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3 Acute Pancreatitis: Non-surgical Therapies Including Gallstone Management
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37. Mowbray NG, Ben-Ismaeil B, Hammoda M, Shingler G, Al-Sarireh B.The microbiology of infected pancreatic necrosis. Hepatobiliary Pancreat Dis Int. 2018;17(5):456–60.
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43. Lee HS, Lee SK, Park DH, Lee SS, Seo DW, Kim MH, etal. Emergence of multidrug resistant infection in patients with severe acute pancreatitis. Pancreatology. 2014;14(6):450–3.
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51. Tse F, Yuan Y.Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis. Cochrane Database Syst Rev. 2012;(5):CD009779.
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55. Schepers NJ, Hallensleben NDL, Besselink MG, Anten MPGF, Bollen TL, da Costa DW, et al. Urgent endoscopic retrograde cholangiopancreatography with sphincterotomy versus conservative treatment in predicted severe acute gallstone pancreatitis (APEC): a multicentre randomised controlled trial. Lancet. 2020;396(10245):167–76.
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49
Chapter 4
Acute Pancreatitis: Surgical Therapies
OsaidAlser, KanakDas, andEdwinOnkendi

Introduction

According the 2012 Revised Atlanta Classication of Acute Pancreatitis (RACAP), acute pancreatitis is classied based on morphology and computed tomography ndings, as interstitial edematous pancreatitis, where the pancreas shows localized or diffuse enlargement on computed tomography (CT) scans, and necrotizing pan­creatitis where necrosis develops in the pancreatic parenchyma or in the peripancre­atic tissues and appears as non-enhancement on contrast-enhanced CT scans. Acute pancreatitis is further classied based on severity as mild, moderately severe, and severe types [1]. These are:
(a) Mild acute pancreatitis, the most common form (estimated incidence is around
80%), has no associated organ failure, local or systemic complications, and usually resolves with no sequelae in the rst week with medical management only [2, 3].
(b) Moderately severe acute pancreatitis (~15%) is dened as acute pancreatitis
associated with the presence of transient organ failure, local complications or exacerbation of comorbid disease.
(c) Severe acute pancreatitis (SAP) (<5%) is dened as acute pancreatitis associ-
ated with persistent organ failure (>48h).
Local complications as per the RACAP 2012 include the following four entities:
1. Acute peripancreatic uid collection (APFC) occurring in the early phase of interstitial pancreatitis with no dened capsule (Fig.4.1a).
O. Alser · K. Das · E. Onkendi (*) Texas Tech University Health Sciences Center, Lubbock, TX, USA e-mail: Edwin.onkendi@ttuhsc.edu
Switzerland AG 2025 E. P. Ceppa et al. (eds.), The SAGES Manual of Evolving Techniques in Pancreatic Surgery, https://doi.org/10.1007/978-3-031-78409-5_4
51© The Author(s), under exclusive license to Springer Nature
52
O. Alser et al.
a
b
c
Fig. 4.1 Evolution of an acute peripancreatic uid collection (APFC) with time. APFC appears as uid that merges into surrounding peripancreatic, peritoneal, and retroperitoneal tissue plains without clear demarcation (a). The pancreas enhances with contrast suggesting maintained perfu­sion and viability. However, it is still difcult to rule out pancreatic necrosis until after the rst week of onset of pancreatitis pain. The APFC evolves into a pseudocyst by developing a wall of granulation tissue 4 or more weeks later (b). Majority of APFCs and pseudocysts will resolve over time without intervention (c)
2. Pancreatic pseudocyst which is a chronic (usually 4weeks or more) sequelae of APFC from interstitial pancreatitis that has developed encapsulation in the form of a well-dened wall formed from non-epithelialized granulation tissues (Figs.4.1b, 4.1c, 4.2, and 4.3).
3. Acute necrotic collection (ANC) in the early phase before demarcation in necro­tizing pancreatitis (Fig.4.4a, b).
4. Walled-off pancreatic necrosis (WOPN), which represents a mature form of ANC where the necrosis is surrounded by a mature wall of granulation tissue between the necrosis and the surrounding tissues. This mature wall typically develops 4 weeks or more from the onset of pancreatitis (Fig. 4.4c, d) (Table4.1) [46].
