Pancreatic Cystoenterostomy: Technique and Rationale for Pseudocyst Treatment

L. William Traverso

Clancy J. Clark

Introduction

Management of cystic lesions of the pancreas requires careful, directed diagnostic evaluation utilizing a multidisciplinary approach (gastroenterology, radiology, interventional radiology, and surgery). Open cystoenterostomy is the backup treatment for managing pancreatic pseudocysts after all other less invasive maneuvers fail. The first-line therapy for symptomatic acute pancreatic pseudocysts should be endoscopic intervention using transenteric or transpapillary drainage. Before discussing the technical aspects of open pancreatic cystoenterostomy, we must convince ourselves that the cystic lesion is a pseudocyst and not a cystic neoplasm of the pancreas. Clinical history, diagnostic imaging, and laboratory studies should be consistent with a pancreatic pseudocyst; otherwise, the pancreatic cyst should be managed with surgical resection or continued observation (e.g., ultrasound, computed tomography, magnetic resonance imaging, or endoscopic ultrasound [EUS]).

Open internal surgical drainage of pancreatic pseudocysts has been the standard of care for symptomatic pseudocysts; more recently, “less invasive” drainage options, such as percutaneous drainage and transluminal or transpapillary endoscopic drainage, have achieved increasing popularity. Based on recent reports of low morbidity, low mortality, and low recurrence, endoscopic drainage by an experienced endoscopist working in a multidisciplinary system should be first-line therapy in managing a symptomatic pancreatic pseudocyst. Additionally, there are case series demonstrating successful laparoscopic pseudocyst drainage using either cystogastrostomy or cystojejunostomy. These newer techniques are not covered in this chapter.

The choice of treatment (open, percutaneous, or endoscopic) depends on multiple factors including size, number, and location of the cyst, the presumed absence of infection or residual necrotic tissue, the presence or absence of a cyst–duct communication, as well as the availability of specialists in endoscopy, interventional radiology, laparoscopy, or pancreatic surgery. Open drainage or resection of pancreatic pseudocyst is indicated in patients with multiple pseudocysts, recurrent pseudocysts, pseudocysts occurring in combination with common bile duct or duodenal stenosis, symptomatic pseudocysts with a dilated pancreatic duct, unfavorable anatomy for an alternative (laparoscopic or endoscopic) approach, or large pseudocysts (greater than 10 cm) for prevention of bleeding or infectious complications.

General Considerations

The management of pancreatic pseudocysts has followed two distinct paths over the last 30 years. The first is a conservative approach with expectant observation reserving intervention to symptomatic patients or those with pseudocysts >6 cm that have failed to resolve over a set time interval (6 wks). The second, driven by technology and innovation, is an aggressive approach with early intervention using percutaneous drainage, endoscopic “decompression” with endoscopic transpapillary drainage or transenteric drainage, or laparoscopic-assisted drainage. We are now more mature in our approach to managing the pancreatic pseudocyst with improvements in our understanding of acute and chronic pancreatitis; cystic neoplasms of the pancreas (including intraductal papillary mucinous neoplasms [IPMN]); the natural history of pseudocyst formation; clear definitions of pancreatic fluid collections, as in the 1992 Atlanta Symposium (Table 1), and advancements in pancreatic imaging with thin-cut multidetector computerized tomography (CT) and EUS.

Etiology and Definition of Pancreatic Pseudocyst

Pancreatic pseudocyst formation requires disruption of the pancreatic ductal system and an inflammatory reaction of surrounding tissues resulting in formation of a fibrous capsule or wall that lacks an epithelial lining, thereby the term “pseudocyst.” Isolated injury due to blunt abdominal trauma or transection of the main pancreatic duct during pancreatic resection can result in extravasation of pancreatic enzymes and a local inflammatory response. Similarly, acute pancreatitis due to alcohol or gallstones can disrupt the pancreatic ductal system, causing acute pancreatic fluid collections. More than 50% of acute pancreatic fluid collections resolve, while in only 5% to 10% of patients with acute pancreatitis a pseudocyst is formed. Based on the 1992 Atlanta Symposium on pancreatic fluid collections, an acute pancreatic pseudocyst must be a collection of pancreatic juice enclosed by a nonepithelialized wall, that is, 4 weeks or more from the onset of injury (Table 1). A chronic pancreatic pseudocyst is defined as a pseudocyst that has formed along with other changes of irreversible fibrosis, that is, chronic pancreatitis.

