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.

Medical Dictionary for the Health Professions and Nursing © Farlex 2012

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).

Epigallocatechin-3-gallate ameliorates lipopolysaccharide-induced acute lung injury by suppression of TLR4/NF-[kappa]B signaling activation

Alveolar fluid clearance in acute lung injury: What have we learned from animal models and clinical studies?

Lipoxin A4 Ameliorates Lipopolysaccharide-Induced A549 Cell Injury through Upregulation of N-myc Downstream-Regulated Gene-1

Yu, "Therapeutic experience of the application of anisodamine on acute lung injury," Journal of Acute Disease, vol.

Mechanism of MCP-1 in Acute Lung Injury and Advanced Therapy by Drug-Loaded Dextrin Nanoparticle

Emin et al., "Mitochondrial transfer from bone-marrow-derived stromal cells to pulmonary alveoli protects against acute lung injury," Nature Medicine, vol.

Shock Wave Therapy Enhances Mitochondrial Delivery into Target Cells and Protects against Acute Respiratory Distress Syndrome

Acute lung injury: a clinical and molecular review.

Molecular and Immune Biomarkers in Acute Respiratory Distress Syndrome: A Perspective From Members of the Pulmonary Pathology Society

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.

Alcohol and the lung

Luce, "Acute lung injury and the acute respiratory distress syndrome," Critical Care Medicine, vol.

Zinc Chloride Smoke Inhalation Induced Severe Acute Respiratory Distress Syndrome: First Survival in the United States with Extended Duration (Five Weeks) Therapy with High Dose Corticosteroids in Combination with Lung Protective Ventilation

Extracellular histones injure endothelial cells causing microvascular thrombosis and hemorrhage in acute lung injury (ALI) [61].

HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis

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