Open access peer-reviewed chapter

Surgical and Interventional Management of Complications Caused by Pancreatitis

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Tommaso Stecca, Bruno Pauletti, Luca Bonariol, Ezio Caratozzolo, Enrico Battistella, Silvia Zilio and Marco Massani

Submitted: February 8th, 2021 Reviewed: February 19th, 2021 Published: March 30th, 2021

DOI: 10.5772/intechopen.96747

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Abstract

Acute pancreatitis has a broad clinical spectrum: from mild, self-limited disease to fulminant illness resulting in multi-organ failure leading to a prolonged clinical course with up to 30% mortality in case of infected necrosis. Management of local complications such as pseudocysts and walled-off necrosis may vary from clinical observation to interventional treatment procedures. Gram negative bacteria infection may develop in up to one-third of patients with pancreatic necrosis leading to a clinical deterioration with the onset of the systemic inflammatory response syndrome and organ failure. When feasible, an interventional treatment is indicated. Percutaneous or endoscopic drainage approach are the first choices. A combination of minimally invasive techniques (step-up approach) is possible in patients with large or multiple collections. Open surgical treatment has been revised both in the timing and in the operating modalities in the last decades. Since 1990s, the surgical treatment of infected necrosis shifted to a more conservative approach. Disruption of the main pancreatic duct is present in up to 50% of patients with pancreatic fluid collections. According to the location along the Wirsung, treatment may vary from percutaneous drainage, endoscopic retrograde pancreatography with sphincterectomy or stenting to traditional surgical procedures. Patients may suffer from vascular complications in up to 23% of cases. Tissue disruption provoked by lipolytic and proteolytic enzymes, iatrogenic complications during operative procedures, splenic vein thrombosis, and pseudoaneurysms are the pathophysiological determinants of bleeding. Interventional radiology is the first line treatment and when it fails or is not possible, an urgent surgical approach should be adopted. Chylous ascites, biliary strictures and duodenal stenosis are complications that, although uncommon and transient, may have different treatment modalities from non-operative, endoscopic to open surgery.

Keywords

  • pancreatic pseudocysts
  • walled-off necrosis
  • infected pancreatic necrosis
  • disconnected pancreatic duct syndrome
  • vascular complications
  • chylous ascites

1. Introduction

The majority of patients suffering from acute pancreatitis will have a mild, self-limited and uncomplicated course. Pancreatic necrosis may develop in up to 10%-20% of patients, because of insufficient perfusion of pancreatic parenchyma to support metabolic requirements, leading to a prolonged clinical course with up to 30% mortality in case of infected necrosis [1]. Local and systemic complications, mild or life-threatening, such as pancreatic and/or peripancreatic fluid collections, walled-off necrosis, infected pancreatic necrosis, disconnected pancreatic duct syndrome and vascular complications can occur. The successful management of these patients needs a multidisciplinary team composed by gastroenterologists, surgeons, interventional radiologists, and specialists in critical care medicine, infectious disease, and nutrition. Intervention is generally required for infected pancreatic necrosis and less commonly in patients with sterile necrosis who are symptomatic (gastric or duodenal outlet or biliary obstruction) [2]. The surgical odyssey in managing necrotizing pancreatitis is a notable example of how evidence-based knowledge leads to improvement in patient care. Open surgical necrosectomy has been the traditional surgical treatment for years. However, although it provides a wide access but it is associated with high morbidity (34%-95%) and mortality (11-39%). In the last decades treatment has moved towards minimally invasive techniques: laparoscopy, retroperitoneal and endoscopic or percutaneous approaches. These can allow open surgery to be postponed in a sub-acute setting or even to avoid it [3, 4, 5, 6].

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2. Pancreatic necrosis and pseudocysts

Local complications such as pancreatic and/or peripancreatic fluid collections can occur after an episode of acute pancreatitis or after recrudescence of chronic pancreatitis or a blunt, penetrating, iatrogenic pancreatic trauma. Peripancreatic fluid collections, with or without a necrotic component, are early manifestations of the pancreatic inflammatory process. They are not delimited by a well-defined inflammatory wall and often remain asymptomatic, ending in spontaneous resolution by a gradual reduction in size. After four weeks from the clinical manifestation, persistent collections usually become wall-defined, encapsulated, with (walled-off necrosis) or without (pancreatic pseudocyst) a necrotic component and a varying degree of pancreatic parenchyma involvement [7].

Management of pseudocysts and walled-off pancreatic necrosis (WOPN) rely on patient’s symptoms, location and characteristics of pancreatic and/or peripancreatic collections, local complications (such as pseudoaneurysm), expertise and availability of a multidisciplinary group [8].

In asymptomatic patients, clinical observation and periodic imaging follow up (every three-six months) represent the most successful management, due to the frequent reduction in size and spontaneous resolution of non-complicated homogeneous collections and to the morbidity associated to interventional (endoscopic or radiologic) treatment procedures. In these cases, it is possible to associate nutritional and pharmacological support (nasoenteric feeding reduces pain and improves nutritional status; proton pump inhibitors and somatostatin-analogue such as octreotide reduce pancreatic secretion).

Infection will develop in about one third of patients with pancreatic necrosis. It may arise at any time during the clinical course but peak incidence is between the 2nd and the 4th week after presentation [2]. Gram-negative bacteria are the main infectious species isolated, the most common of which are Escherichia coliand Pseudomonas aeruginosa[9]. Recently, a trend towards increasing incidence of Gram-positive and multi-resistant bacteria has been demonstrated [10, 11].

Prognosis and management are greatly affected by the recognition between sterile and infected pancreatic necrosis. Clues of suspicion should arise in case of clinical signs of systemic inflammatory response syndrome (SIRS) (new-onset fever, tachycardia, leukocytosis) or organ failure [12]. A blood culture with positive bacterial results and gas in and around the pancreas on a CT scan may give indirect evidence of infection. Prophylactic antibiotic use in patients suffering from acute pancreatitis has not been proven to decrease infection rate and thus, according to the meta-analysis by Wittau et al. [13] it is not recommended a routine prophylaxis. The Cochrane review by Villatoro et al. [14] showed that antibiotic prophylaxis was not associated with a reduced incidence of pancreatic necrosis infection, even though it was associated with significantly decreased mortality. CT- or US-guided fine needle aspiration of pancreatic necrosis for bacteriologic analysis are an accurate, safe and reliable techniques with high accuracy (89.4%-100%) [15, 16].

