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R. W. Parks and E. Gleeson
6 Ongoing Trials andFuture
Directions
Several trials are ongoing that may reveal best
practices for managing idiopathic pancreatitis.
The SpHincterotomy for Acute Recurrent
Pancreatitis (SHARP) trial is currently recruiting
patients with recurrent acute pancreatitis in the
setting of pancreatic divisum to be randomized to
either minor papilla endoscopic sphincterotomy
(miES) or sham surgery. The primary outcome
measure will be risk reduction of subsequent
acute pancreatitis episodes by 33% [60].
The Pancreatitis of Idiopathic origin: Clinical
added value of endoscopic UltraSonography
(PICUS) Study is enrolling patients who have
had their rst episode of presumed idiopathic
acute pancreatitis. All patients will undergo routine EUS. If the diagnostic yield is >10%, the
authors will recommend routine EUS for all
patients with idiopathic acute pancreatitis [61].
In the EFFORT study, patients who have had
at least two episodes of idiopathic acute pancreatitis in the preceding 2years will be randomized to either a “reduced fat diet” (15% fat, 65%
carbohydrate, 20% protein) or a “standard
healthy diet” (30% fat, 50% carbohydrate, 20%
protein according to the World Health
Organization [WHO]). Patients will be followed
for 2years to see if diet can prevent recurrence
of pancreatitis [62].
Future research studies should focus on identifying ways to prevent idiopathic pancreatitis,
calculating the prevalence of occult intraductal
papillary mucinous neoplasm (IPMN) in patients
with idiopathic pancreatitis, determine disparities
in care after diagnosis of idiopathic pancreatitis,
and dene the role of combination etiologies in
the diagnosis of idiopathic pancreatitis [11, 54].
7 Conclusion
In summary, true idiopathic pancreatitis is a diagnosis of exclusion and should account for no
more than 20% of all pancreatitis etiologies.
Initial management of idiopathic acute
pancreatitis is similar to other acute pancreatitis
episodes. Acute pancreatitis may incorrectly be
diagnosed as idiopathic when workup is incompletely performed. Thorough diagnostic studies
should be conducted to identify the cause in order
to provide quality care and prevent recurrence.
These studies include serum IgG4 testing, genetic
testing in appropriate patient populations, EUS,
ERCP with biliary analysis, contrast-enhanced
CT, and MRCP (see Fig.1).
In patients in whom microlithiasis is the etiology, LC should be performed. Future studies
should be conducted to investigate multiple or
interacting factors contributing to idiopathic
acute pancreatitis and to investigate reasons for
incomplete workup, or disparities in care.
Acknowledgments Images 1 and 2 were created with
BioRender.com.
Conicts of Interest The authors have no conicts of
interest.
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Managing Local Complications
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HannahS.Pauw andHjalmarC.van Santvoort
Key Points
1. Local peripancreatic uid complications are
categorized based on symptom duration
(±4weeks), the nature of the content (solid,
liquid, or gas), and whether it is infected.
2. Most sterile peripancreatic uid collections
resolve spontaneously over time and can
therefore be treated conservatively.
3. Infected peripancreatic uid collections, once
walled off by 4weeks, are treated by the step up approach for necrotizing pancreatitis.
According to the step-up approach, invasive
intervention is most effective and associated
with a lower risk of complications when performed after 4 weeks, when necrosis has
become walled off.
1 Introduction
In the majority of patients with acute pancreatitis,
the disease course is mild and self-limiting
requiring supportive care only. However, a wide
H. S. Pauw
Department of Surgery, St. Antonius Hospital,
Nieuwegein, The Netherlands
e-mail: ha.pauw@antoniusziekenhuis.nl
H. C. van Santvoort (*)
Department of Surgery, St. Antonius Hospital,
Nieuwegein, The Netherlands
Department of Surgery, University Medical Center
Utrecht, Utrecht, The Netherlands
e-mail: H.C.vanSantvoort-2@umcutrecht.nl
variety of complications can occur in patients
with acute pancreatitis and these can be classied
as local or systemic. Early detection of complications following acute pancreatitis is essential for
accurate treatment. For this chapter we will only
address the local complications and its management. Chapter “Managing Organ Dysfunction/
Failure” will further address (the management
of) the systemic complications.
Over the past decades, the strategies and techniques for invasive treatment of local complications have greatly evolved. The historical
treatment of acute and infected necrotizing pancreatitis was open surgical debridement in all
patients. For example, Beger et al. promoted
early debridement of sterile necrosis [1]. The
mortality rate for these open surgery strategies
was above the 50%; still it was considered standard treatment till around the 1930s [2]. In the
1980s, a series of prospective studies demonstrated the superior efcacy of conservative treatment over surgical treatment in patients with
sterile necrosis, causing a shift in therapeutic
approach [3–5]. In 1979, the value of abdominal
abscess drainage under ultrasound or CT was discovered, while in 1987, the possibility of using
ultrasound or CT-guided aspiration for early
diagnosis of infected necrosis was realized [6, 7].
