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Presented by-
Dr.RAKESH KARNAWAT
Definition :
Alternative terminology:
 Da Nang Lung
 Transfusion Lung
 Post Perfusion Lung
 Shock Lung
 Traumatic Wet...
Onset Chest
Radiograp
h
Absence of Left
Atrial
Hypertension
Oxygenation
Acute Bilateral
alveolar or
interstitial
infiltrat...
The reliability of chest radiographic criteria has been
demonstrated to be moderate, with substantial inter-
observer vari...
BERLIN CRITERIA
International expert panel met in 2011
The goal of developing the Berlin definition was to try and improve...
CAUSESOFARDS/TYPES
Direct Lung Injury
(PULMONARY)
Indirect Lung Injury (EXTRA
PUL.)
Pneumonia Sepsis
Pulmonary contusion S...
EDEMA
HYALINE
MEMBRANES
INTERSTITIALS
INFLAMMATION
INTERSTITIAL
FIBROSIS
FIBROSIS
EXUDATIVE PROLIFERATIVE FIBROTIC
DAY 0-7...
Up to 1 week
Capillary and alveolar
cells are injured – protein
rich fluid to accumulates in
the interstitial and alveolar...
PROLIFERATIVE
2 to 3rd week
organization of
alveolar
exudates,Type I
alveolar cells get
replaced by type
2 alveolar cells
...
CHEST X-RAY
Progression from diffuse interstitial infiltrates to diffuse, fluffy, alveolar opacities
CT SCAN-ARDS
EXUDATIVE AND FIBROTIC PHASES
Reticular opacities - suggesting the development of interstitial
fibrosis.
MANAGEMENT
 Mechanical ventilation
 Supportive measures
1. Recognition and treatment of the underlying
medical and surgical disorders (e.g., sepsis,
aspiration, trauma)
2. Minimi...
GOALS
 Oxygenation goal: paO2 of 55-80mmHg Or
SpO2 of 88-95%
 Plateau pressure goal:<30cm H2O
 pH goal:7.25-7.45
 I:E ...
NIH ARDS NET MV PROTOCOL
*PART I: Ventilator set up and adjustment
FIRST STAGE:
1. Calculate IBW M=50+2.3(Ht in inches-6o)...
PART II: WEANING
1. RR< 35(may be >35 for < 5 min)
2. Spo2 > 88% (may be <88% for< 15 min)
3. Respiratory distress is abse...
CONDUCT A CPAP TRIAL DAILY WHEN
1.Fio2 < 0.40 and PEEP < 8
2.PEEP and Fio2 < values of previous day
3.Patient has acceptab...
Pressure support weaning procedure
1. Set PEEP=5 and FiO2=0.5
2. Set PS ventilation based on RR during CPAP trial:
If RR<2...
1. Place the pt.on a T-piece or CPAP<5 cm H2O
2. Asses for tolerance for 2 hours
1. RR<35/min
2. SpO2>90 and PaO2>60mmHg
3...
RECRUITMENT MANEUVERS
Traditionally RMs have been delivered as
sustained inflations, with peak inflation
pressures limited...
PEEP
 Increases the end expiratory or baseline airway
pressure to a value greater than atmospheric
pressor on ventilators...
Pressure (cm H2O)
Volume (mL)
Upper Inflection Point
Lower Inflection Point
How to select appropriate
PEEP?
1. Volume-Pres...
This is again a vent.manuveor used in case of refractory
hypoxemia *Oxygenation can be improved by increasing
mean airway ...
Prone PositionMechanisms to improve oxygenation:
Prone position reverses
gravitationally distributed
perfusion to the bett...
Fekri Abroug et al; An updated study-level meta-analysis of
randomised controlled trials on proning in ARDS and acute
lung...
Improves ventilation-perfusion matching and
improves oxygenation by dilating the local pulmonary
capillaries
No improvemen...
KINETIC THERAPY
By continuously rotating critically ill patients from side-to-side to at least
40°, gravitational pressor ...
