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Pancreatic Interventions in Acute Pancreatitis
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Pancreatic Interventions in Acute Pancreatitis: Ascites, Fistulae, Leaks, and Other Disruptions Michael Larsen and Richard A. Kozarek
BACKGROUND Over time, the role of endoscopic retrograde cholangiopancreatography (ERCP) in the setting of acute pancreatitis has evolved.1 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).2 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.3,4 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.5–8 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.
Video for this chapter can be found online at www.expertconsult.com.
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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.5,9 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.10,11 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.11,12 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.13
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.9,13,14 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
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis 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.
BOX 54.1 Key Points: Introduction • With the exception of sphincter of Oddi dysfunction, the use of ERCP to diagnose the etiology of relapsing attacks of pancreatitis has been supplanted by pancreas protocol CT, MRI/MRCP, and EUS. • ERCP in the setting of acute pancreatitis is most commonly performed for biliary tract intervention. • Biliary intervention in pancreatitis may be performed not only to treat biliary calculi but also for palliation of biliary obstruction from pancreatic edema and fluid collections. • Therapeutic pancreatography in acute pancreatitis includes bypass of ductal obstructions and treatment of leaks and their consequences and should be undertaken as one aspect of a multidisciplinary approach. CT, Computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasonography; MRCP, magnetic resonance cholangiopancreatography; MRI, magnetic resonance imaging.
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.14 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.15–19 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.20–24 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
2 Pancreaticoenteric/biliary fistula 5 Pancreatic pleural effusion
6 Pancreatic necrosis
Surgical or percutaneous drain
7 External pancreatic fistula
3 Pseudocyst 1 Bile duct compression by fluid collection/edema
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4 Pancreatic ascites
FIG 54.1 Consequences of pancreatic duct leak. (1) Bile duct compression by fluid collection/edema. (2) Pancreaticoenteric/biliary fistula. (3) Pseudocyst. (4) Pancreatic ascites. (5) Pancreatic pleural effusion. (6) Pancreatic necrosis. (7) External pancreatic fistula.
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BOX 54.2 Endoscopically Amenable
BOX 54.5 Diagnostic Studies in Pancreatic
Biliary Obstruction: Jaundice, Cholangitis • Common bile duct stones • Biliary stenosis from edema, head of pancreas • Extrinsic obstruction from pseudocyst
External Fistulae • High-amylase output through a surgically or percutaneously placed drain • Demonstrable pancreatogram through JP drain
Anatomic Lesions Seen in Acute Pancreatitis
Pancreatic Duct Leak: Exacerbation/Perpetuation of Pancreatitis • Sphincter spasm/stenosis/edema • Pancreatic duct stenosis • Acute, inflammatory • Fixed, fibrotic • Neoplastic • Pancreatic duct stone* *Implies concomitant chronic pancreatitis.
BOX 54.3 Manifestations of Pancreatic
Duct Leak
Internal Fistula • Peripancreatic fluid collection • Pseudocyst • Pancreatic ascites • High-amylase pleural effusion • Pancreaticoenteric/biliary/bronchial fistula • Evolving pancreatic necrosis • Smoldering pancreatitis External Fistula • Pancreaticocutaneous fistula
BOX 54.4 Key Points: Management
Strategies
• The diagnosis of external pancreatic fistulae is usually self-evident. • Pancreas protocol CT scan is most often the best way to define the consequences (fluid collection, necrosis) of an internal pancreatic fistula. • Unless endotherapy can be done at the time of ERCP, secretin-enhanced MRCP may be a better test to define the location or persistence of an internal pancreatic fistula. CT, Computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; MRCP, magnetic resonance cholangiopancreatography.
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) Diagnosis The diagnosis of external pancreatic fistulae is typically straightforward compared with internal fistulae, as diagnostic imaging is usually not needed. A pancreaticocutaneous fistula should be considered in patients with persistent output of clear pancreatic juice after percutaneous drainage of a pseudocyst or peripancreatic fluid collection (Box 54.5).1
Duct Leaks
Internal Fistula • Pseudocyst/evolving pancreatic necrosis • CT • MRI/MRCP • US • EUS • ERCP Pancreatic Ascites • High-amylase fluid with aspiration • Flat film (ground glass appearance) • CT/MRCP* • ERCP* • Ductal disruption versus obstruction/upstream leak High-Amylase Pleural Effusion • ERCP • S-MRCP CT, Computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasonography; JP, Jackson-Pratt; MRCP, magnetic resonance cholangiopancreatography; MRI, magnetic resonance imaging; S-MRCP, secretin-enhanced magnetic resonance cholangiopancreatography; US, ultrasonography. *Concomitant pseudocyst 1/3–1/2.
Similarly, persistent output from a Jackson-Pratt (JP) drain after pancreatic resection, decompression, or peripancreatic surgery (e.g., splenectomy, left nephrectomy, right hemicolectomy, or gastrectomy) is another manifestation of an external PD leak.25 More troublesome, however, may be the patient who sustains a penetrating abdominal injury, such as a knife or gunshot wound, in whom the external fistula is overlooked because of concern for other injuries. Pancreatic injury should be considered in all cases of severe abdominal trauma. The diagnosis of internal fistulae is outlined in Box 54.5. In essence, noninvasive imaging, particularly pancreas protocol computed tomography (CT), remains the best initial diagnostic test in patients with smoldering or severe pancreatitis or in patients with underlying chronic pancreatitis and an acute exacerbation of symptoms.14 Not only will CT define the consequences of pancreatitis (fluid collections, necrosis, effusions, ascites),26 but it can also be used to define the potential etiology (e.g., stones or strictures) and follow the subsequent evolution of pancreatitis. CT remains an imperfect tool, however, in that biliary stone disease is underestimated, the fluid component associated with evolving pancreatic necrosis is overestimated, and leaks are implied rather than defined.27 Further confirmation of a ductal disruption may require sequential scans demonstrating an enlarging fluid collection, aspiration of that fluid collection with measurement of amylase or lipase, an ERCP demonstrating the presence and location of the leak, or secretin-enhanced MRCP (S-MRCP). The latter study has been shown to be predictive of ongoing ductal disruption and clearly minimizes potential ERCP adverse events, such as exacerbation of pancreatitis and iatrogenic infection of an undrained fluid collection.28–30 It may also demonstrate patients with a complete ductal disruption and a disconnected gland syndrome in whom leak closure by ERCP alone is unlikely
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis BOX 54.6 Key Points: Management of
Pancreatic Fistulae
• The appropriate management of pancreatic fistulae should include a multidisciplinary team. • Transpapillary stent placement has a markedly higher success rate in treating internal fistulae if the disruption is bridged. • The role of ERCP in patients with an obvious disconnected gland syndrome is limited. ERCP, Endoscopic retrograde cholangiopancreatography.
to be successful. Finally, use of S-MRCP before ERCP may help to define subsequent endoscopic management comparable to its use in hilar neoplasms of the liver. ERCP, in turn, is usually definitive in showing not only the site of the ductal disruption (if persistent) but also the proximate cause or reason for persistence (PD stones, inflammatory or fibrotic structure).14,31 For the most part, however, diagnostic pancreatography adds an unnecessary risk to the care of acutely or chronically ill patients with presumptive leak, unless endoscopic, percutaneous, or surgical therapy is contemplated.32
MANAGEMENT (BOX 54.6) Indications for Endoscopic Treatment The presence of a presumptive pancreatic fistula alone is not a reason to undertake endotherapy. Important considerations include whether the patient has acute or underlying chronic pancreatitis, whether pancreatic necrosis is present, whether there is superinfection of a fluid collection, whether the presumptive leak is accessible to endoscopic control, and whether the leak is controlled at the time of presentation. For instance, the vast majority of low-volume leaks after pancreatic resection are controlled by a surgically placed JP drain and spontaneously close with or without concomitant octreotide over days or several weeks.33,34 On the other hand, a patient may have rapidly increasing ascites or pleural effusion or concomitant jaundice or cholestasis that demands urgent attention. In general, the following are relative indications for initiation of endoscopic therapy in a patient with a presumed PD leak: 1. An enlarging pancreatic fluid collection (pseudocyst, pancreatic ascites, high-amylase pleural effusion) despite conservative management 2. A symptomatic fluid collection 3. Persistence of an external fistula 4. Inability to refeed the patient without development of recurring pain or pancreatitis14 A fifth indication may be the question of concomitant biliary tract disease. Although the latter may occasionally be a concern for a retained stone in the setting of biliary pancreatitis, it is more commonly seen in patients with jaundice or cholangitis from pancreatic head edema or pseudocyst. Perhaps as important as indications for study are contraindications. Aside from medical instability precluding endoscopy, possibly the most important contraindication to an attempt at endoscopic therapy for a PD leak is the inability to render therapy if a ductal disruption is demonstrated. In this setting the diagnosis of a leak may result in iatrogenic infection of a concomitant fluid collection or necrosis, which ultimately may result in the need for endoscopic, percutaneous, or even surgical drainage. Given the potential for “therapeutic misadventure” and the complexity of patients with pancreatic fistulae, careful planning with the use of high-quality cross-sectional imaging and a multidisciplinary approach to management are essential.
