Acute Lung Injury and ARDS

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Acute Lung InjuryandARDS

• Andreas Crede
• Emergency Medicine Registrar

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Overview

• Introduction
• Definition
• Pathophysiology
• Treatment
• New Stuff
• References

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Introduction

• 1st described 1967 (Ashbaugh et al)
• Incidence 1.5 -7.5/ 100000 population
• 28 day mortality 25 301
• Diagnosis clinical

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Definition

• Acute onset (lt7days) respiratory failure/distress
• Diffuse, bilateral infiltrates on CXR
• Absent left atrial hypertension (PAOP 18mmHg)
• Or absent clinical evidence of left atrial
  hypertension
• PaO2/ FiO2 lt300mmHg (ALI)
• PaO2/ FiO2 lt200mmHg (ARDS)2

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Risk Factors

• Alcoholism
• Genetic predisposition

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Causes

• Direct Injury1
• Pneumonia
• Aspiration
• Drowning
• Amniotic fluid and fat embolism
• Alveolar haemorrhage
• Smoke, toxic gas inhalation
• Reperfusion (incl rapid drainage pleural
  effusion)
• Unilateral lung re-implantation

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Causes

• Indirect Injury1
• Severe Sepsis
• Massive transfusion
• Shock
• Pancreatitis
• Salicylate/ narcotic overdose
• Anaphylaxis
• Cardiopulmonary bypass

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Differential

• LVF
• Fluid overload
• Mitral stenosis
• Lymphangitis carcinomatosis
• Interstitial lung disease1

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Respiratory Failure
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Histologically

• Exudative Phase3
• Neutrophilic Infiltrate
• Alveolar Haemorrhage
• Proteinaceous Pulmonary Oedema
• Cytokines (TNF, IL1,8)
• ? Inflammation
• ? Oxidative Stress and Protease Activity
• ? Surfactant Activity
• Atelectasis

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Histologically

• Elastase- induced capillary and alveolar damage3
• ? Alveolar flooding
• ? Fluid clearance
• Capillary thrombosis
• ? Anticoagulant proteins
• ? Procoagulant proteins (Tissue Factor)
• ? Anti- fibrinolytic Protein (Plasminogen
  Activator Inhibitor)

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Post Acute Phase

• Fibroproliferative Phase3
• Variable time period
• Fibrosis
• Chronic Inflammation
• Neovascularisation
• Resolution3
• Improvement of hypoxaemia
• Improved dead space and lung compliance
• Resolution radiographic abnormalities
• Can take up to 1 year
• Residual restrictive or obstructive picture

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Long Term

• Chronic Respiratory Disease
• Muscle Fatigue
• Muscle Wasting
• Weakness

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Treatment

• Ventilation
• Fluid Management
• Steroids
• Other Stuff

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Ventilation

• Tidal Volumes
• PEEP
• Positioning
• Weaning Protocols

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Tidal Volume

• Recommended 4-6ml/kg4
• High tidal volumes4
• Overdistention of alveoli
• Local inflammatory response resulting in systemic
  inflammation
• TNF, IL6, IL10,

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Tidal Volume4

• Low tidal volume ventilation
• Weight
• Predicted not actual
• Plateau Pressure
• 30cm H2O
• Resp Rate
• Titrated to pH 7.3-7.45
• PEEP and FiO2
• Adjusted to maintain saturation
• Low tidal volume may result in hypercarbia
• ARMA (Respiratory Management in ALI/ARDS Trial)
• NaHCO3 infusions/ hyperventilation to maintain pH

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Tidal Volumes

• Same sedation strategies
• No ? duration of ventilation
• High frequency oscillatory ventilation shown no
  benefit over low tidal volume ventilation
• 30 day mortality not statistically significant
  (37 vs 52, p0.10)
• Earlier recovery from hypoxia
• Only ventilation strategy shown to reduce
  mortality (40 - 31)4

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PEEP

• Recommendation lowest PEEP/ FiO2 to maintain
  saturation
• Recruits collapsed alveoli
• In dependant regions
• Over-distends in non-dependant regions
• ? Repetitive opening/ closing of alveoli ?
  airway damage
• Endothelial/ epithelial stretch injury with
  subsequent capillary injury
• Similar cytokine response as ?tidal volume

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PEEP
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PEEP

• ALVEOLI Trial4
• Higher PEEP improved oxygenation
• In hospital mortality equal btw high and low PEEP
• Time on ventilator similar
• Duration non- pulmonary organ failure equal