At the beginning of this century, the rst study
was published on laparoscopic necrosectomy followed by a study involving endoscopic necrosectomy in 2009 [8, 9]. At the end of the 1990s and
early 2000s, the necessity of surgical debride-
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. A. Windsor et al. (eds.), Acute Pancreatitis, https://doi.org/10.1007/978-981-97-3132-9_16
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H. S. Pauw and H. C. van Santvoort
ment was being questioned when it was shown
that initial conservative therapy, including antibiotic treatment, can be successful in a subgroup of
patients [10]. Mortality in patients managed with
surgery was identical to those managed conservatively [11]. Surgical therapy, when required, was
often delayed to a later stage of disease when the
systemic inammatory response has stabilized
and the necrotic pancreas had become demarcated. In 2010, the randomized PANTER trial
conrmed that a minimally invasive step-up
approach (percutaneous catheter drainage ± minimally invasive debridement) prevents the need
for open surgical debridement in around 30% of
patients [12]. It also demonstrated that drainage
alone was sufcient in 35% of patients. Since
then, the step-up approach has become the standard of care and is recommended in all guidelines
[13–17]. The choice of which intervention strategy is most suitable depends on the location of
the walled-off necrosis, whether there is evidence
of encapsulation, and if there is apparent adherenceto adjacent organs. Endoscopic transgastric
necrosectomy has gained widespread popularity
and has the advantage of internal drainage with
prevention of external pancreatic stula, which is
often seen after percutaneous drainage of surgical intervention [14, 18]. Invasive intervention
can be altogether avoided in some cases, as
shown in the randomized POINTER trial in 2022
[19]. In this study, 39% of patients with infected
necrosis did not require intervention at all and
were successfully treated with antibiotics alone.
Over the years, signicant progress has been
made regarding the optimal timing and type of
treatment to manage the local complications of
acute pancreatitis. With this chapter we aim to
provide the best clinical guidance on how and
when to treat the local complications of acute
pancreatitis.
2 Denitions ofLocal
Complications
The most frequent local complications associated
with acute pancreatitis are pancreatic and/or peripancreatic uid collections. These can arise with
either interstitial or necrotizing pancreatitis. The
collections were dened by the Revised Atlanta
Classication (RAC) based on chronicity, content, and whether they are infected or not (see
Table1) [20]. The content is not well determined
by CT scanning, and ultrasound or MR scanning
is preferred to determine whether the collection
contains solid material (i.e., necrosis). The morphology of the local complications is also important in deciding treatment and is not covered by
this classication. Central collections in the
region of the lesser sac are most common, but
extensions can occur into the small bowel mesentery, and down both paracolic gutters, into the
pelvis, scrotum, and pleura.
2.1 Interstitial Pancreatitis
Interstitial pancreatitis consists of edema and
inammation of the pancreas. CT demonstrates a localized or diffuse enlargement of
the pancreas with homogeneous or slightly heterogeneous enhancement of the pancreatitis
parenchyma. There are no signs of (peri)pancreatic necrosis (hypoperfusion or Hounseld
unit (HU) is <30). Normal pancreatic parenchyma should display a homogeneous increase
Table 1 Morphological classication of local complications(adapted from the Revised Atlanta Classication)
Content
Fluid Acute pancreatic
Solid ± uid Acute necrotic
APFC acute pancreatic uid collection, ANC acute necrotic collection, WON walled-off necrosis
Acute
(<4weeks, no dened wall)
No infection Infection No infection Infection
Infected APFC Pseudocyst Infected pseudocyst
uid collection
Infected ANC Walled-off necrosis Infected WON
collection
Chronic
(>4weeks, dened wall)
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in attenuation with intravenous contrast agent
of 100–150 HU. Parenchymal necrosis is seen
as focal or diffuse zones of non-enhanced or
minimally enhanced (<30HU) pancreatic parenchyma on contrast-enhanced CT [21–24].
2.1.1 Acute Pancreatic Fluid
Collection (APFC)
APFC is dened as anonencapsulated homogeneous peripancreatic collection that develops
within the rst 4weeks of the disease, and only
contains uid APFCs are caused by (peri)pancreatic inammation or as a consequence of rupture
of small peripheral pancreatic side duct branches.
Generally, these collections remain sterile and
will resolve spontaneously over time without the
need for invasive intervention. Infection is
rare. When these collections persist beyond
4weeks, they are referred to as pseudocysts.
