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Updates on Acute respiratory distress syndrome


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These lecture notes were made by Dr. Hamdi Turkey (Pulmonologist at Taiz university)
** Contents:
- Historical view on ARDS
- New definition of ARDS
- Precipitating risk factors
- Pathophysiology of ARDS
- Clinical picture, Diagnosis, Management and Prognosis
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Published in: Health & Medicine

Updates on Acute respiratory distress syndrome

  1. 1. Updates on Acute respiratory distress syndrome Hamdi Turkey - chest physician
  2. 2. I hope you are still awake at the end of this lecture !
  3. 3. Case presentation A 35 year old male patient was r u s h e d i n t o t h e E R complaining of SOB for the past 3 days, he has fever, Tachypnea, pulse 110 bpm,BP 80/50 mmHg, pallor and cyanosed, normal JVP, normal S1 and S2 with no added sounds, on chest auscultation there was bilateral diffuse crackles. SpO2 on room air was 60, ABG : PaO2= 40, Pco2= 40, pH=7.3 What's the diagnosis?
  4. 4. Learning Objectives To know the new definition of ARDS To understand the pathology and pathophysiology of ARDS To devise a ventilation strategy for these patients. To introduce the concept of ventilator induced lung injury To address adjunct and rescue therapy for patients with resistant hypoxemia.
  5. 5. History I n 1 9 6 7 A s h b a u g h a n d colleagues published a case series in the Lancet which described a clinical syndrome, which they (later) termed “Adult R e s p i r a t o r y D i s t r e s s Syndrome” (ARDS). The 12 patients involved complained of acute respiratory distress, cyanosis refractory to oxygen t h e r a py, d e c r e a s e d l u n g c o m p l i a n c e a n d d i f f u s e pulmonary infiltrates on chest x-ray.
  6. 6. Trauma doctors involved in treating victims of war had long been familiar with this syndrome, which came to be known as “wet lung”, “shock lung” or “Da-nang lung”. This problem had been identified during World War II but with the advent of advanced trauma (M.A.S.H. units during the Vietnam war) the prevalence of this form of respiratory failure was truly recognized. Over the past 30 or so years, this syndrome has come to be one of the central problems of intensive care: lung injury arising from a variety of different etiologies, each characterized by bilateral diffuse infiltrates on x-ray, hypoxemia, and non-cardiogenic pulmonary edema. History
  7. 7. In 1988, an expanded definition was proposed that quantified the physiologic respiratory impairment through the use of a four-point lung- injury scoring system that was based on: level of positive end-expiratory pressure ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen static lung compliance degree of infiltration evident on chest radiographs. History
  8. 8. Before research into the pathogenesis and treatment of this syndrome could proceed, it was necessary to formulate a clear definition of the syndrome. Such a definition was developed in 1994 by the American-European Consensus Conference (AECC) on acute respiratory distress syndrome (ARDS). The term “acute respiratory distress syndrome” was used instead of “adult respiratory distress syndrome” because the syndrome occurs in both adults and children. History
  9. 9. The Berlin Definition of ARDS (published in 2012) has replaced the American-European Consensus Conference’s definition of ARDS (published in 1994). However, it should be recognized that most evidence is based upon prior definitions. History
  10. 10. Other terms Shock lung Pump lung Traumatic wet lung Post traumatic atelectasis Adult hyaline membrane disease Progressive respiratory distress Acute respiratory insufficiency syndrome Haemorrhagic atelectasis Hypoxic hyperventilation Postperfusion lung Oxygen toxicity lung Wet lung White lung Transplant lung Da Nang lung Diffuse alveolar injury Acute diffuse lung injury Noncardiogenic pulmonary edema. Progressive pulmonary consolidation
  11. 11. AECC Past definition of ARDS ARDS was defined as: the acute onset of respiratory failure, bilateral infiltrates on chest radiograph, hypoxemia as defined by a PaO2/FiO2 ratio ≤200 mmHg, and no evidence of left atrial hypertension or a pulmonary capillary pressure <18 mmHg (if measured) to rule out cardiogenic edema. In addition, Acute Lung Injury (ALI), the less severe form of acute respiratory failure, was different from ARDS only for the degree of hypoxemia, in fact it was defined by a 200 < PaO2/FiO2 ≤300 mmHg.
