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ARDS

ARDS. ד"ר אלחנן פריד MSMSICU. ARDS. הגדרה (ישנה...) :. First described in 1967 as Adult Respiratory Distress Syndrome שכיח (~100/100,000 שנות אדם), יקר, הורג! American-European Consensus Conference Committee ( AECC 1994 ) criteria Acute onset Bilateral infiltrates in chest radiography

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ARDS

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  1. ARDS ד"ר אלחנן פרידMSMSICU

  2. ARDS הגדרה (ישנה...) : • First described in 1967 as Adult Respiratory Distress Syndrome • שכיח (~100/100,000 שנות אדם), יקר, הורג! • American-European Consensus Conference Committee (AECC 1994) criteria • Acute onset • Bilateral infiltrates in chest radiography • Pulmonary-artery wedge pressure<18 mmHg • Acute lung injury PaO2/FiO2<300 • Acute respiratory distress syndrome PaO2/FiO2<200

  3. Piantadosi, Annals Int Med 2004; 141:460-470

  4. First Berlin definition

  5. Second Berlin fefinition • הפרוגנוזה קשורה לקבוצה:MILD ~27%, MOD ~35%, SEVERE ~45%

  6. ARDS: Causes

  7. ARDS:Epidemiology • Incidence: 80 per 100,000 • Outcomes: • Traditionally 40-60% mortality • Majority of deaths due to MSOF • Low tidal volume ventilation decreases mortality • Other critical care improvements may be involved • Predictive factors for death: CLD, non pulmonary organ dysfunction, sepsis and advance age • Survivors: Most of them will have normal pulmonary function within a year

  8. ARDS:Pathogenesis • ARDS is the manifestation of SIRS in the lungs • Influx of protein rich edema into the air spaces due to increased permeability of the alveolar-capillary barrier • Endothelial damage pathophysiology is similar to that of SIRS/SEPSIS

  9. ARDS:Pathogenesis Insult! Cytokines!! • PMN infiltration – predominate in BAL profilePathology: Exudative Fibroproliferative Fibrotic • Type II Pneumocyte damage – decreased surfactant – atelectasis • Loss of compliance • Shunt, VQ mismatch, Diffusion abnormality: HYPOXEMIA

  10. ARDS: Exudative Phase • The definition applies for the acute “exudative” phase • Rapid onset • Hypoxemia refractory to supplemental oxygen • CXR similar to pulmonary edema • CT Scan: Alveolar filling, consolidation and atelectasis in the dependent lung zones • Pathologic findings: • diffuse alveolar damage with capillary injury and disruption of the alveolar epithelium • hyaline membranes • protein rich fluid edema with neutrophils and macrophages

  11. ARDS:Pathogenesis

  12. ARDS: Exudative Phase • CT Scan During Acute Phase

  13. ARDS: Fibroproliferative phase • Some patients progress to fibrosing alveolitis with persistent hypoxemia, increase alveolar dead space and further decrease in pulmonary compliance • The process may start as early as 5-7 days • The alveolar space becomes filled with mesenchymal cells and their products as well as new blood vessels

  14. ARDS:Pathogenesis

  15. ARDS: Fibroproliferative phase • CT Scan during fibroproliferative phase. • Diffuse interstitial opacities and bullae

  16. DD Infectious causes • Bacteria - Gm neg & pos , mycobacteriae, mycoplasma, rickettsia, chlamydia • Viruses- CMV, RSV, hanta virus, adeno virus, influenza virus • Fungi- H.capsulatum, C.immitis • parasites- pneumocytis carinii, toxoplasma gondii

  17. DD Non infectious causes • CCF • Drugs & toxins (paraquat, aspirin, heroin, narcotics, toxic gas, tricyclic anti depressants, acute radiation pneumonitis) • Idiopathic (esinophilic pneumonia, Acute interstitial pneumonitis, BOOP, sarcoidosis, rapidly involving idiopathic pulmonary fibrosis) • Immunologic (acute lupus pneumonitis, Good Pastures syndrome, hypersensitivity pneumonitis) • Metabolic (alveolar proteinosis) • Miscellaneous (fat embolism, neuro/high altitude pulmonary oedema) • Neoplastic (leukemic infiltration, lymphoma)

  18. ARDS:Treatment • Recent decrease of mortality • Treatment of underlying cause • Better supportive ICU Care • Prevention of infections • Appropriate nutrition • GI prophylaxis • Thromboembolism prophylaxis

  19. ARDS: Treatment • Protective ventilation • Smaller tidal volumes • Avoid overdistention • Tolerate “permissive hypercarbia” • “Open lung” ventilation • Avoid alveolar collapse and reopening

  20. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress SyndromeThe Acute Respiratory Distress Syndrome Network N Engl J Med 2000;342:1301-8 • Study stopped after 2nd interim analysis • Reduction of mortality by 22%

