acute lung injury and ards andreas crede emergency medicine registrar
TRANSCRIPT
Acute Lung Injuryand
ARDS
Andreas CredeEmergency Medicine Registrar
Overview
• Introduction
• Definition
• Pathophysiology
• Treatment
• New Stuff
• References
Introduction
• 1st described 1967 (Ashbaugh et al)
• Incidence 1.5 -7.5/ 100000 population
• 28 day mortality 25 – 30%1
• Diagnosis clinical
Definition
• Acute onset (<7days) respiratory failure/distress• Diffuse, bilateral infiltrates on CXR• Absent left atrial hypertension (PAOP
≤18mmHg)• Or absent clinical evidence of left atrial
hypertension
• PaO2/ FiO2 <300mmHg (ALI)
• PaO2/ FiO2 <200mmHg (ARDS)2
Risk Factors
• Alcoholism
• Genetic predisposition
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
Causes
• Indirect Injury1
• Severe Sepsis• Massive transfusion• Shock• Pancreatitis• Salicylate/ narcotic overdose• Anaphylaxis• Cardiopulmonary bypass
Differential
• LVF
• Fluid overload
• Mitral stenosis
• Lymphangitis carcinomatosis
• Interstitial lung disease1
Physical/ chemical injuryActivation Innate
Inflammatory Cascade
Leakage Protein Rich Oedema FluidInflammatory Cellular
Infiltrates
Diffusion AbnormalitiesV/Q Mismatch
Hypoxia
Respiratory Failure
Physical/ chemical injuryActivation Innate
Inflammatory Cascade
Cellular InfiltrateAtelectasis
Oedema Fluid
Reduced Thoracic Compliance + Vasoconstriction
Hypoxia
Respiratory Failure
Physical/ chemical injuryActivation Innate
Inflammatory Cascade
Small Vessel Thrombosis
Increased Dead Space
Hypoxia
Respiratory Failure
Alveolar Damage
Capillary Damage
Leakage Oedema
Fluid
InflammatoryCellular Infiltrates
V/Q Mismatch
Atelectasis
↓ThoracicCompliance
↑Dead Space
Hypoxic Vasoconstriction
Hypoxia
Respiratory Failure
Atelectasis/ Reduced Lung Compliance
Hypoxaemia↑ Dead Space
Histologically
• Exudative Phase3 • Neutrophilic Infiltrate• Alveolar Haemorrhage• Proteinaceous Pulmonary Oedema• Cytokines (TNF, IL1,8)
» ↑ Inflammation» ↑ Oxidative Stress and Protease Activity» ↓ Surfactant Activity» Atelectasis
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)
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
Long Term
• Chronic Respiratory Disease
• Muscle Fatigue
• Muscle Wasting
• Weakness
Treatment
• Ventilation
• Fluid Management
• Steroids
• Other Stuff
Ventilation
• Tidal Volumes
• PEEP
• Positioning
• Weaning Protocols
Tidal Volume
• Recommended 4-6ml/kg4
• High tidal volumes4
• Overdistention of alveoli• Local inflammatory response resulting in systemic
inflammation• TNF, IL6, IL10,
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
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%, p=0.10)
• Earlier recovery from hypoxia
• Only ventilation strategy shown to reduce mortality (40% - 31%)4
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
PEEP
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
PEEP
Adverse effects of PEEP Cardiac output• Volutrauma Lung water High VA/Q Dead space Endothelial permeability Epithelial permeability Bronchial blood flow
Fessler, ARRD 1993
PEEP + Lung Perfusion
Permutt, JAP 1961
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
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
Supine Ventilation
• ± 40% lung volume under lung, especially patients with large hearts
Prone Ventilation
Effect of Blood Flow in Prone Positioning7
Perc
en
t Flo
w
25
50
0
Supine
MidD ND
Dorsal VentralProne
Ventral Dorsal
D Mid
ND
Positioning
• Prone position4
• Transient improvement PaO2/FiO2
• No improvement: survival/ time on ventilator/ time in ICU
• Role:» High FiO2
» High plateau pressures
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
Fluid Management
Fluid Management
• Fluid movement regulated by:• Starling equation• Vessel wall
– Ability to filter fluid– Selective permeability to proteins
Fluid Management
Fluid Management
• Study of conservative vs liberal fluid management5
• 60 day mortality: 25.5 vs 28.4% p=0.30• 1st 28 days ventilator free: 14.6 vs 12.1 p<0.001• 1st 28 days ICU free: 13.4 vs 11.2 p<0.001• 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
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
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
Emergency Department Summary
• PREVENT!
• Low tidal volume ventilation
• Restrict PEEP
• Restrict Fluids (if possible)
• Initiate Weaning Protocol
• Supine Ventilation
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
Thank You
References• 1. Wheeler, A.P. and Bernard, G.R. 2007,Acute Lung Injury and the Acute
Respiratory Distress Syndrome: A Clinical Review. Lancet; 369: 1553–65• 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; 342:1301-08
• 3 Plantadosi, C.A and Schwartz, D.A. 2004, The Acute Respiratory Distress Syndrome. Ann Intern Med; 141:460-470.
• 4. Girard, T>D> and Bernard,G.R. 2007, Mechanical Ventilation in ARDS: A State-of-the-Art Review. Chest; 131;921-929
• 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; 354:2564-75
• 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; 354:1671-84
• 7. www.slideshare.net