In symptomatic patients, with rapidly enlarging pseudocysts or systemic manifestations of organ failure sustained by an infectious process, an interventional treatment is indicated. In this case endoscopic drainage approach is the first choice, especially when fluid collection is close to gastroduodenal lumen. A combination of techniques is possible in patients with large collections, extended in pelvis and paracolic gutters, or multiple collections [17].

2.1 Endoscopic drainage

Endoscopic drainage of a walled collection is the preferred method when the drainage criteria are met: mature collections delimited by a well-defined inflammatory capsule and with a mostly liquid content; cystic wall adherent to stomach or duodenum; and collection’s size at least 6 cm in size.

This procedure has to be performed by an endoscopist with expertise and when surgical or interventional radiology staffs are available [18]. Contraindications to endoscopic drainage are: presence of pseudoaneurysm due to gastroduodenal or splenic artery erosion, with high risk of bleeding; and collections without a mature wall.

Drainage techniques consist in [19]: transmural drainage: creation of a passage through the stomach or duodenum wall into the cyst lumen. This permits cystic drainage after balloon dilatation and placement of one or more stents. This method is preferred to drain WOPN in order to evacuate solid debris. Transpapillary drainage: placement of a ductal pancreatic stent with or without preliminary sphincterotomy to drain cysts in communication with pancreatic duct, especially when endoscopic retrograde pancreatography demonstrates ongoing ductal leak.

Transmural approach is adopted when large and symptomatic walled-off pancreatic fluid collection is close to gastroduodenal structures. Transmural puncture through gastroduodenal wall (where is endoscopically visible a bulge resulting by apposition to the cyst), is nowadays ecoendoscopically guided. This permits to accurately identify puncture site for cystenterostomy, avoiding vessels or other interposed structures and evaluating real distance to pass through [20]. Self-expanding metal stents or plastic double pig-tail stents can be both used. Lumen Apposing Metal Stent (LAMS) are associated with higher bleeding grade but allow immediate procedures such as endoscopic necrosectomy.

Drainage of turbid necrotic fluid suggests debris presence and can be managed with direct endoscopic debridement and/or with the placement of a naso-cystic catheter for post-procedural lavage. Repeated debridement or association with percutaneous drainage or percutaneous endoscopic gastrostomy can be necessary with unresolved fluid collections [21].

For patients with small pseudocysts derived from main pancreatic duct, transpapillary stent placement is indicated as first drainage approach. This provides continuous drainage of pancreatic fluid, leading to resolution of pancreatic ductal disruption that is responsible of pseudocyst. Follow up with CT or EUS is preferred after four to six weeks if necrotic debridement was not necessary and stents are then removed the fluid cavity is collapsed. More frequent imaging is obtained in patients who underwent necrosectomy, to determine if additional debridement is necessary. When collections are completely evacuated, stents are removed. Long-term stents seem to protect against recurrence allowing ongoing drainage of pancreatic secretions, although cystenterostomy tract matures and persists after eventual stent removal [22].

2.2 Percutaneous drainage

Percutaneous drainage remains an important treatment modality for patients with symptomatic collections. It may be used both as primary therapy or as an adjunct to other techniques. According to the last International [23], American [1] and Japanese [24] guidelines, percutaneous catheter (or endoscopic transmural drainage) should be the first step in the treatment of patients with suspected or confirmed (walled-off) infected necrotizing pancreatitis. This is applied to decompress retroperitoneal fluid collections, to provide a rapid and effective means for source control in patients with infected pancreatic necrosis. It favors clinical stabilization of patients before endoscopic or surgical debridement and is the first choice when endoscopic drainage is unavailable, unsuccessful, or not technically feasible [25].

The positioning can be performed via the transperitoneal or retroperitoneal approaches. It is technically feasible in >95% of patients [26]. Retroperitoneal route is generally preferred because it avoids peritoneal contamination, enteric fistulas and facilitates a possible step-up approach (see “Surgical approach” chapter). Moreover, the catheter tract can act as an entry portal for minimally invasive debridement methods, such as video assisted retroperitoneal or endoscopic debridement [1]. Catheters range from 8 Fr to 30 Fr in diameter; they allow for bedside irrigation and clearance of necrotic material, can be manipulated and replaced according to the evolution of the collections [27].

Percutaneous drainage alone may provide definitive therapy for a subset of patients. The prospective observational multicenter study by Horvath K. et al. in 2010, found that the decrease in the size of the collection of at least 75% after the first 10-14 days predicts successful percutaneous treatment. In 2011, a large prospective multicenter study of treatment outcomes among patients with necrotizing pancreatitis demonstrated that catheter drainage was the first intervention in 63% of cases and did not require additional necrosectomy in 35% of patients [28]. Two prospective randomized trials from the Dutch Pancreatitis Study Group compared various approaches to the management of symptomatic WON. They demonstrated that percutaneous drainage alone was successful in 35%-51% of patients and that a minimally invasive step-up approach was related to a lower rate of pancreatic fistulas, length of hospital stay and death, as compared with open necrosectomy [26, 29].

The risk of pancreatocutaneous fistula formation is the major potential drawback of this technique. The multicentre randomised trial by van Brunschot S. et al. demonstrated that the rate of pancreatic fistula formation was significantly higher in the percutaneous (32%) as compared to the video-assisted retroperitoneal debridement (VARD) group (5%) [29]. The rate is as high as 45% in those with disconnected duct syndrome [30].

2.3 Surgical approach

The surgical odyssey in managing necrotizing pancreatitis is a notable example of how evidence-based knowledge leads to improvement in patient care. In the beginning of the 20th century surgeons such as Mayo Robson, Mickulicz, and Moynihan, in the context of the progression of anesthesia, were induced to deploy laparotomy in an effort to treat complications of severe acute pancreatitis [31]. Over the next decades surgical intervention became the therapy of choice despite a mortality rate greater than 50%. Extensive pancreatic resection became the treatment of choice in the 1960s and 1970s. Innovations and increased accuracy in radiological techniques led to new approaches for management. Surgeons were divided between those who reserved the intervention for cases of infected necrosis by proposing delayed exploration, and those who proposed early debridement for all patients with necrotizing pancreatitis. Since 1990s several studies proved that nonoperative management of patients with sterile pancreatic necrosis was superior to surgical intervention, and that delayed intervention provided improved surgical mortality rates. The treatment of infected necrosis shifted to a more conservative approach also thanks to a comprehensive knowledge of the physio-pathological process of the systemic inflammatory response and the adoption of novel antibiotics in curbing systemic toxicity and protecting against organ failure. Recently, endoscopic debridement and minimally invasive techniques has been introduced [31, 32].