These are fluoro carbons with a high oxygen-
carrying capacity & having intrinsic anti
inflammatory properties which are i...
NONCONVENTIONAL VENTILATORY
SUPPORT
1. HIGH FREQUENCY OSCILLATION
2. EXTRACORPOREAL SUPPORT
HFOV is used again in case of refractory hypoxemia where u
put the pt on high frequency vent.mode techniques using
ventila...
VENTILATION
ROLE OF ECMO
ECMO was proposed to maintain the lung “at rest” while
providing adequate gas exchange & this is found to be
...
FLUID MANAGEMENT
Maintaining a normal or low left atrial filling pressure minimizes
pulmonary edema and prevents further d...
ROLE OF GLUCOCORTICOIDS
The main aim of giving glucocorticoids is to reduce
inflamation process in the lung.
Many attempts...
A BRIEF SUMMARY OF THE AVAILABLE STUDIES-
STEROIDS
*High-dose methylprednisolone (30 mg/ kg) I.V every 6 hours for 4
doses...
Nowaday, the new points are based on clinical
evidences, we should give corticosteroid in the
fibroproliferative phase of ...
ROLE OF SURFACTANT
These are all experimental studies & none of them shown
any clinical benefit in the pts.
Though there a...
ROLE OF ACTIVATED PROTEIN-C
It was used previously as it inactivates Va & VIIa –
limit thrombin generation & fibrinolysis...
Future non-ventilatory therapeutic options
Gene and mesenchymal stem cells therapies- these approaches hold
promise in the...
Evidence-Based Recommendations for
ARDS Therapies
Treatment Recommendationa
Mechanical ventilation
Low tidal volume A
High...
FUTURE PROSPECTIVES
 Numerous pharmacological Rx are
underinvestigation to stop the cascade of events
leading to ARDS
 N...
- Martin J. Tobin, MD
THANK YOU
ARDS
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ARDS

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ARDS

  1. 1. Presented by- Dr.RAKESH KARNAWAT
  2. 2. Definition : Alternative terminology:  Da Nang Lung  Transfusion Lung  Post Perfusion Lung  Shock Lung  Traumatic Wet Lung  Post traumatic Failure  Post traumatic Pulmonary Insufficiency  Wet lung  White Lung Taylor RW et al Res Medica 1983;1:17-21 Incidence: 10% of all ICU admissions 20% of these patients meet ALI criteria. Historical Perspectives: Year: 1967 by Ashbaugh and co – workers Acute respiratory distress in adultss Ashbaugh DG et al .Lancet 1967 REVISION OF DEFINITIONS -1988: by Murray et al.
  3. 3. Onset Chest Radiograp h Absence of Left Atrial Hypertension Oxygenation Acute Bilateral alveolar or interstitial infiltrates PCWP 18 mmHg or no clinical evidence of increased left atrial pressure ALI: PaO2/FIO2 less then 300 mmHg ARDS: PaO2/FIO2 less then 200 mmHg AECCC 1994
  4. 4. The reliability of chest radiographic criteria has been demonstrated to be moderate, with substantial inter- observer variability Hypoxemia criteria can be markedly affected by the patient’s ventilator settings, especially the PEEP level used Wedge pressure can be difficult to interpret and if a patient with ARDS develops a high wedge pressure that should not preclude diagnosing that patient as having ARDS
  5. 5. BERLIN CRITERIA International expert panel met in 2011 The goal of developing the Berlin definition was to try and improve feasibility, reliability, face and predictive validity for mortality compared with the AECC definition JAMA2012;307:2526–2533 1. Lung injury of acute onset, within 1 week of an apparent clinical insult and with progression of respiratory symptoms 2. Bilateral opacities on chest imaging not explained by other pulmonary pathology (e.g. pleural effusion, pneumothorax or nodules) 3. Respiratory failure not explained by heart failure or volume overload 4. Decreased arterial PaO2/FiO2 ratio: Mild: 201 - 300 mmHg (≤ 39.9 kPa) Moderate: 101 - 200 mmHg (≤ 26.6 kPa) severe: ≤ 100 mmHg (≤ 13.3 kPa) IntensiveCareMed 012;38:1573–1582.
