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Acute Respiratory Distress Syndrome ARDS
- 1. Acute Respiratory Distress Syndrome(ARDS) Dr. Prasad Gaikwad Guide- Dr. R.S.Khot Dept of internal Medicine IGGMC, Nagpur
- 2. ARDS • Definition • Etiology •Clinical course and Pathophysiology • Clinical features • Differential diagnosis • Diagnosis • Treatment • Newer modalities- evidence based medicine
- 3. • 1st described1967 (Ashbaugh et al) • Incidence 1.5 -7.5/ 100000 population • 28 day mortality 25 – 44%1
- 4. Other names • Adulthyaline-membrane disease • Adult respiratory insufficiency syndrome • High output respiratory failure • Congestive atelectasis • Hemorrhagic lung syndrome • Stiff-lung syndrome • Shock lung • White lung
- 5. Definition • Clinical syndromeof severe dyspnoea of rapid onset, hypoxemia and diffuse pulmonary infiltrates with absence of left atrial hypertension leading to respiratory failure. • ALI is less severe form but may evolve into ARDS • ALI Po2/Fio2 ratio <300 mmHg. • ARDS Po2/Fio2 ratio <200 mmHg.
- 6. • Berlin definitionof ARDS
- 7. Clinical disorders associatedwith ARDS Direct lung injury 1)pneumonia 2)aspiration of gastric contents 3)pulmonary contusion 4)near drowning 5)toxic inhalation injury Indirect lung injury 1) Sepsis 2)Severe trauma 3)Multiple fractures 4) Multiple blood transfusion 5)Pancreatitis 6) Cardiopulmonary bypass
- 8. Clinical course andPathophysiology • 3 phases 1)Exudative phase- hyaline membrane- 0 to 7 day 2) Proliferative phase- interstitial inflammation- 7 to 21 day 3) Fibrotic phase- fibrosis- after 21 days
- 9. Pathophysiology during exudative phase Direct orindirect injury to the alveolus causes alveolar macrophages to release pro- inflammatory cytokines ↓ Cytokines attract neutrophils into the alveolus and interstitum, where they damage the alveolar-capillary membrane (ACM). ↓ . ACM integrity is lost, interstitial and alveolus fills with proteinaceous fluid, surfactant can no longer support alveolus
- 10. • Exudative Phase •Neutrophilic Infiltrate • Alveolar Haemorrhage • Proteinaceous Pulmonary Oedema • Cytokines (TNF, IL1,8) » ↑ Inflammation » ↑ Oxidative Stress and Protease Activity » ↓ Surfactant Activity » Atelectasis Elastase- induced capillary and alveolar damage3 ↑ Alveolar flooding ↓ Fluid clearance
- 11. Proliferative phase lasts around7-21 days initiation of lung repair organisation of alveolar exudates shift from PMN to lymphocyte rich infiltrate Type II pneumocyte Synthesize surfactant proliferate differentiate into Type I cells reline alveolar walls Fibroblast proliferation interstitial/alveolar fibrosis
- 12. Fibrotic phase Extensive alveolarduct and interstitial fibrosis. Emphysema like changes with bullae formation. Fibrosis may result into progressive vascular occlusion and pulmonary hypertension.
- 13. Consequences of lunginjury include: 1)Impaired gas exchange-due to hyaline membrane V/Q mismatch Related to filling of alveoli Shunting causes hypoxemia Increased dead space Related to capillary dead space and V/Q mismatch Impairs carbon dioxide elimination Results in high minute ventilation 2)Decreased compliance- more in dependent lung portions Hallmark of ARDS Consequence of the stiffness of poorly or nonaerated lung Fluid filled lung becomes stiff/boggy Requires increased pressure to deliver Vt
- 14. 3) Increased pulmonaryarterial pressure Occurs in up to 25% of ARDS patients Results from hypoxic vasoconstriction Positive airway pressure causing vascular compression Can result in right ventricular failure
- 15. Clinical features Symptoms • Acuteonset exertional dyspnoea leading to dyspnoea at rest. • Tachypnea • Anxiety • Agitation • Increased work of breathing Physical examination • Tachypnea • Tachycardia • Increased FiO2 to maintain saturation • May be febrile of hypothermic • Cold extremities • Bilateral crepitation • Manifestation of underlying cause • Cardiogenic pulmonary edema to be ruled out
- 16. Differential diagnosis • Cardiogenicpulmonary edema • Diffuse pneumonia • Alveolar hemorrhage • Acute interstitial pneumonitis • Hypersensitive pneumonitis • Neurogenic pulmonary edema
- 17. Diagnosis Mainly clinical-no specificdiagnostic tests Laboratory tests Diagnostic imaging Hemodynamic monitoring Bronchoscopy
- 18. Lab tests • ABGanalysis PaO2/FIO2 ratio is less than 200. Respiratory acidosis later on metabolic acidosis • To exclude cardiogenic pulmonary edema- B-type natriuretic peptide (BNP) value <100 pg/mL Echocardiogram • Hematological- either leukocytosis or leucopenia • Renal- (ATN) often ensues in the course of ARDS • Hepatic-Liver function abnormalities may be noted in either a pattern of hepatocellular injury
- 19. ABG in ARDS Initialstages PaO2 < 60 mmHg PaCO2 < 35 mmHg pH- may normal or increased showing respiratory alkalosis P/F ratio <200 Late stages PaO2 more falling despite oxygen therapy PaCO2 >45 mmHg showing respiratory acidosis Serum bicarbonates < 22 mEq/L showing metabolic acidosis P/F ratio <200
- 20. Radiological –chest x-ray Showsbilateral alveolar and interstitial opacities involving atleast three- quarters of lung fields. Difficult to d/w from cardiogenic pulmonary edema.