The last guidelines of the Working Group of the International Association of Pancreatology (IAP)/American Pancreatic Association (APA) published in 2013 [23] and of the American Gastroenterological Association (AGA) published in 2020 [1] on the management of acute pancreatitis and pancreatic necrosis list the common indications for intervention. A symptomatic sterile pancreatic necrosis is an indication for intervention (either radiological, endoscopical or surgical). Symptoms can be represented by: gastric, intestinal, or biliary obstruction due to the mass effect of walled-off necrosis, pain, persistent unwellness in patients without signs of infection [1]. In case of infected pancreatic necrosis invasive procedures (e.g. percutaneous catheter drainage, endoscopic transluminal drainage/necrosectomy, minimally invasive or open necrosectomy) should be delayed, where possible, until at least 4 weeks after initial presentation to permit the collection to become “walled-off”. A randomized clinical trial [33] that compared early surgery (within 72 h) and delayed surgery (11 days after onset) demonstrated mortality rates of 56% and 27%, respectively.

Percutaneous drainage, alone or in combination with other minimally invasive approaches, can be an effective means for source control in patients with infected pancreatic necrosis. A significant number of patients (23%–47%) will resolve their necrosis with percutaneous drainage alone. In those with persistent disease, a step up to operative intervention may be undertaken. The tract of the drain is utilized to access the retroperitoneal space for an intracavitary videoscopic necrosectomy by which drains are left in the cavity for lavage and fistula control [26, 34, 35]. The PANTER Study in 2010, a prospective randomized multicenter trial, compared the step-up approach to open necrosectomy and found a higher rate of new-onset multiple-organ failure in the open necrosectomy group (40% vs. 12%) and an equivalent mortality between the groups [26]. Surgical transgastric debridement is similar to endoscopic transgastric debridement, can be done laparoscopically or open, and is performed by an anterior gastrotomy to access the posterior wall of the stomach for transmural access to the necrosis cavity. Open surgical debridement is still an important resource in the management of these patients for the debridement of necrotic tissue.

Before surgical approach, abdominal imaging is helpful to determine intra-abdominal status. Diagnosis of infected pancreatic necrosis is made by identification of air bubbles in retroperitoneal necrosis (areas with lack of contrast enhancement) on CT scan. Diagnosis can be confirmed by CT-guided fine needle aspiration of necrotic material for culture. CT is also indicated to define extent and location of necrotic areas, for example into the mesenteric root and down the paracolic gutters; to demonstrate the presence of a disconnected pancreatic segment (a viable pancreatic portion separated by the rest of pancreas by a necrotic segment, that require external drainage to create a controlled external pancreatic fistula); and to evaluate the presence of other local complications, such as gastric outlet obstruction, splenic or portal vein thrombosis and colonic necrosis. Open debridement with external drainage still plays an important, albeit limited, role. After access to retroperitoneum, fluid is evacuated and necrotic dissection and debridement is made. In biliary pancreatitis, cholecystectomy should be practiced but it is associated with increased incidence of postoperative bile leak or biliary injury. Colon resection and colostomy have to be considered if mesocolon is involved in peripancreatic necrosis. A feeding enteral tube and at least two-four drainage tubes should be placed [36].

Video-assisted retroperitoneal debridement approach requires preoperative percutaneous retroperitoneal access. Radiological catheter insertion is a route to guide the subsequent procedure directly down into necrotic cavity and postoperative lavage. The advantage is minimizing the risk of peritoneal contamination, but the access is limited and precludes other procedures over debridement [34]. Postoperative complications are: intra-abdominal residual fluid collections, derived from pancreatic leak not well controlled by drains; bleeding, due to vascular lesion during debridement maneuvers or rupture of pseudoaneurysm, related to vascular erosion caused by mechanical drain damage or infection associated with uncontrolled pancreatic fistula; pancreatic fistulas: amylase-rich (concentration greater than three times the upper limit of normal serum amylase) fluid coming from drains; biliary injury; and pancreatic endocrine and exocrine insufficiency, that may requires supplemental insulin and oral pancreatic enzyme replacement.

Each approach has distinct peculiarities with pros and cons that must be weighted in each case planning: pattern of disease, physiology of the patient, expertise of the multidisciplinary team, and the resources of the center [1].

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3. Disconnected pancreatic duct syndrome

The term disconnected pancreatic duct syndrome (DPDS) refers to a subset of patients suffering from a disruption of the main pancreatic duct leading to a normal upstream pancreatic gland having no communication with the gastrointestinal tract [1, 37]. Up to 50% of patients with pancreatic fluid collections might have an underlying disconnected duct. It is best recognized using secretin-stimulated magnetic resonance cholangiopancreatography [38]. DPDS can be the result of acute necrotizing pancreatitis, chronic pancreatitis, and pancreatic trauma. Pancreatic juice is still secreted from the disconnected gland resulting in different resolutions that are a continuum of the same pathophysiologic process: recurrent acute pancreatitis, internal persistent pancreatic fistula (most often presenting as a peripancreatic fluid collection), external fistula, pancreatic pleural effusion, pancreatic ascites, or disconnected pancreatic tail syndrome [39, 40].

Internal fistulae are the result of ductal disruptions that are not contained by the inflammatory response. Anterior ductal disruptions result in pancreatic ascites, posterior ones result in pancreatic pleural effusions. Positive testing for a collection rich in pancreatic enzyme gives the secure diagnosis. A percutaneous drainage is the initial treatment to obtain a controlled fistula that in 70-82% of cases results in a spontaneous closure.

External fistulae may develop after pseudocyst percutaneous drainage. The stricture or the obstruction of the Wirsung result in ductal hypertension thus increasing the chance of developing this complication. Endoscopic retrograde pancreatography (ERP) with sphincterotomy or transpapillary stenting should be then performed, both in internal and in external fistulae, to reduce resistance of pancreatic juice flow to the duodenum [41].

If the disruption is in the body or the tail (disconnected pancreatic tail syndrome), open distal pancreatectomy and debridement associated with drainage are the traditional surgical procedures. These are characterized by a high periprocedural morbidity that is counterweighted by the single procedure and a concise overall course. Distal pancreatectomy can be undertaken during the first 30–60 days of illness, in the subacute setting [1].

