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Ards level 3 lecture

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Eric Mugambi
Eric Mugambi

1. Acute respiratory distress syndrome (ARDS) is characterized by acute onset hypoxemia, decreased lung compliance, and bilateral pulmonary infiltrates without evidence of cardiac failure. 2. ARDS is caused by direct lung injury from factors like pneumonia, aspiration, shock, sepsis, or trauma which lead to increased vascular permeability and disruption of the alveolar-capillary barrier. 3. Treatment involves identifying and treating the underlying cause, supportive care including mechanical ventilation with low tidal volumes, and preventing complications.

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Dr. Eric Mugambi
? 1821 ¨C Laennec in ¡®A treatise on diseases of the chest¡¯ ? Idiopathic anasarca of the lungs ? Trauma associated ? World war 1 & 2 ? Vietnam war
? 1950s - Advances in critical care ? Respirators ? Airway access ? Hence the term ¡®respirator lung¡¯ ? Other terms related to inciting agent ? Post-traumatic, shock lung, wet lung, DaNang lung)
? 1967 ¨C Case series of 12 patients ? acute onset ? tachypn?a ? hypox?mia ? loss of compliance Ashbaugh D, Boyd Bigelow D, Petty T, Levine B. ACUTE RESPIRATORY DISTRESS IN ADULTS. The Lancet. 1967;290(7511):319-23.
? Hypoxemia ? Low Pa02 ? Stiff lungs ? Reduced compliance ? Hyaline membranes ? Early fibrosis in patients who died
? Not well characterized due to lack of uniform diagnosis ? Before ICUs ¨C most patients died ? No opportunity for organized investigations ? US data ? 50,000 to 200,000 cases per year (2003) ? 79/100,000 ¨C ALI ? 59/100,000 ¨C ARDS ? 4-9% in ICU settings
? Substantial recovery in lung function occurs within 6-12 months ? In few cases muscle weakness and neuropsychiatric problems may persist ? Mortality has improved significantly from 54% in 1983 to as low as 25% in 2004 but has plateaued since then ? Better prognosis with younger age ? Leading cause of death is multiple organ failure
? 1967 ¨C Ashbaugh et al ? 1988 ¨C Murray and colleagues ? 1992 ¨C American European Consensus Conference (AECC) ? 2012 ¨C Berlin definition
1. Acute onset of respiratory failure 2. Bilateral infiltrates resembling pulmonary edema 3. No evidence of left atrial pressure elevation - PCWP <18mmhg 4. Ratio of PaO2 to FiO2 is <200mmhg ¨C ? ALI ¨C 200<PaO2/FiO2 < 300mmHg (Desaturation)
? ¡°Acute lung injury¡± no longer exists ? Onset of ARDS (diagnosis) must be acute, as defined as within 7 days of some defined event, which may be sepsis, pneumonia, or simply a patient¡¯s recognition of worsening respiratory symptoms. TheARDS DefinitionTask Force: JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669.
? Bilateral opacities consistent with pulmonary edema must be present but may be detected on CT or chest X-ray.
? There is no need to exclude heart failure in the new ARDS definition ? An ¡°objective assessment¡°¨C meaning an echocardiogram in most cases ¡ª should be performed if there is no clear risk factor present like trauma or sepsis. TheARDS DefinitionTask Force: JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669.