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Pancreatic Fluid Collections The endoscopic and nonendoscopic management of pancreatic pseudocysts35–39 and evolving pancreatic necrosis40–45 is covered in Chapter 56. Treatment invariably requires treatment of the underlying ductal disruption, if anatomically feasible, as well as the consequences of that disruption. Thus surgical decompression, percutaneous decompression, and endoscopic decompression of fluid collections have all been variously described.
Pancreatic Ascites and High-Amylase Pleural Effusions Historically, pancreatic ascites and pleural effusions were treated with gut rest and total parenteral nutrition to minimize pancreatic juice stimulation. Diuretics, large-volume thoracentesis and paracentesis, and octreotide have all been used for weeks or months in an attempt to preclude the need for surgical resection or bypass. Successful in less than 50% of these patients, “salvage-type” surgery, usually defined by ERCP preoperatively, consisted of partial pancreatectomy or Roux-en-Y cystojejunostomy in the subset of patients with concomitant pancreatic pseudocysts. Surgical attempts were associated with high morbidity, periprocedural mortality of 8% to 15%, and recurrence rates of 15% to 20%.14 Our group was the first to describe transpapillary stent placement beyond the site of ductal disruption, in conjunction with large-volume paracentesis, as a successful treatment for patients with pancreatic ascites (Fig. 54.2).46 Since our initial publication a number of series have confirmed our findings.47–52 The available literature to date suggests that endoscopic transpapillary stent placement across the site of ductal disruption is successful in resolving pancreatic ascites and pleural effusions in more than 90% of patients and is associated with minimal procedure-related morbidity and close to zero mortality. One of the largest series was published by Telford et al. of 43 patients with PD disruption and a variety of clinical manifestations.53 The etiology was acute pancreatitis in 24 patients, chronic pancreatitis in 9, operative injury in 7, and trauma in 3. Stent placement was successful in resolution of the disruption in 25 patients, unsuccessful in 16 patients, and indeterminate in 2 patients. On univariate analyses, bridging of the ductal disruption and duration of stenting were associated with a statistically significant successful outcome, whereas female gender and acute pancreatitis were negative predictive factors of success. With multivariate analysis, only bridging of the disruption remained statistically significant as a predictor of success (Figs. 54.3, 54.4, and 54.5). Other studies have confirmed the importance of bridging the site of the leak for successful treatment of pancreatic fistulae.54 A similar retrospective series was recently published with data from two tertiary referral centers’ experience with pancreatic leaks of various presentations and etiologies. In this series PD stent placement was successful in 103/107 (96%) of patients, and resolution of the leak was successful in 80 (75%).55 The effectiveness of transpapillary stenting is likely due to a change in the ductal drainage gradient and making the duodenum the path of least resistance to flow. Potential areas of downstream obstruction that are bypassed include the sphincter, possible stones, and the inflammatory or fibrotic stricture frequently associated with a leak (Fig. 54.6). This approach does not work in the setting of a disconnected gland syndrome, in which the bulk of the pancreatic juice that enters the thoracic or abdominal cavity comes from a disconnected PD tail that cannot be reached transpapillarily.14,52
Pancreaticoenteric Fistulae and Acute Pancreatic Trauma Until now, our group has treated more than 30 patients with pancreaticoenteric or biliary fistulae. Although these patients may present with
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B
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FIG 54.2 A, A pancreatogram of a patient with high-amylase ascites demonstrating a ductal disruption in the midbody (arrow). A wire guide is placed across the disruption (B), followed by a bridging pancreatic endoprosthesis (C).
A
C
G
B: 27.1mm C: 9.8mm A: 41.9mm
D
B E
F
FIG 54.3 Computed tomography (CT) demonstrates perisplenic fluid collection (A) and markedly thickened gastric wall (arrow) in a patient with hereditary pancreatitis. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates severe chronic pancreatitis (B) with dilated tail and ductal disruption (C) requiring percutaneous drainage. The stricture is “dilated” with a Soehendra stent extractor (D), followed by balloon dilation (E) and 7-Fr stent placement beyond the ductal disruption (F). Note the improvement on CT scan and persistent dilation of the pancreatic duct tail (G).
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis B
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C
A
D
E
FIG 54.4 A, A large internal fistula (pseudocyst) in the head of the pancreas in a patient with chronic calcific pancreatitis. B, A pancreatogram demonstrates a ductal disruption (arrow) secondary to a high-grade pancreatic duct stricture. C, A pancreatic endoprosthesis is placed across the stenosis and leak (arrowhead). D, A computed tomography scan 6 weeks later demonstrates complete resolution of the pseudocyst after endoscopically placed transduodenal double-pigtail stents. E, A pancreatogram reveals changes of chronic pancreatitis but the leak has resolved.
A
B
C
D
FIG 54.5 Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates pancreatic duct disruption at junction of body and tail (A and B) in a patient with severe left-upper-quadrant/flank pain and splenic vein thrombosis. Pain and ductal disruption are resolved with prosthesis placement (C and D). Disruption recurred 1 year later, requiring distal pancreatectomy/splenectomy.
spontaneous and rapid resolution of a fluid collection for which no treatment is required, a stenosis at the site of ductal disruption may result in relapsing attacks of pancreatitis. Alternatively, fistulization into the bile duct (Fig. 54.7) or colon may result in cholestasis or cholangitis, or recurrent sepsis, respectively.56 In our initial series of eight patients with pancreaticoenteric fistulae, three resolved with downsizing or removing an external drain that had eroded into a contiguous loop of bowel, three resolved with transpapillary stent placement, and two ultimately required surgical resection.57 In the case of pancreaticocolonic fistulae, diverting ileostomy may be necessary to close the fistulae and reduce bacterial translocation and ongoing sepsis.58 Fistulization into the bile duct, in turn, is almost invariably treated successfully by concomitant biliary and PD stenting, assuming that the fistula is not from the upstream disconnected portion of the pancreas (Figs. 54.8 and 54.9).59 In addition to pancreaticoenteric or biliary fistulae that usually occur in the setting of pancreatic necrosis or chronic pancreatitis, ERCP has also been used to treat internal fistulae as a consequence of acute pancreatic trauma. For example, Kim et al. diagnosed normal pancreatograms in 14 of 23 patients with acute abdominal trauma.19 In eight of these patients a leak from the main PD into the parenchyma resolved spontaneously, whereas three had a main PD leak that resolved after bridging with a transpapillary stent. Although the authors of this study suggested that early ERCP was believed to be advantageous in projecting the need for medical, surgical, or endoscopic therapy, it is possible that S-MRCP may evolve to play a diagnostic role, selecting patients who have the greatest potential to benefit from transpapillary therapy.18
External Fistulae As previously discussed, with the exception of penetrating abdominal trauma, the vast majority of external fistulae are iatrogenic. They may occasionally follow partial pancreatic resection or bypass in the setting
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B
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D
E
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FIG 54.6 Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates ductal disruption in the pancreatic head (A) in a patient with huge high-amylase effusion of the right lung (B). The patient is treated with a transpapillary pigtail stent into the fluid collection (C) as well as stenting of the minor papilla to decompress the upstream pancreatic duct (D–F).
D
C
B
A
FIG 54.7 Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates transgastric pigtail stent (arrows, A and B) in a patient with severe necrotizing pancreatitis, portal vein thrombosis, and disconnected pancreatic duct. Note the embolized coils for previous splenic artery aneurysm (arrows, C) and the Jackson-Pratt (JP) drain for persistent colonic fistula into the pancreatic head (D).
B
C
A
FIG 54.8 A, Computed tomography scan demonstrating a dilated bile duct and transduodenal pigtail stents into a peripancreatic fluid collection. B, Cholangiogram demonstrating a communication (arrow) between the bile duct and the pancreatic fluid collection. C, A fully covered metal bile duct stent is placed to seal the fistula.
