acute respiratory distress syndrome
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1) ARDS is an acute lung condition caused by direct or indirect injury to the lungs. It is characterized by inflammation and fluid buildup in the lungs. 2) The pathophysiology involves activation of the innate immune system and release of cytokines, which damage the alveolar-capillary membrane leading to leakage of fluid into the lungs. 3) Treatment focuses on mechanical ventilation with low tidal volumes, application of PEEP, conservative fluid management, prone positioning in severe cases, and treating the underlying cause.
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acute respiratory distress syndrome
- 2. Acute Respiratory Distress Syndrome By Dr. Istikhar Ali Sajjad PGR Pulmonology
- 3. ∗ Review the causes and differentials for ARDS ∗ Briefly discuss the pathophysiology ∗ Discuss the clinical manifestations of ARDS ∗ Understand evidence based treatment options Objectives
- 4. ∗ ARDS is also referred with variety of terms like • Stiff Lung • Shock lung • Wet lung • Post traumatic lung • Adult respiratory distress syndrome • Adult hyaline membrane disease • Capillary leak syndrome & • Congestive atelectasis. Acute Respiratory Distress Syndrome
- 5. June 20, 2012, Vol 307, No. 23 et al. JAMA 2012; 307:2530 -European Society of Intensive Care Medicine with endorsement from American Thoracic Society and Society of Critical Care Medicine -Devised three mutually exclusive severity categories: Mild, Moderate and Severe -Took into account: timing, chest imaging, origin of edema, oxygenation
- 6. et al. JAMA 2012; 307:2530
- 7. Bernard et al. AJRCCM 1994; 149:818 Rice et al. Chest 2007: 132: 410
- 8. ∗ Epidemiology ∗ Annual incidence: 60/100,000 ∗ 20% ICU patients meet criteria for ARDS ∗ Morbidity / Mortality ∗ 26-44%, most (80%) deaths attributed to non-pulmonary organ failure or sepsis ∗ Risk Factors ∗ Advanced age, pre-existing organ dysfunction or chronic medical illness ∗ Patient with ARDS from direct lung injury has higher incidence of death than those from non-pulmonary injury Statistics Levy BD, & Choi AM, Harrison’s Principles of Internal Medicine, 2012
- 9. ∗ Direct Lung Injury ∗ Common causes ∗Aspiration of gastric contents or other substances. ∗Viral/bacterial pneumonia ∗ Less Common causes ∗Chest trauma ∗Embolism: fat, air, amniotic fluid ∗Inhalation of toxic substances ∗Near-drowning ∗O2 toxicity ∗Radiation pneumonitis ETIOLOGY & RISK FACTORS
- 10. ∗ Indirect Lung Injury ∗ Common causes ∗ Sepsis ∗ Severe traumatic injury ∗ Less common causes ∗ Acute pancreatitis ∗ Anaphylaxis ∗ Prolonged Cardiopulmonary bypass surgery ∗ Disseminated intravascular coagulation ∗ Multiple blood transfusions ∗ Narcotic drug overdose (e.g., heroin) ∗ Nonpulmonary systemic diseases ∗ Severe head injury ∗ Shock ∗ Massive blood transfusion. ETIOLOGY & RISK FACTORS
- 11. ∗ Early signs/symptoms ∗ Restlessness ∗ Dyspnea ∗ Low blood pressure ∗ Confusion ∗ Extreme tiredness ∗ Change in patient’s behavior ∗ Mood swing ∗ Disorientation ∗ Change in LOC ∗ If pneumonia is causing ARDS then client may have ∗ Cough ∗ Fever CLINICAL MANIFESTATIONS
- 12. Late signs & symptoms ∗ Severe difficulty in breathing i.e., labored, rapid breathing. ∗ Shortness of breath. ∗ Tachycardia ∗ Cyanosis (blue skin, lips and nails) ∗ Think frothy sputum ∗ Metabolic acidosis ∗ Abnormal breath sounds, like crackles ∗ PaCo2with respiratory alkalosis. ∗ PaO2 CLINICAL MANIFESTATIONS CONTD…………
- 13. ∗ History of above symptoms ∗ On physical examination ∗ Auscultation reveals abnormal breath sounds ∗ The first tests done are : ∗ Arterial blood gas analysis ∗ Bood tests ∗ Chest x-ray ∗ Sputum cultures and analysis ∗ Other tests are : ∗ Chest CT Scan ∗ Echocardiogram DIAGNOSITC EVALUATION