APFC and ANC are indistinguishable in the rst week, usually appearing as homogenous enhancements on contrast-enhanced CT images [7]. Distinction between APFC and ANC becomes possible after the rst week of onset once
4 Acute Pancreatitis: Surgical Therapies
Dilated pancreatic duct
Dilated pancreatic duct
Dilated pancreatic duct
Pseudocyst
Fig. 4.2 Coronal and sagittal CT scan images showing a peripancreatic uid collection 7weeks after onset of pancreatitis. The uid collection is extrapancreatic with pressure effects on the proxi­mal pancreatic duct and the duodenum. The main pancreatic duct is dilated
53
necrosis becomes conuent and demarcated. The distinction between these two is important since APFC is usually self-limited, resolving spontaneously over time (Fig.4.1), and therefore supportive measures alone usually sufcient [8, 9]. Since both pseudocyst and WOPN represent mature forms of acute pancreatitis complica­tions, the distinction is usually easier than APFC and ANC.In contrast to a pseudo­cyst, WOPN contains necrotic pancreatic parenchyma or necrotic fat which appears as solid heterogeneous density within the walled-off cavity on imaging. The ability to differentiate between these pathologies is extremely important since it guides decision-making about their management. The majority of pancreatic uid collec­tions (acute and chronic) remains asymptomatic and resolve spontaneously over time, and therefore do not require any intervention. About 25% become symptom­atic or infected, which necessitates intervention. Any of the above pancreatitis­related collections and complications can be sterile or secondarily infected (Fig. 4.5a–d). Collections that contain solid material are more likely to become infected (i.e., ANC and WOPN) [10]. Infection can be suggested by clinical criteria with signs and symptoms of sepsis as well as on contrast-enhanced CT images by the presence of gas bubbles, which are produced by gas-forming organisms, or from
54
O. Alser et al.
a
Infracolic Pseudocyst
cd e
Pseudocyst Cavitotomy
Fig. 4.3 Intraoperative photos showing the extrapancreatic infracolic pseudocyst (a). Intraoperative ultrasound shows no intracystic solid tissue (b), and this is conrmed by cystic drainage through a cavitotomy (c), with no solid debri found in the cyst cavity (d). A cystojejunostomy is then per­formed for internal drainage (e)
b
Pseudocyst on intraoperative
Pseudocyst
Cavity
US
Cystojejunostomy
stulization into the alimentary tract [11, 12]. Interestingly, SIRS can serve as an early predictor of acute pancreatitis severity and mortality. However, SIRS may result from the development of superimposed infection of pancreatic and/or peri­pancreatic collections [13, 14]. One must differentiate between pure pancreatitis­induced SIRS response and the development of superimposed infection on a pancreatic or peripancreatic collection, which can be difcult especially early in the course (the rst 2weeks from onset of pain) of acute pancreatitis. As we discuss below, the management of these complications requires a multidisciplinary team approach involving gastroenterologists, surgeons (including general surgeons and specialist acute care and hepatopancreatobiliary surgeons), interventional radiolo­gists, infectious disease specialists, etc. The 2012 revised Atlanta classication is summarized in Table4.1 below.
4 Acute Pancreatitis: Surgical Therapies
a b
c
55
d
Fig. 4.4 (a–d) Evolution of pancreatic necrosis. Contrast-enhanced CT 2weeks after onset of pancreatitis pain showing non-enhancement of the pancreatic body and tail due to conuent necro­sis (a). This transforms into an acute necrotic collection 3weeks after onset of pancreatitis pain (b). Patient was discharged asymptomatic. She returned 10weeks after onset of pancreatitis pain, with abdominal pain, nausea, and emesis, and CT showed that the ANC had evolved into a pre­dominantly intraabdominal, 17cm walled-off pancreatic necrosis with local compressive features (c). This was misinterpreted as a pancreatic pseudocyst, and patient underwent endoscopic ultra­sound (EUS)-guided cystogastrostomy (d). EUS, however, showed solid component (necrotic tis­sue) in the collection
56
Chronic peripancreatic collection
(4weeks after onset of pain)
Pancreatic pseudocyst
Homogenous uid density
A well-dened wall, pseudocapsule
Fully encapsulated by a thick wall that demarcates it from surrounding
tissue and structures
Extra-pancreatic with no associated necrosis
No solid tissue in the cavity
Walled-off pancreatic necrosis (WOPN)
Intra-pancreatic with pancreatic parenchymal necrosis with/without
O. Alser et al.
peripancreatic extension of necrosis
Heterogeneous density, with solid component (necrosis)
A well-dened wall completely encapsulates the necrosis, separating it
from the surrounding tissues and structures
Can be sterile or infected
Acute peripancreatic collection
(<4weeks after onset of pain)
Homogenous uid density
No solid or necrotic tissue component
Merges into the peripancreatic tissue planes with
NO clear demarcated encapsulation
No associated pancreatic necrosis
No intra-pancreatic involvement
Types of acute pancreatitis
Table 4.1 Types of acute pancreatitis and its complications. (Adapted from the 2012 Revised Atlanta Classication of Pancreatic and Peripancreatic Fluid
Collections)
Interstitial edematous (85%) Acute peripancreatic uid collection (APFC)
Intra-pancreatic with pancreatic parenchymal
necrosis and/or peripancreatic extension of
necrosis
Heterogeneous density, with solid component
(necrosis)
Not encapsulated yet and no demarcation from
Necrotizing (10%) Acute necrotic collection (ANC)
surrounding tissues and structures
Can be sterile vs. infected
APFC acute peripancreatic uid collection, ANC acute necrotic collection, WON walled-off necrosis