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Minimally Invasive Debridement andLavage ofNecrotizing Pancreatitis
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268
Figure30.3 Debridement of necrotic pancreatic tissue under
direct vision using an operating nephroscope.
Figure30.4 A 12F Ryles nasogastric tube and 28F chest drain are
placed into the cavity at the end of the procedure and used as an
irrigating drainage system to continuously flush the necrotic
cavity with 0.9% saline solution at a rate of 125 mL/h.
the commonest minimal access technique, though endoscopic approaches have become first line in many institutions as part of a step- up approach strategy. Most data
published in the form of comparative studies and trials
compare open surgery with minimally invasive strategies. Hence why the largest cohort study of MARPN
remains of 274 patients published from the pancreatic
unit in Liverpool in 2016[11]. They describe a procedurespecific complication rate of 20.4% with a conversion
rate to open necrosectomy of 13.1% due to technical difficulties in maintaining a tract, bleeding during the procedure, and inaccessible collections.
One of the most important complications is that of
bleeding during or after the procedure; the incidence of
this is 11–21% [8,10,11]. Primary bleeding during the
procedure is from contact with granulating tissue or
avulsion of a vessel, with the rare possibility of injury to
the splenic artery. If cessation of the procedure and irrigation fails to stem the bleeding then the cavity requires
closing by a pack, suture, or drain clamp in order to facilitate tamponade. Secondary bleeding can occur at any
time in the postoperative period from an erosion into a
vessel or a pseudoaneurysm rupture. If clamping the
drain does not prevent cardiovascular instability then an
urgent CT angiography investigation needs to be performed with a view to a mesenteric angiogram and
embolization of a bleeding vessel.
Subsequent procedures may prove difficult and a
period of conservative management is advocated to
ensure there is no further bleeding.
Fistulation to the GI tract has been reported but the
incidence remains very low. Approximately 1% can occur
from erosion of necrosis into the lumen of the bowel or
the development of focal ischemia as tributaries of mesenteric vessels become occluded[12]. It may also become
apparent from the medial border of the duodenum
as necrosectomy of the head of the pancreas reveals
thedefect. Management of this is on a case by case basis
and may require cessation of intervention, keeping the
patient starved and commencing total parenteral nutrition. Fistulation from the pancreas duct occurs in 5–28%
of patients from the remnant healthy pancreas and is
managed conservatively providing flow proximally is not
obstructed[8,11]. An endoscopic retrograde cholangiopancreatography (ERCP) and pancreatic duct stent may
treat an established fistula.
Compared to open surgery, MARPN has significantly
lower complications (35.4% vs. 51.7%), less incidence of
multiorgan failure (12–20% vs. 35–40%) but mortality
rates remain similar (23.1% vs. 22.9%), respectively[8,11,13,14]. The difficulty in comparing techniques
in the management of necrotizing pancreatitis is that the
development of novel drainage strategies has provided
multiple options. In previous cohort studies, it has been
reported that the use of MARPN is not suitable in 30% of
cases in some studies and one quarter of all patients will
require additional percutaneous drains[8,11]. This implies
that as good as MARPN is as a technique, there will be
areas of walled-
off necrosis that may not be accessible.

Modern Management ofNecrotizing Pancreatitis 269
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Thus is the nature of necrotizing pancreatitis and why
the development of different drainage techniques has
improved management.
Single Port Pancreatic Necrosectomy
There has been a single report published reviewing the
use of a single port for necrosectomy in seven patients[15].
It is important to state that this technique is used for
extrapancreatic walled- off collections, predominantly
those that are accessible using a three- channel SILS port.
A percutaneous drain is inserted radiologically into the
collection under local anesthetic and then the patient is
given a general anesthetic where a 3 cm cut- down incision
is made over the drain site to afford the SILS port. A zerodegree nephroscope is then inserted through one channel
and an articulating grasper through the other, with a 0.9%
saline irrigation channel. A necrosectomy is performed
under direct vision and an irrigation nasogastric tube is
then placed for further lavage and drainage. The case
series is small, a morbidity rate is not possible to accurately calculate and the post- procedural median length of
stay was 47days[15]. Though this is a technically feasible
technique, it is for a specific, difficult to access, area of
necrosis of critically unwell patients. It should become
part of an array of minimal access techniques for patients
with complex necrotizing pancreatitis.
