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OVERVIEW
Acute Respiratory Distress Syndrome (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.
The term acute lung injury (ALI) has been discarded
See ARDS Definitions
DEFINITION
SEVERITY
RISK FACTORS
Direct Indirect
Classical phases
Injury
Exudative alveolar capillary membrane disruption with inflammatory cell infiltrate and high protein
exudate to form hyaline membranes
Proliferative proliferation of abnormal Type II alveoli cells and inflammatory cells
Fibrotic infiltration with fibroblasts which replace alveoli and alveolar ducts with fibrosis
Resolution slow and incomplete repair and restoration of architecture
Complex interplay:
damage with bidirectional flow (proteins and fluid in to alveoli, surfactant and alveolar cytokines into
plasma)
surfactant dysfunction
proliferation of type II cells
-> the balance between repair and fibrosing alveolitis
Inflammatory infiltrates
migration of neutrophils into alveoli with activation -> release of oxygen species, cytokines, eicasanoids,
proteases -> tissue damage
pulmonary endothelial cells, platelets, interstitial and alveolar macrophages also play important roles in
alveolar inflammation.
Surfactant dysfunction
Effects
MANAGEMENT
General
diagnosis and appropriate treatment to minimise physiological impact of cause (drain collection,
antibiotics, resuscitate, splint fractures)
feed
standard ICU prophylaxis
Mechanical ventilation
ARDS Network protective lung ventilation strategy (from the ARMA study)
controlled ventilation
TV 6mL/kg
avoid overstretch (volutrauma) and inadequate recruitment (atelectrauma)
PEEP
Plateau pressure <30 cmH20 (higher than this contributes to VILI from overstretching and
hyperinflation of the functional baby lung)
mode of ventilation: generally no difference
PCV tends to be used c/o plateau pressure approximates peak pressure, with VC plateau pressure
needs to be measured
no role for inverse ratio ventilation (I:E ratio > 1) -> increased mean airway pressure +
haemodynamic instability + regional hyperinflation
oxygenation target: SpO2 > 90%, PaO2 >60mmHg
carbon dioxide target: ARDSnet aimed for a normal CO2 -> but lung is exposed to repeated tidal stretch,
ideally hypercapnia should be minimised but there isnt compelling data to suggest it is harmful unless
there is an obvious reason (raised ICP, pregnancy).
Pharmacological therapy
PROGNOSIS