Natural History of A Pancreatic Pseudocyst

A pancreatic pseudocyst requires at least 4 weeks to develop the mature fibrous wall that defines a pancreatic pseudocyst. Bradley et al. at Grady Memorial Hospital in Atlanta were the first to document the natural history of pancreatic pseudocysts using ultrasound and learned that resolution is uncommon after 7 to 12 weeks from onset of symptoms. They reported increased complication rates for unoperated pseudocysts after 12 weeks, leading to a recommendation that all pseudocysts should be treated with drainage. With the emergence of CT, Yeo et al. reported that asymptomatic pseudocysts can safely be monitored with resolution of pseudocyst in 60% of patients. They found that pseudocysts larger than 6 cm were more likely to require surgical intervention. Vitas and Sarr confirmed that asymptomatic pancreatic pseudocysts can be managed successfully without intervention. Interestingly, 35% (24 of 68) of patients eventually developed symptoms requiring operative intervention and 9% (6 of 68) had a serious complication. We can conclude from these studies that asymptomatic, small (<6 cm) pancreatic pseudocysts should be monitored with interval imaging and do not warrant drainage.

History and Physical Examination

When a clear timeline from pancreatic duct injury to pseudocyst formation is not available, we must rely on a carefully obtained clinical history and high-quality imaging.
Typical symptoms include nausea, vomiting, dyspepsia, epigastric abdominal pain, weight loss, and anorexia. Small, and sometimes even large, pancreatic pseudocysts may be entirely asymptomatic and discovered incidentally. Pertinent history of gallstones, alcoholism, acute and chronic pancreatitis, abdominal trauma, or abdominal operation (e.g., splenectomy) should be sought. If absent, an alternative diagnosis should be considered. Records from a previous hospitalization documenting pancreatitis can help outline a timeline from injury to pseudocyst formation. History of steatorrhea and diabetes can suggest underlying pancreatic dysfunction particularly due to the irreversible changes of chronic pancreatitis.

Table 1 1992 Atlanta International Symposium: Clinical Definition of Pancreatic Fluid Collections

	Acute pancreatic fluid collections	Acute pancreatic pseudocysts
Definition	Acute fluid collections occur early in the course of acute pancreatitis, are located in or near the pancreas, and always lack a wall of granulation or fibrous tissue.	A pseudocyst is a collection of pancreatic juices that arises as a consequence of acute pancreatitis, pancreatic trauma, or chronic pancreatitis, and is enclosed by a nonepithelialized wall.
Clinical manifestations	Acute fluid collections are common in patients with severe pancreatitis, occurring in 30% to 50% of cases. However, more than half of the lesions regress spontaneously. They are rarely demonstrable by physical findings and are usually discovered by imaging techniques. Often irregular in shape, acute fluid collections do not demonstrate a defined wall.	Pseudocysts in patients with acute pancreatitis are rarely palpable and are most often discovered by imaging techniques. They are usually round or ovoid in shape and have a well-defined wall, as demonstrated by computed tomography or sonography.
Pathology	The precise composition of such collections is not known. Bacteria are variably present. The critical clinical distinction between an acute fluid collection and a pseudocyst (or a pancreatic abscess) is the lack of a defined wall.	The presence of a well-defined wall composed of granulation or fibrous tissue distinguishes a pseudocyst from an acute fluid collection. A pseudocyst is usually rich in pancreatic enzymes and is most often sterile.
Discussion	Acute fluid collections represent an early point in the development of acute pseudocysts or pancreatic abscesses. Why most acute fluid collections regress but others progress to become pseudocysts or abscesses is not known.	Formation of a pseudocyst generally requires 4 or more wks from the onset of acute pancreatitis. In this regard, an acute pseudocyst is a fluid collection that arises in association with an episode of acute pancreatitis, is of more than 4 wks’ duration, and is surrounded by a defined wall. Fluid collections less than this age that lack a defined wall are more properly termed acute fluid collections. In contrast, chronic pseudocysts have a well-defined wall but arise in patients with chronic pancreatitis and lack an antecedent episode of acute pancreatitis. Bacteria may be present in a pseudocyst but often are of no clinical significance because they represent contamination and not clinical infection. When pus is present, the lesion is more correctly termed a pancreatic abscess.