Laparoscopic Approaches
toPancreatic Necrosectomy
Many small volume case series have been reported over
the past couple of decades but the technique remains low
in popularity and there are no large volume studies published[16]. The peritoneal approach has been commonly
reported and the pancreatic cavity is approached from
either the mesocolon or through the greater omentum
into the lesser sac. It is also possible to enter transgastrically once the collection/necrosis is walled- off and ready
to drain through a cystgastrostomy[17]. The major benefit is that only single operation is needed for necrosectomy, though it has been reported that 20% of patients
require a further procedure[16]. Other reported benefits
include a morbidity rate of 21% and the simultaneous
ability to perform a cholecystectomy [16,18]. The only
comparative study between laparoscopic and open techniques of necrosectomy was published in 2012, which
stated that there was a lower complication rate, less blood
loss, and a shorter length of stay[19]. The operation duration was longer, which leads to specific respiratory
complications from prolonged abdominal insufflation.
There is a further risk of introducing a contained
collection into a previously sterile peritoneal compartment. Many units prefer to approach necrosectomy
through the retroperitoneum. There has been a retroperitoneal laparoscopic approach described where two
ports are placed into the necrotic cavity over percutaneous drains. This allows insufflation of carbon dioxide and
necrosectomy can be performed using laparoscopic
instruments and clips and diathermy can be used to control bleeding[20]. The major advantage of this technique
is that it requires only two procedures, compared to other
retroperitoneal techniques, with a lower median time to
discharge of 44days. There remains a complication rate
of 38% and the series was of only 13 patients [20]. The
retroperitoneal is still an important aspect of pancreatic
necrosectomy, though the MARPN technique remains
the most commonly used minimally invasive strategy.
Modern Management ofNecrotizing
Pancreatitis
In 2016 a Cochrane review was published comparing
interventions in necrotizing pancreatitis and summarized that there was low to very low quality evidence to
compare minimally invasive step approaches to open
necrosectomy [21]. This highlights the difficulties in
comparing techniques and establishing the role of
MARPN with a solid evidence base. More recent studies
have established that minimally invasive step- up
approaches have significantly fewer deaths than open
surgery (2% vs. 10%), respectively and a risk ratio of
0.7 [22]. Two randomized control trials have been
reported from the Dutch Pancreatitis Group. The Panter
trial, which compared open necrosectomy with a minimally invasive step- up approach and found the latter to
be superior in terms of mortality, postoperative complications, and pancreatitis insufficiency [23]. Van
Brunschot etal. published a randomized trial reviewing
surgical step- up and endoscopic step- up approaches and
determined that there was no difference in mortality or
major complications. The only differences reported was
a short length of stay and few pancreatic fistulae in the
endoscopic step- up group. It was concluded that there
should be a shift toward endoscopic approaches[10].
As the evidence bases slowly improves, the primary use
of open necrosectomy becomes less recommended and
minimally invasive strategies have become first line. The
advent of endoscopic therapies has further shifted management from surgically minimally invasive techniques,
especially MARPN. Given these advances a modern pancreas unit should be able to provide multiple strategies
and afford a multidisciplinary decision- making process,
where patient factors, collection distribution and timing
can be discussed in order to tailor personalized
management.

Minimally Invasive Debridement andLavage ofNecrotizing Pancreatitis
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270
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Halloran CM. Single port retroperitoneal pancreatic
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31
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Open Surgical Debridement ofNecrotizing Pancreatitis: Late Postoperative
Morbidity andOutcome
Dongya Huang1, Zipeng Lu1, and Yi Miao
1
Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
2
Pancreas Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, China
1,2
271
Introduction
Open surgical debridement, once considered as the firstline treatment for necrotizing pancreatitis, is now
reserved as the final step in contemporary treatment
algorithms with the “step- up” approach and is needed in
fewer than 20% of cases[1]. However, an open approach
may have advantages over minimally invasive debridement techniques in the following conditions: (i) infeasible for minimally invasive approaches, due to solid
material constituting majority of the necrosis, or unfavorable anatomic location of the necrosis; (ii) complications including abdominal compartment syndrome,
enteric fistula, ileus, and massive intra- abdominal hemorrhage; (iii) additional surgical procedures are needed
(e.g., cholecystectomy for biliary etiology); (iv) efficient
removal of necrotic tissue and rapid control of systemic
infection are warranted, particularly in critically ill
patients with severe sepsis. In selected cases, a “stepjump” open surgery first approach, by skipping the precedent treatments in the “step- up” approach including
percutaneous catheter drainage and minimally invasive
debridement, may be beneficial[2].