  21. VARIABLES Ventilator mode Tidal Volume Plateau Pressure Ventilation rate/pH goal Inspiration flow, I:E Oxygenation goal FIO2/PEEP Weaning PROTOCOL Volume assist control < 6mL/Kg body weight <30 cm H2O 6-35/min adjusted for pH of 7.30 if possible Adjust to 1:1-1:3 PaO2>55 and or SpO2>88% Combinations PS wean when FiO2/PEEP<.40/8 NIH/ARDS Network

  22. Hypercarbic acidosis Hypoxemia Respiratory failure and arrest Decrease myocardial contractility Cerebral vasodilatation Decrease seizure threshold Hyperkalemia Permissive hypercapnia Supplemental oxygen overcomes CO2 induced hypoxia No evolution to respiratory arrest Lack of significant deleterious effects Is hypercarbia beneficial? ARDS:Permissive Hypercapnia

  23. Optimal “PEEP” • Positive end-expiratory pressure should be high enough to shift the end-expiratory pressure above the lower inflection point by 2-3 cm H2O (usually 12-15 cm H2O) • Allows maximal alveolar recruitment • Decreases injury by repeated opening and closing of small airways

  24. ARDS: Treatment • Recruiting maneuvers • NO • Prone positioning • Steroids • APRV • ECMO • Volume cycle vs. pressure cycle • Inverse-Ratio Ventilation • Non invasive Positive Pressure Ventilation • High-Frequency Ventilation • Tracheal Gas Insufflation • Extracorporeal gas exchange • Fluorocarbon Liquid Gas Exchange

  25. APRV • It uses a release of airway pressure from an elevated baseline to simulate expiration. • The elevated baseline facilitates oxygenation avoids collapsing of alveoli and the timed releases aid in carbon dioxide removal. • Potential advantages of APRV include lower airway pressures, lower minute ventilation, minimal adverse effects on cardio-circulatory function. • Airway pressure release ventilation is consistent with lung protection strategies that strive to limit lung injury associated with mechanical ventilation, particularly recruitment/derecruitment • More (larger) studies are needed to define its role in ALI/ARDS

  26. ARDS:Treatment • Inhaled nitric oxide and other vasodilators • Most ARDS/ALI patient may have mild to moderate pulmonary HTN • Improvement in oxygenation was small and not sustained • No change on mortality or duration of mechanical ventilation • May be used as “rescue” therapy • Surfactant • Successful in neonatal respiratory distress syndrome

  27. Recruitment maneuvers • Lung recruitment in patients with ARDS GattinoniNEJM 2006;354:1175-86 • Sixty eight patients with ALI/ARDS underwent whole lung CT Scan during breath holding session at airway pressures of 5, 15 and 45 cm of water • The percentage of potentially recruitable lung was defined as the proportion of lung tissue in which aeration was restored (Recruited)

  28. Recruitment • Knowing the % of recruitable lung might be the key to the effects of PEEP • PEEP in patients with limited recruitable areas might be of little benefit or harmful • Overdistention • Worsening of Shunt • Authors suggest PEEP of 15 for those recruitables and 10 for those who are not

  29. ARDS Treatment • Gattinoni et al, NEJM 2001;345:568-573 • 304 patients with ARDS • Prone group: at least six hours/day for ten days • Better oxygenation in the prone patients • Similar incidence of complications • No improvement in survival • However patient only prone for 7 hours a day and up to 10 days

  30. ARDS Treatment • Fluid and hemodynamic management • Optimal fluid management is controversial • There is data supporting fluid restriction as a mean to minimize lung edema • However maintenance and preservation of oxygen delivery may require fluid administration • Euvolemia, judicious use of vasopressors • Effects of ventilation in circulation • To Swan or not to Swan

  31. ARDS: Treatment • Glucocorticoids • No benefits in acute phase • Some evidence of improvement during proliferative phase (Meduri et al JAMA 1998;280:159-165) • Methylprednisolone 2mg/kg initially for 32 days • Improvement in Lung injury scores, MOSD scores and mortality • Benefits may be noticed by day 3 • High risk of infection • ? May consider a short course of high dose as rescue therapy

  32. ARDS: Treatment • Omega-3 (immunonutrition) • Prostacyclines • Surfactant • NMA • Ketoconazole • Pentoxifylline • Antioxidants, NAC

  33. Swan and ARDS • PAC versus CVP to guide treatment of ALI NEJM 2006; 354: 2213-2224 • 1000 patients • Mortality at 60 days was similar between groups, as well as the ventilator free days and days not spent in the ICU • Fluid balances were similar among the groups • PAC had double complications mainly arrhythmias

  34. ARDS- Survival & Follow-up • One year post discharge, 49% of survivors had returned to work, most to prior positions • Those not returning: - persistent weakness & fatigue - job stress - poor mobility - poor functional statusHerridge et al NEJM 2003; 348(8)683-93

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