2.1.2 Pseudocysts
Pseudocysts are lled with uid which consists
of uiddebris, blood, and inammatory cells, no
solid necroticmaterial, and they are walled off by
a thick brous wall. They can be either asymptomatic or symptomatic: causing biliary or gastric outlet obstruction, bleeding, or secondary
infection. It is a complication most often seen in
chronic pancreatitis patients, but it also occurs in
a small proportion (approximately 10–20%) of
patients with acute pancreatitis. The majority of
the pseudocysts will spontaneously resolve over
time. Indication for intervention depends on
symptomsand less on the size. Interventions are
only needed in a small subset of patients with
pseudocysts.
2.2 Necrotizing Pancreatitis
Approximately 5–10% of the patients will
develop necrotizing pancreatitis (NP). This is
characterized by necrosis of the pancreatic or
peripancreatic tissue, as seen on contrastenhanced CT scanning. There are three different
subgroups of NP as dened by the Revised
Atlanta Classication depending on the involvement of the pancreas: pancreatic parenchymal
necrosis alone, peripancreatic necrosis alone, and
acute pancreatic parenchymal necrosis with peripancreatic necrosis. In most patients with necrotizing pancreatitis (approximately 75–80%), the
combined type is seen. Necrosis of the pancreatic
or peripancreatic tissue is sterile at rst but may
become secondarily infected. The risk of secondary infection is around 30% [25, 26].
2.2.1 Acute Necrotic Collection (ANC)
In necrotizing pancreatitis, collections that
develop during the rst 4weeks from the onset of
disease are referred to as acute necrotic collections. These collections contain variable amounts
of uid and solid necrotic debris which distinguish them from APFCs. Necrosis usually
involves both the pancreas and peripancreatic tissue, and in approximately 50% of necrotic collections, it is located outside of the pancreas
without apparent direct involvement of the pancreatic parenchyma [27].The process of encapsulation (formation of inammatory brotic
capsule)starts to developduring the arbitrary 4
week period that is used for the denition.
2.2.2 Walled-o Necrosis (WON)
When ANC matures and encapsulates, they are
referred to as walled-off necrosis (WON).
Usually this happens after 4weeks in the disease.
In contrast to ANC, WON is surrounded by a
brotic capsule. These collections can vary in
size and may or may not become secondarily
infected.
2.2.3 Infected Walled-oNecrosis
Infected necrosis is suspected when a patient
clinically deteriorates despite maximal conservative support and other sources of infection are
ruled out. CT imaging may show gas in the
necrotic collections in around 40% of patients
[28], as shown in Fig.1d. Infected necrosis usually takes up to 2–4weeks to develop, but it can
also occur in the rst week of pancreatitis or
much later [14].
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H. S. Pauw and H. C. van Santvoort
Fig. 1 Contrast-enhanced computerized tomography
scans of patients with acute pancreatitis, with application of
specialist interventions for pancreatic necrosis. (a)
Uncomplicated acute edematous pancreatitis(OP) is seen
with perfusion of the pancreatic parenchyma, surrounded
by inammation. (b) Acute necrotizing pancreatitis(NP)
with loss of most of the parenchyma, excepting a small portion in the head and separate small portion of the tail of the
gland. This scan was taken 2weeks into the attack and the
necrosis with associated inammation is diffuse and poorly
localized. (c) More than 4weeks after the onset of acute
pancreatitis in the same patient as in b, the walled- off
necrosis (WON) (designated NC in Figure) has become
localized and walled off close to the posterior wall of the
stomach, making it suitable for endoscopic drainage. (d) In
the same patient as in b, infection has supervened, identied by the presence of radiolucent black gas bubbles within
the collection, which was treated by endoscopic necrosectomy (EN). The endoscopically inserted self- expanding
metal stent between the stomach and necrotic cavity is visible as a radiopaque white ring; ushing the cavity endoscopically every 7–10days was necessary to empty and
allow collapse of the cavity, following which the stent was
removed. (Reprinted from Szatmary etal. [76])
Managing Local Complications
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3 Management ofLocal
Complications: Interstitial
Edematous Pancreatitis
3.1 Acute Peripancreatic Fluid
Collection (APFC)
In general, the vast majority of acute pancreatic
or peripancreatic uid collections resolve spontaneously in the rst few weeks after onset. They
do not require invasive intervention. Drainage of
sterile collections can do harm by introducing
iatrogenic infection [29].
3.2 Pseudocysts
In general, the indication for intervention of pancreatic pseudocysts is determined by the presence of symptoms (e.g., persistent abdominal
pain, anorexia, a new abdominal mass after an
episode of pancreatitis) and/or the presence of
complications (e.g., gastric and/or biliary outlet
obstruction, bleeding, or secondary infection)
[30]. Current guidelines do not recommend intervention based on the diameter of pseudocysts.