Historically, open surgical debridement with large
incision and extensive necrosectomy resulted in a high
incidence of complications and mortality after surgery[3,4]. A better understanding of the natural course
of disease, advances in medical treatment especially in
critical care, incorporating a “step- up” strategy, and
accumulation of expertise in high- volume centers significantly improved clinical outcomes after open surgical
debridement for necrotizing pancreatitis [5–11].
Improvement of surgical techniques also played an
important role in continuous optimization of patients’
prognosis in this clinical setting. Traditional open
surgical procedures for necrotizing pancreatitis included
debridement and continuous closed lavage[12], debridement and open packing/staged laparotomy[13], debridement and closed packing[14]. Nowadays, the tendency
of minimalization in open surgery for necrotizing pancreatitis is remarkable, and reported techniques included
open transgastric necrosectomy[5,8] and small incision
retroperitoneal debridement[15].
Late complications in necrotizing pancreatitis are common and have a significant impact on patients’ long- term
wellness (Table31.1). In a recent report involving 578 consecutive cases of necrotizing pancreatitis with a median
follow- up time of 46 months, 85% of the patients developed ≥1 long- term complication, and 59% of them
required invasive interventional treatment[16]. In an earlier cohort of patients with necrotizing pancreatitis after
surgical debridement with a median follow- up time of
28.9 months, 62% of the patients developed a long- term
complication and 26% of them required intervention[17].
The following paragraphs will focus on individual
long- term complications closely related to the procedure
of open debridement.
Pancreatocutaneous Fistula
Pancreatic leakage develops in necrotizing pancreatitis
when the main pancreatic duct or its branches are
destructed and subsequent pancreatic juice extravasates
to the peripancreatic space. Any transcutaneous interventions including open surgery with postoperative
drainage may cause pancreatocutaneous fistula [18].
Another form of pancreatic fistula in necrotizing pancreatitis is internal fistula, which is less associated with
necrosectomy, thus is not discussed in this chapter.
The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Fourth Edition. Edited by Hans G. Beger, Markus W. Büchler,
RalphH. Hruban, Julia Mayerle, John P. Neoptolemos, Tooru Shimosegawa, Andrew L. Warshaw, David C. Whitcomb, and Yupei Zhao.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/beger/thepancreas4e

Table31.1 Clinical results andlong- term complications after open surgical debridement fornecrotizing pancreatitis.
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First author
Surgery
period
Surgical
technique Patient N
Short- term
mortality
a
rate % Follow-
up time
Hemorrhage %Pancreatic
fistula %
Enteric
fistula %
Incisional
hernia %
Endocrine
insufficiency
%
Exocrine
insufficiency %Supplementary
enzyme use %
Tsiotos[21,41] 1983–1995 OD & SL 44/72 25 mean: 60mo 18.1 19.4 23.6 27.3 36.4 25 25
Tzovaras[22] 1987–1999 mixed 21/44 18.3 median: 48mo NA 9.1 13.6 47.6 47.6 9.5 NA
Rodriguez[10] 1990–2005 OD & CP 167 12 NA 4 41 15 NA 16 20 NA
Cinquepalmi[42] 1990–2005 OD & CL 32/35 22 median: 85mo NA NA NA 91 29 NA NA
Busse[49] 2003–2012 TGOD 50 20 NA NA NA NA NA 35 NA 20
Hollemans[19,34] 2005–2008 OD & CL 38/45 16 mean: 86mo 27 38 22 53 56 56 42
Luckhurst[6] 2006–2019 OD & CL 88 10
b
12mo 9 73 NA NA 26 NA 14
Chandrasekaran[48] 2009–2010 OD & SL 21 NA >12mo NA NA NA NA 61.9 57.1 80.9
Jones[35] 2010–2015 mixed 33 21.9
b
12mo 9.1 30.3 9.1 9.1 NA 48.5
Zhang[15] 2010–2019 SIOD 31 16 6mo 6 16 6 6 13 NA 10
a
Patient number included in long- term follow- up/patient number after necrosectomy; b90- day mortality rate.
