruitment occurs in the first 10s, with haemodynamic compromise occurring later

36. 36 Various rescue ventilatory strategies: Prone Positioning ECMO HFOV

37. 37 PRONE POSITION VENTILATION: Benefits: 1. Relieves the cardiac and abdominal compression 2. Makes regional V/Q ratio and chest elastance more uniform 3. Facillitates drainage of Secretion 4. Potentiates the beneficial effects of Recruitment maneuver

38. 38 Patients with severe ARDS (Pao2 /Fio2 < 150 mm Hg) Early in the course (ideally within 48 h) Best outcomes reported when prone positioning is used in combination with both low tidal volume ventilation (6 cc/kg) and neuromuscular blockade. Successful trials use at least 16 hours of daily proning.

39. 39 Contraindication: Patients with facial/neck trauma or spinal instability Patients with recent sternotomy or large ventral surface burn Patients with elevated intracranial pressure Patients with massive hemoptysis Patients at high risk of requiring CPR or defibrillation

40. 40 Potential complications: Temporary increase in oral and tracheal secretions occluding airway ETT migration or kinking Vascular catheter kinking Elevated intraabdominal pressure Increased gastric residuals Facial pressure ulcers, facial edema, lip trauma from ETT, brachial plexus injury (arm extension)

41. 41 High-frequency oscillatory ventilation (HFOV): This improves oxygenation by promoting alveolar recruitment and reducing overdistension. It uses a small tidal volume (1–3 mL/kg) with a high rate of 100–600/min at higher mean airway pressures. Patients must be deeply sedated to prevent inspiratory efforts. Though HFOV offers a theoretical advantage, the overall impact on an ARDS patient’s outcomes is still controversial. Thus, routine use of HFOV is not recommended

42. 42 INVERSE RATION VENTILATION (IRV) Oxygenation can also be improved by increasing mean airway pressure with IRV The Inspiratory (I) time is lengthened so that it is longer than the expiratory (E) Time (I:E > 1:1) With diminished time to exhale, Dynamic hyperinflation leads to increase end –expiratory pressure, similar to PEEP given by Ventillator Decrease fio2 to 0.6 to avoid possible oxygen toxicity But no mortality benefit in ARDS has been demonstrated

43. 43 Fluid and hemodynamic management in ARDS: Pulmonary edema is the final endpoint of ARDS pathophysiology; hence, fluid conservative strategies may help in oxygenation and outcome. But the presence of circulatory shock in severe ARDS needs adequate fluid resuscitation to maintain the peripheral perfusion. The Fluids and Catheters Treatment Trial (FACTT) found that in hemodynamically stable ARDS patients, the fluid conservative strategy improves the lung function and increases mechanical ventilation–free days without increasing nonpulmonary organ failure but no difference in 60 days’ mortality.

44. 44 Currently, the recommended approach is to achieve the lowest intravascular volume that maintains adequate tissue perfusion as measured by urine output, other organ perfusion, and metabolic acid–base status. Once the shock has resolved, patients should be managed with a conservative fluid strategy with the goal of zero fluid balance.

45. 45 Role of Steroids: The ARDSnet–STEROID study found no difference in 60-day mortality after steroid treatment. There was increased mortality in patients who started on steroids at least 14 days after diagnosis. DEXA-ARDS Trial (2020) and RECOVERY Trial (2020) have found mortality benefits and more ventilator-free days using dexamethasone in ARDS patients. The steroids are more efficient at reversing the inflammatory process in early ARDS but are ineffective in the fibrotic phase.

46. 46 Spontaneous breathing trial in an ARDS patient? Weaning is a continuous process; it involves daily interruption of sedation and daily screening for readiness for spontaneous breathing trial (SBT). Should be started when all the following criteria are met: 1. Resolution of the acute phase of the disease 2. FiO2 < 0.40 and PEEP < 8 cmH2O 3. Not receiving neuromuscular blocking agents 4. The patient is awake and following commands. 5. Systolic arterial pressure >90 mm Hg without vasopressor support 6. Tracheal secretions are minimal, and the patient has a good cough and gag reflex

47. 47 TRIALS

48. 48 PROSEVA Trial: 2013 Prone positioning in Severe ARDS PROTOCOL Early proning Patients with paO2 : FiO2 ratio of < 150 with FiO2 of 0.6 were proned for at least 16 hrs a day Lung protective Ventilation PEEP selected from PEEP :FiO2 table

49. 49 CRITERIA FOR STOPPING PRONE VENTILATION . PaO2:FiO2 ratio > 150 with PEEP < 10 cmh2o and FiO2 < 0.6 in supine position after 4 hrs CONCLUSION Early aplication of prolonged prone positioning session significantly decrease mortality.

50. 50 ACURASYS Trial: 2010 Neuromuscular blockers in early ARDS Neuromuscular blockers are used in ARDS to facilitate Mechanical Ventilation Previous studiers have shown improvement in oxygenation and non significant improvement in mortality Look for mortality benefit with neuromuscular blockers

51. 51 METHODS Lung protective ventilation Cisatracurium vs Saline 15 mg bolus , continuous infusion of 37.5 mg / hr for 48 hrs

52. 52 OSCILLATE Trial: METHODS New onset , moderate to severe ARDS HFOV vs Controlled ventilation strategy with the use of low volume and high PEEP CONCLUSION In moderate to severe ARDS , early application of HFOV may increase in hospital mortality

53. 53 OSCAR Trial: High Frequency Oscillation for ARDS METHODS Adults requiring mechanical ventilation for ARDS to undergo either HFOV with Novalung R100 ventilator ( Metran ) or usual ventilatory care . Pao2:FiO2 of 200 mmhg or less and expected duration of ventilation of at least 2 days

54. 54 CONCLUSION The use of HFOV had no significant effect on 30 day mortality in patients undergoing mechanical ventilation for ARDS No benefit, No harm

55. 55 CESAR Trial: METHODS Continued Conventional management versus referral to consideration for treatment by ECMO CONCLUSION Transferring of adult patients with Severe but potentially reversible respiratory failure to a centre with an ECMO based management protocol significantly improves survival without severe disability

56. 56 Thank You