In severe acute pancreatitis, the early phase is associated with a systemic inflammatory response syndrome. One third of the deaths occurs during this early phase, and 50% of those deaths are associated with severe lung injury. The second phase of severe pancreatitis is closely related to the development of complications in the injured pancreas. These complications include fat necrosis, pseudocyst formation, and pancreatic abscess. Each of these complications can be related to the release of activated digestive enzymes. Release of lipase leads to adipose tissue injury and fat necrosis that usually takes place in peripancreatic tissue. The extraductal collection of pancreatic secretions, resulting from ductal rupture, forms a pseudocyst. The more severe complication is abscess, which is associated with substantial morbidity and mortality. Pancreatic abscess includes peripancreatic necrosis of connective tissue and contains both activated digestive enzymes and a mixed flora of bacteria. Local and systemic infections can contribute to the worsening or the persistence of preexisting ARDS. The delay between hospital admission and pulmonary complications was investigated by Berry et al. On hospital admission, radiologic abnormalities were present in 15% (5 of 33 patients) with acute pancreatitis. There were 71% additional patients (20 of 28 patients) with new radiologic abnormalities after day 5.
Two studies including a small number of patients showed that cytokine overproduction might participate to the pathogenesis of severe lung injury during acute pancreatitis. Among seven patients with acute pancreatitis at risk for acquiring the ARDS, lung injury developed in only one patient. In the BAL, the concentration of interleukin (IL)-8 was significantly higher on hospital admission in this single patient who acquired ARDS than in the six patients who did not. Because the thoracic duct drainage has been proposed as an alternative to remove proteolytic and lipolytic enzymes released by the injured pancreas, Montravers et al measured in plasma and thoracic duct the proinflammatory concentrations of cytokines on days 0 (24 h after the diagnosis of acute lung injury), 2, 4, and 8. There were high concentrations of tumor necrosis factor (TNF)-a, IL-1, IL-6, neutrophil enzymes, and pancreatic enzymes including amylase, lipase, and trypsin in plasma. A moderate increase in lymph-to-plasma gradient was observed for IL-6, lipase, and trypsin, while other mediators had similar concentrations in the plasma and lymph.