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ALI
is a diffuse heterogeneous lung injury characterized by hypoxemia, non
cardiogenic pulmonary edema, low lung compliance and widespread
capillary leakage.
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ALI
is caused by any stimulus of local or systemic inflammation, principally
sepsis.
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Acute
Lung Injury (ALI) & Acute Respiratory Distress Syndrome (ARDS) are
defined as:
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Primary ALI is caused by a direct injury to the lung
(e.g. pneumonia). Secondary ALI is caused by an indirect insult (e.g.
pancreatitis).
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There
are two stages – the acute phase characterized by disruption of the
alveolar-capillary interface, leakage of protein rich fluid into the
interstitium and alveolar space and extensive release of cytokines and
migration of neutrophils. A later reparative phase is characterized by
fibroproliferation, and organization of lung tissue.
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The
patient has low lung volumes, atelectasis, loss of compliance,
ventilation-perfusion mismatch (increased deadspace) and right to left
shunt.
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Clinical features are - severe dyspnea, tachypnea and resistant
hypoxemia. There are two diagnoses to be made: the syndrome of Acute
Lung Injury and the underlying cause. ALI is a clinical diagnosis. There
are probably two forms of ALI – primary ALI, caused by a direct injury
to the lung, and secondary ALI, caused by an indirect injury to the
lung.
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The cornerstone of treatment is to keep the PaO2 >60mmHg,
without causing injury to the lungs with excessive O2 or volutrauma.
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Pressure control ventilation is more versatile than volume control: but
a volume limited strategy should be used.
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A
number of adjunct therapies are available, none have proven effective.
Of these, inhaled nitric oxide and prone positioning are most frequently
used.
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Current ventilation strategies involve using low tidal volumes with or
without high levels of PEEP. The open lung approach attempts to optimize
lung mechanics and minimize phasic damage by strategically placing PEEP
above Pflex.
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Ventilator induced lung injury is caused by volutrauma and excessive use
of oxygen.
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Steroids may have a role in chronic ARDS in patients,
without infection, with high O2 requirements days to weeks into the
disease process.
Copyright Patrick Neligan
2001-2002 |
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