Pancreatic pseudocysts are rarely palpable and physical examination is frequently unrevealing. However, massive pancreatic pseudocysts are well documented in the literature and, historically before modern imaging, abdominal distension was common on presentation. Jaundice due to obstruction of the biliary tree is infrequent and typically seen in patients with a history of chronic pancreatitis. A tender abdomen should not be present and would suggest infected pseudocyst or pancreatic abscess.

Imaging and Laboratory Studies

Imaging of the pancreatic pseudocyst is vital to devise management. Transabdominal ultrasound is useful for following established asymptomatic pancreatic pseudocysts because of its low cost, wide availability, and lack of radiation exposure. However, initial imaging should be obtained with high-quality pancreas protocol CT. CT can provide detailed information on pseudocyst size and number, wall thickness, relation to mesenteric vessels, portal or splenic vein thrombosis, portal hypertension and collateralization, pancreatic atrophy, pancreatic calcifications, pancreatic duct disruption, pancreatic duct dilation, and biliary dilation and obstruction. Magnetic resonance cholangiopancreatography might provide additional detail of pancreatic ductal anatomy and cyst content.

EUS, although operator dependent and not readily available, can provide invaluable information to rule out cystic neoplasms including cyst content, wall nodularity, vascularity, and septations. EUS also allows for fine needle aspiration of the cyst. Cytology, mucin content, viscosity, amylase, and carcinoembryonic antigen (CEA) can help differentiate pseudocysts from cystic neoplasms. Additional tumor markers including CA 72–4, CA 125, CA 19–9, and CA 15–3 have been investigated but are not routinely used. Although no single test can exclude a cystic neoplasm lined with mucinous epithelium like IPMN or mucinous cystadenoma, low CEA, no mucin, and smooth cyst wall support diagnosis of pancreatic pseudocyst. Low amylase in cyst fluid could suggest either mucinous or serous cystadenoma. A useful summary of the differential diagnosis is provided in Table 2.

Routine preoperative laboratory studies should include serum amylase, lipase, liver function tests (coagulation studies, albumin), and CA 19–9. Smoldering pancreatitis marked by persistently elevated amylase or lipase, as well as peripancreatic inflammation on CT would suggest an interval of observation prior to intervention. Acute or
chronic pancreatitis associated with alcohol can be complicated by portal hypertension, portal vein thrombosis, and cirrhosis warranting careful perioperative planning. Stool elastase may also be useful to objectively document pancreatic exocrine insufficiency in setting of chronic pancreatitis and allow improvement with enzyme replacement.

Table 2 Cystic Neoplasms versus Pseudocyst

	SCA	MCT	IMPN	Pseudocyst
Patient sex	Women (3:1)	Exclusively women	Male (2.2:1)	Both
Cytology	Cuboidal or flattened epithelium	Mucin-secreting epithelium (ovarian stroma)	Mucin-secreting columnar cells	No mucin
Cyst aspiration CEA	Near 0	>200	>200	0
Cyst aspiration amylase	None	Low	High	High or none
Mural nodules by EUS, MRI, or CT	None	Uncommon	Possible	No nodules but debris common
Several cysts	Rare	Rare	Common	Uncommon
Central stellate scar	Yes	No	No	No
Calcification of pancreatic parenchyma	No	Rare	No	Common
CEA, carcinoembryonic antigen; CT, computed tomography; EUS, endoscopic ultrasound; IMPN, intraductal mucinous papillary neoplasm; MCT, mucinous cystic tumor (includes mucinous cystadenoma, borderline, and cystadenocarcinoma); MRI, magnetic resonance imaging; SCA, serous cyst adenoma (includes serous cystadenoma, microcystic serous cystadenoma with honeycomb-like appearance, oligocystic serous cystadenoma with multiple large cysts, and cystadenocarcinomas.