When drainage is indicated, it should preferably
be performed 4–6 weeks after onset of disease
because the collection is usually fully encapsulated by then which reduces the risk of procedure
relatedcomplications [20, 31]. The rst choice of
treatment is endoscopic transluminal drainage. If
there is communication with the main pancreatic
duct, additional transpapillary drainageor stenting should be considered. An alternative would be
laparoscopic cystogastrostomy or Roux-en-Y cystojejunostomy, which may required depending on
the location and morphologyof the pseudocyst.
4 Management ofLocal
Complications: Necrotizing
Pancreatitis
The majority of patients with sterile pancreatic
or peripancreatic necrosis can be successfully
treated conservatively, regardless of the size
and extension of the collections. Most acute
necrotic collections will resolve spontaneously
over time. In some cases (e.g., ongoing organ
failure for several weeks, or ongoing [arbitrarily >4–8weeks after onset of pancreatitis]
gastric outlet, intestinal, or biliary obstruction
due to mass effect from large walled-off necrosis), intervention is indicated without the suspicion or documented infection of the necrotizing
pancreatitis [14]. Invasive intervention is generally only indicated in patients who are deteriorating despite the best conservative
management and in whom infected necrosis is
suspected (Fig.2). Clinical decision-making on
timing and type of invasive intervention can be
complex and requires a multidisciplinary team
approach. The different strategies and techniques, as part of a step-up approach, are discussed below and summarized in a treatment
algorithm.
4.1 Investigation forSuspected
Infected Pancreatic Necrosis
Infected pancreatic necrosis can be suspected
based on clinical deterioration (persisting sepsis,
new/prolonged organ failure, increased need for
cardiovascular and/or respiratory and/or renal
support, leukocytosis, elevated or increasing
C-reactive protein [CRP], and fever) despite adequate support, in the absence of an alternative
source of infection [32]. In case of clinical deterioration, we recommend to perform a CT scan to
further investigate the possibility of infection of
the pancreatic necrosis and to evaluate other possible local complications (such as extrapancreatic
necrosis, arterial pseudoaneurysms, venous
thrombosis). On CT, presence of extraluminal
gas in the pancreatic and/or peripancreatic tissues
can be seen as a sign of infection [33]. To formally diagnose infection of the pancreatic necrosis, tissue obtained from percutaneous,
endoscopic, or surgical drainage should test positive for bacteria and/or fungi on Gram stain or
culture.
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ETD/ETN
extension
Peri-gastric/duodenal
collection(s) without deep
H. S. Pauw and H. C. van Santvoort
Necrotizing pancreatitis: either ANC or WONInterstitial pancreatitis
If deterioration:
inflammatory markers)
necrosis (gas), pseudoaneurysms
Maximum supportive treatment, with active patient
monitoring (serial clinical examination for signs of SIRS,
pancreatitis, morphology and extent collections, signs of infected
-CT-scan to diagnose local complications: interstitial or necrotizing
If possible, delay intervention until > 4 weeks (preferably until encapsulation)
even detoriation
Not clinically improving or
Start antibiotics
Suspected* or proven infection
Clinically
stable/improving
+
Ongoing organ failure or
ongoing symptoms due to
Sterile collection(s)
symptoms
Clinically stable/no
APFC
obstruction
extension
Peri-gastric/duodenal
collection(s) with deep
stomach/duodenum
Collections distant from
PCD or ETD ± STE PCD ± STE ETD/ETN and PCD ± STE
If failure
Surgical necrosectomy
(minimally invasive or open)
weeks, or ongoing [arbitrarily >4–8weeks after onset of pancreatitis] gastric outlet,
intestinal, or biliary obstruction due to mass effect from large walled-off necrosis
Abbreviations: ANC acute necrotic collection, WON walled-off necrosis, APFC
acute peripancreatic uid collection, PCD percutaneous catheter drainage, ETD
endoscopic transluminal drainage, STE step-up approach; endoscopic
Ongoing organ failure for several
+
Pseudocyst
- Symptomatic?
Yes No
Drainage Supportive treatment
Fig. 2 Algorithm for managing suspected infected pancreatic necrosis. Denitions
and further explanation: * Infected pancreatic necrosis can be suspected based on
clinical deterioration (persisting sepsis, new/prolonged organ failure, increased need
for cardiovascular and/or respiratory and/or renal support, leukocytosis, elevated or
increasing C-reactive protein [CRP], and fever) despite adequate support, in the
absence of an alternative source of infection.
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