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis A
B
C
D
E
F
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10x7pd stent &10x7biliary stent
FIG 54.9 High-grade bile duct stricture in a patient with pancreatic necrosis and intramural pancreatic ductal disruption. Note contrast in colon (A), deformed edematous papilla (B), and biliary stent placement (C). Small arrows demonstrate intraduodenal abscess and the large arrow demonstrates dilated pancreatic duct (D). Note the dual-stent placement (E and F), which resolved jaundice and concomitant PD disruption and obstruction.
of a downstream stricture. Most, however, are a consequence of a disconnected gland after percutaneous or surgical drainage of a pancreatic fluid collection or necrosis.14 Our group initially reported a series of patients undergoing transpapillary stenting for amenable external fistulae more than a decade ago.60 Since that time, multiple additional series have been published or abstracted.14,61,62 By way of summarizing the available series, 86% of patients (50 of 58) could be successfully stented and 46 of those patients (92%) had resolution of their fistulae. Procedural adverse events were limited to mild flares of pancreatitis, although there were two deaths in the series by Costamagna et al.,61 neither related to the fistula or its endoscopic treatment. No recurrences were reported in patients undergoing successful fistula closure at follow-up ranging from 12 to 36 months. Our approach to endotherapy of pancreaticocutaneous fistulae has evolved over the past decade. Whereas endoscopic therapy was initially reserved for postoperative or percutaneously drained patients whose external fistulae did not respond to several weeks of clear liquids, total parenteral nutrition, and octreotide, our current practice is to study patients with high-volume fistulae with S-MRCP if they have a marginal decrease in fistula volume after several days of somatostatin analog. ERCP and transpapillary stent placement are undertaken unless imaging documents a disconnected gland syndrome (Fig. 54.10; see also Fig. 54.7).
Disconnected Pancreatic Duct Syndrome Our experience has taught us that prevention of disconnected PD syndrome (DPDS) is paramount, because treatment is complex. It is clear that a significant number of patients who have WOPN treated
with percutaneous drainage alone will develop pancreaticocutaneous fistulae secondary to disconnected duct syndrome. Our group has devised a treatment for WOPN, which is termed “dual-modality drainage,” in order to prevent such fistulae from developing. This technique involves the placement of both a percutaneous drain and endoscopic transluminal stents into areas of WOPN, with subsequent removal of the percutaneous drain once the necrosis resolves.63 If it is determined that there is no DPDS, the transluminal drains are also removed. However, if the patient has DPDS, the transmural stents are left in place indefinitely to prevent recurrent fluid collections. This combined approach has reduced our cutaneous fistula rate to zero when treating WOPN.64,65 Historically, patients with disconnected gland syndrome and pancreaticocutaneous fistulae have required distal pancreatectomy.14 More recently, less invasive approaches have been described, with varying levels of success.66 Interventional radiologist–administered cyanoacrylate injection into the disconnected tail has been described. This requires guidewire placement into the PD tail through the fistulous tract, placement of a microcatheter over the wire, and injection of the entire disconnected portion of the duct to include side branches. Mild postprocedural pancreatitis has been noted in approximately 50% of patients, and recurrent fistulae may occur unless the entire duct and its side branches are sealed. This procedure works best when there is only 3 to 4 cm of disconnected gland and is less likely to be successful when the glandular disconnection is at the genu, which requires a significant portion of the gland to be glued shut. In addition to the percutaneous approach to the disconnected gland, as well as the surgical approach using glue injection to minimize
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B
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D
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H
(2)7fr-3cm transgastric stents
FIG 54.10 A, Computed tomography scan demonstrating a percutaneous drain adjacent to the body of the pancreas in a patient with a history of severe acute pancreatitis and central gland necrosis. The drain had a high output of amylase-rich fluid on a daily basis. B, Magnetic resonance cholangiopancreatography demonstrates a dilated pancreatic duct in the tail (arrow) with no communication with the head of the gland, suggesting disconnected pancreatic duct syndrome. C, The fistula tract is accessed percutaneously using a TIPS needle, which is directed across the gastric wall. D, Wire guides are placed through the needle and grasped using an endoscopic snare. E, Dilation across the gastric wall is performed using a controlled radial expansion balloon dilator followed by the placement of two double-pigtail stents (F and G). Injection of contrast through the fistula tract opacifies the stomach, thus demonstrating an alternate route for the flow of pancreatic juice from the fistula tract (H). TIPS, transjugular intrahepatic portosystemic shunt.
postpancreatectomy leak,67 Soehendra’s group has used transpapillary injection of methyl-butyl cyanoacrylate into the distal duct at the site of glandular disruption.68 Eight of 11 patients in their series had resolved disruptions without recurrence, although all had concomitant PD stents or drains and endoscopic transmural drainage of associated fluid collections. This group also used glue injection as an adjunct in patients with severe pancreatic necrosis undergoing aggressive endoscopic drainage using EUS-directed lavage or debridement.69 Our group has also devised a combined endoscopic and percutaneous rendezvous approach to internalization of chronic pancreaticocutaneous fistulae in patients with disconnected gland syndrome (see Fig. 54.8). This technique involves an interventional radiologist initially accessing the fistula tract using a transjugular intrahepatic portosystemic shunt (TIPS) needle. The needle is then passed under fluoroscopic and endoscopic control into the stomach. The tract is then dilated using an 8-Fr microcatheter, and two guidewires are passed through the catheter, grasped using an endoscopic
snare, and pulled through the endoscope. Further dilation of the tract is then performed using a controlled radial expansion balloon dilator, subsequent to which two double-pigtail stents are placed across the gastric wall into the fistula tract. The resultant “redirection” of pancreatic juice into the stomach has been used to close fistulae in 15 patients treated at our institution. During long-term follow-up, recurrent pancreatic fluid collections developed in two patients because of migrated stents and were treated with endoscopic cystgastrostomy.70 Despite the success with glue injection and the combined approach described above, these are small case series performed at centers with significant experience in managing patients with complicated pancreatitis. The widespread application of these nonsurgical techniques requires additional critical assessment before widespread adoption can be advocated. However, they do provide “proof-of-principle” that viable alternatives to long-term drain placement and surgery are very much on the horizon.
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ADVERSE EVENTS (BOX 54.7) (SEE CHAPTER 8)
the time of ERCP. As such, all patients with a presumptive internal fistula should receive a broad-spectrum antibiotic before undergoing diagnostic ERCP and may require more prolonged treatment afterward, particularly in the setting of pancreatic necrosis. Moreover, clearly contaminated fluid collections should be considered for concomitant endoscopic or percutaneous drainage of necrosis, as described in Chapter 53. Note that our group has previously demonstrated that bacterial contamination within the PD is invariable in patients with indwelling stents and that stent occlusion is a necessary but not sufficient cause of pancreatic sepsis.73 Stent occlusion may also be associated with obstructive pancreatitis, and it is for this reason, as well as fear of iatrogenic duct injury,74 that indwelling stents should be retrieved quickly after external fistula closure and after 4 to 6 weeks of treating an internal PD fistula.14
Immediate Adverse Events
Chronic Adverse Events
The immediate adverse events of transpapillary stent placement are those of diagnostic ERCP and include drug reaction, aspiration, cardiopulmonary events, pancreatitis from contrast injection or sphincter manipulation, and cholangitis in patients with underlying endoscopically untreated concomitant biliary stenosis. Bleeding and iatrogenic perforation can occasionally be seen if sphincterotomy is performed to facilitate stent placement.71 Pancreatitis flare approximates 10% in normal ducts and is uncommon in patients who have ductal changes of chronic pancreatitis. It may approach 50% in the setting of unsuccessful stenting when multiple accessories and guidewires have been placed into the PD to facilitate bridging the area of the leak. This pancreatitis is usually attenuated, however, if a short transpapillary stent is left to preclude ductal obstruction by an edematous papilla or traumatized sphincter.72 Pancreatitis is more common in the setting of an improperly sized prosthesis for the duct, even if the disruption can be bridged. Examples include placement of a 7-Fr stent into a 5-Fr-diameter duct or placement of a 12-cm prosthesis to bridge a ductal leak 3 cm from the papilla.
Although iatrogenic ductal injury is listed under chronic adverse events, PD prostheses (other than short-term prophylactic for prevention of post-ERCP pancreatitis) never belong in the pancreas, particularly in patients with otherwise normal PDs. A number of procedural and stent modifications have decreased trauma to the major PD and minimized side-branch occlusion over the past several years. These modifications include use of 3-Fr-diameter to 4-Fr-diameter stents, elimination of internal stent flanges, and recognition that stents that apply significant pressure proximally (toward the tail), especially when in an angulated position, may cause duct ulceration and subsequent fibrosis.74,75 Despite this, 3-Fr unflanged pigtail stents almost always spontaneously migrate within a week or two and are probably appropriate only in the patient in whom bridging of the disruption was unsuccessful, and then only to prevent or ameliorate post-ERCP pancreatitis. Iatrogenic ductitis should be anticipated and minimized by selecting a prosthesis that has a smaller diameter than the PD downstream from the leak, is the appropriate length to bridge the disruption without an inordinate stent length beyond the site of the leak, and avoids upstream impaction or angulation on the ductal wall.