The high morbidity and mortality associated with open surgical procedures, especially for poor surgical candidates, recommend a minimally invasive endoscopic [42]. Partial duct disruption can be treated with endoscopic transpapillary stent bridging with a fistula resolution rate of 56%, according to Varadarajulu et al. [43]. One possible endoscopic approach in case of complete duct disruption is the use of permanent indwelling transmural stents that allow the creation and maintenance of a fistulous tract into the gastrointestinal lumen [42].

Correct choice of procedure, as well as correct choice of timing of intervention, are mandatory for success.

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4. Vascular complications (haemorrhage, pseudoaneurysm and thrombosis)

Haemorrhage, pseudoaneurysm and thrombosis are the main vascular complications with an incidence ranging from 1% to 23% in patients with acute pancreatitis. Arterial complications are less frequent than venous complications (1.3-10% vs. 22%) [44].

The etiopathology of bleeding in patients with severe pancreatitis can be summarized in four main causes. The first one is due to the local spreading of lipolytic and proteolytic enzymes during a severe pancreatitis or necrosis that leads to the disruption of the tissue and the release of pancreatic fluids thus resulting in the arterial wall damage [45]. The second cause is related to a iatrogenic damage: improper surgical management of acute pancreatitis with an early operation for non-infected necrosis has been reported in Literature as a possible cause of wall arterial weakening thus leading to bleeding due to the activated enzymes [46]. Another iatrogenic source of damage is associated to the radiological positioning of drains that could give a direct trauma to the vessels and a continuous local inflammation that can diminish arterial wall integrity [47]. A third pathogenic mechanism is splenic vein thrombosis due to the necrotizing process, pseudocyst and severe inflammation that could lead to portal hypertension and, as a late sequelae, to esophageal varices formation [45]. The last remarkable pathogenic mechanism is the formation of a pseudoaneurysm that derived from the rupture of a vessels into a long-standing pseudocyst [48]. Symptoms are gastrointestinal bleeding, abdominal pain and splenomegaly and they depend on the localization of pseudoaneurysm. The most common vessels are splenic (35-50%), gastroduodenal (20%), and pancreaticoduodenal (20%) artery. Other vessels involved are tributaries of the gastric, colic and hepatic bloodstream [40, 49].

Ultrasound (US) and Computed Tomography (CT) are the gold standard to diagnose a vascular complication. Specially, CT imaging showed a higher sensibility in the diagnosis of pseudo-aneurysm, and US has an important role in identifying thrombosis or in patients with iodine allergy or renal insufficiency [50]. Enhanced-contrast CT locates necrotic areas, abscess cavity, pseudocysts, and bleeding site. Angiography is the gold standard technique for the location and the control of the bleeding [45]. Interventional radiology is the first line treatment in both elective and emergency management of vascular complications. Angiography followed by trans-arterial embolization (TAE) is the gold standard management [51]. Different techniques can be used: the one preferred is the sandwich technique with coil located proximally and distally to the pseudoaneurysm to minimize the risk of potential rebleeding [52]. Haemostasis can be implemented with glue, N-butyl cyanoacrylate (NBCA), thrombin, ethiodised oil or gelfoam. Patients with unsuccessful TAE or in which is technically impossible, an emergency haemostatic surgery should be performed. Ligation of bleeding arteries is the technique of choice although related to a high rate of rebleeding. In extreme cases, open packing or salvage emergency pancreatectomy may represent the only chances for survival [45].

Vascular complications are rare but potentially fatal with a difficult management that is why they should be treated in a tertiary centre.

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5. Chylous ascites

Pancreatitis is a rare cause of chylous ascites (CA) and in Literature, only few cases about acute pancreatitis are reported since its discovered in 1984 [53, 54]. Other causes related to CA are abdominal trauma, malignancies, sarcoidosis, lymphangiomatosis, yellow nail syndrome, cirrhosis, and mycobacterial infections [55]. CA diagnosis is based on the presence of a milky triglyceride- rich fluid collection in the peritoneal cavity. Patients complain about abdominal pain, distension, weight loss, oedema, anorexia, and weakness.

Diagnosis requires peritoneal fluid sampling with documentation of a lipid rich fluid, triglyceride concentration > 1.2 mM (110 mg/dl), peritoneal-to-plasma protein concentration ratio of >0.5 and presence of microscopic fat. The minimum daily volume of CA considered significant ranges between 100 ml to 600 ml [56, 57].

The pathogenesis is not completely clarified especially when CA is due to acute pancreatitis. The main possible reason is the spreading of proteolytic and lipolytic enzymes associated to necrosis of pancreatic tissue that damage the lymphatic vessels thus provoking a lymph leakage. Other possible reasons are AP related and include: splenic vein thrombosis leading to portal vein hypertension thus causing the rupture of lymphatic vessels; and the severe inflammation that could cause lymphatic vessels obstruction and lymphatic exudation [58, 59].

CA treatment is multimodal. Conservative treatment is based on total parenteral nutrition (TPN) or medium chain triglyceride (MCT)-high protein enteral feeding with or without addition of octreotide and reaches the resolution in two to six weeks in 60-100% of cases [60, 61]. Interventional and surgical approaches should be reserved for cases in which conservative treatment has failed. A second line therapy is bipedal lymphangiography (BPLAG) with lipiodol. This technique permits to identify the normal lymphatic stream and locate the leakage site or the obstruction site. The accumulation of injected lipiodol determines an inflammatory response that acts as an embolic agent and determines leakage resolution in up to 70% of cases [62].

Van der Gaag and colleagues has considered any duration of chylous ascites, longer than 14 days despite therapy, a requirement for surgical intervention [63]. Surgical treatment may vary from a peritoneovenous shunt to open surgical ligation of the leaking lymphatics [64]. Surgical approach should be chosen only in case of persistent CA despite treatment, symptomatic patients, or impossibility to perform interventional radiology.

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6. Biliary and duodenal complications

Biliary stricture (BS) and duodenal stenosis (DS) are uncommon complication of AP. Pathogenesis of these events is strictly related to the anatomical position between the pancreatic head, the common bile duct and the duodenum. BS and DS are, in most cases, early and transient conditions associated to severe inflammation [65]. The main causes for temporary BS are inflammatory oedema and pseudocyst formation and enlargement in the area proximal to the pancreatic head that create a compression of the common bile duct, thus causing jaundice, nausea, vomit, abdominal pain, pruritus, and fatigue to the patient [66].

