Acute Pancreatitis-Associated Lung Injury: Pathophysiological Mechanisms and Potential Future Therapies

Acute pancreatitis is a relatively frequent condition with a yearly incidence reported usually in the range of 30 patients per 100,000 inhabitants per year (1, 2). Mortality in the severe necrotizing form is reported in 15%– 25% of patients (3, 4) and seems to occur essentially with two peaks, the Ž rst occurring early, i.e. within the Ž rst 7 days, and then related to the development of organ dysfunction. The second peak occurs late, i.e. after the second week, when multiple organ dysfunction is frequently combined with sepsis/peripancreatic infection (4–7). Respiratory dysfunction in acute pancreatitis is a major component of the multiple organ dysfunction syndrome (MODS) and there is frequently a need for ventilatory support (7–10). Adult respiratory distress syndrome (ARDS), including diffuse pulmonary inŽ ltrates, progressive hypoxaemia and increased pulmonary endothelial barrier permeability, has been reported to contribute to early death in patients with severe acute pancreatitis (6, 11, 12). Pulmonary injury following induction of experimental acute pancreatitis has been characterized by pulmonary endothelial barrier dysfunction (e.g. tissue oedema, plasma exudation, cell activation and barrier failure), leucocyte sequestration, release of mediators and morphological injury, pulmonary haemorrhage and pneumocyte damage. Our aim in this review was to discuss the potential mechanisms responsible for pancreatitis-associated lung injury and potential ways for novel prevention and treatment.