BOX 54.7 Key Points: Adverse Events • The risk of procedural or postprocedural adverse events in treating pancreatic duct fistulae endoscopically should be weighed against the risk of persistent fistula or alternative treatments. • Procedural pancreatitis and iatrogenic infection of a concomitant fluid collection are the major risks in endoscopically treating internal pancreatic duct fistulae. • Iatrogenic “ductitis,” including irreversible stricture formation, can follow pancreatic duct stenting, especially when the size of the selected stent is greater than the caliber of the duct.
Subacute Adverse Events Subacute adverse events are usually infectious and result from iatrogenic introduction of bacteria into a fluid collection or necrotic debris at
SUMMARY 1. Pancreatic duct leaks are a consequence of acute inflammation with duct disruption, downstream obstruction, or both. 2. Minor leaks in the setting of acute pancreatitis or necrosis are probably common and respond to conservative therapy. 3. The consequences of major ductal disruptions include internal fistulae (pseudocysts, necrosis, pancreatic ascites, pancreatic pleural effusions, pancreaticoenteric or biliary communication) and external fistulae. 4. Treatment of internal fistulae requires treatment of the leak and/or the sequelae/consequences of the leak.
5. Bridging the site of ductal disruption with a transpapillary prosthesis is more likely to result in resolution of the disruption unless there is disconnected gland syndrome. 6. The complexity of most pancreatic leaks requires management by a multidisciplinary team with expertise in pancreatic diseases. This is particularly true in the setting of DPDS. The complete reference list for this chapter can be found online at www.expertconsult.com.
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis
REFERENCES 1. Kozarek R. Role of ERCP in acute pancreatitis. Gastrointest Endosc. 2002;56:S231–S236. 2. Testoni PA, Mariani A, Curioni S, et al. MRCP-secretin test-guided management of idiopathic recurrent pancreatitis: long-term outcomes. Gastrointest Endosc. 2008;67:1028–1034. 3. Easler JJ, Sherman S. Endoscopic retrograde cholangiopancreatography for the management of common bile duct stones and gallstone pancreatitis. Gastrointest Endosc Clin N Am. 2015;25:657–675. 4. van Geenen EJ, van Santvoort HC, Besselink MG, et al. Lack of consensus on the role of endoscopic retrograde cholangiography in acute biliary pancreatitis in published meta-analyses and guidelines: a systematic review. Pancreas. 2013;42:774–780. 5. Larsen M, Kozarek R. Management of pancreatic ductal leaks and fistulae. J Gastroenterol Hepatol. 2014;29:1360–1370. 6. Larsen M, Kozarek R. Management of ductal leaks. In: Forsmark C, Gardner T, eds. Prediction and Management of Severe Acute Pancreatitis. New York: Springer Science + Business Media; 2015:151–167. 7. Delhaye M, Matos C, Deviere J. Endoscopic technique for the management of pancreatitis and its complications. Best Pract Res Clin Gastroenterol. 2004;18:155–181. 8. Varadarajulu S, Noone T, Hawes RH, et al. Pancreatic duct stent insertion for functional smoldering pancreatitis. Gastrointest Endosc. 2003;58:438–441. 9. Kozarek RA, Traverso LW. Pancreatic fistulas and ascites. In: Brandt JL, ed. Textbook of Clinical Gastroenterology. Philadelphia: Current Medicine; 1998:1175–1181. 10. Chebli JM, Gaburri PD, de Souza AF, et al. Internal pancreatic fistulas: proposal of a management algorithm based on a case series analysis. J Clin Gastroenterol. 2004;38:795–800. 11. Lau ST, Simchuk EJ, Kozarek RA, et al. A pancreatic ductal leak should be sought to direct treatment in patients with acute pancreatitis. Am J Surg. 2001;181:411–415. 12. Uomo G, Molino D, Visconti M, et al. The incidence of main pancreatic duct disruption in severe biliary pancreatitis. Am J Surg. 1998;176:49–52. 13. Andrén-Sandberg Å, Dervenis C. Pancreatic pseudocysts in the 21st century: part I: classification, pathophysiology, anatomic considerations and treatment. JOP. 2004;5:8–24. 14. Kozarek RA. Pancreatic duct leaks and pseudocysts. In: Ginsberg G, Kochman M, Norton I, et al, eds. Clinical Gastrointestinal Endoscopy. 2nd ed. Philadelphia: Elsevier; 2011:692–705. 15. Poon RT, Lo SH, Fong D, et al. Prevention of pancreatic anastomotic leakage after pancreaticoduodenectomy. Am J Surg. 2002;183:42–52. 16. Sheehan MK, Beck K, Creech S, et al. Distal pancreatectomy: does the method of closure influence fistula formation? Am Surg. 2002;68:264–267. 17. Freeny PC, Hauptmann E, Althaus SJ, et al. Percutaneous CT-guided catheter drainage of infected acute necrotizing pancreatitis: techniques and results. AJR Am J Roentgenol. 1998;170:969–975. 18. Memis A, Parildar M. Interventional radiological treatment in complications of pancreatitis. Eur J Radiol. 2002;43:219–228. 19. Kim HS, Lee DK, Kim IW, et al. The role of endoscopic retrograde pancreatography in the treatment of traumatic pancreatic duct injury. Gastrointest Endosc. 2001;54:49–55. 20. Oksuz MO, Altehoefer C, Winterer JT, et al. Pancreatico-mediastinal fistula with a mediastinal mass lesion demonstrated by MR imaging. J Magn Reson Imaging. 2002;16:746–750. 21. Sakorafas GH, Sarr MG, Farnell MB. Pancreaticobiliary fistula: an unusual complication of necrotising pancreatitis. Eur J Surg. 2001;167:151–153. 22. De Backer AI, Mortele KJ, Vaneerdeweg W, et al. Pancreatocolonic fistula due to severe acute pancreatitis: imaging findings. JBR-BTR. 2001;84:45–47. 23. Salih A. Massive pleural effusion. Postgrad Med J. 2001;77:536–547. 24. Ito H, Matsubara N, Sakai T, et al. Two cases of thoracopancreatic fistula in alcoholic pancreatitis: clinical and CT findings. Radiat Med. 2002;20:207–211. 25. Bassi C, Dervenis C, Butturini G, et al. Postoperative pancreatic fistula: an international study group (ISGPF) definition. Surgery. 2005;138:8–13.
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26. Zhao K, Adam SZ, Keswani RN, et al. Acute pancreatitis: revised Atlanta classification and the role of cross-sectional imaging. AJR Am J Roentgenol. 2015;205:W32–W41. 27. Baron TH, Morgan DE. Acute necrotizing pancreatitis. N Engl J Med. 1999;340:1412–1417. 28. Matos C, Bali MA, Delhaye M, et al. Magnetic resonance imaging in the detection of pancreatitis and pancreatic neoplasms. Best Pract Res Clin Gastroenterol. 2006;20:157–178. 29. Gillams AR, Kurzawinski T, Lees WR. Diagnosis of duct disruption and assessment of pancreatic leak with dynamic secretin-stimulated MR cholangiopancreatography. AJR Am J Roentgenol. 2006;186:499–506. 30. O’Toole D, Vullierme MP, Ponsot P, et al. Diagnosis and management of pancreatic fistulae resulting in pancreatic ascites or pleural effusions in the era of helical CT and magnetic resonance imaging. Gastroenterol Clin Biol. 2007;31:686–693. 31. Kozarek RA. Endoscopic therapy of complete and partial pancreatic duct disruptions. Gastrointest Endosc Clin N Am. 1998;8:39–53. 32. Szentes MJ, Traverso LW, Kozarek RA, et al. Invasive treatment of pancreatic fluid collections with surgical and nonsurgical methods. Am J Surg. 1991;161:600–605. 33. Kaman L, Behera A, Singh R, et al. Internal pancreatic fistulas with pancreatic ascites and pancreatic pleural effusions: recognition and management. ANZ J Surg. 2001;71:221–225. 34. Gurusamy KS, Koti R, Fusai G, et al. Somatostatin analogues for pancreatic surgery. Cochrane Database Syst Rev. 2013;(4):CD008370. 35. Gurusamy KS, Pallari E, Hawkins N, et al. Management strategies for pancreatic pseudocysts. Cochrane Database Syst Rev. 2016;(4):CD011392. 36. Kozarek RA, Brayko CM, Harlan J, et al. Endoscopic drainage of pancreatic pseudocysts. Gastrointest Endosc. 1985;31:322–327. 37. Ge PS, Weizmann M, Watson RR. Pancreatic pseudocysts: advances in endoscopic management. Gastroenterol Clin North Am. 2016;45:9–27. 38. Siddiqui AA, Adler DG, Nieto J, et al. EUS-guided drainage of peripancreatic fluid collections and necrosis by using a novel lumenapposing stent: a large retrospective, multicenter U.S. experience (with videos). Gastrointest Endosc. 2016;83:699–707. 39. Kozarek RA, Ball TJ, Patterson DJ, et al. Endoscopic transpapillary therapy for disrupted pancreatic duct and peripancreatic fluid collections. Gastroenterology. 1991;100:1362–1370. 40. Sharaiha RZ, Tyberg A, Khashab MA, et al. Endoscopic therapy with lumen-apposing metal stents is safe and effective for patients with pancreatic walled-off necrosis. Clin Gastroenterol Hepatol. 2016;[Epub ahead of print]. 41. Thompson CC, Kumar N, Slattery J, et al. A standardized method for endoscopic necrosectomy improves complication and mortality rates. Pancreatology. 2016;16:66–72. 42. Pannala R, Ross AS. Pancreatic endotherapy and necrosectomy. Curr Treat Options Gastroenterol. 2015;13:185–197. 43. Fisher JM, Gardner TB. Endoscopic therapy of necrotizing pancreatitis and pseudocysts. Gastrointest Endosc Clin N Am. 2013;23:787–802. 44. Baron TH, Thaggard WG, Morgan DE, et al. Endoscopic therapy for organized pancreatic necrosis. Gastroenterology. 1996;111:755–764. 45. Baron TH, Harewood GC, Morgan DE, et al. Outcome differences after endoscopic drainage of pancreatic necrosis, acute pancreatic pseudocysts, and chronic pancreatic pseudocysts. Gastrointest Endosc. 2002;56:7–17. 46. Kozarek RA, Jiranek GC, Traverso LW. Endoscopic treatment of pancreatic ascites. Am J Surg. 1994;168:223–226. 47. Bracher GA, Manocha AP, DeBanto JR, et al. Endoscopic pancreatic duct stenting to treat pancreatic ascites. Gastrointest Endosc. 1999;49:710–715. 48. Pai CG, Suvarna D, Bhat G. Endoscopic treatment as first-line therapy for pancreatic ascites and pleural effusion. J Gastroenterol Hepatol. 2009;24:1198–1202. 49. Wronski M, Slodkowski M, Cebulski W, et al. Optimizing management of pancreaticopleural fistulas. World J Gastroenterol. 2011;17:4696–4703. 50. Bakker OJ, van Baal MC, van Santvoort HC, et al. Endoscopic transpapillary stenting or conservative treatment for pancreatic fistulas in necrotizing pancreatitis: multicenter series and literature review. Ann Surg. 2011;253:961–967.