mo: months; NA: not applicable; OD & CL: open debridement & continuous closed lavage; OD & CP: open debridement & closed packing; OD & SL: open debridement & open packing/staged laparotomy;
SIOD:small incision open debridement; TGOD: transgastric open debridement.

Pancreatic fistula rate after surgical debridement in
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necrotizing pancreatitis was 8−73% from different studies[6,7,9–11,15,19–26]. Transgastric necrosectomy has
the innate advantage of minimizing risk of external fistula by creating durable internal drainage for potential
gland leaks, and the reported pancreatic fistula rate after
open transgastric necrosectomy was 2.0−4.7% [5,8].
When postoperative pancreatic fistula persists, underlying anatomical deformity of the pancreatic duct secondary to parenchymal necrosis should be suspected. When
duct stricture or disconnected pancreatic duct syndrome
(DPDS) presented, persistent pancreatic fistula after
pancreatic debridement increased from 27% in cases
with normal duct to 54% and 85%, respectively [27].
Disconnected left pancreatic remnant on preoperative
CT scan was also found to be a risk factor for the development of pancreatic fistula after necrosectomy[7].
Around two- thirds of the post- necrosectomy pancreatic fistula will close spontaneously after noninterventional treatments at around 4months after surgery[18,28].
Conservative treatments included optimized drainage,
somatostatin analogues, antibiotics, and nutritional support. If the fistula is refractory to medical treatment, the
choice between different interventional modalities currently lacks strong evidence support. Endoscopic transpapillary duct drainage [29], surgical interventions
including fistulojejunostomy, pancreaticojejunostomy,
and left pancreatectomy[30] are among the physician’s
arsenal and were reported with a satisfactory safety and
efficacy profile. Changes in ductal morphology may provide helpful information in clinical decision- making to
choose the appropriate treatment[31]. Simultaneous left
pancreatectomy resection with the index debridement
for cases with DPDS were also recommended[7].
Hemorrhage
Hemorrhage is one of the most fatal complications and
contributes to a substantial mortality rate in necrotizing
pancreatitis. Late hemorrhage in necrotizing pancreatitis is related to the presence of residual peripancreatic or
pancreatic necrosis, long- standing pseudocyst, and gastrointestinal varicosis following thrombosis and obstruction of the portosplenomesenteric vein. Too aggressive
or expectant timing for debridement and traumatic
manipulation during necrosectomy may also increase
the risk of postoperative bleeding. The common sites of
hemorrhage in necrotizing pancreatitis include splenic
artery, gastroduodenal or pancreaticoduodenal artery,
portal vein, spleen, and unspecified peripancreatic vessels[32,33]. Isolated vessels or even vascular stumps in
the necrotic cavity are frequently found during necrosectomy; proper ligation or transfixation of the vessel or its
Hemorrhage 273
Figure31.1 Isolated vascular stumps (arrows) in necrotic cavity
during open debridement, which require proper management
with ligation or transfixation.
stump is required, and surgical debridement holds technical advantages in this respect (Fig.31.1).
Various studies have reported a rate of postoperative
hemorrhage of 2.7−10.1% after open pancreatic necrosectomy[6–10,15,19–21,23–26,34–36]. In the extended
observational study of a randomized controlled trial,
two more patients (5%) had intra- abdominal bleeding
requiring intervention during the long- term follow- up
period, making an overall hemorrhage rate of 27% in the
open surgery arm[34]. As regards a different but closely
related disease entity, the visceral artery pseudoaneurysm was reported to be 4.3% in all patients with
necrotizing pancreatitis with a median incidence timing
of 63.5days after disease onset and 21% of the patients
were diagnosed based on incidental CT findings [37].
