Surgical and Interventional Management of Complications Caused by Pancreatitis

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.

Full text

Selection of our books indexed in the Book Citation Index
in Web of Science™ Core Collection (BKCI)
Interested in publishing with us?
Contact book.department@intechopen.com
Numbers displayed above are based on latest data collected.
For more information visit www.intechopen.com
Open access books available
Countries delivered to Contributors from top 500 universities
International authors and editor s
Our authors are among the
most cited scientists
Downloads
We are IntechOpen,the world’s leading publisher ofOpen Access booksBuilt by scientists, for scientists
12.2%
128,000
150M
TOP 1%
154
5,200

1
Chapter
Surgical and Interventional
Management of Complications
Caused by Pancreatitis
TommasoStecca, BrunoPauletti, LucaBonariol,
EzioCaratozzolo, EnricoBattistella, SilviaZilio
and MarcoMassani
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 infec-
tion 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 syn-
drome 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 sphincterec-
tomy or stenting to traditional surgical procedures. Patients may suffer from vascu-
lar 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

Pancreatitis
2
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 syn-
drome 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 man-
aging necrotizing pancreatitis is a notable example of how evidence-based knowl-
edge 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: laparos-
copy, retroperitoneal and endoscopic or percutaneous approaches. These can allow
open surgery to be postponed in a sub-acute setting or even to avoid it [3–6].
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 resolu-
tion 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 peripan-
creatic 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 (endo-
scopic 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 coli
and 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

3
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
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 accu-
rate, 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 inflamma-
tory 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 drain-
age: placement of a ductal pancreatic stent with or without preliminary sphinc-
terotomy 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, trans-
papillary 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

Pancreatitis
4
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 neces-
sary. 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” chap-
ter). 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 pro-
spective 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 fistu-
las, length of hospital stay and death, as compared with open necrosectomy [26, 29].
The risk of pancreatocutaneous fistula formation is the major potential draw-
back 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

5
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
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 mor-
tality 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 curb-
ing 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 with-
out signs of infection [1]. In case of infected pancreatic necrosis invasive procedures
(e.g. percutaneous catheter drainage, endoscopic transluminal drainage/necrosec-
tomy, 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 identi-
fication 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

Pancreatitis
6
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 obstruc-
tion, 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 associ-
ated with increased incidence of postoperative bile leak or biliary injury. Colon
resection and colostomy have to be considered if mesocolon is involved in peripan-
creatic 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 postopera-
tive 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 uncon-
trolled 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].
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 under-
lying disconnected duct. It is best recognized using secretin-stimulated magnetic
resonance cholangiopancreatography [38]. DPDS can be the result of acute necro-
tizing 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

7
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
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 tradi-
tional surgical procedures. These are characterized by a high periprocedural morbid-
ity 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 endo-
scopic [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 mainte-
nance 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.
4. Vascular complications (haemorrhage, pseudoaneurysm and
thrombosis)
Haemorrhage, pseudoaneurysm and thrombosis are the main vascular complica-
tions 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 sum-
marized 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 inflam-
mation 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 pan-
creaticoduodenal (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.

Pancreatitis
8
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 pack-
ing 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.
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 collec-
tion 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.

9
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
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 cre-
ate 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 abnor-
mal 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 cholangiopancrea-
tography (ERCP) to localize the leakage and positioning a stent [69]. If this proce-
dure 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].
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 special-
ists 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.

Pancreatitis
10
Author details
TommasoStecca*, BrunoPauletti, LucaBonariol, EzioCaratozzolo,
EnricoBattistella, SilviaZilio and MarcoMassani
Surgery Department, First Surgical Unit, Treviso Regional Hospital, Azienda
ULSS2 Marca Trevigiana, Italy
*Address all correspondence to: tommaso.stecca@aulss2.veneto.it
Conflict of interest
The authors declare no conflict of interest.
© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms
of the Creative Commons Attribution License (http://creativecommons.org/licenses/
by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.

11
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
References
[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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] Wittau M, Mayer B, Scheele J,
Henne-Bruns D, Dellinger EP, et al.

Pancreatitis
12
Systematic review and meta-analysis
of antibiotic prophylaxis in severe
acute pancreatitis. Scandinavian
Journal of Gastroenterology. DOI
:10.3109/00365521.2010.53148
6. Epub ahead of print 2011. DOI:
10.3109/00365521.2010.531486.
[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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] Keane MG, Sze SF, Cieplik N,
Murray S, Johnson GJ, et al. Endoscopic
versus percutaneous drainage
of symptomatic pancreatic fluid

13
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
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] 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] 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] 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] 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] 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] 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] Banks PA. Acute pancreatitis:
Landmark studies, management
decisions, and the future. Pancreas.
2016; 45: 633-640. DOI:10.1097/
MPA.0000000000000632.
[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] 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] 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] 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] Kozarek RA, Ball TJ, Patterson DJ,
Freeny PC, Ryan JA, et al. Endoscopic
transpapillary therapy for disrupted
pancreatic duct and peripancreatic
fluid collections. Gastroenterology.

Pancreatitis
14
DOI:10.1016/0016-5085(91)90790-r.
Epub ahead of print 1991. DOI:
10.1016/0016-5085(91)90790-r.
[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] DiMaio CJ. Management of
complications of acute pancreatitis.
Curr Opin Gastroenterol. 2018;
34: 336-342. DOI:10.1097/
MOG.0000000000000462.
[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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] Zhang C, Li A, Luo T, Li J, Liu D,
et al. Strategy and management of

15
Surgical and Interventional Management of Complications Caused by Pancreatitis
DOI: http://dx.doi.org/10.5772/intechopen.96747
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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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.

Pancreatitis
16
[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] 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] Creaghe SB, Roseman DM,
Saik RP. Biliary obstruction in chronic
pancreatitis: Indications for surgical
intervention. Am Surg.
[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] 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] 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] 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] 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.