Endoscopic Therapy for Pancreatic Duct Leaks and Disruptions

Pancreatitis, whether acute or chronic, can lead to a plethora of complications, such as fluid collections, pseudocysts, fistulas, and necrosis, all of which are secondary to leakage of secretions from the pancreatic ductal system. Partial and side branch duct disruptions can be managed successfully by transpapillary pancreatic duct stent placement, whereas patients with disconnected pancreatic duct syndrome require more complex endoscopic interventions or multidisciplinary care for optimal treatment outcomes. This review discusses the current status of endoscopic management of pancreatic duct leaks and emerging concepts for the treatment of disconnected pancreatic duct syndrome.

Key points

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Pancreatic duct (PD) disruption can lead to pseudocysts, pancreatic ascites/pleural effusion, and external pancreatic fistulas.
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Endoscopic transpapillary drainage is a safe and effective treatment modality for treating PD disruptions.
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The best results following endoscopic transpapillary drainage are obtained if the PD disruption is partial and is bridged by the endoprosthesis.
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Pseudocyst occurring as a consequence of PD disruptions can also be treated with endoscopic transmural drainage, with or without endoscopic ultrasound (EUS) guidance.
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For patients with disconnected pancreatic duct syndrome (DPDS) and an associated peripancreatic fluid collection, placement of permanent indwelling transmural stents is effective for drainage of the upstream gland.
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For patients with DPDS and an external fistula, in the absence of an associated peripancreatic fluid collection, the “outside-in” transluminal puncture technique or EUS-guided PD stent placement may be considered for drainage of the upstream gland.

Pancreatic duct (PD) disruption with leakage of pancreatic juice is a complication resulting from episodes of acute or chronic pancreatitis, pancreatic malignancy, or abdominal trauma, or following abdominal surgery. The PD disruption may involve the main PD or one of its side branches. The clinical consequences of PD disruption depend on several factors including the etiology, site and extent of disruption, rate of secretion of pancreatic juice, location of the leak relative to anatomic tissue planes, ability of the systemic inflammatory response in containing the leak, and the presence of downstream obstruction of the PD by strictures/calculi. A normal PD with a small leak of pancreatic juice from one of the side branches may resolve spontaneously, whereas a persistent leak from a major main PD disruption may be complicated by pseudocyst formation, internal fistula formation causing ascites or pleural effusion, or external pancreatic fistulas (EPFs).

Following PD disruption, the pancreatic secretions leak from the ductal defect and collect in the peripancreatic area. This pancreatic fluid collection (PFC) evolves and, depending on the path the pancreatic juice takes, leads to formation of a pseudocyst, internal pancreatic fistula (IPF), or EPF. If the pancreatic juice remains confined to the retroperitoneum, mediastinum, or lesser sac, it subsequently becomes enclosed by a well-formed nonepithelialized wall and evolves into a pseudocyst over a 4- to 6-week period. If the pancreatic secretions track into internal spaces like peritoneal or pleural cavities, an IPF is created. An anterior PD rupture leads to leakage of the pancreatic juice into the peritoneal cavity with development of pancreatic ascites, whereas a posterior PD disruption directs the pancreatic juice superiorly into the mediastinum through the aortic or esophageal hiatus and into the pleural cavity, resulting in pleural effusion. The IPFs can occasionally communicate with other spaces such as the pericardium or organs such as bronchus, stomach, and small or large bowel. The pancreatic juice can also find its way externally to the skin surface, and an EPF develops as a consequence. This process may occur spontaneously but usually follows a surgical or radiologic intervention of the PFC.

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