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A R D S. Jhansi Nalamati MD FCCP Asst. Prof. Of Medicine, AECOM BRONX NY. Definition. Acute Respiratory Distress Syndrome First described in 1967 in Lancet as Adult Respiratory Distress Syndrome by Asbaugh et.al.

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A R D S

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  1. A R D S Jhansi Nalamati MD FCCP Asst. Prof. Of Medicine, AECOM BRONX NY

  2. Definition • Acute Respiratory Distress Syndrome • First described in 1967 in Lancet as Adult Respiratory Distress Syndrome by Asbaugh et.al. • 12 pts. had developed acute respiratory distress, cyanosis , diffuse pulmonary infiltrates decreased lung compliance and was refractory to Oxygen therapy • Also called as “wet lung”, “shock lung” and “Da Nang lung”

  3. Incidence • Crude estimates of 78.9/100,000 person years • In patient mortality 38.5% • 190,600 cases/year in the US with 74,500 deaths and 3.6 million hospital days

  4. ARDS and ALI (Acute Lung Injury) in 1992 • Defined by American European Consensus • “Acute Lung Injury” is an umbrella term for “ Hypoxemia Respiratory Failure” , a severe version of which is “ARDS”. • Bilateral Infiltrates • PCWP< 18mm Hg • PaO2/FiO2< 300 = ALI • PaO2/FiO2<200 =ARDS

  5. ALI/ARDS ( Addl. Features) • Bilateral widespread infiltrates on CXR • Airway collapse ( low lung Volumes) • Surfactant deficiency • Reduced lung compliance

  6. Etiology • Direct insult to the lungs- bacterial, viral, fungal agents, lung contusion, Fat embolism • Systemic medical and surgical conditions- trauma, shock, sepsis, burns, pancreatitis • Noxious agents- exposure to smoke , aspiration

  7. PATHOPHYSIOLOGY • Altered Pulmonary Capillary Permeability secondary to endothelial injury • Altered alveolar diffusion capacity • Increased intrapulmonary shunt • Degree of epithelial injury can predict outcome

  8. Patho-physiology(contd.) • Loss of epithelial integrity and injury to type II alveolar cells can disrupt fluid transport thereby leading to impairing the removal of fluid from alveolar space • Injury to type II pneumocytes can reduce the production of surfactant which leads to worsening atelectasis and gas exchange

  9. Histo-pathological phases • 1) Exudative Phase: 1-3 days- diffuse alveolar damage ( DAD) with majority of type I pneumocyte necrosis, diffuse microvascular injury and influx of inflammatory cells and proteinaceous fluid into the interstitium

  10. Fibroproliferative phase • Day 3-7- repair manifested by type I pneumocyte hyperplasia and proliferation of fibroblasts

  11. Treatment of ARDS • Corner stone of treatment is to keep PaO2 >60mm Hg, without causing injury to lung with excessive O2 or excessive TV ( FiO2 < 60% and TV of 6ml/kg) • Plateau pressure should not exceed 30mmHg and minimal TV should be at least 4ml/kg ( irrespective of MAP or plateau pressure) • “Avoid Volutrauma and Barotrauma”

  12. ATS recommendations • Minimize O2 toxicity • Recruit alveoli • Minimize high airway pressures • Prevent atelectasis • Use sedation and paralysis judiciously

  13. Tx of ARDS/ALI • “SUPPORTIVE CARE” • “SUPPORTIVE CARE” • “SUPPORTIVE CARE”

  14. Low Tidal Volume Ventilation with or without High PEEP • Minimizes the amount of phasic stretch of lung units in inspiration to prevent VILI( Ventilator Induced Lung Injury) • Proven to be effective in an NIH coordinated multi center trial( NEJM ), patients ventilated with TV of 6ml/kg had a 22% reduction in mortality compared to patients ventilated with TV of 10-12ml/kg

  15. Open Lung approach • Attempts to optimize lung mechanics and minimize phasic damage by strategically placing PEEP above Pflex. • Quasi- Static Volume Pressure curve- the lungs are said to be most compliant between the lower inflection point and the upper inflection point, beyond which over distension occurs

  16. PCV( Pressure Controlled ventilation) • Better gas distribution than volume control ventilation by avoiding over distension of low complaint units • Plateau pressure not to exceed 30mm of Hg • Reverse I:E Ratio

  17. APRV ( Airway pressure release ventilation) • Sets pressure high and pressure low and time high and time low • Patient can spontaneously breathe within these limits, minimizing sedation requirements • Unclear what is the PEEP ( ? Pressure high, ? Pressure low, ? Mean)

  18. HFV ( High frequency ventilation) • Reduces barotrauma and improves VQ mismatch • Potential complications- inspication of mucus, airway damage due to high gas velocities and over distension causing alveolar injury and worsening ALI

  19. Tx ( contd.) • Prone Positioning • Permissive Hypercapnia ( potential complications include pulmonary vasoconstriction, pulmonary HTN, proarrhythmic effects, cerebral vasodilatation, increasing ICP) • Prophylactic Bil. chest tubes

  20. Inhaled Nitric Oxide • Improves oxygenation and decreases Pulmonary Vascular Resistance • Dose varies from 1.25 to 40ppm • NO clear benefit in limited randomized controlled trials • Needs to be given for days to weeks • Sensitization can occur • Can cause renal dysfunction, immunosuppression, potentially mutagenic , can cause methhemoglobinemia and NO2 concentration

  21. Steroids in ARDS • Controversial • Cytokines decline over the first week in survivors of ARDS, but persist in non survivors

  22. Steroid regimen( Prednisone) • 2mg/kg day 1-14 • 1mgkg day 15-21 • 0.5mg/kg day 22-28 • 0.25mg/kg day 29-30 • 0.125mg/kg day 31-32 • Not to be started before 7days of ALI or admission or beyond 28days of ALI or admission

  23. Novel therapies for ARDS • Albuterol • Salmetrol • Surfactant • Pentoxyfylline • Cyclooxygenase inhibitors • Antioxidants • TNF antibodies infusion • PAF inhibitors and receptor antagonists • Antiproteases

  24. Cause of death • Underlying cause • Secondary complications- sepsis from ventilator associated pneumonia, GI bleed, multi organ failure

  25. Management of secondary effects • Judicious use of sedation and neuromuscular blockade • Hemodynamic management • Nutritional support • Glucose control • Nosocomial pneumonia prevention and Tx • GI and DVT prophylaxis

  26. Nosocomial Pneumonia • 60% of pts with ARDS in 30days • Can occur as early as 10days • Prevention strategies include-continuous subglottic aspiration of secretions, selective GI tract decontamination ( does not prevent pseudomonas) elevation of head 30 degrees, mouth care, avoiding vent. Circuit changes or clearing the condensate

  27. Nosocomial pneumonia (contd.) • Closed suction is of no benefit • Avoid unnecessary antibiotics • No use of antibiotic or silver impregnated ETT tubes

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