  12. 12. The 1994 AECC definition became globally accepted, but had limitations The current definition is the ‘Berlin Definition’ published in 2013, which was created by a consensus panel of experts convened in 2011 (an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine) AECC Past definition of ARDS
  13. 13. ARDS BERLIN DEFINITION ARDS is an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue… [ w i t h ] h y p o x e m i a a n d b i l a t e r a l radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance.
  14. 14. The goal of developing the Berlin definition was to try and improve feasibility, reliability, face and predictive validity ARDS BERLIN DEFINITION
  15. 15. Timing of acute onset The timing of acute onset of respiratory failure to make diagnosis of ARDS is clearly defined in Berlin definition. It defines the exposure to a known risk factor or worsening of the respiratory symptoms within one week. It is important to identify risk factors that explain the context of acute respiratory failure arised from
  16. 16. Oxygenation In the Berlin definition, there is no use of the term Acute Lung Injury (ALI). The committee felt that this term was used inappropriately in many contexts and hence was not helpful. In the Berlin definition, ARDS was classified as mild, moderate and severe according to the value of PaO2/FiO2 ratio. Importantly, the PaO2/FiO2 ratio value is considered only with a CPAP or PEEP value of at least 5 cmH2O.
  17. 17. The chest radiograph is characterized by bilateral opacities involving at least 3 quadrants that are not fully explained by pleural effusions, atelectasis and nodules. In the absence of known risk factors, a cardiogenic origin of edema is to be excluded by objective evaluation of cardiac function with echocardiography. Consequently, the wedge pressure measurement was abandoned because ARDS may coexist with hydrostatic edema caused by fluid overload or cardiac failure. Chest X-ray
  18. 18. Key components acute, meaning onset over 1 week or less bilateral opacities consistent with pulmonary edema must be present but may be detected on CT or chest radiograph PF ratio <300mmHg with a minimum of 5 cmH20 PEEP (or CPAP) must not be fully explained by cardiac failure or fluid overload,” in the physician’s best estimation using available information — an “objective assessment“ (e.g. echocardiogram) should be performed in most cases if there is no clear cause such as trauma or sepsis.
  19. 19. Severity *on PEEP 5+; **observed in cohort ARDS is categorized as being mild, moderate, or severe: ARDS Severity PaO2/FiO2* Mortality** Mild 200 – 300 27% Moderate 100 – 200 32% Severe < 100 45%
  20. 20. Changes from the 1994 AECC definition the term acute lung injury was abandoned measurement of the PaO2/FIO2 ratio was changed to require a specific minimum amount of PEEP 3 categories of ARDS were proposed (mild, moderate, and severe) based on the PaO2/FIO2 ratio Radiographic criteria were changed to improve interrater reliability PCWP criterion was removed and additional clarity was added to improve the ability to exclude cardiac causes of bilateral infiltrates
  21. 21. 1994 AECC DEFINITION Now obsolete
  22. 22. Shortcoming of the AECC definition acute is ill defined PF ratio can be manipulated by adjusting PEEP CXR interpretation is unreliable PACs are rarely used PCWP may oscillate above and below the cut-off and may be elevated for reasons other than heart failure ALI was used inconsistently, just PF ratio 200 to 300, or all patients <300 including ARDS?
