Pancreatic Interventions in Acute Pancreatitis: Ascites, Fistulae, Leaks, and Other Disruptions

Background

Over time, the role of endoscopic retrograde cholangiopancreatography (ERCP) in the setting of acute pancreatitis has evolved. Previously, ERCP was commonly used after resolution of an acute attack, or more commonly multiple attacks, in an attempt to define pancreatic ductal anatomy and determine an etiology for unexplained pancreatitis. Congenital variants, including duodenal duplication, anomalous pancreaticobiliary union, annular pancreas, and pancreas divisum, can be diagnosed, as can other anatomic causes of pancreatitis, such as ampullary adenoma or surreptitious stone disease. For the most part, less invasive approaches to imaging the pancreatic duct (PD), such as endoscopic ultrasonography (EUS), magnetic resonance imaging (MRI), and magnetic resonance cholangiopancreatography (MRCP), have supplanted the need for ERCP (see Chapter 34 ), a procedure that can actually cause the disease for which it is being applied (see Chapter 52 ).

As advanced imaging has nearly eliminated the need for diagnostic ERCP, the role of ERCP has become primarily therapeutic. The main role of ERCP in the acute setting is in the treatment of acute biliary pancreatitis. This subject is covered in detail in Chapter 53 . However, selective use of ERCP in patients with presumed biliary pancreatitis who have high suspicion for choledocholithiasis or biliary sepsis is common clinical practice.

Another situation where ERCP can provide therapy is in patients with “idiopathic” relapsing acute pancreatitis. Most series suggest that sphincter of Oddi dysfunction is the most common etiology when other diagnostic studies have been exhausted (see Chapter 47 ). As such, there remains a significant role for ERCP in conjunction with sphincter of Oddi manometry (SOM) (see Chapter 16 ) in such patients ( Box 54.1 ).

In addition to its application in conjunction with SOM in patients with acute relapsing pancreatitis and its selective application in biliary pancreatitis, ERCP has been used as a means to provide pancreatic endotherapy in the setting of ductal disruptions caused by acute pancreatitis. PD leaks can manifest in various ways, including smoldering pancreatitis, pseudocysts, fistulae, pancreatic ascites, and high amylase pleural effusions. The mainstay of treatment for these conditions is the placement of a PD stent to bridge the area of disruption (when possible) during ERCP. Disconnected duct syndrome represents the most severe form of a PD disruption that commonly occurs in the setting of severe acute pancreatitis, but the role of ERCP in this setting is limited. Management of this condition is covered in Chapter 55 . This chapter will focus on the role of ERCP in the management of ductal disruptions. Ductal disruptions are seen in a background of chronic and acute pancreatitis.

Epidemiology of Ductal Disruption

The majority of cases of ductal disruption in the setting of acute pancreatitis are likely secondary effects of damage to the ductular epithelium from the underlying inflammation rather than the initial cause of the pancreatitis. However, acute sphincter obstruction in the setting of a common bile duct stone may increase intraductal pressure, leading to side branch or acinar leak with resultant pancreatitis. Likewise, any other downstream obstruction may increase upstream duct pressure, leading to PD blowout and perpetuation or exacerbation of pancreatitis. In patients with acute pancreatitis this is most commonly caused by severe edema, whereas in chronic pancreatitis, disruptions are usually the consequence of a downstream stricture or stone and resultant upstream ductal hypertension. In the setting of severe pancreatic necrosis, ductal disruption is almost invariable, although whether the ductal disruption is the cause or the consequence of the necrosis remains unclear. The presence of a peripancreatic fluid collection does not imply a significant ongoing leak in all instances. Whereas up to 40% of patients with acute pancreatitis develop acute fluid collections, less than 5% of these patients develop a pseudocyst.

Classification

PD leaks are typically defined anatomically by the location of the ductal disruption within the pancreas. The location, in conjunction with the size of the leak and the presence or absence of concomitant necrosis, often determines the clinical manifestations ( Fig. 54.1 ). Low-grade leaks will typically result in intrapancreatic fluid collections that can result in smoldering pancreatitis or remain asymptomatic. Larger leaks are more likely to result in significant pancreatic or peripancreatic necrosis and can cause abdominal fluid collections, high-amylase pleural effusions, pancreatic ascites, and even mediastinal involvement.

A large leak of the PD tail may cause an acute perisplenic fluid collection with or without a high-amylase left-pleural effusion. Alternatively, pancreatic juice may follow anatomic pathways around the left kidney and even into the pelvis, with resultant scrotal or labial edema. In some situations, fluid collections from pancreatic tail leaks can fistulize to either the small bowel near the ligament of Treitz or to the descending colon.

Ductal disruptions in the head of the pancreas have a variety of different manifestations depending on the body's ability to contain the output. Often this results in organized fluid collections in the right upper quadrant, which may be associated with C-loop edema and gastric outlet obstruction with biliary compression, or even with pancreaticobiliary fistulization. In larger leaks the fluid can track more remotely and result in right perinephric fluid accumulation and dissection into the pelvis or perihilar area.

Central disruptions typically result in fluid collections within the lesser sac and are commonly seen in the setting of severe acute pancreatitis with walled-off pancreatic necrosis (WOPN) and often result in a permanently disconnected duct/gland syndrome. Leaks in this area can also result in dissection into the mediastinum or pericardium, or pancreatic ascites. Patients with pancreatic ascites will experience abdominal pain with abdominal distension and occasionally develop bacterial peritonitis.

In addition to being classified by the location of origin, PD leaks (fistulae) are also typically classified as either internal or external. External leaks represent pancreatocutaneous or pancreaticocutanous fistulae and are most typically a consequence of trauma, surgery, or interventional radiologic drainage procedures. Internal fistulae, in turn, classically have included pseudocysts, pancreatic ascites, high-amylase pleural effusions, and erosion of pancreatic fluid collections into contiguous organs, resulting in pancreaticoenteric, gastric, colonic, or biliary fistulae. They also include evolving pancreatic necrosis, in which variable amounts of high-amylase fluid collect, usually in the context of central pancreatic necrosis. Anatomic classifications based on the presence of an acute or chronic PD leak are outlined in Box 54.2 .

Although this chapter focuses on PD leaks and their endoscopic treatment, Box 54.3 summarizes some of the other pancreatitis-related endoscopically amenable lesions that endoscopists see in a busy ERCP practice. They include bile duct obstruction from stones, edema within the head of the pancreas, and neoplasms that occasionally present with pancreatitis. From a pancreatic standpoint, they include neoplastic obstruction of the papilla or duct, edema or spasm of the sphincter mechanism, and an inflammatory PD stenosis.

Management Strategies ( Box 54.4 )