A duodenal early complication is gastric outlet obstruction related to the abnormal peristaltic wave and following ileus caused by the severe inflammation and the possible compression of the duodenal loop by the enlarged neck of the pancreas that cause a lumen obstruction [67].

BS ad DS usually solve with a conservative treatment intended to overcome the acute inflammatory phase. Pseudocyst management is resumed in previous chapters.

In many studies, late BS is associated to pancreatic duct disruption (PDD) with pancreatic juice leakage when duct of the head/neck of pancreas is involved in pancreatic necrosis [68]. When PDD is suspected, contrast-enhanced CT should be performed to confirm it and after that an endoscopic retrograde cholangiopancreatography (ERCP) to localize the leakage and positioning a stent [69]. If this procedure failed, and a progression of the common duct stricture has developed, surgical procedure is indicated [53].

The process that leads a transient DS to an irreversible one is still unclear. Literature suggests that the underlaying cause is a possible ischemic and thrombotic event. Indeed, inflammation may induce arterial narrowing and/or thrombosis of the pancreaticoduodenal circulation producing local ischemia and resulting in chronic fibrosis [70]. Patients who present intermittent symptomatic episodes of upper gastrointestinal tract obstruction should undergo surgical bypass, chosen considering the pathophysiology (gastrojejunostomy or gastroenterostomy with vagotomy to prevent marginal ulcer)[71].

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7. Conclusion

The majority of patients suffering from acute pancreatitis will have a mild, self-limited and uncomplicated course. Local and systemic complications, mild or life-threatening, such as pancreatic and/or peripancreatic fluid collections, walled-off necrosis, infected pancreatic necrosis, disconnected pancreatic duct syndrome and vascular complications can occur.

The successful management of these patients needs a multidisciplinary team composed by gastroenterologists, surgeons, interventional radiologists, and specialists in critical care medicine, infectious disease, and nutrition. However, it must be considered that the requisite technical expertise and judgment for many of these procedures is not widely available in all centres. Intervention is generally required for infected pancreatic necrosis and less commonly in patients with sterile necrosis who are symptomatic. The surgical odyssey in managing necrotizing pancreatitis has been described. Operative approaches to the treatment of acute pancreatitis complications have undergone a dramatic transformation over the past few decades. Prospective, randomized trials have further clarified the value of the latest minimally invasive approaches to the treatment of this disease. This is the notable example of how evidence-based knowledge leads to improvement in patient care.

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Conflict of interest

The authors declare no conflict of interest.