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51. Kurumboor P, Varma D, Rajan M, et al. Outcome of pancreatic ascites in patients with tropical calcific pancreatitis managed using a uniform treatment protocol. Indian J Gastroenterol. 2009;28:102–106. 52. Gomez-Cerezo J, Barbado CA, Suarez I, et al. Pancreatic ascites: study of therapeutic options by analysis of case reports and case series between the years 1975 and 2000. Am J Gastroenterol. 2003;98:568–577. 53. Telford JJ, Farrell JJ, Saltzman JR, et al. Pancreatic stent placement for duct disruption. Gastrointest Endosc. 2002;56:18–24. 54. Varadarajulu S, Noone TC, Tutuian R, et al. Predictors of outcome in pancreatic duct disruption managed by endoscopic transpapillary stent placement. Gastrointest Endosc. 2005;61:568–575. 55. Das R, Papachristou GI, Slivka A, et al. Endotherapy is effective for pancreatic ductal disruption: a dual center experience. Pancreatology. 2016;16:278–283. 56. Heeter ZR, Hauptmann E, Crane R, et al. Pancreaticocolonic fistulas secondary to severe acute pancreatitis treated by percutaneous drainage: successful nonsurgical outcomes in a single-center case series. J Vasc Interv Radiol. 2013;24:122–129. 57. Wolfsen HC, Kozarek RA, Ball TJ, et al. Pancreaticoenteric fistula: no longer a surgical disease? J Clin Gastroenterol. 1992;14:117–121. 58. Mohamed SR, Siriwardena AK. Understanding the colonic complications of pancreatitis. Pancreatology. 2008;8:153–158. 59. Carrere C, Heyries L, Barthet M, et al. Biliopancreatic fistulas complicating pancreatic pseudocysts: a report of three cases demonstrated by endoscopic retrograde cholangiopancreatography. Endoscopy. 2001;33:91–94. 60. Kozarek RA, Ball TJ, Patterson DJ, et al. Transpapillary stenting for pancreaticocutaneous fistulas. J Gastrointest Surg. 1997;1:357–361. 61. Costamagna G, Mutignani M, Ingrosso M, et al. Endoscopic treatment of postsurgical external pancreatic fistulas. Endoscopy. 2001;33:317–322. 62. Saeed ZA, Ramirez FC, Hepps KS. Endoscopic stent placement for internal and external pancreatic fistulas. Gastroenterology. 1993;105:1213–1217. 63. Gluck M, Ross A, Irani S, et al. Endoscopic and percutaneous drainage of symptomatic walled-off pancreatic necrosis reduces hospital stay and radiographic resources. Clin Gastroenterol Hepatol. 2010;8:1083–1088.
64. Gluck M, Ross A, Irani S, et al. Dual modality drainage for symptomatic walled-off pancreatic necrosis reduces length of hospitalization, radiological procedures, and number of endoscopies compared to standard percutaneous drainage. J Gastrointest Surg. 2012;16:248–256. 65. Ross AS, Irani S, Gan SI, et al. Dual-modality drainage of infected and symptomatic walled-off pancreatic necrosis: long-term clinical outcomes. Gastrointest Endosc. 2014;79:929–935. 66. Murage KP, Ball CG, Zyromski NJ, et al. Clinical framework to guide operative decision making in disconnected left pancreatic remnant (DLPR) following acute or chronic pancreatitis. Surgery. 2010;148:847–856. 67. Suc B, Msika S, Fingerhut A, et al. Temporary fibrin glue occlusion of the main pancreatic duct in the prevention of intra-abdominal complications after pancreatic resection: prospective randomized trial. Ann Surg. 2003;237:57–65. 68. Seewald S, Brand B, Groth S, et al. Endoscopic sealing of pancreatic fistula by using N-butyl-2-cyanoacrylate. Gastrointest Endosc. 2004;59:463–470. 69. Seewald S, Groth S, Omar S, et al. Aggressive endoscopic therapy for pancreatic necrosis and pancreatic abscess: a new safe and effective treatment algorithm. Gastrointest Endosc. 2005;62:92–100. 70. Irani S, Gluck M, Ross A, et al. Resolving external pancreatic fistulas in patients with disconnected pancreatic duct syndrome: using rendezvous techniques to avoid surgery (with video). Gastrointest Endosc. 2012;76:586–593, e1–e3. 71. Kozarek RA, Ball TJ, Patterson DJ, et al. Endoscopic pancreatic duct sphincterotomy: indications, technique, and analysis of results. Gastrointest Endosc. 1994;40:592–598. 72. Fazel A, Quadri A, Catalano MF, et al. Does a pancreatic duct stent prevent post-ERCP pancreatitis? A prospective randomized study. Gastrointest Endosc. 2003;57:291–294. 73. Kozarek R, Hovde O, Attia F, et al. Do pancreatic duct stents cause or prevent pancreatic sepsis? Gastrointest Endosc. 2003;58:505–509. 74. Smith MT, Sherman S, Ikenberry SO, et al. Alterations in pancreatic ductal morphology following polyethylene pancreatic stent therapy. Gastrointest Endosc. 1996;44:268–275. 75. Raijman I. Biliary and pancreatic stents. Gastrointest Endosc Clin N Am. 2003;13:561–592.
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Pancreatic Interventions in Acute Pancreatitis: Ascites, Fistulae, Leaks, and Other Disruptions Michael Larsen and Richard A. Kozarek
BACKGROUND Over time, the role of endoscopic retrograde cholangiopancreatography (ERCP) in the setting of acute pancreatitis has evolved.1 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).2 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.3,4 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.5–8 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.
Video for this chapter can be found online at www.expertconsult.com.
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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.5,9 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.10,11 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.11,12 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.13
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.9,13,14 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
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis 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.
BOX 54.1 Key Points: Introduction • With the exception of sphincter of Oddi dysfunction, the use of ERCP to diagnose the etiology of relapsing attacks of pancreatitis has been supplanted by pancreas protocol CT, MRI/MRCP, and EUS. • ERCP in the setting of acute pancreatitis is most commonly performed for biliary tract intervention. • Biliary intervention in pancreatitis may be performed not only to treat biliary calculi but also for palliation of biliary obstruction from pancreatic edema and fluid collections. • Therapeutic pancreatography in acute pancreatitis includes bypass of ductal obstructions and treatment of leaks and their consequences and should be undertaken as one aspect of a multidisciplinary approach. CT, Computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasonography; MRCP, magnetic resonance cholangiopancreatography; MRI, magnetic resonance imaging.