Age >50 years, presence of any organ failure, and
previous endoscopic transluminal necrosectomy with
lumen- opposing metal stent were reported to be risk
factors for visceral pseudoaneurysm in necrotizing
pancreatitis[37,38].
Recognition of early signs of hemorrhage and/or pseudoaneurysm is critical for prompt intervention and successful treatment; these include blood in drainage, acute
onset of abdominal pain, gastrointestinal bleeding, and
early presentations of hemorrhagic shock. Visceral angiography is considered as the first step in management of
bleeding after necrosectomy if the patient is hemodynamically stable, which could provide detailed information on bleeding sites. And further intravascular
embolization with a coil or covered stent would provide
definite treatment or a bridging measure for surgery[33,37]. Emergent open laparotomy for hemostasis
is a lifesaving procedure for patients with catastrophic
intra- abdominal bleeding or failed percutaneous vascular embolization, and has the advantage of eliminating
underlying causes of bleeding including residual infected
necrosis and direct compression from the drainage tube,

Open Surgical Debridement ofNecrotizing Pancreatitis: Late Postoperative Morbidity andOutcome
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274
and so on. Extensive blood oozing into the necrotic cavity represents another challenging scenario, in which
gauze packing may be the only choice of treatment.
Postoperative hemorrhage would have a profoundly detrimental impact on a patient’s outcome with a mortality
rate of 34.1%[32].
Enteric Fistula
Multiple factors were involved in the pathogenesis of
enteric fistula in necrotizing pancreatitis, which include
organ ischemia secondary to vascular thrombosis due to
enzyme- rich and inflammatory exudates involvement,
colonic ischemia in hypoperfusion status in splanchnic
blood supply, direct autodigestion from extravasated
pancreatic juice, and iatrogenic causes during interventions[28]. Enteric fistula was reported with an incidence
rate of 6−23.6% after surgical debridement from various
studies [7,9,10,15,19–23,25]. The incidence of enteric
fistula in necrotizing pancreatitis was associated with
organ failure, presence of extensive necrosis, and operative intervention[16,39].
Once the diagnosis of enteric fistula is established,
timely interventional management is essential to stabilize
the patients. Percutaneous catheter drainage, endoscopic
stenting, enterostomy, enteric resection, enteric fixation,
or proximal diversion of the gastrointestinal tract is indicated for different clinical settings. Although surgery is
still the mainstay treatment for enteric fistula, nonsurgical interventions have been increasingly applied in recent
years. In one report focused on colonic fistula after
necrosectomy for infected pancreatic necrosis, 34.8% of
the cases with colonic fistula closed spontaneously[40].
Once colonic ischemia is suspected during surgical
debridement, it is recommended that a prophylactic loop
ileostomy be constructed [20]. Necrotizing pancreatitis
complicated with gastrointestinal fistula represents a
treatment challenge, as studies have found out that the
disease course is significantly prolonged, and mortality is
substantially high in this group of patients[16,40].
Incisional Hernia
Risk factors for the development of incisional hernia including wound infection, repeated laparotomies, obesity, diabetes mellitus, malnutrition are commonly seen in patients
after open debridement. Various incidence rates of incisional hernia after traditional transperitoneal surgical
debridement were reported with a wide range of 9.1% to
91% [22,25,34–36,41,42]. Patients with incisional hernia
increased from 24% to 53% if the follow- up time was
extended from 6months to an average of over 7 years after
open necrosectomy[19,34]. In a retrospective study specifically focused on long- term hernia development after laparotomy for necrotizing pancreatitis, elder age was found to
be the only risk factor for hernia development[43].
Hernias are more common when marsupialization of
thelesser sac is used as a controlled laparostomy[44,45].