References

  1. 1. Baron TH, DiMaio CJ, Wang AY, Morgan KA. American Gastroenterological Association Clinical Practice Update: Management of Pancreatic Necrosis. Gastroenterology. 2020; 158: 67-75.e1. DOI:10.1053/j.gastro.2019.07.064
  2. 2. Bugiantella W, Rondelli F, Boni M, Stella P, Polistena A, et al. Necrotizing pancreatitis: A review of the interventions. Int J Surg. 2016; 28: S163–S171. DOI:10.1016/j.ijsu.2015.12.038
  3. 3. Traverso LW, Kozarek RA. Pancreatic necrosectomy: Definitions and technique. J Gastrointest Surg. DOI:10.1016/j.gassur.2004.05.013. Epub ahead of print 2005. DOI: 10.1016/j.gassur.2004.05.013
  4. 4. Tan V, Charachon A, Lescot T, Chafaï N, Le Baleur Y, et al. Endoscopic transgastric versus surgical necrosectomy in infected pancreatic necrosis. Clin Res Hepatol Gastroenterol. DOI:10.1016/j.clinre.2014.06.016. Epub ahead of print 2014. DOI: 10.1016/j.clinre.2014.06.016
  5. 5. Freeman ML, Werner J, Van Santvoort HC, Baron TH, Besselink MG, et al. Interventions for necrotizing pancreatitis: Summary of a multidisciplinary consensus conference. Pancreas. DOI:10.1097/MPA.0b013e318269c660. Epub ahead of print 2012. DOI: 10.1097/MPA.0b013e318269c660
  6. 6. Raraty MGT, Halloran CM, Dodd S, Ghaneh P, Connor S, et al. Minimal access retroperitoneal pancreatic necrosectomy: Improvement in morbidity and mortality with a less invasive approach. Ann Surg. DOI:10.1097/SLA.0b013e3181d96c53. Epub ahead of print 2010. DOI: 10.1097/SLA.0b013e3181d96c53
  7. 7. Cui ML, Kim KH, Kim HG, Han J, Kim H, et al. Incidence, risk factors and clinical course of pancreatic fluid collections in acute pancreatitis. Dig Dis Sci. DOI:10.1007/s10620-013-2967-4. Epub ahead of print 2014. DOI: 10.1007/s10620-013-2967-4
  8. 8. Bradley EL, Howard TJ, Van Sonnenberg E, Fotoohi M. Intervention in necrotizing pancreatitis: An evidence-based review of surgical and percutaneous alternatives. J Gastrointest Surg. DOI:10.1007/s11605-007-0445-z. Epub ahead of print 2008. DOI: 10.1007/s11605-007-0445-z
  9. 9. Lu J Di, Cao F, Ding YX, Wu YD, Guo YL, et al. Timing, distribution, and microbiology of infectious complications after necrotizing pancreatitis. World J Gastroenterol. DOI:10.3748/wjg.v25.i34.5162. Epub ahead of print 2019. DOI: 10.3748/wjg.v25.i34.5162
  10. 10. Schmidt PN, Roug S, Hansen EF, Knudsen JD, Novovic S. Spectrum of microorganisms in infected walled-off pancreatic necrosis - Impact on organ failure and mortality. Pancreatology. DOI:10.1016/j.pan.2014.09.001. Epub ahead of print 2014. DOI: 10.1016/j.pan.2014.09.001
  11. 11. Lee HS, Lee SK, Park DH, Lee SS, Seo DW, et al. Emergence of multidrug resistant infection in patients with severe acute pancreatitis. Pancreatology. DOI:10.1016/j.pan.2014.10.003. Epub ahead of print 2014. DOI: 10.1016/j.pan.2014.10.003
  12. 12. Rau BM, Bothe A, Kron M, Beger HG. Role of Early Multisystem Organ Failure as Major Risk Factor for Pancreatic Infections and Death in Severe Acute Pancreatitis. Clin Gastroenterol Hepatol. DOI:10.1016/j.cgh.2006.05.030. Epub ahead of print 2006. DOI: 10.1016/j.cgh.2006.05.030
  13. 13. Wittau M, Mayer B, Scheele J, Henne-Bruns D, Dellinger EP, et al. Systematic review and meta-analysis of antibiotic prophylaxis in severe acute pancreatitis. Scandinavian Journal of Gastroenterology. DOI:10.3109/00365521.2010.531486. Epub ahead of print 2011. DOI: 10.3109/00365521.2010.531486
  14. 14. Villatoro E, Mulla M, Larvin M. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. DOI:10.1002/14651858.cd002941.pub3. Epub ahead of print 2010. DOI: 10.1002/14651858.cd002941.pub3
  15. 15. Banks PA, Gerzof SG, Langevin RE, Silverman SG, Sica GT, et al. CT-guided aspiration of suspected pancreatic infection - Bacteriology and clinical outcome. Int J Pancreatol. DOI:10.1007/BF02784951. Epub ahead of print 1995. DOI: 10.1007/BF02784951
  16. 16. Rau B, Pralle U, Mayer JM, Beger HG. Role of ultrasonographically guided fine-needle aspiration cytology in the diagnosis of infected pancreatic necrosis. Br J Surg. DOI:10.1046/j.1365-2168.1998.00707.x. Epub ahead of print 1998. DOI: 10.1046/j.1365-2168.1998.00707.x
  17. 17. Werner J, Feuerbach S, Uhl W, Büchler MW. Management of acute pancreatitis: From surgery to interventional intensive care. Gut. DOI:10.1136/gut.2003.035907. Epub ahead of print 2005. DOI: 10.1136/gut.2003.035907
  18. 18. Muthusamy VR, Chandrasekhara V, Acosta RD, Bruining DH, Chathadi K V., et al. The role of endoscopy in the diagnosis and treatment of inflammatory pancreatic fluid collections. Gastrointest Endosc. DOI:10.1016/j.gie.2015.11.027. Epub ahead of print 2016. DOI: 10.1016/j.gie.2015.11.027
  19. 19. Binmoeller KF, Seifert H, Walter A, Soehendra N. Transpapillary and transmural drainage of pancreatic pseudocysts. Gastrointest Endosc. DOI:10.1016/S0016-5107(95)70095-1. Epub ahead of print 1995. DOI: 10.1016/S0016-5107(95)70095-1
  20. 20. Park DH, Lee SS, Moon SH, Choi SY, Jung SW, et al. Endoscopic ultrasound-guided versus conventional transmural drainage for pancreatic pseudocysts: A prospective randomized trial. Endoscopy. DOI:10.1055/s-0029-1215133. Epub ahead of print 2009. DOI: 10.1055/s-0029-1215133
  21. 21. Seewald S, Groth S, Omar S, Imazu H, Seitz U, et al. Aggressive endoscopic therapy for pancreatic necrosis and pancreatic abscess: A new safe and effective treatment algorithm (videos). Gastrointest Endosc. DOI:10.1016/S0016-5107(05)00541-9. Epub ahead of print 2005. DOI: 10.1016/S0016-5107(05)00541-9
  22. 22. Weckman L, Kylänpää ML, Puolakkainen P, Halttunen J. Endoscopic treatment of pancreatic pseudocysts. Surg Endosc Other Interv Tech. DOI:10.1007/s00464-005-0201-y. Epub ahead of print 2006. DOI: 10.1007/s00464-005-0201-y
  23. 23. Iap WG, Acute APA, Guidelines P. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013; 13: 1-15. DOI:10.1016/j.pan.2013.07.063
