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  2. 2. BERLIN DEFINITION: Syndrome characterised by Onset within 1 wk of clinical insult B/L radio graphic opacities not explained by pleural effusions, atelectasis or nodules Respiratory failure not explained by cardiac failure or overload Poor systemic oxygenation PaO2/FiO2≤300 mmHG on PEEP ≥5 cm H2O
  3. 3. 3 categories of ARDS: Mild ARDS 200< PaO2/FiO2> 300 mmHg Moderate ARDS 100< PaO2/FiO2>200 mmHg Severe ARDS PaO2/FiO2 ≤ 100 mmHg
  4. 4. • ARDS results primarily from an increase in lung vascular permeability. • Accumulation of fluid and protein increases when the lung endothelial and epithelial barriers are injured. • Increased permeability pulmonary edema.
  6. 6. MECHANISM OF LUNG INJURY • Lung injury is caused by an imbalance of pro- inflammatory and anti- inflammatory mediators. • Nuclear factor kB (NF-kBfactor) , a transcription factor, whose activation shifts the balance in favor of a pro inflammatory state.
  7. 7. • As early as 30 minutes after an acute insult, there is increased synthesis of IL-8, a potent neutrophil chemotactic and activating agent, by pulmonary macrophage. • IL1 and TNF lead to endothelial activation and pulmonary micro vascular sequestration and activation of neutrophil. • Activated neutrophils release- oxidants, protease, PAF &Leukotriene . This leads to tissue damage, accumulation of edema fluid, surfactant inactivation, hyaline membrane formation.
  8. 8. • The destructive forces unleashed by the neutrophils can be counteracted by endogenous anti-protease, antioxidants and anti inflammatory cytokines (IL-10). • Coagulating pathway itself is a powerful pro inflammatory signal. (Thrombin promotes adhesion of neutrophils to endothelium). • It is the balance between the destructive and protective factors that determines the degree of tissue injury and clinical severity of ARDS.
  9. 9. RESOLUTION • Macrophage removes the exudate and tissue debris. • Type 2 pneumocytes give rise to type 1 cells. • Endothelial restoration occurs both by migration from uninjured capillaries and marrow derived progenitor cells. • Macrophage release fibrogenic cytokines (TGF- β, PDGF) which stimulates the fibroblast growth and collagen deposition.
  10. 10. EARLY AND LATE PHASE OF LUNG INJURY EARLY (EXUDATIVE PHASE) • First few hours or days. • Interstitial and alveolar edema, • Capillary congestion, • Intra-alveolar hemorrhage. • Protein-rich pulmonary edema. • Hyaline membranes containing condensed fibrin and plasma proteins form over the next several days. • Later,in the exudative phase, inflammatory cells become more numerous within the lung interstitium. • Extensive necrosis of type I alveolar epithelial cells “Diffuse alveolar damage (DAD)”.
  11. 11. • Alveolar edema and alveolar collapse, that is, atelectasis due to loss of normal surfactant- related stabilization of alveoli, interfere with oxygenation. • Surfactant is washed out of alveoli and inactivated by the alveolar edema.
  12. 12. LATE(PROLIFERATIVE PHASE) • 7 to 10 days after initial injury. • Type II alveolar cells, fibroblasts and myofibroblasts proliferate. • Increased dead-space fraction, • High minute ventilation requirement, • Pulmonary hypertension • Further reduction in lung compliance.
  13. 13. CLINICAL FEATURES • Rapid course, occurring within 12 to 72 hours of the predisposing event. • Patient will be anxious, agitated, and dyspneic
  14. 14. • Inflammatory changes→ decrease lung compliance, ↑ WOB, tachypnea, ↓TV • ABG → PaO2 ≤ 50 to 55 mm Hg & SPO2 < 85%
  15. 15. • The hallmark of ARDS is hypoxemia that is resistant to oxygen therapy • Large right-to-left shunt. • Initially compensate by hyperventilating • Maintain an acceptable PaO2 with an acute respiratory alkalosis. • Deteriorate over several hours, requiring endotracheal intubation and mechanical ventilation.
  16. 16. When large portions of the lung are nonventilated due to alveo- lar collapse or flooding (hatched area), blood flow to these units with mixed venous P O 2 (Pv O 2 ) of 40 mm Hg and content of 15 vol. percent is effectively “shunted” through the lungs without being resaturated. Thus, despite a high concentration of supplemental oxygen (100% in this example) and high alveolar P O 2 in ventilated unit, these blood flows mix in accord with their oxygen contents, that is, the resulting left atrial blood has an oxygen content that is the weighted mean of the oxygen content of the shunted and nonshunted blood. In this example of a 50% shunt, the left atrial and systemic arteries have an arterial P O 2 of 60 mm Hg. Ca O 2 , arterial oxygen content; C CO 2 capillaryoxygen content; Cv O 2 , mixed venous oxygen content; P a , alveolar pressure; Pa O 2 , arterial P O 2 ; Pv O 2 , partial pressure of oxygen in the mixed venous blood.