- 21. Initial patchy peripheral distributionbut later on progresses to ground glass alveolar opacities.
- 22. Radiological CT thorax heterogeneity ofalveolar involvement is apparent on CT scan
- 23. Invasive Hemodynamic Monitoring •Hemodynamic monitoring with a pulmonary artery (Swan- Ganz) catheter may be helpful in selected cases for distinguishing cardiogenic from noncardiogenic pulmonary edema. • This allows measurement of RA pressure, RV pressure, PA pressure and pulmonary artery occlusion pressure (PAOP). • A PAOP lower than 18 mm Hg is usually consistent with noncardiogenic pulmonary edema. • However their use is controversial. • One large retrospective cohort study of ICU showed that patients with pulmonary artery catheters had an increased mortality rate, hospital cost, and length of stay. • Hence not indicated for routine patients.
- 24. Bronchoscopy • May beconsidered to evaluate the possibility of infection, alveolar hemorrhage, or acute eosinophilic pneumonia in patients acutely ill with bilateral pulmonary infiltrates • >10000 organisms/mL is significant for diagnosis of ARDS for patients who are not treated with antibiotics. • Presence of neutrophils in the BAL fluid with the presence of intracellular organisms is helpful in diagnosis of ARDS • Analysis of the types of cells present in the BAL fluid may be helpful in the differential diagnosis of patients with ARDS. >20% eosinophils-acute eosinophilic pneumonia high proportion of lymphocytes may be observed in acute hypersensitivity pneumonitis, sarcoidosis, or bronchiolitis obliterans-organizing pneumonia (BOOP)
- 25. Management of ARDS •Treat the underlying cause. • Conservative fluid management. • Non invasive ventilation. • Mechanical ventilation. • Other modalities.
- 26. Treating underlying cause Theunderlying cause may be treated with broad spectrum antibiotic as with patients having pneumonia, pancreatitis and severe sepsis Surgical intervention if needed should be carried out
- 27. Fluid management • Aggressiveattempts to reduce left atrial filling pressure-will help in minimizing pulmonary edema and improved arterial oxygenation • Can be achieved by fluid restriction and diuresis • Approach limited by hypotension Hypoperfusion of end organs Secondary ARDS due to remote infection and inflammation
- 28. Non-invasive ventilation • ContinuousCPAP or Non invasive ventilation using BiPAP mask may be beneficial in early course of disease. • But often patients unable to maintain saturation , get drowsy, develop altered sensorium • Very little data available for its use • Invasive mechanical ventilation is mandatory
- 29. Mechanical ventilation • Goalsof mechanical ventilation Low tidal volume ventilation to avoid volutrauma Maintain O2 saturation between 85-90% Minimizing FiO2 < 0.65 within first 48 hrs of ventilation Optimum PEEP Minimal plateau pressures
- 30. Mechanical ventilation Low TidalVolume Ventilation • ONLY RECOMMENDED BEST THERAPEUTIC APPROACH OVER 4 DECADES • 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
- 31. • ARDS affectsthe lung in a heterogeneous fashion • Normal alveoli- can cope up with normal or higher vt • Injured alveoli -can potentially participate in gas exchange, susceptible to damage from opening and closing of higher vt • Damaged alveoli-filled with fluid, do not participate in gas exchange • High tidal volumes • Overdistention of alveoli • Local inflammatory response resulting in systemic inflammation with release of inflammatory cytokines • Recommended 4-6ml/kg
- 32. Optimum PEEP • Empiricallyset to a level that it will minimize FiO2 and maximize PaO2. • On most modern mechanical ventilators it is possible to set static pressure –volume curves. • Titration of PEEP to the lower inflection point on pressure – volume curve- keeps lungs open, improves oxygenation, minimizes barotrauma. • Optimum PEEP for most of patients ranges from 12-15 mmHg
- 33.