  24. 24. Isaji S, Takada T, Kawarada Y, Hirata K, Mayumi T, et al. JPN Guidelines for the management of acute pancreatitis: Surgical management. J Hepatobiliary Pancreat Surg. 2006; 13: 48-55. DOI:10.1007/s00534-005-1051-7
  25. 25. Keane MG, Sze SF, Cieplik N, Murray S, Johnson GJ, et al. Endoscopic versus percutaneous drainage of symptomatic pancreatic fluid collections: a 14-year experience from a tertiary hepatobiliary centre. Surg Endosc. DOI:10.1007/s00464-015-4668-x. Epub ahead of print 2016. DOI: 10.1007/s00464-015-4668-x
  26. 26. van Santvoort HC, Besselink MG, Bakker OJ, Hofker HS, Boermeester MA, et al. A Step-up Approach or Open Necrosectomy for Necrotizing Pancreatitis. N Engl J Med. DOI:10.1056/nejmoa0908821. Epub ahead of print 2010. DOI: 10.1056/nejmoa0908821
  27. 27. Mortelé KJ, Girshman J, Szejnfeld D, Ashley SW, Erturk SM, et al. CT-guided percutaneous catheter drainage of acute necrotizing pancreatitis: Clinical experience and observations in patients with sterile and infected necrosis. Am J Roentgenol. DOI:10.2214/AJR.08.1116. Epub ahead of print 2009. DOI: 10.2214/AJR.08.1116
  28. 28. Van Santvoort HC, Bakker OJ, Bollen TL, Besselink MG, Ahmed Ali U, et al. A conservative and minimally invasive approach to necrotizing pancreatitis improves outcome. Gastroenterology. DOI:10.1053/j.gastro.2011.06.073. Epub ahead of print 2011. DOI: 10.1053/j.gastro.2011.06.073
  29. 29. van Brunschot S, van Grinsven J, van Santvoort HC, Bakker OJ, Besselink MG, et al. Endoscopic or surgical step-up approach for infected necrotising pancreatitis: a multicentre randomised trial. Lancet. DOI:10.1016/S0140-6736(17)32404-2. Epub ahead of print 2018. DOI: 10.1016/S0140-6736(17)32404-2
  30. 30. Ross A, Gluck M, Irani S, Hauptmann E, Fotoohi M, et al. Combined endoscopic and percutaneous drainage of organized pancreatic necrosis. Gastrointest Endosc. DOI:10.1016/j.gie.2009.06.037. Epub ahead of print 2010. DOI: 10.1016/j.gie.2009.06.037
  31. 31. Bradley EL, Dexter ND. Management of severe acute pancreatitis: A surgical odyssey. Annals of Surgery. DOI:10.1097/SLA.0b013e3181c72b79. Epub ahead of print 2010. DOI: 10.1097/SLA.0b013e3181c72b79
  32. 32. Banks PA. Acute pancreatitis: Landmark studies, management decisions, and the future. Pancreas. 2016; 45: 633-640. DOI:10.1097/MPA.0000000000000632
  33. 33. Mier J, Luque-De León E, Castillo A, Robledo F, Blanco R. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg. DOI:10.1016/S0002-9610(96)00425-4. Epub ahead of print 1997. DOI: 10.1016/S0002-9610(96)00425-4
  34. 34. Horvath K, Freeny P, Escallon J, Heagerty P, Comstock B, et al. Safety and efficacy of video-assisted retroperitoneal debridement for infected pancreatic collections: A multicenter, prospective, single-arm phase 2 study. Arch Surg. DOI:10.1001/archsurg.2010.178. Epub ahead of print 2010. DOI: 10.1001/archsurg.2010.178
  35. 35. Freeny PC, Hauptmann E, Althaus SJ, Traverso LW, Sinanan M. Percutaneous CT-guided catheter drainage of infected acute necrotizing pancreatitis: Techniques and results. Am J Roentgenol. DOI:10.2214/ajr.170.4.9530046. Epub ahead of print 1998. DOI: 10.2214/ajr.170.4.9530046
  36. 36. Uhl W, Warshaw A, Imrie C, Bassi C, McKay CJ, et al. IAP Guidelines for the Surgical Management of Acute Pancreatitis. Pancreatology. DOI:10.1159/000071269. Epub ahead of print 2003. DOI: 10.1159/000071269
  37. 37. Kozarek RA, Ball TJ, Patterson DJ, Freeny PC, Ryan JA, et al. Endoscopic transpapillary therapy for disrupted pancreatic duct and peripancreatic fluid collections. Gastroenterology. DOI:10.1016/0016-5085(91)90790-r. Epub ahead of print 1991. DOI: 10.1016/0016-5085(91)90790-r
  38. 38. Bang JY, Wilcox CM, Navaneethan U, Hasan MK, Peter S, et al. Impact of Disconnected Pancreatic Duct Syndrome on the Endoscopic Management of Pancreatic Fluid Collections. Ann Surg. DOI:10.1097/SLA.0000000000002082. Epub ahead of print 2018. DOI: 10.1097/SLA.0000000000002082
  39. 39. DiMaio CJ. Management of complications of acute pancreatitis. Curr Opin Gastroenterol. 2018; 34: 336-342. DOI:10.1097/MOG.0000000000000462
  40. 40. Martin RF, Hein AR. Operative Management of Acute Pancreatitis. Surgical Clinics of North America. DOI:10.1016/j.suc.2013.02.007. Epub ahead of print 2013. DOI: 10.1016/j.suc.2013.02.007
  41. 41. Morgan KA, Adams DB. Management of Internal and External Pancreatic Fistulas. Surgical Clinics of North America. DOI:10.1016/j.suc.2007.08.008. Epub ahead of print 2007. DOI: 10.1016/j.suc.2007.08.008
  42. 42. Nadkarni NA, Kotwal V, Sarr MG, Vege SS. Disconnected pancreatic duct syndrome endoscopic stent or surgeon’s knife? Pancreas. DOI:10.1097/MPA.0000000000000216. Epub ahead of print 2015. DOI: 10.1097/MPA.0000000000000216
  43. 43. Varadarajulu S, Noone TC, Tutuian R, Hawes RH, Cotton PB. Predictors of outcome in pancreatic duct disruption managed by endoscopic transpapillary stent placement. Gastrointest Endosc. DOI:10.1016/S0016-5107(04)02832-9. Epub ahead of print 2005. DOI: 10.1016/S0016-5107(04)02832-9
  44. 44. Evans RPT, Mourad MM, Pall G, Fisher SG, Bramhall SR. Pancreatitis: Preventing catastrophic haemorrhage. World Journal of Gastroenterology. DOI:10.3748/wjg.v23.i30.5460. Epub ahead of print 2017. DOI: 10.3748/wjg.v23.i30.5460
  45. 45. Flati G, Andrén-Sandberg Å, La Pinta M, Porowska B, Carboni M. Potentially fatal bleeding in acute pancreatitis: Pathophysiology, prevention, and treatment. Pancreas. DOI:10.1097/00006676-200301000-00002. Epub ahead of print 2003. DOI: 10.1097/00006676-200301000-00002
  46. 46. Tsiotos GG, Juarez MM, Sarr MG. Intraabdominal hemorrhage complicating surgical management of necrotizing pancreatitis. Pancreas. DOI:10.1097/00006676-199603000-00003. Epub ahead of print 1996. DOI: 10.1097/00006676-199603000-00003
  47. 47. Beger HG, Büchler M, Bittner R, Block S, Nevalainen T, et al. Necrosectomy and postoperative local lavage in necrotizing pancreatitis. Br J Surg. DOI:10.1002/bjs.1800750306. Epub ahead of print 1988. DOI: 10.1002/bjs.1800750306
