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ARDS
Acute Respiratory distress Syndrome
Introduction
• ALI or ARDS was first described by Ashbaugh and
Petty in 1967
• 1994 AECC (American European Consensus
conference ) definition became globally accepted,
but had limitations
• The current definition is the ‘Berlin Definition’
published in 2013
• Created by a consensus panel of experts
• European Society of Intensive Care Medicine
endorsed by the American Thoracic Society and
the Society of Critical Care Medicine
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…[with]
hypoxemia and bilateral radiographic
opacities, associated with increased venous
admixture, increased physiological dead space
and decreased lung compliance
Risk factors
• Bacteremia
• Sepsis
• Trauma, with or without pulmonary contusion
• Fractures, particularly multiple fractures and long bone
fractures
• Burns
• Massive transfusion
• Pneumonia
• Aspiration
• Drug overdose
• Near drowning
• Postperfusion injury after cardiopulmonary bypass
• Pancreatitis
• Fat embolism
Pathophysiology
• Initial "exudative" stage-diffuse alveolar damage
within the first week
• “Proliferative" stage-resolution of pulmonary
edema, proliferation of type II alveolar cells,
squamous metaplasia, and early deposition of
collagen.
• Some patients progress to a third "fibrotic" stage,
characterized by obliteration of normal lung
architecture, diffuse fibrosis, and cyst formation
Clinical features
The defining features of ARDS are:
1. Severe refractory (resistant to treatment)
hypoxemia
2. Presence of pulmonary oedema with normal
hydrostatic pressure in the pulmonary
vasculature
3. Appearance of diffuse bilateral pulmonary
infiltrates on chest X-ray
4. Falling pulmonary compliance (<50 mL/cmH2O).
Clinical features
• Increased breathlessness
• Tachypnea
• Hypoxemia
• Patients struggle to breathe through lungs
that feel like a wet sponge
Investigations
• ABG analysis – PaO2 decreased 60 mmHg
– PaCO2 initially normal than later increased
• PFT – FRC, VC, VT reduced
• Chest X ray – symmetrical bilateral and diffuse
snowstorm infiltrates
• CT scan – opacities of atelectasis
• Auscultation – rales more common, some time wheeze
Management
• Treatment divided in four areas, they are
1. Treat the cause of ARDS
2. Treatment for hypoxemia
3. Supporting treatment like nutritional
4. Prevent and treat complications
Management
• Treat the cause of ARDS
– Based on cause treat the root cause of ARDS
• Treatment for hypoxemia
– Support adequate gas exchange and tissue
oxygenation
– Ventilator with PEEP
• Supporting treatment
– Management of patient nutritional status and fluid
balance
– Management of input and output
Management
• Prevent and treat complications
– Common complication are:
– Nosocomial infections
– Barotrauma
– Coagulation disturbances
Pharmacology
• Surfactant replacement therapy
• Inhaled B2-agonists which may improve lung
compliance (Moriiia, 1997)
• Steroids are sometimes given In the later
stages but tend to encourage infection in
critically ill patients (Bass et ai., 1997)

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Ards

  • 2. Introduction • ALI or ARDS was first described by Ashbaugh and Petty in 1967 • 1994 AECC (American European Consensus conference ) definition became globally accepted, but had limitations • The current definition is the ‘Berlin Definition’ published in 2013 • Created by a consensus panel of experts • European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine
  • 3. 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…[with] hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance
  • 4. Risk factors • Bacteremia • Sepsis • Trauma, with or without pulmonary contusion • Fractures, particularly multiple fractures and long bone fractures • Burns • Massive transfusion • Pneumonia • Aspiration • Drug overdose • Near drowning • Postperfusion injury after cardiopulmonary bypass • Pancreatitis • Fat embolism
  • 5. Pathophysiology • Initial "exudative" stage-diffuse alveolar damage within the first week • “Proliferative" stage-resolution of pulmonary edema, proliferation of type II alveolar cells, squamous metaplasia, and early deposition of collagen. • Some patients progress to a third "fibrotic" stage, characterized by obliteration of normal lung architecture, diffuse fibrosis, and cyst formation
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  • 7. Clinical features The defining features of ARDS are: 1. Severe refractory (resistant to treatment) hypoxemia 2. Presence of pulmonary oedema with normal hydrostatic pressure in the pulmonary vasculature 3. Appearance of diffuse bilateral pulmonary infiltrates on chest X-ray 4. Falling pulmonary compliance (<50 mL/cmH2O).
  • 8. Clinical features • Increased breathlessness • Tachypnea • Hypoxemia • Patients struggle to breathe through lungs that feel like a wet sponge
  • 9. Investigations • ABG analysis – PaO2 decreased 60 mmHg – PaCO2 initially normal than later increased • PFT – FRC, VC, VT reduced • Chest X ray – symmetrical bilateral and diffuse snowstorm infiltrates • CT scan – opacities of atelectasis • Auscultation – rales more common, some time wheeze
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  • 12. Management • Treatment divided in four areas, they are 1. Treat the cause of ARDS 2. Treatment for hypoxemia 3. Supporting treatment like nutritional 4. Prevent and treat complications
  • 13. Management • Treat the cause of ARDS – Based on cause treat the root cause of ARDS • Treatment for hypoxemia – Support adequate gas exchange and tissue oxygenation – Ventilator with PEEP • Supporting treatment – Management of patient nutritional status and fluid balance – Management of input and output
  • 14. Management • Prevent and treat complications – Common complication are: – Nosocomial infections – Barotrauma – Coagulation disturbances
  • 15. Pharmacology • Surfactant replacement therapy • Inhaled B2-agonists which may improve lung compliance (Moriiia, 1997) • Steroids are sometimes given In the later stages but tend to encourage infection in critically ill patients (Bass et ai., 1997)