  23. 23. Incidence and outcome ■ 20-75 per 100,000 ■ 30% mortality ■ Recovery may take 6-12 months ■ Residual: Restriction Obstruction Gas- Exchange Abnormalities Reduced Quality of Life
  24. 24. Direct pneumonia aspiration of gastric contents lung contusion fat embolism Amniotic fluid embolism near drowning inhalational injury reperfusion injury non-pulmonary sepsis multiple trauma massive transfusion pancreatitits Salicylate or narcotic overdose cardiopulmonary bypass Indirect Risk factors
  25. 25. Cardiogenic Vs non cardiogenic pulmonary edema Cardiogenic Non-Cardiogenic Patchy infiltrates in bases Effusions Kerley B lines Cardiomegaly Pulmonary vascular redistribution Excess fluid in alveoli Homogenous fluffy shadows No effusion No Kerley B lines No cardiomegaly No pulmonary vascular redistribution Protein, inflammatory cells, fluid
  26. 26. Cardiogenic Non-Cardiogenic
  27. 27. Cardiogenic Non-Cardiogenic
  28. 28. Pathophysiology Classical phases Injury Exudative – alveolar capillary membrane disruption with inflammatory cell infiltrate and high protein exudate to form hyaline membranes Proliferative – proliferation of abnormal Type II alveoli cells and inflammatory cells Fibrotic – infiltration with fibroblasts which replace alveoli and alveolar ducts with fibrosis Resolution – slow and incomplete repair and restoration of architecture
  29. 29. Pathophysiology Based on the histological appearance - Exudative phase (0-4 days) • Alveolar and interstitial edema • Capillary congestion • Destruction of type I alveolar cells • Early hyaline membrane formation Proliferative Phase (3-10 days) • Increased type II alveolar cells • Cellular infiltration of alveolar septum • Organisation of hyaline membranes Fibrotic Phase (>10 days) • Fibrosis of hyaline membranes and alveolar septum • Alveolar duct fibrosis
  30. 30. Findings on Light Microscopy and Electron Microscopy during the Acute Phase (Panels A and D) and the Fibrosing- Alveolitis Phase (Panels B, C, and E) of Acute Respiratory Distress Syndrome.
  31. 31. Pathophysiology Mechanisms in early phase - • Release of inflammatory cytokines – TNF alpha, IL- 1,6,8 • Failure of alveolar edema clearance, epithelial and endothelial damage • Increased permeability of alveolo – capillary membrane • Neutrophil migration and oxidative stress • Procoagulant shift – fibrin deposition • Surfactant dysfunction Mechanism in late (repair) phase – • Fibroproliferation -TGF beta, MMPs, thombospondin, plasmin, ROS • Remodelling - matrix and cell surface proteoglycans, MMP, imbalance of coagulation and fibrinolysis.
  32. 32. Pathophysiology
  33. 33. Complex interplay pulmonary oedema from damage to the alveolocapillary barrier inflammatory infiltrates surfactant dysfunction It is essential to understand that although ALI is a diffuse process, it is also a heterogeneous process, and not all lung units are affected equally: normal and diseased tissue may exist side-by-side.
  34. 34. Effects hypoxaemia (V/Q mismatch, impaired hypoxic pulmonar y vasoconstriction) increase in dependent densities (surfactant dysfunction, alveolar instabilities) decreased compliance (surfactant dysfunction, decreased lung volume, fibrosis) collapse/consolidation (increased compression of dependent lung) increased minute ventilation (increased in alveolar dead space) increased work of breathing (increased elastance, increased minute volume requirement) pulmonary hypertension (vasoconstriction, microvascular thrombi, fibrosis, PEEP)
  35. 35. Host factors increasing the risk of ARDS Clinical variables found to be associated with an increased risk of ARDS Diabetes mellitus decreases the risk of ALI. chronic alcohol abuse hypoproteinemia advanced age, increased severity,and extent of injury or illness as measured by injury severity score (ISS) or APACHEscore hyper-transfusion of blood products cigarette smoking.