  17. 17. CHEST X RAY • Diffuse, bilateral alveolar infiltrates. • LACK OF: 1. increased heart size, 2.increased width of the vascular pedicle 3.vascular redistribution toward upper lobes 4.presence of septal lines, 5. perihilar (bat’s wing) distribution of the edema Along with patchy peripheral infiltrates that extend to the lateral lung margins, suggests ARDS.
  18. 18. CT CHEST • Ground-glass opacification frequent pattern , although a nonspecific sign • A reticular pattern at follow-up is the most common CT pattern in ARDS survivors.
  19. 19. LABORATORY STUDIES 1. ABG- To confirm the diagnosis. Hallmark of ARDS – hypoxemia not responding to O2 therapy. EARLY STAGE: Respiratory alkalosis. If respiratory muscle fatigue, then hypercapnea. LATE STAGE: increased in minute ventilation due to increased dead space fraction.
  20. 20. 2. CPK and TROP I 3.NT PRO –BNP 4.ECG and ECHO 5.Invasive Hemodynamic monitoring. (PA catheterisation) 6. Bronchoalveolar lavage (BAL): a) For the evaluation of patients who have ARDS of unclear origin. b) To rule in or rule out acute processes that may have specific therapies. C/I of BAL: a)Those with a very low Pa O 2 b)Those requiring high levels of PEEP.
  21. 21. 7. LUNG BIOPSY: For a highly selective group of patients where alternative diagnoses are possible and would significantly change management and prognosis.
  22. 22. Goals of Management of Patients with ARDS Treatment of respiratory system abnormalities • Diagnose and treat the precipitating cause of ARDS. • Maintain oxygenation, preferably using non toxic FiO2 (<0.7),PEEP, or mechanical ventilation. • Prevent ventilator-induced lung injury (VILI) by using a low tidal volume ventilatory strategy with a limit (≤30 cm H2O) on plateau pressure
  23. 23. • Keep pH in normal range without compromising goal to prevent VILI • Enhance patient–ventilator synchrony and patient comfort by use of sedation, amnesia, opioid analgesia, and pharmacologic paralysis. • Wean from mechanical ventilation when patient can breathe without assisted ventilation.
  24. 24. Treatment of nonrespiratory system abnormalities • Support or treat other organ system dysfunction or failure • General critical care (preventive and homeostatic measures) • Adequate early nutritional support
  25. 25.  Face mask usually ineffective  PEEP :CPAP/BiPAP/Mechanical ventilation The effect of PEEP-induced improvement in arterial oxygenation is attributed predominantly to recruitment of collapsed alveoli. • Application of PEEP may also mediate a redistribution of alveolar fluid into the interstitium and decrease the absolute magnitude of shunt by reducing cardiac output. • Also allow to lower FiO2 from high, potentially MAINTAINING ADEQUATE OXYGENATION
  26. 26. LUNG PROTECTIVE VENTILATION GOAL : To avoid volume truama and atelect truama.
  27. 27. ARMA TRIAL • Randomized trial • Mid-to-late 1990s • Hypothesis -low tidal volume ventilation, combined with limited end-inspiratory (plateau) pressure, would lower mortality and ventilator days among survivors of ARDS compared with use of traditional tidal volumes. • The trial included 861 subjects. • The low tidal volume arm consisted of a tidal volume of 6 mL/kg predicted body weight, as long as the end- inspiratory pressure (Pplat) was ≤30 cm H2O. • The traditional tidal volume arm used a tidal volume of 12 mL/kg predicted body weight, as long as the Pplat remained <50 cm H2O.
  28. 28. ARMA TRIAL: • Low tidal volume + low plateau pressure ventilation will decreases the mortality. • P plat ≤30 cm of H2O is safe.
  29. 29. ROLE OF HIGHER PEEP • ALVEOLI; LOVS & EXRESS TRIAL showed no mortality benefits with high PEEP • Meta analysis combining the data from above three trial showed mortality benefit in those with PaO2/FiO2<200
  30. 30. Lung protective ventilation low tidal volume High PEEP minimum of 5cm H2O Plateau pressure <30cm h2o Oxygenation goal PaO2 55-80mmhg Spo2 88-95% P plateau goal <30cm H2o PH goal. 7.30-7.45 VENTILATION TARGETS
  31. 31. SETTINGS Calculate Predicted Body Weight(PBW) Males: PBW (kg) = • 50 + 2.3[(height in inches) − 60] Females: PBW (kg) = • 45.5 + 2.3[(height in inches) − 60]
  32. 32. VENTILATOR MODE: • Low TV VCV is preferred. • PCV is also preferred as it can limit Pplat and Ppeak. • Inverse ratio ventilation – giving more time for inspiration, can improve oxygenation (salvage mode ventilation) • BIPAP and APRV modes that allows spontaneous breathing during positive pressure ventilation
  33. 33. • High frequency oscillatory ventilator - Supported by rapid pressure oscillations that generate small tidal volumes also called ultimate low tidal volume ventilator. Commonly used in RD in newborn.