Transverse incision resulted in less incisional hernia when
compared with midline incision[46,47]. However, a retrospective case- control study in necrotizing pancreatitis did
not find a difference in hernia development between various types of incision[43]. Minimalization of the incision in
open necrosectomy may help to avoid the risk of incisional
hernia[15]. In the authors’ institution, we now use uni- /
bilateral flank incision (retroperitoneal) and/or mini transverse incision (transperitoneal) instead of a midline incision for open debridement. The choice of incision is flexible
and depends on the location and extension of necrosis
(Fig.31.2). A minimally invasive “step- up” approach could
significantly reduce the chance of hernia development by
avoiding laparotomy in some patients[19,34].
Incisional hernia is a condition that frequently requires
surgical reintervention and 52−86.5% of the patients
whodeveloped incisional hernia subsequently received
hernia repair[16,22,41,43].
New- Onset Endocrine Insufficiency
Acute necrosis of the pancreatic parenchyma, extensive
debridement, and subsequent chronic inflammation
after acute onset will cause permanent loss of functional
unit both in the endocrine and exocrine compartment of
the pancreata. Pancreatic functional loss in necrotizing
pancreatitis seems to be progressive and irreversible in
long- term follow- up[16,34].
Endocrine insufficiency after open necrosectomy
was reported with an incidence rate of 9.1−61.9% after
various follow- up times [6,10,15,22,34,35,41,42,48,49].
Endocrine insufficiency occurs early in necrotizing pancreatitis, as serum glucose greater than 200
included in Ranson’s score. Worth noting, over one- third
of euglycemic patients at the time of acute attack resolution further developed endocrine insufficiency, after
follow- up time was extended from 6months to 86months
in the PANTER trial[19,34]. And this finding was supported by other observations[16,41].
Studies have suggested that functional loss of the pancreas was more dependent on the severity of the attack
rather than on the action of debridement [16,50].
Development of organ failure, infection other than sterile necrosis, higher computed tomography (CT) severity
index, and more extensive necrosis during acute onset of
necrotizing pancreatitis were associated with the development of endocrine insufficiency afterward[16,41,48].
mg/dL was

References 275
(a) (b)
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Figure31.2 Minimalization of incision in open debridement. (a) Extensive pancreatic necrosis was found in a preoperative computed
tomography (CT) exam of a patient with infected necrotizing pancreatitis. (b) Epigastric 7- cm transverse incision (arrow heads) with
bilateral flank incisions (arrows) in open necrosectomy for this patient (drainage tubes were introduced via the flank incisions).
New- Onset Pancreatic Exocrine
Insufficiency (PEI)
The incidence of PEI after open debridement for necrotizing pancreatitis varied from 9.5% to 57.1%[10,22,34,41,48],
and the percentage of patients who relied on enzyme supplementation was reported to be 10−80.9%[6,15,19,34,35,
41,48,49]. Different diagnostic criteria will lead to different estimations of the burden of exocrine insufficiency.
One study used fecal elastase- 1 <200 μg/g and found the
incidence rate of long- term PEI after open necrosectomy
to be 56% [34], while exocrine insufficiency was diagnosed in 25–57.1% of patients when fecal fat excretion
>7 g/24 h was used[41,48].
Direct open debridement was reported to increase the
risk of longwith the minimally invasive step- up approach both in
functional test and supplementary enzyme dependence[34]. The extent and infection status of the necrosis,
and no or incomplete visualization of the main pancreatic duct are associated with the incidence of exocrine
insufficiency[41,48]. In another study, renal failure and
term exocrine insufficiency when compared
cardiovascular failure during the acute phase were found
to be independent risk factors for long-
term PEI devel-
opment in patients with necrotizing pancreatitis[16].
Summary
Late complications are common in patients with necrotizing pancreatitis and after open surgical debridement.
Long- term follow- up in these patients is essential and
warranted to identify potential complications and initiate
treatment promptly. In a contemporary treatment algorithm, the role of open surgery for necrotizing pancreatitis has fundamentally changed but remains indispensably
important, as it seems to be decisive for the fate in a subset of patients with necrotizing pancreatitis, not only as a
bail-
out procedure after failed minimally invasive interventions but maybe also as a first choice in selected
patients. In future, novel treatment strategy and surgical
techniques for necrotizing pancreatitis should be tested
in well- designed clinical trials focusing on both shortterm outcomes and long- term morbidities.
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