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PEEP

• Adverse effects of PEEP
• ? Cardiac output
• Volutrauma
• ? Lung water
• ? High VA/Q
• ? Dead space
• ? Endothelial permeability
• ? Epithelial permeability
• ? Bronchial blood flow

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Fessler, ARRD 1993
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PEEP Lung Perfusion
Permutt, JAP 1961
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PEEP

• Some Endpoints
• Best PaO2
• Lowest Shunt
• Best O2 delivery
• Best lung perfusion
• Plateau Pressure 30cm H2O
• Optimise aeration on CT
• Pressure/ volume curve becomes concave

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Positioning

• Prone positioning1,4
• Redistribution of blood ventilation to least
  affected areas of lung
• Secretion clearance
• Shifts mediastinum anteriorly assists
  recruitment of atelectatic areas
• ? reduce lung injury
• Reduced lung compression by abdominal contents

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Supine Ventilation

• 40 lung volume under lung, especially patients
  with large hearts

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Prone Ventilation
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Effect of Blood Flow in Prone Positioning7
50
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Percent Flow
0
Dorsal
Ventral
Supine
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Positioning

• Prone position4
• Transient improvement PaO2/FiO2
• No improvement survival/ time on ventilator/
  time in ICU
• Role
• High FiO2
• High plateau pressures

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Weaning Protocols

• Reduce duration of mechanical ventilation vs
  patients managed by IMV protocol4
• Daily spontaneous breathing trial4
• 30-120 mins unassisted ventilation
• 4 Criteria before commencement
• Some reversal of underlying cause
• PEEP 8cm H2O/ FiO2 50
• Haemodynamic stability
• Ability to initiate inspiratory effort

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Fluid Management
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Fluid Management

• Fluid movement regulated by
• Starling equation
• Vessel wall
• Ability to filter fluid
• Selective permeability to proteins

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Fluid Management
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Fluid Management

• Study of conservative vs liberal fluid
  management5
• 60 day mortality 25.5 vs 28.4 p0.30
• 1st 28 days ventilator free 14.6 vs 12.1 plt0.001
• 1st 28 days ICU free 13.4 vs 11.2 plt0.001
• Difference in organ failure and need for dialysis
  not statistically significant
• No specific mention of CVP/ PAOP levels which to
  aim for
• Conservative 4mmHg Liberal 10-14mmHg CVP

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Steroids

• Theoretical use to ?inflammatory response
  associated with ARDS6
• 2006 study6
• No ?60 day mortality (28.6 vs 29.2 p 0.10)
• Use of steroids 14 days post onset ? mortality
• ? need for vasopressors
• ? ventilator and shock free days
• ? neuromuscular weakness
• Short term improvement in oxygenation

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Other stuff

• Extracorporeal membrane oxygenation
• Improvement in oygenation
• No ? long term survival
• Vasodilators
• Improved oygenation
• No ? long term survival
• Ketoconazole
• Pentoxyfilline
• Nutritional modification
• Antioxidants
• Surfactant
• B2 stimulants1

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Emergency Department Summary

• PREVENT!
• Low tidal volume ventilation
• Restrict PEEP
• Restrict Fluids (if possible)
• Initiate Weaning Protocol
• Supine Ventilation

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Conclusion

• Many theoretical therapies
• Only proven strategy to improve survival is low
  tidal volume ventilation
• Therapies to reduce number of days needing scarce
  resources valuable in our setting

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Thank You
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References

• 1. Wheeler, A.P. and Bernard, G.R. 2007,Acute
  Lung Injury and the Acute Respiratory Distress
  Syndrome A Clinical Review. Lancet 369 155365
• 2. The Acute Respiratory Distress Syndrome
  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
  3421301-08
• 3 Plantadosi, C.A and Schwartz, D.A. 2004, The
  Acute Respiratory Distress Syndrome. Ann Intern
  Med 141460-470.
• 4. Girard, TgtDgt and Bernard,G.R. 2007, Mechanical
  Ventilation in ARDS A State-of-the-Art Review.
  Chest 131921-929
• 5. The National Heart, Lung and Blood Institue
  Acute Respiratory Distress Syndrome Clinical
  Trials Network. 2006, Comparison of Two
  Fluid-Management Strategies in Acute Lung Injury.
  N Engl J Med 3542564-75
• 6. The National Heart, Lung and Blood Institue
  Acute Respiratory Distress Syndrome Clinical
  Trials Network. 2006, Efficacy and Safety of
  Corticosteroids for Persistent Acute Respiratory
  Distress Syndrome. N Engl J Med 3541671-84
• 7. www.slideshare.net