Acute Respiratory Distress Syndrome

1. Acute Respiratory Distress Syndrome Susie Gerik, MD Children’s Special Services

2. Objectives • Describe features of ARDS • List possible inciting conditions • Describe pathophysiology • Discuss treatment strategies • Address morbidity and mortality

3. History • Described by William Osler in 1800 • Asbaugh et al., Lancet 1967 • Observed in adults and children

4. Definition • Condition characterized by acute inflammatory lung injury resulting in widespread pulmonary edema as a result of increased alveolar capillary permeability and epithelial destruction.

5. Features • Acute respiratory distress • Cyanosis refractory to oxygen • Decreased lung compliance • Diffuse infiltrates on CXR

7. 1988 Lung Injury Score • PEEP • PaO2/FIO2 ratio • Static lung compliance • Degree of infiltrates

8. 1994 Consensus • Acute onset • PaO2/FIO2 < 200 • Bilateral infiltrates • PCWP < 18

9. 1994 Consensus • Two categories: • Acute lung injury: PaO2/FIO2 ratio < 300 • ARDS: PaO2/FIO2 < 200

10. Incidence • Acute Lung Injury: 17.9/100,000 • ARDS: 13.5/100,000 • ~1% of all PICU admissions

11. Causes • Shock • Aspiration • Trauma • Infections • Inhaled fumes • Drugs and poisons • Miscellaneous

12. Ventilator-induced Lung Injury • Barotrauma • large lung volumes • Atalectrauma • shear forces • Biotrauma • activation of effector cells to release mediators

13. Indirect Injury • Sepsis syndrome • Severe nonthoracic trauma • Post cardiopulmonary bypass • Post hemodialysis • Disseminated intravascular coagulation • Pancreatitis • Antiphospholipid syndromes

15. Pathogenesis • Inflammatory mediators • damage to microvascular endothelium • damage to alveolar epithelium • increased alveolar permeability • accumulation of alveolar edema fluid

16. Pathogenesis • Neutrophils and macrophages • Complement • Cytokines • Platelet activating factor • Eicosanoids • Free radicals

18. Pathophysiology • Abnormalities in gas exchange • Abnormalities in oxygen delivery and consumption • Abnormalities in cardiopulmonary interactions • Multiple organ involvement

19. Gas Exchange - Hypoxemia • Increased capillary permeability • Interstitial and alveolar exudate • Intrapulmonary shunting • Reduced ventilation-perfusion matching • Diffusion defect with right to left shunt

20. Pulmonary Mechanics • Reduced lung volume (FRC) • Reduced lung compliance • Impaired function of surfactant

21. Pathologic Flow • Uncoupling of oxidative dependency • Oxygen utilization by non-ATP producing oxidase systems • Increased diffusion distance for O2 between capillary and alveolus

22. Cardiopulmonary Interactions • Pulmonary hypertension -> increased RV afterload • High PEEP -> decreased preload • Results in decreased cardiac output

24. Non-pulmonary Abnormalities • Multi-organ system failure • Bio-trauma • Pathologic oxygen-supply dependency

25. Max O2 extraction VO2 Critical DO2 DO2 Normal VO2 = DO2 X O2ER Substrate utilization Max O2 extraction VO2 Critical DO2 DO2 Septic Shock/ARDS Abnormal Flow Dependency

26. Acute, Exudative Phase • Rapid respiratory failure after trigger • Diffuse alveolar damage with inflammatory infiltrate • Hyaline membrane formation • Capillary injury • Protein-rich edema fluid in alveoli • Disruption of alveolar epithelium

27. Subacute, Proliferative Phase • Persistent hypoxemia • Development of hypercarbia • Fibrosing alveolitis • Further decrease in pulmonary compliance • Pulmonary hypertension

28. Chronic Phase • Obliteration of alveolar and bronchiolar spaces and pulmonary capillaries

29. Recovery Phase • Gradual resolution of hypoxemia • Improved lung compliance • Resolution of CXR abnormalities

30. Goals of Treatment • Optimize gas exchange and O2 delivery • Minimize ventilator-induced lung injury • Treat etiology • Avoid multisystem organ failure

31. Treatment: Respiratory Support • Mechanical ventilation • High frequency ventilation • ECMO • Nitric oxide • Liquid ventilation • Exogenous surfactant

32. Treatment: Monitoring • Respiratory • Hemodynamic • Metabolic • Infections • Fluid/electrolytes

33. Optimize VO2/D02 Relationship • DO2 • hemoglobin • mechanical ventilation • oxygen (PEEP) • VO2 • preload • afterload • contractility

34. Ventilation Strategies • Oxygen • PEEP • Inverse I:E ratio • Lower TV • Prone position

35. PEEP • Displaces edema fluid into interstitium • Decreases atalectasis • Decreases right to left shunt • Improves compliance • Improves oxygenation

36. Nitric Oxide • Pulmonary vasodilation • Selectively improves perfusion of ventilated areas • Reduces intrapulmonary shunting • Improves arterial oxygenation • No systemic hemodynamic effects

37. Prone Position • Improved gas exchange • Uniform alveolar ventilation • Recruitment of segments in dorsal region • Improved postural drainage • Redistribution of perfusion away from edematous, dependent regions

38. High Frequency Ventilation • Raises MAP • Recruits lung volume • Small changes in TV • Impedes venous return

40. Liquid Ventilation • Perflubron • 20x O2 and 30x CO2 solubility • Heavier than water • Higher spreading coefficient • Improved compliance and gas exchange

42. Mortality • 40-60% • Multiorgan failure/sepsis • Decreasing because of better vetilatory strategies and earlier recognition and treatment

43. Iatrogenic Contributors to Morbidity/Mortality • Inadequate nutrition • Fluid overload • Inappropriate sedation • Neuromuscular blocking agents • Complications from medical procedures • Medical errors

44. Prognostic Factors • Underlying medical condition • Presence of multiorgan failure • Severity of illness

45. Thank you!