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ARDS

ARDS. ICU nurses course 2004 Tim Smith. History. WW1 deaths from respiratory problems after non-thoracic injury Ashbaugh 1967 Series 12 similar cases reported “Adult Respiratory Distress Syndrome” 1988 Murray’s Lung Injury Score 1994 AECC “Acute Respiratory Distress Syndrome”

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ARDS

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  1. ARDS ICU nurses course 2004 Tim Smith

  2. History • WW1 deaths from respiratory problems after non-thoracic injury • Ashbaugh 1967 • Series 12 similar cases reported • “Adult Respiratory Distress Syndrome” • 1988 Murray’s Lung Injury Score • 1994 AECC • “Acute Respiratory Distress Syndrome” • “Acute Lung Injury”

  3. Definitions • Diagnosis: • Acute onset respiratory failure • History of risk factor • Severe hypoxaemia • Bilateral pulmonary infiltrates • Not cardiogenic pulmonary oedema • ARDS if PaO2:FiO2 <200 • ALI if PaO2:FiO2 <300

  4. Pathogenesis • Inflammatory process • Diffuse damage to alveoli and to vascular endothelium • Multiple possible inciting events • Multiple inflammatory mediators • IL-1, IL-8, TNF • Balance of pro vs anti inflammatory mediators probably important

  5. Pathology

  6. Pathophysiology • ’d interstitial and alveolar fluid • Decreased surfactant (type II cells) • Hyaline membrane formation • Impaired gas exchange • Alveolar collapse (V/Q mismatch) • Decreased lung compliance

  7. Causes Direct Lung Injury • Pneumonia • Aspiration • Lung contusion • Fat embolus • Near drowning • Inhalational Injury • Reperfusion Injury Indirect Lung Injury Sepsis Trauma Transfusion Overdose Pancreatitis

  8. Incidence • USA estimate 1977: • 75/100,000/y • Scandinavian study 1999: • ARDS 13.5 /100,000/y • ALI 17.9 /100,000/y • ARDSnet suggests may be higher in USA even with new criteria.

  9. Outcome • Apparently improving. • Seattle: • 1983-1987 mortality 53-68% • 1993 mortality 36% • UK: • 1990-1993 mortality 66% • 1994-1997 mortality 34% • Why? • Better general care? • Better treatment of sepsis? • Better ventilation strategies?

  10. Prognostic Factors • All negative: • Advanced age • Non-pulmonary organ dysfunction • Chronic liver disease • Sepsis • Failure to improve during 1st week • Initial PaO2:FiO2 ratio not predictive • Initial lung injury score not predictive

  11. Sequelae • Resolution • most survivors • gradual but full recovery • normal or near normal lung function in 1y • Fibrosing alveolitis • 10-13% of survivors • healing by scarring not re-epithelialisation • Persistent poor compliance • Increased alveolar dead space • Continuing hypoxia

  12. Clinical History • Often unobtainable 1st hand • Progressive dyspnoea • Important to enquire after cause • May not be obvious • Usually 12-48h before onset of illness

  13. Physical Signs • Non-specific • Febrile/Hypothermic • Tachypnoea • Tachycardia • Cyanosis • Chest auscultation may be normal • Manifestations of underlying disease • Examine carefully for septic foci • Lines • Wounds • Etc • Exclude cardiogenic pulmonary oedema

  14. Laboratory Analyses • Non-specific • Signs of underlying disease • Monitor liver and renal function • Often leukocytosis or leukopenia • Inflammatory markers often raised

  15. Blood Gas Analysis • Hypoxaemia • Initially: • may see respiratory alkalosis • Underlying disease: • metabolic acidosis • As respiratory function worsens: • respiratory/mixed acidosis

  16. Chest X Ray • Bilateral infiltrates • Symmetric/Asymmetric • Patchy/Diffuse • Initially often peripheral • Immediate changes max severity 3d • Poor correlation with hypoxaemia

  17. Chest X ray 1

  18. Chest X ray 2

  19. Chest X Ray 3

  20. CT Scan • May give important additional info • BUT possible high risk transfer • Better detection of: • Pneumothoraces • Pneumomediastinum • Effusions • Cavitation • Pulmonary Interstitial Oedema

  21. CT scan 1

  22. CT scan 2

  23. Treatment • Respiratory support • Treatment of the cause • Supportive care • Fluid management • Nutrition • Stress ulcer prevention • Specific treatments disappointing

  24. Respiratory Support • Aim to maintain SaO2>85% • Whilst keeping FiO2 <0.6 • O2 via facemask usually ineffective • NIV may avoid IPPV in some cases • IPPV usually required • CO2 retention often a feature

  25. Problems with IPPV • Barotrauma • Damage due to high pressures • Pneumothorax • Pneumomediastinum • Surgical emphysema • Volutrauma • Cyclical opening of collapsed alveoli • Shear forces increase inflammation • VILI • Worsening ARDS

  26. Protective Ventilation • NIH ARDSnet study (2000): VT 12ml/kg Pplat 50 cmH2O vs VT 6ml/kg Pplat 30 cmH2O • Mortality 39.8% vs 31% • 22% reduction in mortality with low VT • Previous studies did not show effect • Methodological differences? • Underpowered? • Difficult to achieve in practice

  27. PEEP • Open lung vs. Closed lung • Amato et al 1998 • PEEP above lower inflection point • Decreased 28 d mortality • No change in hospital mortality • BUT small study • PEEP does maintain recruited lung • High PEEP may allow lower FiO2 • New ARDSnet trial

  28. Permissive Hypercapnia • Limitation of VT may cause CO2 • High CO2 causes respiratory acidosis • CO2 may be protectivein hypoxia • Outcome studies show benefit

  29. Prone Position • Improved PaO2 in 65% patients • No way to predict responders • Benefit may persist after proning • Safe but labour intensive • Improves V/Q matching • Outcome benefit not demonstrated • but only 6h proning • trials of longer peroids needed

  30. High Frequency Oscillation Very small VT High frequency Increases MAWP Normalises CO2 No outcome benefit shown

  31. ECMO Extracorporeal Membrane Oxygenation Successful in IRDS No outcome benefit in ARDS

  32. Liquid Ventilation • Perflurocarbon • High O2 and CO2 capacity • Low surface tension • PLV vs TLV • Improved ventilatory dynamics in animal models • No outcome difference in human trial • High number of older patients in study group

  33. Fluid Management • Infiltrates improve with diuresis • Oxygenation may improve • Some evidence for improved outcome with fluid restriction • Concerns about hypoperfusion • Current study: • Liberal vs conservative fluid strategy • Current advice do not overhydrate

  34. Steroids • Ineffective in early ARDS • Case reports and small RCT suggest benefit in late ARDS • Current study by ARDSnet • Interim results suggest benefit • Final results awaited

  35. Surfactant • Effective in IRDS • Inconsistent results in ARDS • Delivery methods • Disease severity • Surfactant/fraction used • Ongoing RCT with natural surfactant

  36. Nitric Oxide/Prostacyclin • Inhaled vasodilators • Preferentially delivered to better ventilated lung areas • Aim to improve V/Q mismatch • Improves oxygenation • No improvement in outcome

  37. Other Agents • Ketoconazole • Lisophylline Tried and failed • Ibuprofen • 2 agonists • Decrease neutrophil activity • Improve alveolar fluid clearance • Enhance syrfactant secretion Watch this space

  38. Summary • ARDS/ALI is lung inflammation • 2º to various insults • Outcome appears to be improving • No proven specific treatment exists • Treatment of cause • Supportive care • Appropriate fluid management • Low VT strategy decreases mortality

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