  36. 36. Causative factors in ARDS Primary injury Host response Consequences of therapy
  37. 37. Clinical features
  38. 38. Symptoms Acute respiratory distress syndrome (ARDS) is characterized by the development of acute dyspnea and hypoxemia within hours to days of an inciting event, such as trauma, sepsis, drug overdose, massive transfusion, acute pancreatitis, or aspiration. In many cases, the inciting event is obvious, but, in others (eg, drug overdose), it may be harder to identify. Patients developing ARDS are critically ill, often with multisystem organ failure, and they may not be capable of providing historical information. Typically, the illness develops within 12-48 hours after the inciting event, although, in rare instances, it may take up to a few days. With the onset of lung injury, patients initially note dyspnea with exertion. This rapidly progresses to severe dyspnea at rest, tachypnea, anxiety, agitation, and the need for increasingly high concentrations of inspired oxygen.
  39. 39. Physical findings Physical findings often are nonspecific and include tachypnea, tachycardia, and the need for a high fraction of inspired oxygen (FIO2) to maintain oxygen saturation. The patient may be febrile or hypothermic. Because ARDS often occurs in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be present. Cyanosis of the lips and nail beds may occur. Examination of the lungs may reveal bilateral rales. Rales may not be present despite widespread involvement. Because the patient is often intubated and mechanically ventilated, decreased breath sounds over 1 lung may indicate a pneumothorax or endotracheal tube down the right main bronchus. Manifestations of the underlying cause (eg, acute abdominal findings in the case of ARDS caused by pancreatitis) are present.
  40. 40. Symptoms and signs that suggest a cause of ARDS
  41. 41. Laboratory investigations Routine blood counts RFT LFT Blood culture BNP ABG BAL ECHO Chest CT scan PCWP
  42. 42. Classic Chest X Ray of a patient with ARDS, although the lung injury appears diffuse, when you look at the CT scan of the same patient on the right you can see that the lower lobes are densely consolidated and the upper lobes relatively spared. Nevertheless, this patient was severely hypoxic, and responded well to prone positioning.
  43. 43. Management
  44. 44. Therapy- goals Treatment of the underlying cause Cardio-pulmonary support Specific therapy targeted at lung therapy Supportive therapy
  45. 45. Diagnosis and appropriate treatment of the underlying cause to minimise physiological impact of cause (drain collection, antibiotics, resuscitate, splint fractures) Nutritional support Standard ICU prophylaxis Stress ulcer prophylaxis Prevention of nosocomial infections CVP monitoring with CV line with appropriate fluid therapy General measures
  46. 46. Goal of management of a patient with ARDS
  47. 47. Treatable inciting causes of ARDS
  48. 48. Lung protective strategy in ARDS A myth or a fact!
  49. 49. Mechanical ventilation
  50. 50. Therapy- mechanical ventilation The Problem: Ventilator- Induced Lung Injury ■ High volumes and pressures: Stress ( barotrauma) ■ Overdistension & Alveolar Cracking ( volumtrauma) ■ Cyclic Opening and closing of atelectatic alveoli ( atelectrauma) Cause increased permeability and alveolar damage
  51. 51. The Problem: Oxygen Toxicity ■ Free Radicals ■ Oxygen Washout and De-Recruitment High FiO2 can lead to further alveolar damage Therapy- mechanical ventilation
  52. 52. ■ Intubation almost always necessary ■ In past, goal was to normalize pH, PaCO2, PaO2 ■ High volumes and pressures were used ■ Worse outcomes Therapy- mechanical ventilation
  53. 53. Lung protective strategy Amato et al. 1998, Effects of a protective- ventilation strategy on mortality in the acute respiratory distress syndrome. N. Engl. J. Med. 338:347-54 ■ 53 pts with early ARDS ■ Compared “conventional” ventilation of 12ml/kg to “protective” 6ml/kg ■ Low PEEP. PaCO2 35-38 ■ Improved survival at 28 days ■ Higher percentage of ventilator weaning ■ Less barotrauma
  54. 54. The Acute Respiratory Distress Network. 2000. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N. Engl. J. Med. 342:1301-8 ■ Larger Trial. 861 patients ■ Compared 12 ml/kg vs. 6ml/kg ventilation. ■ Plateau pressures 50 cm H2O vs. 30 cm H2O. ■ Trial ended early: ■39.8% mortality vs. 31% mortality THIS HAS CHANGED CLINICAL PRACTICE Lung protective strategy
  55. 55. Mechanical ventilation ARDS Network protective lung ventilation strategy (from the ARMA study) controlled ventilation TV 6mL/kg avoid overstretch (volutrauma) and inadequate recruitment (atelectrauma) PEEP 5-15 Plateau pressure <30 cmH20 (higher than this contributes to VILI from overstretching and hyperinflation of the functional ‘baby lung’)
  56. 56. mode of ventilation: generally no difference PCV tends to be used c/o plateau pressure approximates peak pressure, with VC plateau pressure needs to be measured no role for inverse ratio ventilation (I:E ratio > 1) -> increased mean airway pressure + haemodynamic instability + regional hyperinflation oxygenation target: SpO2 88-95%, PaO2 > 55-80 mmHg carbon dioxide target: ARDSnet aimed for a normal CO2 -> but lung is exposed to repeated tidal stretch, ideally hypercapnia should be minimised but there isn’t compelling data to suggest it is harmful unless there is an obvious reason (raised ICP, pregnancy).