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.14 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.15–19 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.20–24 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
2 Pancreaticoenteric/biliary fistula 5 Pancreatic pleural effusion
6 Pancreatic necrosis
Surgical or percutaneous drain
7 External pancreatic fistula
3 Pseudocyst 1 Bile duct compression by fluid collection/edema
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4 Pancreatic ascites
FIG 54.1 Consequences of pancreatic duct leak. (1) Bile duct compression by fluid collection/edema. (2) Pancreaticoenteric/biliary fistula. (3) Pseudocyst. (4) Pancreatic ascites. (5) Pancreatic pleural effusion. (6) Pancreatic necrosis. (7) External pancreatic fistula.
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BOX 54.2 Endoscopically Amenable
BOX 54.5 Diagnostic Studies in Pancreatic
Biliary Obstruction: Jaundice, Cholangitis • Common bile duct stones • Biliary stenosis from edema, head of pancreas • Extrinsic obstruction from pseudocyst
External Fistulae • High-amylase output through a surgically or percutaneously placed drain • Demonstrable pancreatogram through JP drain
Anatomic Lesions Seen in Acute Pancreatitis
Pancreatic Duct Leak: Exacerbation/Perpetuation of Pancreatitis • Sphincter spasm/stenosis/edema • Pancreatic duct stenosis • Acute, inflammatory • Fixed, fibrotic • Neoplastic • Pancreatic duct stone* *Implies concomitant chronic pancreatitis.
BOX 54.3 Manifestations of Pancreatic
Duct Leak
Internal Fistula • Peripancreatic fluid collection • Pseudocyst • Pancreatic ascites • High-amylase pleural effusion • Pancreaticoenteric/biliary/bronchial fistula • Evolving pancreatic necrosis • Smoldering pancreatitis External Fistula • Pancreaticocutaneous fistula
BOX 54.4 Key Points: Management
Strategies
• The diagnosis of external pancreatic fistulae is usually self-evident. • Pancreas protocol CT scan is most often the best way to define the consequences (fluid collection, necrosis) of an internal pancreatic fistula. • Unless endotherapy can be done at the time of ERCP, secretin-enhanced MRCP may be a better test to define the location or persistence of an internal pancreatic fistula. CT, Computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; MRCP, magnetic resonance cholangiopancreatography.
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) Diagnosis The diagnosis of external pancreatic fistulae is typically straightforward compared with internal fistulae, as diagnostic imaging is usually not needed. A pancreaticocutaneous fistula should be considered in patients with persistent output of clear pancreatic juice after percutaneous drainage of a pseudocyst or peripancreatic fluid collection (Box 54.5).1
Duct Leaks
Internal Fistula • Pseudocyst/evolving pancreatic necrosis • CT • MRI/MRCP • US • EUS • ERCP Pancreatic Ascites • High-amylase fluid with aspiration • Flat film (ground glass appearance) • CT/MRCP* • ERCP* • Ductal disruption versus obstruction/upstream leak High-Amylase Pleural Effusion • ERCP • S-MRCP CT, Computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasonography; JP, Jackson-Pratt; MRCP, magnetic resonance cholangiopancreatography; MRI, magnetic resonance imaging; S-MRCP, secretin-enhanced magnetic resonance cholangiopancreatography; US, ultrasonography. *Concomitant pseudocyst 1/3–1/2.
Similarly, persistent output from a Jackson-Pratt (JP) drain after pancreatic resection, decompression, or peripancreatic surgery (e.g., splenectomy, left nephrectomy, right hemicolectomy, or gastrectomy) is another manifestation of an external PD leak.25 More troublesome, however, may be the patient who sustains a penetrating abdominal injury, such as a knife or gunshot wound, in whom the external fistula is overlooked because of concern for other injuries. Pancreatic injury should be considered in all cases of severe abdominal trauma. The diagnosis of internal fistulae is outlined in Box 54.5. In essence, noninvasive imaging, particularly pancreas protocol computed tomography (CT), remains the best initial diagnostic test in patients with smoldering or severe pancreatitis or in patients with underlying chronic pancreatitis and an acute exacerbation of symptoms.14 Not only will CT define the consequences of pancreatitis (fluid collections, necrosis, effusions, ascites),26 but it can also be used to define the potential etiology (e.g., stones or strictures) and follow the subsequent evolution of pancreatitis. CT remains an imperfect tool, however, in that biliary stone disease is underestimated, the fluid component associated with evolving pancreatic necrosis is overestimated, and leaks are implied rather than defined.27 Further confirmation of a ductal disruption may require sequential scans demonstrating an enlarging fluid collection, aspiration of that fluid collection with measurement of amylase or lipase, an ERCP demonstrating the presence and location of the leak, or secretin-enhanced MRCP (S-MRCP). The latter study has been shown to be predictive of ongoing ductal disruption and clearly minimizes potential ERCP adverse events, such as exacerbation of pancreatitis and iatrogenic infection of an undrained fluid collection.28–30 It may also demonstrate patients with a complete ductal disruption and a disconnected gland syndrome in whom leak closure by ERCP alone is unlikely
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis BOX 54.6 Key Points: Management of
Pancreatic Fistulae
• The appropriate management of pancreatic fistulae should include a multidisciplinary team. • Transpapillary stent placement has a markedly higher success rate in treating internal fistulae if the disruption is bridged. • The role of ERCP in patients with an obvious disconnected gland syndrome is limited. ERCP, Endoscopic retrograde cholangiopancreatography.
to be successful. Finally, use of S-MRCP before ERCP may help to define subsequent endoscopic management comparable to its use in hilar neoplasms of the liver. ERCP, in turn, is usually definitive in showing not only the site of the ductal disruption (if persistent) but also the proximate cause or reason for persistence (PD stones, inflammatory or fibrotic structure).14,31 For the most part, however, diagnostic pancreatography adds an unnecessary risk to the care of acutely or chronically ill patients with presumptive leak, unless endoscopic, percutaneous, or surgical therapy is contemplated.32
MANAGEMENT (BOX 54.6) Indications for Endoscopic Treatment The presence of a presumptive pancreatic fistula alone is not a reason to undertake endotherapy. Important considerations include whether the patient has acute or underlying chronic pancreatitis, whether pancreatic necrosis is present, whether there is superinfection of a fluid collection, whether the presumptive leak is accessible to endoscopic control, and whether the leak is controlled at the time of presentation. For instance, the vast majority of low-volume leaks after pancreatic resection are controlled by a surgically placed JP drain and spontaneously close with or without concomitant octreotide over days or several weeks.33,34 On the other hand, a patient may have rapidly increasing ascites or pleural effusion or concomitant jaundice or cholestasis that demands urgent attention. In general, the following are relative indications for initiation of endoscopic therapy in a patient with a presumed PD leak: 1. An enlarging pancreatic fluid collection (pseudocyst, pancreatic ascites, high-amylase pleural effusion) despite conservative management 2. A symptomatic fluid collection 3. Persistence of an external fistula 4. Inability to refeed the patient without development of recurring pain or pancreatitis14 A fifth indication may be the question of concomitant biliary tract disease. Although the latter may occasionally be a concern for a retained stone in the setting of biliary pancreatitis, it is more commonly seen in patients with jaundice or cholangitis from pancreatic head edema or pseudocyst. Perhaps as important as indications for study are contraindications. Aside from medical instability precluding endoscopy, possibly the most important contraindication to an attempt at endoscopic therapy for a PD leak is the inability to render therapy if a ductal disruption is demonstrated. In this setting the diagnosis of a leak may result in iatrogenic infection of a concomitant fluid collection or necrosis, which ultimately may result in the need for endoscopic, percutaneous, or even surgical drainage. Given the potential for “therapeutic misadventure” and the complexity of patients with pancreatic fistulae, careful planning with the use of high-quality cross-sectional imaging and a multidisciplinary approach to management are essential.
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Pancreatic Fluid Collections The endoscopic and nonendoscopic management of pancreatic pseudocysts35–39 and evolving pancreatic necrosis40–45 is covered in Chapter 56. Treatment invariably requires treatment of the underlying ductal disruption, if anatomically feasible, as well as the consequences of that disruption. Thus surgical decompression, percutaneous decompression, and endoscopic decompression of fluid collections have all been variously described.