- 15. ∗ Common complications are; ∗ Nosocomial pneumonia: ∗ Barotrauma ∗ Renal failure ∗ Other complications are : ∗ O2 toxicity, ∗ stress ulcers, ∗ Tracheal ulceration, ∗ Blood clots leading to deep vein thrombosis & ∗ pulmonary embolism. COMPLICATIONS
- 16. ∗ Left ventricular failure/volume overload ∗ Mitral stenosis ∗ Pulmonary veno-occlusive disease ∗ Lymphangitic spread of malignancy ∗ Interstitial and/or airway disease ∗ Hypersensitivity pneumonia ∗ Acute eosinophilic pneumonia ∗ Acute interstitial pneumonitis Differentials
- 17. Pathophysiology 1. Direct or indirect injury to the alveolus causes alveolar macrophages to release pro- inflammatory cytokines Ware et al. NEJM 2000; 342:1334
- 18. Pathophysiology 2. Cytokines attract neutrophils into the alveolus and interstitum, where they damage the alveolar-capillary membrane (ACM). Ware et al. NEJM 2000; 342:1334
- 19. Pathophysiology 3. ACM integrity is lost, interstitial and alveolus fills with proteinaceous fluid, surfactant can no longer support alveolus Ware et al. NEJM 2000; 342:1334
- 20. Physical/ chemical injury Activation Innate Inflammatory Cascade Leakage Protein Rich Oedema Fluid Inflammatory Cellular Infiltrates Diffusion Abnormalities V/Q Mismatch Hypoxia Respiratory Failure
- 21. Physical/ chemical injury Activation Innate Inflammatory Cascade Cellular Infiltrate Atelectasis Oedema Fluid Reduced Thoracic Compliance + Vasoconstriction Hypoxia Respiratory Failure
- 22. Physical/ chemical injury Activation Innate Inflammatory Cascade Small Vessel Thrombosis Increased Dead Space Hypoxia Respiratory Failure
- 23. ∗ Exudative Phase ∗ Neutrophilic Infiltrate ∗ Alveolar Haemorrhage ∗ Proteinaceous Pulmonary Oedema ∗ Cytokines (TNF, IL1,8) ∗ ↑ Inflammation ∗ ↑ Oxidative Stress and Protease Activity ∗ ↓ Surfactant Activity ∗ Atelectasis Histologically
- 24. ∗ Elastase- induced capillary and alveolar damage ∗ ↑ Alveolar flooding ∗ ↓ Fluid clearance ∗ Capillary thrombosis ∗ ↓ Anticoagulant proteins ∗ ↑ Procoagulant proteins (Tissue Factor) ∗ ↑ Anti- fibrinolytic Protein (Plasminogen Activator Inhibitor) Histologically
- 25. ∗ Fibroproliferative Phase ∗ Variable time period ∗ Fibrosis ∗ Chronic Inflammation ∗ Neovascularisation ∗ Resolution3 ∗ Improvement of hypoxaemia ∗ Improved dead space and lung compliance ∗ Resolution radiographic abnormalities ∗ Can take up to 1 year ∗ Residual restrictive or obstructive picture Post Acute Phase
- 26. ∗ Chronic Respiratory Disease ∗ Muscle Fatigue ∗ Muscle Wasting ∗ Weakness Long Term
- 27. ∗ Treat the underlying cause ∗ Low tidal volume ventilation ∗ Use PEEP ∗ Conservative fluid management ∗ Positioning ∗ Reduce potential complications Evidence based management of ARDS
- 28. Hypothesis: In patients with ALI, ventilation with smaller tidal volumes (6 mL/kg) will result in better clinical outcomes than traditional tidal volumes (12 mL/kg) ventilation. ARDS Network N Engl J Med 2000; 342:1301
- 29. • When compared to larger tidal volumes, Vt of 6ml/kg of ideal body weight: • Decreased mortality • Increased number of ventilator free days • Decreased extrapulmonary organ failure • Mortality is decreased in the low tidal volume group despite these patients having: • Worse oxygenation • Increased pCO2 (permissive hypercapnia) • Lower pH ARDSnet. NEJM 2000; 342: 1301 Low Tidal Volume Ventilation
- 30. Low Tidal Volume Ventilation ARDS affects the lung in a heterogeneous fashion • Normal alveoli • Injured alveoli can potentially participate in gas exchange, susceptible to damage from opening and closing • Damaged alveoli filled with fluid, do not participate in gas exchange