  6. 6. CAUSESOFARDS/TYPES Direct Lung Injury (PULMONARY) Indirect Lung Injury (EXTRA PUL.) Pneumonia Sepsis Pulmonary contusion Severe trauma Aspiration Multiple bone fractures Near-drowning Flail chest Toxic inhalation injury Head trauma Burns Multiple transfusions Drug overdose Pancreatitis
  7. 7. EDEMA HYALINE MEMBRANES INTERSTITIALS INFLAMMATION INTERSTITIAL FIBROSIS FIBROSIS EXUDATIVE PROLIFERATIVE FIBROTIC DAY 0-7 14 21.. Clinical courseand pathophysiology Lancet 2007; 369:1553-65
  8. 8. Up to 1 week Capillary and alveolar cells are injured – protein rich fluid to accumulates in the interstitial and alveolar spaces – Hyaline membrane Chemicals (cytokines TNF-a, IL-1b, IL-6 and chemokines Neutrophils, macrophages, prostacyclin, leukotrienes, thromboxane, Free radicals) Interferes in gas exchange
  9. 9. PROLIFERATIVE 2 to 3rd week organization of alveolar exudates,Type I alveolar cells get replaced by type 2 alveolar cells Lymphocytes Most patients get recovered FIBROTIC Beyond 3rd week Remodeling by collagenous tissue, arterial thickening, obliteration of pre-capillary vessels. abnormal tissue repair, Type III collagen Long term MV support and O2 therapy Increased morbidity and
  10. 10. CHEST X-RAY Progression from diffuse interstitial infiltrates to diffuse, fluffy, alveolar opacities
  11. 11. CT SCAN-ARDS EXUDATIVE AND FIBROTIC PHASES Reticular opacities - suggesting the development of interstitial fibrosis.
  12. 12. MANAGEMENT  Mechanical ventilation  Supportive measures
  13. 13. 1. Recognition and treatment of the underlying medical and surgical disorders (e.g., sepsis, aspiration, trauma) 2. Minimise procedures and their complications 3. Prophylaxis against venous thromboembolism, gastrointestinal bleeding, and central venous catheter, arterial lines, urinary catheters infection…etc. 4. Recognition of nosocomial infections 5. Provision of adequate nutrition
  14. 14. GOALS  Oxygenation goal: paO2 of 55-80mmHg Or SpO2 of 88-95%  Plateau pressure goal:<30cm H2O  pH goal:7.25-7.45  I:E goal: 1:1 to 1:3
  15. 15. NIH ARDS NET MV PROTOCOL *PART I: Ventilator set up and adjustment FIRST STAGE: 1. Calculate IBW M=50+2.3(Ht in inches-6o), F=45.5+2.3(Ht in inches 50) 2. Select ACMV & Set initial TV to 8ml/kg 3.Add PEEP to 5-7 cm H2O 4. Reduce TV by 1 ml/kg at intervals of <2hours until TV=6ml/kg 5. Set RR < 35bpm 6. Set inspiratory flow rate above pt. demand(>80L/min) JAMA 2010;303:865– 873 SECOND STAGE: When TV=6ml/kg Measure Plateau Pressure:Target <30cm H2o If Ppl;>30cm H2o Decrease TV in 1 ml/kg steps until Ppl drops <30cm H2o or TV down to 4ml/kg. THIRD STAGE: Monitor arterial blood gases for respiratory acidosis pH GOAL: 7.30-7.45 If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 If pH < 7.15: Increase RR to 35. If pH remains < 7.15, TV may be increased in 1 ml/kg steps until pH > 7.15 . Can give NaHCO3 Alkalosis Management: (pH > 7.45) Decrease vent rate if possible. ARDS Network,NEJM, 342:2000
  16. 16. PART II: WEANING 1. RR< 35(may be >35 for < 5 min) 2. Spo2 > 88% (may be <88% for< 15 min) 3. Respiratory distress is absent pulse<120 absence of sweating no dyspnea no abdominal paradox no marked use of accessory muscles of respiration.