Pancreatic Ascites and High-Amylase Pleural Effusions Historically, pancreatic ascites and pleural effusions were treated with gut rest and total parenteral nutrition to minimize pancreatic juice stimulation. Diuretics, large-volume thoracentesis and paracentesis, and octreotide have all been used for weeks or months in an attempt to preclude the need for surgical resection or bypass. Successful in less than 50% of these patients, “salvage-type” surgery, usually defined by ERCP preoperatively, consisted of partial pancreatectomy or Roux-en-Y cystojejunostomy in the subset of patients with concomitant pancreatic pseudocysts. Surgical attempts were associated with high morbidity, periprocedural mortality of 8% to 15%, and recurrence rates of 15% to 20%.14 Our group was the first to describe transpapillary stent placement beyond the site of ductal disruption, in conjunction with large-volume paracentesis, as a successful treatment for patients with pancreatic ascites (Fig. 54.2).46 Since our initial publication a number of series have confirmed our findings.47–52 The available literature to date suggests that endoscopic transpapillary stent placement across the site of ductal disruption is successful in resolving pancreatic ascites and pleural effusions in more than 90% of patients and is associated with minimal procedure-related morbidity and close to zero mortality. One of the largest series was published by Telford et al. of 43 patients with PD disruption and a variety of clinical manifestations.53 The etiology was acute pancreatitis in 24 patients, chronic pancreatitis in 9, operative injury in 7, and trauma in 3. Stent placement was successful in resolution of the disruption in 25 patients, unsuccessful in 16 patients, and indeterminate in 2 patients. On univariate analyses, bridging of the ductal disruption and duration of stenting were associated with a statistically significant successful outcome, whereas female gender and acute pancreatitis were negative predictive factors of success. With multivariate analysis, only bridging of the disruption remained statistically significant as a predictor of success (Figs. 54.3, 54.4, and 54.5). Other studies have confirmed the importance of bridging the site of the leak for successful treatment of pancreatic fistulae.54 A similar retrospective series was recently published with data from two tertiary referral centers’ experience with pancreatic leaks of various presentations and etiologies. In this series PD stent placement was successful in 103/107 (96%) of patients, and resolution of the leak was successful in 80 (75%).55 The effectiveness of transpapillary stenting is likely due to a change in the ductal drainage gradient and making the duodenum the path of least resistance to flow. Potential areas of downstream obstruction that are bypassed include the sphincter, possible stones, and the inflammatory or fibrotic stricture frequently associated with a leak (Fig. 54.6). This approach does not work in the setting of a disconnected gland syndrome, in which the bulk of the pancreatic juice that enters the thoracic or abdominal cavity comes from a disconnected PD tail that cannot be reached transpapillarily.14,52
Pancreaticoenteric Fistulae and Acute Pancreatic Trauma Until now, our group has treated more than 30 patients with pancreaticoenteric or biliary fistulae. Although these patients may present with
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B
C
FIG 54.2 A, A pancreatogram of a patient with high-amylase ascites demonstrating a ductal disruption in the midbody (arrow). A wire guide is placed across the disruption (B), followed by a bridging pancreatic endoprosthesis (C).
A
C
G
B: 27.1mm C: 9.8mm A: 41.9mm
D
B E
F
FIG 54.3 Computed tomography (CT) demonstrates perisplenic fluid collection (A) and markedly thickened gastric wall (arrow) in a patient with hereditary pancreatitis. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates severe chronic pancreatitis (B) with dilated tail and ductal disruption (C) requiring percutaneous drainage. The stricture is “dilated” with a Soehendra stent extractor (D), followed by balloon dilation (E) and 7-Fr stent placement beyond the ductal disruption (F). Note the improvement on CT scan and persistent dilation of the pancreatic duct tail (G).
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis B
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C
A
D
E
FIG 54.4 A, A large internal fistula (pseudocyst) in the head of the pancreas in a patient with chronic calcific pancreatitis. B, A pancreatogram demonstrates a ductal disruption (arrow) secondary to a high-grade pancreatic duct stricture. C, A pancreatic endoprosthesis is placed across the stenosis and leak (arrowhead). D, A computed tomography scan 6 weeks later demonstrates complete resolution of the pseudocyst after endoscopically placed transduodenal double-pigtail stents. E, A pancreatogram reveals changes of chronic pancreatitis but the leak has resolved.
A
B
C
D
FIG 54.5 Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates pancreatic duct disruption at junction of body and tail (A and B) in a patient with severe left-upper-quadrant/flank pain and splenic vein thrombosis. Pain and ductal disruption are resolved with prosthesis placement (C and D). Disruption recurred 1 year later, requiring distal pancreatectomy/splenectomy.
spontaneous and rapid resolution of a fluid collection for which no treatment is required, a stenosis at the site of ductal disruption may result in relapsing attacks of pancreatitis. Alternatively, fistulization into the bile duct (Fig. 54.7) or colon may result in cholestasis or cholangitis, or recurrent sepsis, respectively.56 In our initial series of eight patients with pancreaticoenteric fistulae, three resolved with downsizing or removing an external drain that had eroded into a contiguous loop of bowel, three resolved with transpapillary stent placement, and two ultimately required surgical resection.57 In the case of pancreaticocolonic fistulae, diverting ileostomy may be necessary to close the fistulae and reduce bacterial translocation and ongoing sepsis.58 Fistulization into the bile duct, in turn, is almost invariably treated successfully by concomitant biliary and PD stenting, assuming that the fistula is not from the upstream disconnected portion of the pancreas (Figs. 54.8 and 54.9).59 In addition to pancreaticoenteric or biliary fistulae that usually occur in the setting of pancreatic necrosis or chronic pancreatitis, ERCP has also been used to treat internal fistulae as a consequence of acute pancreatic trauma. For example, Kim et al. diagnosed normal pancreatograms in 14 of 23 patients with acute abdominal trauma.19 In eight of these patients a leak from the main PD into the parenchyma resolved spontaneously, whereas three had a main PD leak that resolved after bridging with a transpapillary stent. Although the authors of this study suggested that early ERCP was believed to be advantageous in projecting the need for medical, surgical, or endoscopic therapy, it is possible that S-MRCP may evolve to play a diagnostic role, selecting patients who have the greatest potential to benefit from transpapillary therapy.18
External Fistulae As previously discussed, with the exception of penetrating abdominal trauma, the vast majority of external fistulae are iatrogenic. They may occasionally follow partial pancreatic resection or bypass in the setting
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B
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D
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FIG 54.6 Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates ductal disruption in the pancreatic head (A) in a patient with huge high-amylase effusion of the right lung (B). The patient is treated with a transpapillary pigtail stent into the fluid collection (C) as well as stenting of the minor papilla to decompress the upstream pancreatic duct (D–F).
D
C
B
A
FIG 54.7 Endoscopic retrograde cholangiopancreatography (ERCP) demonstrates transgastric pigtail stent (arrows, A and B) in a patient with severe necrotizing pancreatitis, portal vein thrombosis, and disconnected pancreatic duct. Note the embolized coils for previous splenic artery aneurysm (arrows, C) and the Jackson-Pratt (JP) drain for persistent colonic fistula into the pancreatic head (D).
B
C
A
FIG 54.8 A, Computed tomography scan demonstrating a dilated bile duct and transduodenal pigtail stents into a peripancreatic fluid collection. B, Cholangiogram demonstrating a communication (arrow) between the bile duct and the pancreatic fluid collection. C, A fully covered metal bile duct stent is placed to seal the fistula.
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis A
B
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10x7pd stent &10x7biliary stent
FIG 54.9 High-grade bile duct stricture in a patient with pancreatic necrosis and intramural pancreatic ductal disruption. Note contrast in colon (A), deformed edematous papilla (B), and biliary stent placement (C). Small arrows demonstrate intraduodenal abscess and the large arrow demonstrates dilated pancreatic duct (D). Note the dual-stent placement (E and F), which resolved jaundice and concomitant PD disruption and obstruction.
of a downstream stricture. Most, however, are a consequence of a disconnected gland after percutaneous or surgical drainage of a pancreatic fluid collection or necrosis.14 Our group initially reported a series of patients undergoing transpapillary stenting for amenable external fistulae more than a decade ago.60 Since that time, multiple additional series have been published or abstracted.14,61,62 By way of summarizing the available series, 86% of patients (50 of 58) could be successfully stented and 46 of those patients (92%) had resolution of their fistulae. Procedural adverse events were limited to mild flares of pancreatitis, although there were two deaths in the series by Costamagna et al.,61 neither related to the fistula or its endoscopic treatment. No recurrences were reported in patients undergoing successful fistula closure at follow-up ranging from 12 to 36 months. Our approach to endotherapy of pancreaticocutaneous fistulae has evolved over the past decade. Whereas endoscopic therapy was initially reserved for postoperative or percutaneously drained patients whose external fistulae did not respond to several weeks of clear liquids, total parenteral nutrition, and octreotide, our current practice is to study patients with high-volume fistulae with S-MRCP if they have a marginal decrease in fistula volume after several days of somatostatin analog. ERCP and transpapillary stent placement are undertaken unless imaging documents a disconnected gland syndrome (Fig. 54.10; see also Fig. 54.7).
