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In respiratory care and nursing circles, benefits from frequent repositioning of the bedridden patient and actively clearing fluids and secretions in the lower airway are seldom challenged. When clearance of retained mucus is needed, I couldn't agree more.
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However, my own clinical experience suggests that very early in the course of non-symmetrical lung injury and pneumonia--when fluids are more freely mobile--this "stirring up" might actually help spread inflammation and even transform limited disease into full-blown acute respiratory distress syndrome (ARDS).
Unintended Spread of Initially Localized Injury
Current teaching holds that diffuse lung injury (acute lung injury or ARDS) begins synchronously throughout the lung, mediated by inhalation, massive aspiration or indirect injury from blood-borne leukocytes, inflammatory mediators, immune complexes or bacteria. In most instances, this perception is undoubtedly justified. But relatively little attention has been paid to the possibility that inflammatory injury may begin focally and propagate via the airways, unintentionally aided by the well meaning nurse, physician or respiratory care practitioner.
We do know that poorly chosen ventilatory patterns--those involving high tidal volumes, high plateau pressures and low levels of PEEP--exacerbate injury. Research into the damage caused by mechanical ventilation (ventilator-induced lung injury) has been focused largely on the primacy of repeated stresses and strains encountered by the lung parenchyma and unsupported small airways during tidal breathing.
Any edema that forms as a result of the primary injury or VILI, however, might also play an important and perhaps preventable role in determining the extent and distribution of damage. The acutely injured lung is comprised of units of two types, functional and damaged. Our thought is that, if uncontained, inflammatory edema may transform some of the former into the latter, thereby extending ("propagating") trouble.