  17. 17. CONDUCT A CPAP TRIAL DAILY WHEN 1.Fio2 < 0.40 and PEEP < 8 2.PEEP and Fio2 < values of previous day 3.Patient has acceptable spontaneous breathing efforts 4.Systolic BP > 90 mmHg without vasopressor support CONDUCTING THE TRIAL Set CPAP = 5cm H2O, FiO2=0.5 If RR<35 for 5min advance to PSV. If CPAP trial is not tolerated then return to previous ACMV.
  18. 18. Pressure support weaning procedure 1. Set PEEP=5 and FiO2=0.5 2. Set PS ventilation based on RR during CPAP trial: If RR<25: set PS=5cm H2O and if tolerated for more than 2hrs,asses for unassisted breathing trial If RR=25-35:set PS=20cm H2O then reduce by 5cm H2O at <5min interval for 1-3hrs, then go to unassisted trial If initial PS not tolerated return to previous ACMV
  19. 19. 1. Place the pt.on a T-piece or CPAP<5 cm H2O 2. Asses for tolerance for 2 hours 1. RR<35/min 2. SpO2>90 and PaO2>60mmHg 3. Spontaneous TV>4ml/kg of IBW 4. Signs of respiratory distress are absent 3. If tolerated well - consider for extubation 4. If not tolerated, resume pre-weaning settings.
  20. 20. RECRUITMENT MANEUVERS Traditionally RMs have been delivered as sustained inflations, with peak inflation pressures limited to between 30 and 40 cm H2O, typically held for a period ranging from 15 to 40 seconds with the intention of reopening collapsed regions of the lung NEJM 2007; 354: 1775-1786 However, due to the unusually high surface tension within affected alveoli, the benefit is often transient especially if not followed by sufficiently high levels of PEEP.
  21. 21. PEEP  Increases the end expiratory or baseline airway pressure to a value greater than atmospheric pressor on ventilators.  Improves oxygenation prevents end exp collapse of alveoli increase FRC recruites nonventilated/poorly ventilated alveoli  Creates hydrostatic force,shift fluid from alveoli to interstitium,relieves pulm.oedema
  22. 22. Pressure (cm H2O) Volume (mL) Upper Inflection Point Lower Inflection Point How to select appropriate PEEP? 1. Volume-Pressure Curve 2. Incremental increase in PEEP value 3. FiO2/PEEP ratio Principle for FiO2 and PEEP Adjustment FiO2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 PEEP 5 5-8 8-10 10 10-14 14 14-18 18-24
  23. 23. This is again a vent.manuveor used in case of refractory hypoxemia *Oxygenation can be improved by increasing mean airway pressure with "inverse ratio ventilation." In this technique, the inspiratory (I) time is lengthened so that it is longer than the expiratory (E) time (I:E 1:1 to I.E. I:3). With diminished time to exhale, dynamic hyperinflation leads to increased end-expiratory pressure, just like PEEP. *This mode of ventilation has the advantage of improving oxygenation with lower peak pressures than conventional ventilation. Although inverse ratio ventilation can improve oxygenation and help in reducing FIO2 to 0.60 to avoid possible oxygen toxicity. No mortality benefit or survival benefit in ARDS has been demonstrated. INVERSE RATIO VENTILATION
  24. 24. Prone PositionMechanisms to improve oxygenation: Prone position reverses gravitationally distributed perfusion to the better- ventilated ventral lung regions and improved ventilation of previously dependent dorsal lung, both of which would improve ventilation/perfusion matching. More efficient drainage of secretions Improvement in oxygenation is immediate but there is no difference in mortality. Optimum timing or duration ? Because of the lack of clear benefit in survival and the potential complications of prone positioning,we believe that there is not enough evidence to support its routine use in all patients with acute lung injury and ARDS Gattinoni et al., NEJM, 2001;45:568–573
  25. 25. Fekri Abroug et al; An updated study-level meta-analysis of randomised controlled trials on proning in ARDS and acute lung injury.Critical Care 2011, 15; 6 Analysis showed that prone ventilation significantly reduces ICU mortality in ARDS patients and suggested that long prone durations should be applied Two large RCT’s compared the effect of prone vs supine positioning on mortality Conclusion: Both studies showed that prone positioning does not improve survival and that it may be associated with harmful effects such as decubitus ulcers and self- extubation
  26. 26. Improves ventilation-perfusion matching and improves oxygenation by dilating the local pulmonary capillaries No improvement on survival Nitric Oxide Routine use is not recommended Nitric Oxide Taylor R W E et.al.LOW-DOSE INHALED NITRIC OXIDE IN PATIENTSWITHACUTE LUNG INJURY: JAMA 2004; 291:1603–1609.
