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Acute Lung Injury and ARDS. Andreas Crede Emergency Medicine Registrar. Overview. Introduction Definition Pathophysiology Treatment New Stuff References. Introduction. 1 st described 1967 (Ashbaugh et al) Incidence 1.5 -7.5/ 100000 population 28 day mortality 25 – 30% 1

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acute lung injury and ards

Acute Lung InjuryandARDS

Andreas Crede

Emergency Medicine Registrar

overview
Overview
  • Introduction
  • Definition
  • Pathophysiology
  • Treatment
  • New Stuff
  • References
introduction
Introduction
  • 1st described 1967 (Ashbaugh et al)
  • Incidence 1.5 -7.5/ 100000 population
  • 28 day mortality 25 – 30%1
  • Diagnosis clinical
definition
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
Risk Factors
  • Alcoholism
  • Genetic predisposition
causes
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
causes1
Causes
  • Indirect Injury1
      • Severe Sepsis
      • Massive transfusion
      • Shock
      • Pancreatitis
      • Salicylate/ narcotic overdose
      • Anaphylaxis
      • Cardiopulmonary bypass
differential
Differential
  • LVF
  • Fluid overload
  • Mitral stenosis
  • Lymphangitis carcinomatosis
  • Interstitial lung disease1
histologically
Histologically
  • Exudative Phase3
      • Neutrophilic Infiltrate
      • Alveolar Haemorrhage
      • Proteinaceous Pulmonary Oedema
      • Cytokines (TNF, IL1,8)
          • ↑ Inflammation
          • ↑ Oxidative Stress and Protease Activity
          • ↓ Surfactant Activity
          • Atelectasis
histologically1
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
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
Long Term
  • Chronic Respiratory Disease
  • Muscle Fatigue
  • Muscle Wasting
  • Weakness
treatment
Treatment
  • Ventilation
  • Fluid Management
  • Steroids
  • Other Stuff
ventilation
Ventilation
  • Tidal Volumes
  • PEEP
  • Positioning
  • Weaning Protocols
tidal volume
Tidal Volume
  • Recommended 4-6ml/kg4
  • High tidal volumes4
      • Overdistention of alveoli
      • Local inflammatory response resulting in systemic inflammation
      • TNF, IL6, IL10,
tidal volume 4
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
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
slide25
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
slide27
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
slide28
PEEP

Adverse effects of PEEP

  •  Cardiac output
  • Volutrauma
  •  Lung water
  •  High VA/Q
  •  Dead space
  •  Endothelial permeability
  •  Epithelial permeability
  •  Bronchial blood flow
peep lung perfusion
PEEP + Lung Perfusion

Permutt, JAP 1961

slide31
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
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
Supine Ventilation
  • ± 40% lung volume under lung, especially patients with large hearts
effect of blood flow in prone positioning 7

D

Mid

ND

D

Mid

ND

Ventral

Dorsal

Prone

Effect of Blood Flow in Prone Positioning7

50

25

Percent Flow

0

Dorsal

Ventral

Supine

positioning1
Positioning
  • Prone position4
      • Transient improvement PaO2/FiO2
      • No improvement: survival/ time on ventilator/ time in ICU
      • Role:
          • High FiO2
          • High plateau pressures
weaning protocols
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 management1
Fluid Management
  • Fluid movement regulated by:
      • Starling equation
      • Vessel wall
        • Ability to filter fluid
        • Selective permeability to proteins
fluid management3
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
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
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
Emergency Department Summary
  • PREVENT!
  • Low tidal volume ventilation
  • Restrict PEEP
  • Restrict Fluids (if possible)
  • Initiate Weaning Protocol
  • Supine Ventilation
conclusion
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
references
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