The pancreatic pseudocyst is a collection of pancreatic secretions contained within a fibrous sac comprised of chronic inflammatory cells and fibroblasts in and adjacent to the pancreas contained by surrounding structures. Why a fibrous sac filled with pancreatic fluid is the source of so much interest, speculation, and emotion amongst surgeons and gastroenterologists is indeed hard to understand. Do we debate so vigorously about bilomas, urinomas, or other abdominal collections of visceral secretions? Perhaps it is because the pancreatic pseudocyst represents a sleeping tiger, which though frequently harmless, still can rise up unexpectedly and attack with its enzymatic claws into adjacent visceral and vascular structures and cause lifethreatening complications.
Another part of the debate and puzzlement about pancreatic pseudocysts is related to confusion about pancreatic pseudocyst definition and nomenclature. The Atlanta classification, developed in 1992, was a pioneering effort in describing and defining morphologic entities in acute pancreatitis. Since then, a working group has been revising this system to incorporate more modern experience into the terminology. In the latest version of this system, pancreatitis is divided into acute interstitial edematous pancreatitis (IEP) and necrotizing pancreatitis (NP), based on the presence of pancreatic tissue necrosis. The fluid collections associated with these two “types” of pancreatitis are also differentiated. Early (<4 weeks into the disease course) peripancreatic fluid collections in IEP are referred to as acute peripancreatic fluid collections (APFC), whereas in NP, they are referred to as postnecrotic peripancreatic fluid collections (PNPFC). Late (>4 weeks) fluid collections in IEP are called pancreatic pseudocysts, and in NP, they are called walled-off pancreatic necrosis (WOPN).
Acute pancreatitis represents a broad spectrum of disease. Although the disease course may smolder, typically an initial inciting event results in organ injury, which sets into play the evolving clinical course. The early phase of disease is marked by the inflammatory mediators from damaged pancreatic tissue, resulting in variable degrees of systemic inflammatory response. The later phase is determined by the morphology of organ injury, specifically with regard to tissue ischemia and necrosis. The outcome of this later phase is often impacted by local or systemic infection. Peripancreatic fluid collections can occur in both the early and the late phases of disease. They presumably occur from injury to or ischemia of the main pancreatic duct or a side branch duct, although some, particularly early on, may be the result of third-space edema fluid. Peripancreatic fluid collections represent a heterogeneous entity.