  27. 27. KINETIC THERAPY By continuously rotating critically ill patients from side-to-side to at least 40°, gravitational pressor can help in improving ventilation perfusion mismatch , increased FRC & thus helpful to improve oxygenation and benefit patients with ALI/ARDS.
  28. 28. These are fluoro carbons with a high oxygen- carrying capacity & having intrinsic anti inflammatory properties which are injected in the lung to improve the oxygenation but none of these shown any benefit in the pt.
  29. 29. NONCONVENTIONAL VENTILATORY SUPPORT 1. HIGH FREQUENCY OSCILLATION 2. EXTRACORPOREAL SUPPORT
  30. 30. HFOV is used again in case of refractory hypoxemia where u put the pt on high frequency vent.mode techniques using ventilation frequencies of greater than 60 breath per minute and tidal volumes between 1 to 5ml/kg Highfrequency oscillatory ventilation improves gas exchange, inflates the lungs uniformly,reduces ventilator-induced lung injury, and reduces levels of systemic inflammatory mediators. Patients in the high-frequency oscillatory ventilation group showed an earlier improvement in the PaO2/FiO2 ratio compared with in the PaO2/FiO2 ratio compared with those on conventional ventilation, although the difference did not persist for more than 24 hours. AMJ RESPIRCRIT CARE MED 2002;166:801–808.
  31. 31. VENTILATION
  32. 32. ROLE OF ECMO ECMO was proposed to maintain the lung “at rest” while providing adequate gas exchange & this is found to be efficient in removing 20% of CO2 • Substantial risk of infection and bleeding • Not routinely recommended • No improvement on survival • Recent trial ; A modified technique (low-frequency positive- pressure ventilation with extracorporeal CO2 removal [LFPPV-ECCO2R]) is proposed to inflate the lungs to moderate pressures to maintain FRC while CO2 removal is ensured by a low flow partial venovenous bypass.
  33. 33. FLUID MANAGEMENT Maintaining a normal or low left atrial filling pressure minimizes pulmonary edema and prevents further decrements in arterial oxygenation and lung compliance, improves pulmonary mechanics, shortens ICU stay and the duration of mechanical ventilation, and is associated with a lower mortality. ARDSNet05: Fluid and Catheter Treatment Trial (FACTT) These results support the use of a conservative strategy of fluid management in patients with acute lung injury untill unless pt is having hypotension or hypoperfusion of critical organs. Am J Respir Crit Care Med 2012;186:1256–1263. Hypoalbuminemic patients should receive coloids whereas all other patients should receive crystalloid fluids to decrease the pulmonary congestion
  34. 34. ROLE OF GLUCOCORTICOIDS The main aim of giving glucocorticoids is to reduce inflamation process in the lung. Many attempts have been made to treat both early and late ARDS pt.with glucocorticoids to reduce this potentially deleterious pulmonary inflammation but only few studies have shown the benefitial effect. *Current evidence does not support the use of glucocorticoids in the care of early ARDS patients. *Glucocorticoids can be used in the late phase of ARDS to decrease fibrotic tissue formation.