  34. 34. ADJUVANTS TO PROTECTIVE MECHANICAL VENTILATION • PERMISSIVE HYPERCAPNOEA – recommented as core ventilator strategy. C/I of permissive hypercapnoea: 1.Increased ICP 2. A/C stroke 3. A/C or C/C MI 4.Severe PAH 5. RVF 6. Uncontrolled metabolic acidosis 7. Sickle cell Anemia 8 TCA overdose 9 Pregnancy
  35. 35. • FLUID AND HEMODYNAMIC Mx ARDSNet FACTT Trial • Results of the study support the use of a conservative fluid strategy in managing patients with ARDS who are not in shock. • Based on the results, the FACTT investigators also recommend using a CVC to guide hemodynamic and fluid management.
  36. 36. PRONE POSITIONING • Improve the O2 by ; Increase FRC Change in diaphragmatic motion Perfusion redistribution Increase clearance of secretion.
  37. 37. DISADVANTAGES • Accidental extubation • Pressure sores • Increase requirement forsedation • Retinal ischemia in hypotensive patients • Cardiac arrythmia/hemodynamic instability
  38. 38. • Unresponsive cerebral hypertension • Unstable bone fractures • Left heart failure • Hemodynamic instability • Active intra abdominal pathology CONTRA INDICATIONS
  39. 39. • RECRUITMENT MANEUVER Application of CPAP to recruit or open partially or totally collapsed alveoli using high level of PEEP CPAP at 35-40 cm of H2O for 30 sec.
  40. 40. • INHALED NITRIC OXIDE Vasodilation of pulmonary capillaries or arterioles. Divert blood flow to alveoli and away from shunt (by lowering pul.artery pressure and pul. Vas. resist).
  41. 41. • Improves oxygenation • Rapidly inactivated by hemoglobin • Requires continuous delivery • No improvement in mortality • costly • Only used as a salvage therapy
  42. 42. INHALED PROSTACYCLIN • Epoprostenol/Iloprost • Less cost • Improve oxygenation to the same degree
  43. 43. TRACHEAL GAS INSUFFLATION (TGI) • Delivering fresh gas through modified endotracheal tube at point just above carina. • Removes CO2 from trachea and small airways. • Reduce anatomical dead space. As a salvage intervention for patients with high levels of PaCO2 (e.g., >100 mm Hg)
  44. 44. • EXTRACORPORAL LIFE SUPPORT External artificial membrane and a mechanical pump to provide gas exchange and systemic perfusion.
  45. 45. • CORTICOSTEROIDS Little role in treatment of ARDS High dose benificial during proliferative phase of ARDS, it prevents lungs scarring
  46. 46. NEUROMUSCULAR BLOCKING AGENTS • To improve ventilator synchrony and improve oxygenation. • Associated with prolonged neuromuscular weakness in survivors of ARDS. • May be useful for short term use in severe ARDS
  47. 47. • OTHER THERAPIES Statin Beta agonist Macrolides
  48. 48. CLINICAL COURSE AND DURATION • The median duration of mechanical ventilation is approximately 5 days, 7 days, and 9 days for mild, moderate, and severe ARDS, respectively. • Most ARDS-related deaths occur within the first 2 weeks, with one-third occurring by day 7, two-thirds by day 14, and three- fourths to four-fifths by day 28. • The mortality rate of patients on
  49. 49. CAUSES OF DEATH • Underlying disease or injury • Most common cause is SEPSIS associated with multiple organ system failure • Only a relatively small fraction of patients – 10% to 20% of all patients with ARDS – die a respiratory death due to irreversible
  50. 50. PULMONARY SEQUELAE • In the Toronto ARDS Outcomes study, spirometry and lung volumes improved rapidly among survivors, reaching normal in most subjects by 6 months • Diffusion capacity is mildly impaired in many patients after ARDS, but it may return to normal by 2 to 5 years among survivors.
  51. 51. PHYSICALAND NEUROMUSCULAR SEQUELAE • Low exercise capacity, weakness, and decreased physical quality of life as far as 5 years after their acute illness. • Risk factors for these findings –multiorgan dysfunction in the ICU – prolonged duration of ARDS – treatment with corticosteroids during the ICU stay
  52. 52. • Critical illness polyneuropathy, • ICU-acquired myopathy (critical illness myopathy) • Entrapment neuropathy • Heterotopic ossification
  53. 53. COGNITIVE AND PSYCHOLOGICAL SEQUELAE • Impaired memory, reduced attention, and concentration and processing speed • Depression and Anxiety • PTSD
  54. 54. DIFFERENTIAL DIAGNOSIS • Pulmonary edema due to left heart failure • DAH • Acute eosinophilic pneumonia • Lupus pneumonitis • AIP • Pulmonary alveolar proteinosis • BOOP/COP • Hypersensitivity pneumonitis • Leukemic infiltration • Drug induced pulmonary edema and pneumonitis • Acute major pulmonary embolus • Sarcoidosis • Interstitial pulmonary fibrosis
  55. 55. To conclude • ARDS is a manifestation of an underlying pathology with 50% mortality • Early recognition and proper ventilatory management is the only solution now
  56. 56. THANK YOU