Course and Pathogenesis

Abstract

The distinction between acute and chronic pancreatic pseudocysts according to the Atlanta classification (2) is confusing, if “the definition of chronicity is based, not on the age of the cyst, but rather on the underlying illness“(1). According to this article, acute pancreatic pseudocysts arise from acute pancreatitis and chronic pseudocysts to chronic pancreatitis. This may sound semantically plausible, but pathogenetically it is controversial. Further to rare traumatic causes, pancreatic pseudocysts are usually due to enzymatic necrotic episodes in the context of acute and/or chronic pancreatitis—in both types of pancreatitis, acute pseudocysts are always present, showinga delicate wall consisting of detritus, resorptive inflammation, and new granulating tissue. The subsequent reparative inflammation leads to a dense wall in the pseudocysts consisting of mature collagenized granulating tissue with fibrosis as an indicator of a chronic pseudocyst. Chronic pseudocysts can therefore develop subsequently to acute as well as chronic pancreatitis (with an acute episode)—without initial enzymatic necrosis, no pseudocyst will develop! In addition to the listed traditional complications associated with pseudocysts (1), an earlier observation is worth sharing (3). A shipbuilder developed a pancreatic pseudocyst subsequent to trauma; this pseudocyst had arroded the inferior vena cava and to flushing of enzymes into the blood circulation. Extremely raised pancreatic enzymes in the serum triggered necrotizing panniculitis and enzymatic bone necroses with secondary polyarthropathy and secondary sepsis (3). Such disease courses can occur on rare occasions subsequent to pancreatitis and in acinar cell cancers of the pancreas.