acute lung injury


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adult respiratory distress syndrome

A condition due to a diffuse infiltrative process in the lungs, which affects ±150,000/year (US), and is characterised by acute pulmonary oedema and respiratory failure, poor oxygenation, increased functional residual capacity and decreased compliance; ARDS may accompany various medical and surgical conditions, and may be associated with interstitial pneumonitis—usual, desquamative and lymphoid types.
 
Aetiology
Gram-negative sepsis, pneumonia, shock, gastric acid aspiration, trauma, drug overdose, toxic gas (chlorine, NO2, smoke) exposure, severe metabolic derangement, pancreatitis.
 
Clinical findings
A 6–24-hour latency period is followed by hypoxia, decreased aeration, dyspnoea, severe SOB and “stiff” lungs—i.e., decreased pulmonary compliance.

Imaging
Extensive, diffuse bilateral fluffy infiltrates.
 
Management
Nitric oxide (NO), 18 ppm, may reduce mean pulmonary artery pressure; 37 to 30 mm Hg, may reduce intrapulmonary shunting (36% to 31%), increase ratio of partial pressure of arterial O2 to inspired O2 (PaO2/FiO2), an index of arterial oxygenation efficiency (±152 to ±199); other management strategies include PEEP.
 
Prognosis
The outcome of ARDS is a function of underlying cause.
 
Mortality
± 60%, the cause of death has shifted from hypoxia to multiple organ failure.

a·cute lung in·ju·ry

(ă-kyūt' lŭng in'jŭr-ē)
Any acute decline in lung function of sudden onset, whether traumatic or related to disease state; may be life threatening.

acute lung injury

Abbreviation: ALI.
A clinically severe, sudden decline in lung function, marked by infiltrates in both lung fields and significantly diminished arterial oxygen saturation. There is no evidence that the condition is caused by left-sided heart failure. The disease is similar to adult respiratory distress syndrome (ARDS). Like ARDS, ALI may be life threatening. ALI is distinguished from ARDS by the severity of hypoxemia. ALI = PaO2/FIO2 ratio of < 300, ARDS = PaO2/FIO2 < 200.
See also: injury
References in periodicals archive ?
Effect of epigallocatechin-3-gallate (EGCG) pretreatment on TLR-4/NF-[kappa]B signaling after acute lung injury induced by lipopolysaccharide (LPS).
Alveolar fluid clearance in acute lung injury: What have we learned from animal models and clinical studies?
Yu, "Therapeutic experience of the application of anisodamine on acute lung injury," Journal of Acute Disease, vol.
Emin et al., "Mitochondrial transfer from bone-marrow-derived stromal cells to pulmonary alveoli protects against acute lung injury," Nature Medicine, vol.
Summers, "Acute lung injury results from failure of neutrophil de-priming: a new hypothesis," European Journal of Clinical Investigation, vol.
The recognition that excessive chronic alcohol ingestion has such a dramatic and independent effect on the risk of acute lung injury prompted a search for the underlying mechanisms.
Extracellular histones injure endothelial cells causing microvascular thrombosis and hemorrhage in acute lung injury (ALI) [61].
Matthay, "Acute lung injury: epidemiology, pathogenesis, and treatment," Journal of Aerosol Medicine and Pulmonary Drug Delivery, vol.
Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome, are defined as severe complications with systemic inflammatory responses in the air spaces and lung parenchyma [1].
Bilheimer et al., "Prognostic and pathogenetic value of combining clinical and biochemical indices in patients with acute lung injury," Chest, vol.

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