  48. 48. M.A. V, E. V, F. P, F. S, L. F, et al. Pseudoaneurysm of the gastroduodenal artery secondary to chronic pancreatitis. Annals of Vascular Surgery
  49. 49. Bergert H, Hinterseher I, Kersting S, Leonhardt J, Bloomenthal A, et al. Management and outcome of hemorrhage due to arterial pseudoaneurysms in pancreatitis. Surgery. DOI:10.1016/j.surg.2004.10.009. Epub ahead of print 2005. DOI: 10.1016/j.surg.2004.10.009
  50. 50. Chiang KC, Chen TH, Hsu J Te. Management of chronic pancreatitis complicated with a bleeding pseudoaneurysm. World J Gastroenterol. 2014; 20: 16132-16137. DOI:10.3748/wjg.v20.i43.16132
  51. 51. Zhang C, Li A, Luo T, Li J, Liu D, et al. Strategy and management of severe hemorrhage complicating pancreatitis and post-pancreatectomy. Diagnostic Interv Radiol. DOI:10.5152/dir.2018.18283. Epub ahead of print 2019. DOI: 10.5152/dir.2018.18283
  52. 52. Kirby JM, Vora P, Midia M, Rawlinson J. Vascular complications of pancreatitis: Imaging and intervention. Cardiovasc Intervent Radiol. DOI:10.1007/s00270-007-9138-y. Epub ahead of print 2008. DOI: 10.1007/s00270-007-9138-y
  53. 53. Karakayali FY. Surgical and interventional management of complications caused by acute pancreatitis. World J Gastroenterol. 2014; 20: 13412-13423. DOI:10.3748/wjg.v20.i37.13412
  54. 54. Goldfarb JP. Chylous Effusions Secondary to Pancreatitis: Case Report and Review of the Literature. Am J Gastroenterol. DOI:10.1111/j.1572-0241.1984.tb05101.x. Epub ahead of print 1984. DOI: 10.1111/j.1572-0241.1984.tb05101.x
  55. 55. Steinemann DC, Dindo D, Clavien PA, Nocito A. Atraumatic chylous ascites: Systematic review on symptoms and causes. Journal of the American College of Surgeons. DOI:10.1016/j.jamcollsurg.2011.01.010. Epub ahead of print 2011. DOI: 10.1016/j.jamcollsurg.2011.01.010
  56. 56. Weniger M, D’Haese JG, Angele MK, Kleespies A, Werner J, et al. Treatment options for chylous ascites after major abdominal surgery: a systematic review. Am J Surg. DOI:10.1016/j.amjsurg.2015.04.012. Epub ahead of print 2016. DOI: 10.1016/j.amjsurg.2015.04.012
  57. 57. Cárdenas A, Chopra S. Chylous ascites. American Journal of Gastroenterology. DOI:10.1016/S0002-9270(02)04268-5. Epub ahead of print 2002. DOI: 10.1016/S0002-9270(02)04268-5
  58. 58. Al-Ghamdi MY, Bedi A, Reddy SB, Tanton RT, Peltekian KM. Chylous ascites secondary to pancreatitis: Management of an uncommon entity using parenteral nutrition and octreotide. Dig Dis Sci. DOI:10.1007/s10620-006-9734-8. Epub ahead of print 2007. DOI: 10.1007/s10620-006-9734-8
  59. 59. Poo S, Pencavel TD, Jackson J, Jiao LR. Portal hypertension and chylous ascites complicating acute pancreatitis: The therapeutic value of portal vein stenting. Ann R Coll Surg Engl. DOI:10.1308/rcsann.2017.0078. Epub ahead of print 2018. DOI: 10.1308/rcsann.2017.0078
  60. 60. Gómez-Martín JM, Martínez-Molina E, Sanjuanbenito A, Martín-Illana E, Arrieta F, et al. Chylous ascytes secondary to acute pancreatitis: a case report and review of literature. Nutr Hosp. DOI:10.1590/S0212-16112012000100044. Epub ahead of print 2012. DOI: 10.1590/S0212-16112012000100044
  61. 61. Gurusamy KS, Koti R, Fusai G, Davidson BR. Somatostatin analogues for pancreatic surgery. Cochrane Database of Systematic Reviews. DOI:10.1002/14651858.CD008370.pub3. Epub ahead of print 2013. DOI: 10.1002/14651858.CD008370.pub3
  62. 62. Tabchouri N, Frampas E, Marques F, Blanchard C, Jirka A, et al. Chylous Ascites Management After Pancreatic Surgery. World J Surg. DOI:10.1007/s00268-016-3772-y. Epub ahead of print 2017. DOI: 10.1007/s00268-016-3772-y
  63. 63. van der Gaag NA, Verhaar AC, Haverkort EB, Busch ORC, van Gulik TM, et al. Chylous Ascites after Pancreaticoduodenectomy: Introduction of a Grading System. J Am Coll Surg. DOI:10.1016/j.jamcollsurg.2008.07.007. Epub ahead of print 2008. DOI: 10.1016/j.jamcollsurg.2008.07.007
  64. 64. Assumpcao L, Cameron JL, Wolfgang CL, Edil B, Choti MA, et al. Incidence and management of chyle leaks following pancreatic resection: A high volume single-center institutional experience. J Gastrointest Surg. DOI:10.1007/s11605-008-0619-3. Epub ahead of print 2008. DOI: 10.1007/s11605-008-0619-3
  65. 65. Vijungco JD, Prinz RA. Management of Biliary and Duodenal Complications of Chronic Pancreatitis. World Journal of Surgery. DOI:10.1007/s00268-003-7246-7. Epub ahead of print 2003. DOI: 10.1007/s00268-003-7246-7
  66. 66. Creaghe SB, Roseman DM, Saik RP. Biliary obstruction in chronic pancreatitis: Indications for surgical intervention. Am Surg
  67. 67. BRUST RJ, CHEN KC. Acute hemorrhagic pancreatitis complicated by duodenalobstruction. Report of a case. Am J Roentgenol Radium Ther Nucl Med. 1962; 87: 732-735
  68. 68. Sugimoto M, Sonntag DP, Flint GS, Boyce CJ, Kirkham JC, et al. Biliary stenosis and gastric outlet obstruction: Late complications after acute pancreatitis with pancreatic duct disruption. Pancreas. DOI:10.1097/MPA.0000000000001064. Epub ahead of print 2018. DOI: 10.1097/MPA.0000000000001064
  69. 69. Bill JG, Mullady DK. Stenting for Benign and Malignant Biliary Strictures. Gastrointestinal Endoscopy Clinics of North America. DOI:10.1016/j.giec.2018.12.001. Epub ahead of print 2019. DOI: 10.1016/j.giec.2018.12.001
  70. 70. Archer S, Levitt S, Drury P. DUODENAL NECROSIS AND INTRAMURAL HAEMATOMA COMPLICATING ACUTE PANCREATITIS. Aust N Z J Surg. DOI:10.1111/j.1445-2197.1991.tb00286.x. Epub ahead of print 1991. DOI: 10.1111/j.1445-2197.1991.tb00286.x
  71. 71. Sharma H, Marwah S, Singla P, Garg A, Bhukkal B. Roux-en-Y duodenojejunostomy for surgical management of isolated duodenal obstruction due to chronic pancreatitis. Int J Surg Case Rep. DOI:10.1016/j.ijscr.2017.01.008. Epub ahead of print 2017. DOI: 10.1016/j.ijscr.2017.01.008

Written By

Tommaso Stecca, Bruno Pauletti, Luca Bonariol, Ezio Caratozzolo, Enrico Battistella, Silvia Zilio and Marco Massani

Submitted: February 8th, 2021 Reviewed: February 19th, 2021 Published: March 30th, 2021