Ards level 3 lecture
? Hypoventilation ? Ventilation perfusion mismatch ? Right to left shunt ? Diffusion impairment ? Reduced inspired oxygen tension (Pio2) ? Very low cardiac output
? Common causes (mnemonic PAST) ? Pneumonia ? Aspiration ? Shock ? Sepsis ? Trauma ? *Transfusion (multiple)
? Lung ? Contusion ? Near drowning ? Inhalational injury ? Reperfusion pulmonary edema ? Other ? Cardio-pulmonary bypass ? Drug overdose ? Acute pancreatitis (alcohol increases risk!) ? Transfusion of blood products
? Endothelial injury ? Increased vascular permeability ¨C hallmark ? Epithelial disruption ? Alveolar flooding ? Disorganized repair leads to fibrosis ? Septic shock in patients with bacterial pneumonia ? Loss of type 2 cells ? Impaired fluid transit ¨C no fluid removal ? Loss of surfactant ? Loss of type 1 progenitor cells
? Impaired gas exchange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic dead space ? Decreased lung compliance ¨C due to the stiffness of poorly or non-aerated lung ? Pulm HTN ¨C 25% of pts, due to hypoxic vasoconstriction,Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction
Ards level 3 lecture
Ards level 3 lecture
Ards level 3 lecture
Normal BGB
Small bronchiole and alveolae
Alveoli and capillaries
Ards level 3 lecture
? Acute onset within 12-36 hrs of inciting event, upto 5- 7days ? Dyspnoea, tachypnoea, hypoxemia, dry cough chest pain ? O/E: tachycardia, cyanosis, tachypnoea, diffuse rales, ? BGAs: resp alkalosis, hypoxemia ? CXR: bilateral alveolar infiltrates over 75% of lung fields ? No pulm venous congestion, no kerley b lines, no cardiomegaly, pleural effusions
Ards level 3 lecture
Ards level 3 lecture
1. Pneumonia 2. Diffuse alveolar hemorrhage 3. Idiopathic acute eosinophilic pneumonia 4. Cryptogenic organising pneumonia 5. Acute interstitial pneumonia 6. Rapidly progressive cancer 7. Cardiogenic pulmonary edema
? Investigations ? Guided by clinical suspicion of underlying illness (ddx) ? For monitoring progress in patients with critical illness ? Routine e.g. ABGs ? Tests of Organ function
? Treat underlying illness ? Minimize procedures ? Prevent complications ? Barotrauma ? DVT ? Stress ulcers ? Promptly recognize nosocomial infections ? Provide adequate nutrition
THERAPY RECOMMENDATION Low tidal volume A (strong evidence from RCTs) Minimize left atrial filling pressures B (limited clinical data) High PEEP C (recommended only as alternative) Prone positioning C Recruitment maneuvers C ECMO C High frequency ventilation D (Not recommended) Glucocorticoids D Surfactant, Inhaled NO, other anti- inflammatory D
? Gene therapy ? Mesenchymal stem cells
? Impaired gas exhange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic deadspace ? Decreased lung compliance ¨C due to the stiffness of poorly or nonaerated lung ? Pulm HTN ¨C 25% of pts, due to hypoxic vasoconstriction,Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction

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Ards level 3 lecture

  • 2. ? 1821 ¨C Laennec in ¡®A treatise on diseases of the chest¡¯ ? Idiopathic anasarca of the lungs ? Trauma associated ? World war 1 & 2 ? Vietnam war
  • 3. ? 1950s - Advances in critical care ? Respirators ? Airway access ? Hence the term ¡®respirator lung¡¯ ? Other terms related to inciting agent ? Post-traumatic, shock lung, wet lung, DaNang lung)
  • 4. ? 1967 ¨C Case series of 12 patients ? acute onset ? tachypn?a ? hypox?mia ? loss of compliance Ashbaugh D, Boyd Bigelow D, Petty T, Levine B. ACUTE RESPIRATORY DISTRESS IN ADULTS. The Lancet. 1967;290(7511):319-23.
  • 5. ? Hypoxemia ? Low Pa02 ? Stiff lungs ? Reduced compliance ? Hyaline membranes ? Early fibrosis in patients who died
  • 6. ? Not well characterized due to lack of uniform diagnosis ? Before ICUs ¨C most patients died ? No opportunity for organized investigations ? US data ? 50,000 to 200,000 cases per year (2003) ? 79/100,000 ¨C ALI ? 59/100,000 ¨C ARDS ? 4-9% in ICU settings
  • 7. ? Substantial recovery in lung function occurs within 6-12 months ? In few cases muscle weakness and neuropsychiatric problems may persist ? Mortality has improved significantly from 54% in 1983 to as low as 25% in 2004 but has plateaued since then ? Better prognosis with younger age ? Leading cause of death is multiple organ failure
  • 8. ? 1967 ¨C Ashbaugh et al ? 1988 ¨C Murray and colleagues ? 1992 ¨C American European Consensus Conference (AECC) ? 2012 ¨C Berlin definition
  • 9. 1. Acute onset of respiratory failure 2. Bilateral infiltrates resembling pulmonary edema 3. No evidence of left atrial pressure elevation - PCWP <18mmhg 4. Ratio of PaO2 to FiO2 is <200mmhg ¨C ? ALI ¨C 200<PaO2/FiO2 < 300mmHg (Desaturation)
  • 10. ? ¡°Acute lung injury¡± no longer exists ? Onset of ARDS (diagnosis) must be acute, as defined as within 7 days of some defined event, which may be sepsis, pneumonia, or simply a patient¡¯s recognition of worsening respiratory symptoms. TheARDS DefinitionTask Force: JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669.
  • 11. ? Bilateral opacities consistent with pulmonary edema must be present but may be detected on CT or chest X-ray.
  • 12. ? There is no need to exclude heart failure in the new ARDS definition ? An ¡°objective assessment¡°¨C meaning an echocardiogram in most cases ¡ª should be performed if there is no clear risk factor present like trauma or sepsis. TheARDS DefinitionTask Force: JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669.
  • 14. ? Hypoventilation ? Ventilation perfusion mismatch ? Right to left shunt ? Diffusion impairment ? Reduced inspired oxygen tension (Pio2) ? Very low cardiac output
  • 15. ? Common causes (mnemonic PAST) ? Pneumonia ? Aspiration ? Shock ? Sepsis ? Trauma ? *Transfusion (multiple)
  • 16. ? Lung ? Contusion ? Near drowning ? Inhalational injury ? Reperfusion pulmonary edema ? Other ? Cardio-pulmonary bypass ? Drug overdose ? Acute pancreatitis (alcohol increases risk!) ? Transfusion of blood products
  • 17. ? Endothelial injury ? Increased vascular permeability ¨C hallmark ? Epithelial disruption ? Alveolar flooding ? Disorganized repair leads to fibrosis ? Septic shock in patients with bacterial pneumonia ? Loss of type 2 cells ? Impaired fluid transit ¨C no fluid removal ? Loss of surfactant ? Loss of type 1 progenitor cells
  • 18. ? Impaired gas exchange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic dead space ? Decreased lung compliance ¨C due to the stiffness of poorly or non-aerated lung ? Pulm HTN ¨C 25% of pts, due to hypoxic vasoconstriction,Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction
  • 26. ? Acute onset within 12-36 hrs of inciting event, upto 5- 7days ? Dyspnoea, tachypnoea, hypoxemia, dry cough chest pain ? O/E: tachycardia, cyanosis, tachypnoea, diffuse rales, ? BGAs: resp alkalosis, hypoxemia ? CXR: bilateral alveolar infiltrates over 75% of lung fields ? No pulm venous congestion, no kerley b lines, no cardiomegaly, pleural effusions
  • 29. 1. Pneumonia 2. Diffuse alveolar hemorrhage 3. Idiopathic acute eosinophilic pneumonia 4. Cryptogenic organising pneumonia 5. Acute interstitial pneumonia 6. Rapidly progressive cancer 7. Cardiogenic pulmonary edema
  • 30. ? Investigations ? Guided by clinical suspicion of underlying illness (ddx) ? For monitoring progress in patients with critical illness ? Routine e.g. ABGs ? Tests of Organ function
  • 31. ? Treat underlying illness ? Minimize procedures ? Prevent complications ? Barotrauma ? DVT ? Stress ulcers ? Promptly recognize nosocomial infections ? Provide adequate nutrition
  • 32. THERAPY RECOMMENDATION Low tidal volume A (strong evidence from RCTs) Minimize left atrial filling pressures B (limited clinical data) High PEEP C (recommended only as alternative) Prone positioning C Recruitment maneuvers C ECMO C High frequency ventilation D (Not recommended) Glucocorticoids D Surfactant, Inhaled NO, other anti- inflammatory D
  • 33. ? Gene therapy ? Mesenchymal stem cells
  • 34. ? Impaired gas exhange leading to severe hypoxemia - 2/2 ventilation-perfusion mismatch, increase in physiologic deadspace ? Decreased lung compliance ¨C due to the stiffness of poorly or nonaerated lung ? Pulm HTN ¨C 25% of pts, due to hypoxic vasoconstriction,Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction
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