- 34. Inverse ratio ventilation I:Eratio > 1:1 Inspiratory time lengthened and expiratory time shortened. Same strategy like increasing ventilator prescribed PEEP May help to keep FiO2 < 0.6 to avoid oxygen induced toxicity Long term survival benefit is questionable.
- 35. Airway Pressures inARDS • Plateau pressure is most predictive of lung injury • Goal- plateau pressure < 30, the lower plateau pressure the better is outcome • 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
- 36. • Assess causeof high Plateau Pressures • Always represents some pathology: – heart failure – Pneumothorax – Auto-peeping – Mucus Plug – Right main stem intubation – Chest wall fat / Obesity
- 37. Permissive hypercapnia • It’sa consequence of low Vt ventilation. • Patients often develop hypercapnia and respiratory acidosis. • Small studies in favour of PaCO2 levels as high as 375mmHg and pH as low as 6.6 • However recent meta-analysis suggest that PaCO2 of 60-70 mmHg and pH range 7.2-7.25 are sufficient to avoid volutrauma. • Troublesome part- patients often develop hyperventilation and ventilator asynchrony; needs managed with neuromuscular blockade.
- 38. Ventilatory parameters First stage 1)Calculatepatient’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 8 mL/kg 3)Add PEEP of 5-7 cm H2O 4)Reduce Vt every 2hrs by 1 mL/kg till 6mL/kg PBW Second stage Now set target plateau pressure <30 cmH2O by adjusting Vt till 4mL/kg Third stage 1)Target pH= 7.30-7.45 2)If pH <7.30 then adjust RR till 35br per minute
- 39. Weaning • Daily CPAPbreathing trial – FiO2 <.40 and PEEP <8 – Patient has acceptable spontaneous breathing efforts – No vasopressor requirements, • 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
- 40. Weaning • Tolerating BreathingTrial? – 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 • No Accessory muscle use • No Abdominal Paradox • No Diaphoresis • No Marked Dyspnea – If tolerated, consider extubation
- 41. Other modalities • Proneposition ventilation • High frequency ventilation • Partial liquid ventilation • Extracorporeal membrane oxygenation(ECMO) • Systemic glucocorticoids • Surfactant replacement • Inhaled nitric oxide
- 42. • Prone positionventilation • 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
- 43. Hypothesis: Early applicationof 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.
- 44. • High frequencyoscillation ventilation(HFOV) uses small tidal volumes(1-2 mL/kg) at a very fast rate(5-20 cycles per second) Had been useful in animal studies Lack proven benefit in human. Instead hazardous
- 45. -Randomized control trial,stopped with 548 of 1200 patients -Found early initiation of HFOV does not reduce hospital mortality and may increase hospital mortality
- 46. • Extracorporeal membraneoxygenation(ECMO) had proven benefit for neonatal respiratory syndrome but not for ARDS • Partial liquid ventilation uses high density , inert liquid of per-fluorocarbon which solubilizes oxygen and carbon dioxide; thought to improve oxygenation. No clear benefit on survival
- 47. Inhaled nitric oxide canbe of help in early course of treatment to improve oxygenation but no improved survival benefit Glucocorticoids To suppress inflammation in early ARDS did not have any have any evidence based recommendation Instead deleterious effect on pulmonary inflammation
- 48. • Enrolled 282patients with aerosolized albuterol and saline placebo with primary outcome as ventilator free days. • Conclusion -aerosolized albuterol does not improve clinical outcomes in patients with ALI. Routine use of b2-agonist therapy in mechanically ventilated patients with ALI can not be recommended
- 49. Evidence –based recommendationsfor ARDS therapies Treatment Recommendation Low tidal volume A Minimize left atrial filling pressure B High PEEP C Prone position C ECMO C High frequency ventilation D glucocorticoids D Surfactant replacement and inhaled nitric oxide D A- recommended on evidence based RCTs B- recommended based on supportive but limited clinical trials C- recommended only as alternative therapy D- not recommended as evidence is against efficacy
- 50. Prognosis • Mortality rangesfrom 26-44% • Mostly attributable to underlying cause of ARDS • Age is most important predictor of mortality • Other predictors- presence of liver damage, alcohol abuse, APACHE III score, presence of kidney injury • Patients >60yrs have threefold mortality than <60yrs • Patients having direct lung injury have twofold more mortality than indirect lung injury.
- 51. Sequelae • Patients usuallyrecover complete lung functions within 6 months. • One third of Survivors have normal spirometry and diffusion capacities after 6 months. • Significant rates of depression and post traumatic stress disorder amongst survivors.
- 52.