  35. 35. A BRIEF SUMMARY OF THE AVAILABLE STUDIES- STEROIDS *High-dose methylprednisolone (30 mg/ kg) I.V every 6 hours for 4 doses) given to patients within 24 hours of the diagnosis of ARDS has not improved outcome or reduced mortality *In fact, one study showed a higher mortality associated with early steroid therapy in ARDS (Bone 1987) *Secondary infection are increased in patients receiving high dose methyl-prednisolone for ARDS (Bone 1987) *High-dose methylprednisolone (2-3 mg/kg/day) given to 25 patients with late ARDS (2 weeks duration) resulted in a beneficial response in 21 patients and an 86% survival in the responders (Meduri 1994) *Medurri: The surviving patients treated with corticosteroids had significant reductions in plasma levels of chemical mediators like TNF-a , IL-1b, IL-6, and IL-8
  36. 36. Nowaday, the new points are based on clinical evidences, we should give corticosteroid in the fibroproliferative phase of ARDS, 7-14 days, without evidence of infection Treated patients had: - earlier reduction in lung injury score - reduced time on vent [p=.002] - reduced ICU stay [p =.007] - reduced ICU mortality [21% vs 43%] p=.03 - lower rate of ICU infections [p = .0002]
  37. 37. ROLE OF SURFACTANT These are all experimental studies & none of them shown any clinical benefit in the pts. Though there are many evidences in support of surfactant replacement therapy for neonatal respiratory distress syndrome but the results from its use in adult ARDS patients have not shown any clinical benefits.
  38. 38. ROLE OF ACTIVATED PROTEIN-C It was used previously as it inactivates Va & VIIa – limit thrombin generation & fibrinolysis. It also has anti-inflam.activity but because of its more adverse effects ex. Increase risk of bleeding (3.5% vs 2.0%) it is no longer used now a days.
  39. 39. Future non-ventilatory therapeutic options Gene and mesenchymal stem cells therapies- these approaches hold promise in the treatment of ARDS.  Gene therapy for ALI/ARDS Lung injury in ARDS is characterized by a pro-inflammatory increase in vascular permeability and neutrophil infiltration, which sustain alveolar edema and damage to alveolar barrier. Lung gene transfer encoding for IL10 has been shown to reduce the release of inflammatory cytokines with improvement in oxygenation & pulmonary vascular resistance. Similar anti- inflammatory effects have been found with the delivery of genes encoding anti-inflammatory cytokines such as interferon protein 10 (IP-10), IL 12, Heme oxygenases (HO) and transforming growth factor beta-1 (TGF-β1)  Mesenchymal stem cells Mesenchymal stem cells (MSC) are multipotent stromal cells that can differentiate into a variety of cells types, having regenerative properties and may repair damaged tissues & this properties make them promising as a therapeutic approach in ARDS. In addition, they can release many molecules, which contribute to immunomodulatory and anti-inflammatory effects. Although all these strategies have demonstrated to improve oxygenation, their impact on mortality is controversial.
  40. 40. Evidence-Based Recommendations for ARDS Therapies Treatment Recommendationa Mechanical ventilation Low tidal volume A High-PEEP or "open-lung" C Prone position C Recruitment maneuvers C High-frequency ventilation and ECMO D Surfactant replacement, inhaled nitric oxide, and other antiinflammatory therapy e.g., ketoconazole, PGE1, NSAIDs D Glucocorticoids Fluid Therapy C B
  41. 41. FUTURE PROSPECTIVES  Numerous pharmacological Rx are underinvestigation to stop the cascade of events leading to ARDS  Neutrrophil inhibitors  Interleukin-1 receptor antagonist  Pulmonary specific vasodilator  Surfactant replacement therapy  Antisepsis agent  Gene Therapy
  42. 42. - Martin J. Tobin, MD
  43. 43. THANK YOU

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