  57. 57. Ventilator strategy in ARDS
  58. 58. Ventilator settings for lung protection
  59. 59. Complications related to MV
  60. 60. Other techniques to improve oxygenation prone posture: improves oxygenation and mortality in severe ARDS recruitment manoeuvres (e.g. PEEP 30-40cmH2O held for 30 seconds or staircase recruitment manouvre) -> can improve oxygenation but controversial, not everyone responds inhaled iNO: optimisation of V/Q mismatch, 1-60ppm, on 40-70% will respond, monitor for metHb inhaled prostacycline (PGI2): optimisation of V/Q mis-match, 1-50ng/kg/min, as effective as iNO
  61. 61. Pharmacological therapy surfactant replacement therapy: theoretically good, improves oxygenation but no improvement in mortality, problems with distribution to alveoli Diuretics : liberal vs conservative strategy glucocorticoids: improvement in ventilator free days and shock, no improvement in mortality and increase in weakness ketoconazole: antifungal that inhibits thromboxane synthase and 5-lipooxygenase -> early data but not confirmed. others: cytokine antagonism, NSAIDS, scavengers of O2 radicals, lisofylline -> no success Seek and treat underlying causes and complications
  62. 62. A randomized, clinical trial determined that simvastatin, a hydroxymethylglutaryl-coenzyme A reductase inhibitor, improved oxygenation and respiratory mechanics in patients with ALI. Further studies are needed, but treatment with simvastatin appears safe and may be associated with improved organ dysfunction in patients with ALI. Statins Pharmacological therapy Activated protein C Drotrecogin alfa was withdrawn from the worldwide market October 25, 2011. In the Recombinant Human Activated Protein C Worldwide Evaluation in Severe Sepsis (PROWESS)-SHOCK clinical trial, drotrecogin alfa failed to demonstrate a statistically significant reduction in 28-day all-cause mortality in patients with severe sepsis and septic shock. Trial results observed a 28-day all-cause mortality rate of 26.4% in patients treated with activated drotrecogin alfa compared with 24.2% in the placebo group of the study.
  63. 63. In these critically ill patients, pay careful attention to early recognition of potential complications in the intensive care unit (ICU), including pneumothorax, IV line infections, skin breakdown, inadequate nutrition, arterial occlusion at the site of intra-arterial monitoring devices, DVT and pulmonary embolism (PE), retroperitoneal hemorrhage, gastrointestinal (GI) hemorrhage, erroneous placement of lines and tubes, and the development of muscle weakness.
  64. 64. Prognosis pulmonary function returns to normal at 6-12 months in survivors occasionally patient have severe restrictive lung disease although this is the case, many patient have a severe reduction and pulmonary QOL -> depression, anxiety and PTSD are common patient often have cognitive impairment -> these correlate with the period and severity of hypoxia
  65. 65. Thank you