- 31. ∗ Protective measure to avoid over distention of normal alveoli ∗ Uses low (normal) tidal volumes ∗ Minimizes airway pressures ∗ Uses Positive end-expiratory pressure (PEEP) Low Tidal Volume Ventilation
- 32. Hypothesis: In patients with ALI ventilated with 6 mL/kg, higher levels of PEEP will result in better clinical outcomes than lower levels of PEEP. N Engl J Med 2004; 351:327
- 33. ∗ Higher levels of PEEP/FiO2 does not improve outcomes ∗ may negatively impact outcomes: ∗ Causing increased airway pressure ∗ Increase dead space ∗ Decreased venous return ∗ Barotrauma PEEP
- 34. • Positive End Expiratory Pressure • Every ARDS patient needs it • Goal is to maximize alveolar recruitment and prevent cycles of recruitment/derecruitment PEEP
- 35. Meade, M et al, JAMA. 2008; 299(6):637-645 -983 patients, randomized into control group with ALI protocol, low Vt and PEEP vs. Open lung group with low Vt, higher PEEP and recruitment maneuvers -No statistically significant difference in mortality outcomes
- 36. Mercatt, M, et al. JAMA. 2008; 299(6):646-655. -Multicenter randomized trial, 767 patients. Set a PEEP aimed to increase alveolar recruitment while limiting hyperinflation -Randomly assigned two groups: moderate PEEP (5-9cm H2O) vs. level of PEEP to reach a plateau pressure of 28-30cm H2O -Found that it didn’t significantly reduce mortality; however, it did improve lung function and decreased days on vent and organ failure duration
- 37. ∗ As FiO2 increases, PEEP should also increase PEEP ARDSnet. NEJM 2004; 351,
- 38. ∗ Plateau pressure is most predictive of lung injury ∗ Goal plateau pressure < 30, the lower the better • Decreases alveolar over-distention and reduces risk of lung strain ∗ Adjust tidal volume to ensure plateau pressure at goal ∗ It may be permissible to have plateau pressure > 30 in some cases • Obesity • Pregnancy • Ascites Airway Pressures in ARDS Terragni et al. Am J Resp Crit Care Med. 2007; 175(2):160
- 39. ∗ Assess cause of high Plateau Pressures ∗ Always represents some pathology: ∗ Stiff, non-compliant lung: ARDS, heart failure ∗ Pneumothorax ∗ Auto-peeping ∗ Mucus Plug ∗ Right main stem intubation ∗ Compartment syndrome ∗ Chest wall fat / Obesity Permissible Plateau Pressures
- 40. Airway Pressures Peak Inspiratory Pressure Plateau Pressure PEEP Airway Pressures Time
- 41. N Engl J Med 2006; 354: 2213 Fluid and Catheter Treatment Trial --No need for routine PAC use is ALI patients --Support use of conservative strategy fluid management in patients with ALI
- 42. ∗ Using the data from a PAC compared to that from a CVC in an explicit protocol: ∗ Did not alter survival. ∗ Did not improve organ function. ∗ Did not change outcomes for patients entering in shock compared to those without shock. ∗ PAC use resulted in more non-fatal complications, mostly arrhythmias. Results N Engl J Med 2006; 354: 2213
- 43. N Engl J Med. 2006;354:2564 ~Hypothesis: Diuresis or fluid restriction may improve lung function but could jeopardize extrapulmonary organ perfusion ~Conclusion: Conservative fluid management improved lung function and shortened mechanical ventilation times and ICU days without increasing nonpulmonary organ failures
- 44. Fluid Management • Increased lung water is the underlying cause of many of the clinical abnormalities in ARDS (decreased compliance, poor gas exchange, atelectasis) • After resolution of shock, effort should be made to attempt diuresis • CVP used as guide, goal <4 • Shortens time on vent and ICU length of stay (13 days vs 11 days) ARDSnet. NEJM 2006; 354: 2564
