Acute lung injury

Consists of acute hypoxia, respiratory failure with bilateral lung infiltrates not primarily due to left atria hypertension.

Defined as the ratio of arterial oxygen pressure (Pao2) to fraction of inspired oxygen (Fio2) of 300 or less, compared to a ratio of 200 or less for ARDS.

Incidence of 86 cases per 100,000 person-years and mortality rate of 39%.

Estimated 190,000 cases annually with approximately 74,000 deaths.

Includes a variety of lesions involving the epithelial and endothelial changes caused by a number of etiologies.

Susceptibility appears to heritable and mediators include cytokines, oxidants, and growth factors, interleukins, TNF, and transforming growth factor.

Pro-inflammatory and pro-thrombotic fatty acid eicosanoid derivatives of cyclooxygenase and 5-lipoxygenase are enzymes are mediators of pathogenesis.

Manifests as lung congestion, edema, surfactant disruption, atelectasis and can progress to respiratory failure and acute interstitial pneumonia.

Results from a cascade of events from either infectious or noninfectious inflammatory processes.

Characterized by neutrophilic the lung inflammation, permeability, intravascular and alveolar fibrin deposition ( Abraham E).

Elevated proinflammatory mediators combined with decreased expression of antinflammatory mechanisms are essential components of lung inflammation.

Proinflammatory genes regulated by transcriptional apparatus, particularly NF-κB.

Within 30 minutes of insult an increase in IL-8 by lung macrophages, a neutrophil chemotactic and activating agent, occurs.

IL-2 and TNF are released with activation and collection of neutrophils.

Neutrophils play significant role in pathogenesis.

Early in the process the lungs show increased numbers of neutrophils in the interstitial space, the alveoli and in the vascular space.

Activated leukocytes release oxidants, proteases, leukotrienes, and platelet activating factor to cause tissue damage and initiate the inflammatory cascade of events.

Use of positive end-expiratory pressure (PEEP) to prevent alveoli collapse is used while delivering small tidal volumes to protect the uninjured lung from overdistension.

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