Disconnected Pancreatic Duct Syndrome Our experience has taught us that prevention of disconnected PD syndrome (DPDS) is paramount, because treatment is complex. It is clear that a significant number of patients who have WOPN treated
with percutaneous drainage alone will develop pancreaticocutaneous fistulae secondary to disconnected duct syndrome. Our group has devised a treatment for WOPN, which is termed “dual-modality drainage,” in order to prevent such fistulae from developing. This technique involves the placement of both a percutaneous drain and endoscopic transluminal stents into areas of WOPN, with subsequent removal of the percutaneous drain once the necrosis resolves.63 If it is determined that there is no DPDS, the transluminal drains are also removed. However, if the patient has DPDS, the transmural stents are left in place indefinitely to prevent recurrent fluid collections. This combined approach has reduced our cutaneous fistula rate to zero when treating WOPN.64,65 Historically, patients with disconnected gland syndrome and pancreaticocutaneous fistulae have required distal pancreatectomy.14 More recently, less invasive approaches have been described, with varying levels of success.66 Interventional radiologist–administered cyanoacrylate injection into the disconnected tail has been described. This requires guidewire placement into the PD tail through the fistulous tract, placement of a microcatheter over the wire, and injection of the entire disconnected portion of the duct to include side branches. Mild postprocedural pancreatitis has been noted in approximately 50% of patients, and recurrent fistulae may occur unless the entire duct and its side branches are sealed. This procedure works best when there is only 3 to 4 cm of disconnected gland and is less likely to be successful when the glandular disconnection is at the genu, which requires a significant portion of the gland to be glued shut. In addition to the percutaneous approach to the disconnected gland, as well as the surgical approach using glue injection to minimize
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B
C
D
E
F
G
H
(2)7fr-3cm transgastric stents
FIG 54.10 A, Computed tomography scan demonstrating a percutaneous drain adjacent to the body of the pancreas in a patient with a history of severe acute pancreatitis and central gland necrosis. The drain had a high output of amylase-rich fluid on a daily basis. B, Magnetic resonance cholangiopancreatography demonstrates a dilated pancreatic duct in the tail (arrow) with no communication with the head of the gland, suggesting disconnected pancreatic duct syndrome. C, The fistula tract is accessed percutaneously using a TIPS needle, which is directed across the gastric wall. D, Wire guides are placed through the needle and grasped using an endoscopic snare. E, Dilation across the gastric wall is performed using a controlled radial expansion balloon dilator followed by the placement of two double-pigtail stents (F and G). Injection of contrast through the fistula tract opacifies the stomach, thus demonstrating an alternate route for the flow of pancreatic juice from the fistula tract (H). TIPS, transjugular intrahepatic portosystemic shunt.
postpancreatectomy leak,67 Soehendra’s group has used transpapillary injection of methyl-butyl cyanoacrylate into the distal duct at the site of glandular disruption.68 Eight of 11 patients in their series had resolved disruptions without recurrence, although all had concomitant PD stents or drains and endoscopic transmural drainage of associated fluid collections. This group also used glue injection as an adjunct in patients with severe pancreatic necrosis undergoing aggressive endoscopic drainage using EUS-directed lavage or debridement.69 Our group has also devised a combined endoscopic and percutaneous rendezvous approach to internalization of chronic pancreaticocutaneous fistulae in patients with disconnected gland syndrome (see Fig. 54.8). This technique involves an interventional radiologist initially accessing the fistula tract using a transjugular intrahepatic portosystemic shunt (TIPS) needle. The needle is then passed under fluoroscopic and endoscopic control into the stomach. The tract is then dilated using an 8-Fr microcatheter, and two guidewires are passed through the catheter, grasped using an endoscopic
snare, and pulled through the endoscope. Further dilation of the tract is then performed using a controlled radial expansion balloon dilator, subsequent to which two double-pigtail stents are placed across the gastric wall into the fistula tract. The resultant “redirection” of pancreatic juice into the stomach has been used to close fistulae in 15 patients treated at our institution. During long-term follow-up, recurrent pancreatic fluid collections developed in two patients because of migrated stents and were treated with endoscopic cystgastrostomy.70 Despite the success with glue injection and the combined approach described above, these are small case series performed at centers with significant experience in managing patients with complicated pancreatitis. The widespread application of these nonsurgical techniques requires additional critical assessment before widespread adoption can be advocated. However, they do provide “proof-of-principle” that viable alternatives to long-term drain placement and surgery are very much on the horizon.
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis
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ADVERSE EVENTS (BOX 54.7) (SEE CHAPTER 8)
the time of ERCP. As such, all patients with a presumptive internal fistula should receive a broad-spectrum antibiotic before undergoing diagnostic ERCP and may require more prolonged treatment afterward, particularly in the setting of pancreatic necrosis. Moreover, clearly contaminated fluid collections should be considered for concomitant endoscopic or percutaneous drainage of necrosis, as described in Chapter 53. Note that our group has previously demonstrated that bacterial contamination within the PD is invariable in patients with indwelling stents and that stent occlusion is a necessary but not sufficient cause of pancreatic sepsis.73 Stent occlusion may also be associated with obstructive pancreatitis, and it is for this reason, as well as fear of iatrogenic duct injury,74 that indwelling stents should be retrieved quickly after external fistula closure and after 4 to 6 weeks of treating an internal PD fistula.14
Immediate Adverse Events
Chronic Adverse Events
The immediate adverse events of transpapillary stent placement are those of diagnostic ERCP and include drug reaction, aspiration, cardiopulmonary events, pancreatitis from contrast injection or sphincter manipulation, and cholangitis in patients with underlying endoscopically untreated concomitant biliary stenosis. Bleeding and iatrogenic perforation can occasionally be seen if sphincterotomy is performed to facilitate stent placement.71 Pancreatitis flare approximates 10% in normal ducts and is uncommon in patients who have ductal changes of chronic pancreatitis. It may approach 50% in the setting of unsuccessful stenting when multiple accessories and guidewires have been placed into the PD to facilitate bridging the area of the leak. This pancreatitis is usually attenuated, however, if a short transpapillary stent is left to preclude ductal obstruction by an edematous papilla or traumatized sphincter.72 Pancreatitis is more common in the setting of an improperly sized prosthesis for the duct, even if the disruption can be bridged. Examples include placement of a 7-Fr stent into a 5-Fr-diameter duct or placement of a 12-cm prosthesis to bridge a ductal leak 3 cm from the papilla.
Although iatrogenic ductal injury is listed under chronic adverse events, PD prostheses (other than short-term prophylactic for prevention of post-ERCP pancreatitis) never belong in the pancreas, particularly in patients with otherwise normal PDs. A number of procedural and stent modifications have decreased trauma to the major PD and minimized side-branch occlusion over the past several years. These modifications include use of 3-Fr-diameter to 4-Fr-diameter stents, elimination of internal stent flanges, and recognition that stents that apply significant pressure proximally (toward the tail), especially when in an angulated position, may cause duct ulceration and subsequent fibrosis.74,75 Despite this, 3-Fr unflanged pigtail stents almost always spontaneously migrate within a week or two and are probably appropriate only in the patient in whom bridging of the disruption was unsuccessful, and then only to prevent or ameliorate post-ERCP pancreatitis. Iatrogenic ductitis should be anticipated and minimized by selecting a prosthesis that has a smaller diameter than the PD downstream from the leak, is the appropriate length to bridge the disruption without an inordinate stent length beyond the site of the leak, and avoids upstream impaction or angulation on the ductal wall.
BOX 54.7 Key Points: Adverse Events • The risk of procedural or postprocedural adverse events in treating pancreatic duct fistulae endoscopically should be weighed against the risk of persistent fistula or alternative treatments. • Procedural pancreatitis and iatrogenic infection of a concomitant fluid collection are the major risks in endoscopically treating internal pancreatic duct fistulae. • Iatrogenic “ductitis,” including irreversible stricture formation, can follow pancreatic duct stenting, especially when the size of the selected stent is greater than the caliber of the duct.
Subacute Adverse Events Subacute adverse events are usually infectious and result from iatrogenic introduction of bacteria into a fluid collection or necrotic debris at
SUMMARY 1. Pancreatic duct leaks are a consequence of acute inflammation with duct disruption, downstream obstruction, or both. 2. Minor leaks in the setting of acute pancreatitis or necrosis are probably common and respond to conservative therapy. 3. The consequences of major ductal disruptions include internal fistulae (pseudocysts, necrosis, pancreatic ascites, pancreatic pleural effusions, pancreaticoenteric or biliary communication) and external fistulae. 4. Treatment of internal fistulae requires treatment of the leak and/or the sequelae/consequences of the leak.
5. Bridging the site of ductal disruption with a transpapillary prosthesis is more likely to result in resolution of the disruption unless there is disconnected gland syndrome. 6. The complexity of most pancreatic leaks requires management by a multidisciplinary team with expertise in pancreatic diseases. This is particularly true in the setting of DPDS. The complete reference list for this chapter can be found online at www.expertconsult.com.
CHAPTER 54 Pancreatic Interventions in Acute Pancreatitis
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