- 45. Hypothesis: Early application of prone positioning would improve survival in patients with severe ARDS. Conclusion: Early application of prolonged prone positioning significantly decreased 28 day and 90 mortality in patients with severe ARDS. Guerin et al. NEJM. 2013; 368:2159
- 46. ∗ Prone positioning ∗ Redistribution of blood & ventilation to least affected areas of lung ∗ Secretion clearance ∗ Shifts mediastinum anteriorly – assists recruitment of atelectatic areas ∗ ? reduce lung injury ∗ Reduced lung compression by abdominal contents Positioning
- 47. Supine Ventilation ∗ ± 40% lung volume under lung, especially patients with large hearts
- 49. PATIENT LYING PRONE ON VOLLMAN PRONE POSITIONER 49
- 50. ∗ Daily CPAP breathing trial ∗ FiO2 <.40 and PEEP <8 ∗ Patient has acceptable spontaneous breathing efforts ∗ No vasopressor requirements, use judgement ∗ Pressure support weaning ∗ PEEP 5, PS at 5cm H2O if RR <25 ∗ If not tolerated, RR, Vt – return to A/C↑ ↓ ∗ Unassisted breathing ∗ T-piece, trach collar ∗ Assess for 30minutes-2 hours Weaning
- 51. ∗ Tolerating Breathing Trial? ∗ SpO2 ≥90 ∗ Spontaneous Vt ≥4ml/kg PBW ∗ RR ≤35 ∗ pH ≥7.3 ∗ Pass Spontaneous Awakening Trial (SAT) ∗ No Respiratory Distress ( 2 or more) ∗ HR > 120% baseline ∗ Accessory muscle use ∗ Abdominal Paradox ∗ Diaphoresis ∗ Marked Dyspnea ∗ If tolerated, consider extubation Weaning
- 52. 1) Calculate patient’s predicted body weight: • Men (kg) = 50 + 2.3(height in inches – 60) • Females (kg) = 45.5 + 2.3(height in inches – 60) 2) Set Vt = predicted body weight x 6cc 3) Set initial rate to approximate baseline minute ventilation (RR x Vt) 4) Set FiO2 and PEEP to obtain SaO2 goal of >=88% 5) Diurese after resolution of shock 6) Refer to ARDSnet guidelines Putting it all together
- 54. ∗ Mechanical Trouble (tubing, ventilator, ptx, plugging) ∗ Neuromuscular blockade ∗ Recruitment maneuvers – positioning, “good lung down” optimizes V/Q mismatch ∗ Increase PEEP ∗ Inhaled epoprostenol sodium (Flolan) ∗ When inhaled, the vasodilator reaches the normal lung, is concentrated in normal lung segments and recruits blood flow to functional alveoli where it is oxygenated. This decreases shunting and hypoxemia ∗ High frequency ventilation Refractory Hypoxia
- 55. Papazian, L, et al. NEJM 2010; 363: 1107-1116. -Neuromuscular blocking agents may increase oxygenation and decrease ventilator associated lung injury in severe ARDS patients -Multicenter double blind trial with 340 patients; received 48hrs of cisatracurium (Nimbex) or placebo -Found that early administration of NBA improved 90 day survival and increased time off vent without increase in muscle weakness
- 56. ∗ Treat underlying infection ∗ DVT prophylaxis / stress ulcer prevention ∗ Hand washing ∗ Use full barriers with chlorhexadine ∗ Sedation / analgesia ∗ Feeding protocol ∗ Avoid contrast nephropathy ∗ Pressure ulcer prevention, turning Q2h ∗ Avoid steroid use Supportive Therapies
- 57. ~No benefit of corticosteroids on survival ~When initiated 2 weeks after onset of ARDS, associated with significant increase in mortality rate compared to placebo group N Engl J Med. 2006; 354:1671
- 58. ∗ Recovery dependent on health prior to onset ∗ Within 6 months, will have reached max recovery ∗ At 1 year post-extubation, >1/3 have normal spirometry • Significant burden of emotional and depressive symptoms with increased depression in ARDS survivors ∗ Survivor clinic catches symptoms early by screening patients ∗ New treatment modalities, lung protective ventilation Conclusion Levy BD, & Choi AM, Harrison’s Principles of Internal Medicine, 2012
Editor's Notes
- Non-cardiogenic pulmonary edema Profound hypoxemia – difference between ali and ards.