The ARDS is an important cause of mortality in critically ill patients. Its exact incidence is unknown but may be as high as 75 per 100,000 population in the United States. The risk factors for developing this syndrome include pneumonia, gastric aspiration, sepsis, shock, and multiple transfusions, as well as less common causes such as multiple trauma, multiple fractures, cardiopulmonary bypass, drug overuse, and acute pancreatitis. Although acute pancreatitis represents one of the less common clinical disorders associated with ARDS, severe attacks of pancreatitis are frequently associated with acute lung injury and respiratory failure.
Acute pancreatitis is an inflammatory process that usually occurs in a normal organ and is diagnosed mainly by acute abdominal pain associated with a concomitant increase in the serum amylase and lipase concentrations. Gallstone migration into the common bile duct and alcohol abuse account for most of the etiologies of the disease in western countries. The injury is usually mild, but severe pancreatic injury develops in 20% of patients, and 15 to 25% of these patients will die.
Studies have examined the clinical spectrum of lung injury associated with acute pancreatitis. Although these clinical reports have provided some insights into the pathogenesis of acute respiratory insufficiency associated with acute pancreatitis, several experimental studies have provided new understanding of the pathophysiology of acute pancreatitis-associated lung injury. The objective of this article is to review the clinical studies, including the original descriptions published > 30 years ago, as well as the recent experimental findings that have used either pharmacologic blockade or genetically modified animals.
The incidence of the pulmonary complications varies from 15 to 55%, and their severity varies from mild hypoxemia without clinical or radiologic abnormalities to severe ARDS. Approximately 10% of patients show alveolar edema on the chest radiograph, and progressive hypoxemia develops in one third of patients, a finding that is evident within hours or may appear within 2 to 3 days. Pulmonary vascular resistance does not increase as an immediate consequence of pancreatitis, and the pulmonary edema results from an increase in lung microvascular permeability. In one study published in 1972, 9 of 50 patients (18%) with acute pancreatitis had diffuse pulmonary infiltrates consistent with lung injury. Five patients (10%) died of the ARDS, and four survivors recovered with normal pulmonary function.