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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_734_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Disclaimer
- •Contents
- •Contributors
- •Embryology
- •Lymphatics
- •Nerves
- •Clinically Relevant Anatomic Variations
- •Duodenum Inversum
- •Pancreas Divisum
- •Annular Pancreas
- •Ectopic Pancreas
- •Ansa Pancreatica
- •Pancreaticobiliary Maljunction
- •Duplication Anomalies
- •Physiology
- •Duodenal Physiology
- •Mechanical Function
- •Endocrine Function
- •Pancreatic Physiology
- •Exocrine Physiology
- •Normal Anatomy
- •Duodenal Anatomy
- •Pancreatic Anatomy
- •Ductal Anatomy
- •Vasculature
- •Endocrine Physiology
- •References
- •Etiology
- •Pathophysiology
- •Diagnosis
- •Clinical Presentation
- •Laboratory Tests
- •Imaging
- •Medical Management
- •Fluid Resuscitation
- •Analgesics
- •Prophylactic Antibiotics
- •Nutrition
- •Complications
- •Long-Term Sequelae of Acute Pancreatitis
- •References
- •Introduction
- •Initial Treatment
- •Reducing Severity of Acute Pancreatitis
- •Fluid Resuscitation
- •Pain Management
- •Nutrition
- •Preventing Infectious Complications
- •References
- •Introduction
- •Sterile Pancreatic Necrosis
- •Antibiotic Therapy
- •Catheter Drainage
- •Video-Assisted Retroperitoneal Drainage (VARD) Procedure
- •Sinus Tract Necrosectomy
- •Open Necrosectomy
- •Open Trans-Gastric Cystogastrostomy
- •Disconnected Distal Pancreatic Duct Syndrome
- •Introduction
- •References
- •Introduction
- •Venous Thrombosis
- •Intra-Abdominal Hypertension
- •Thoracic Complications
- •Gastrointestinal Complications
- •References
- •Pain
- •Endocrine Dysfunction
- •Exocrine Dysfunction
- •Conclusion
- •References
- •Background
- •Postoperative Care
- •References
- •Background
- •Head-Dominant Disease
- •Tail-Dominant Disease
- •Perioperative Management
- •Procedure Steps
- •Open Whipple
- •MIS Whipple
- •Open Distal Pancreatectomy
- •MIS Distal Pancreatectomy
- •Pearls
- •References
- •Introduction
- •Procedures
- •Indications
- •Contraindications
- •Preoperative Workup
- •Pediatrics
- •Patient Selection
- •Contraindications
- •Key Steps
- •Common Steps
- •Pitfalls/Tricks
- •Local Complications
- •Systemic Complications
- •References
- •History/Introduction
- •Indications
- •Adults
- •Procedural Aspects
- •Preoperative Care
- •Total Pancreatectomy
- •Islet Infusion
- •Minimally Invasive Surgery (MIS)
- •Postoperative Care
- •Outcomes
- •Perioperative Data
- •Perioperative Complications
- •Endocrine Function
- •References
- •Introduction
- •Duodenal Adenomas
- •Duodenal Adenocarcinomas
- •Duodenal Neuroendocrine Tumors (D-NETs)
- •Other Non-neoplastic Epithelial Lesions
- •Duodenal Gastrointestinal Stromal Tumors (DGISTs)
- •Leiomyoma
- •Lipoma
- •Choledochal Cysts
- •Duodenal Lymphoma
- •Conclusion
- •References
- •Introduction
- •Pre-procedural Considerations
- •Indications
- •Resection Techniques
- •Sporadic Non-ampullary Adenomas: Cold Snare Polypectomy
- •Sporadic Non-ampullary Adenomas: EMR
- •Sporadic Non-ampullary Adenomas: ESD
- •Sporadic Non-ampullary Adenomas: Full-Thickness Resection Device
- •Ampullary Adenomas: Endoscopic Papillectomy
- •Sporadic Non-ampullary Adenomas: Cold Snare Polypectomy
- •Sporadic Non-ampullary Adenomas: EMR
- •Endoscopic Papillectomy
- •Surveillance
- •References
- •Introduction
- •Benign Tumors
- •Genetic Syndromes
- •Pre-Malignant Tumors
- •Low-Grade Malignancies
- •Alternatives
- •Inclusion Criteria
- •Preoperative Planning
- •Open Transduodenal Ampullectomy
- •Minimally Invasive (Robotic-Assisted) Transduodenal Ampullectomy
- •Outcomes
- •Conclusions
- •References
- •Introduction
- •Anatomy
- •Laparoscopic Segmental Duodenectomy
- •Robotic Segmental Duodenectomy
- •Technique
- •Open Segmental Duodenectomy
- •Patient Positioning
- •Technique
- •Conclusion
- •References
- •Overview
- •Intraductal Papillary Mucinous Neoplasm (IPMN)
- •General Concepts
- •Novel Biomarkers
- •DNA-Based Biomarkers
- •MiRNA
- •Protein-Based Biomarkers
- •IPMNs
- •MCNs
- •SCNs
- •SPTs
- •Guidelines
- •Surveillance Discontinuation
- •Follow-Up Strategy
- •The Verona Policy
- •Conclusions
- •References
- •Introduction
- •Pathophysiology
- •Work-Up
- •Tissue Diagnosis
- •Serum Tumor Markers
- •Multidisciplinary Decision-Making
- •Adjuvant Trials
- •Systemic Chemotherapy
- •Chemoradiation
- •Neoadjuvant Trials
- •Chemotherapy
- •Chemoradiation
- •Pancreatectomy
- •Summary
- •References
- •Introduction
- •Diagnosis
- •Imaging
- •Functionality
- •Insulinoma
- •Gastrinoma
- •VIPoma
- •Glucagonoma
- •Staging/Surgical Decision-Making
- •Nonmetastatic Disease
- •Metastatic Disease
- •Multidisciplinary Decision-Making
- •Surgical Resection
- •Systemic Treatments
- •Open Trials
- •Surveillance
- •References
- •Renal Cell Carcinoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Outcome
- •Colorectal Carcinoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Prognosis
- •Melanoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Prognosis
- •Sarcoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Prognosis
- •Conclusion
- •References
- •Preoperative Considerations
- •Key Steps
- •Staging Laparoscopy
- •Specimen Removal
- •Vascular Resection
- •Reconstruction
- •Pancreaticojejunostomy
- •Hepaticojejunostomy
- •Gastro- or Duodeno-Jejunostomy
- •Final Steps
- •References
- •Randomized Controlled Trials
- •Surgical Technique
- •Resection Phase
- •Reconstruction Phase
- •Postoperative Course
- •Conclusions
- •References
- •Introduction
- •Preoperative Workup
- •Preoperative Planning
- •Surgical Management
- •Patient Preparation
- •Surgical Steps
- •Step 1: Kocher Maneuver
- •Step 4: Pancreatic Transection
- •Reconstruction
- •Hepaticojejunostomy
- •Pancreaticojejunostomy
- •Duodenojejunostomy
- •References
- •Introduction
- •Preoperative Planning
- •Diagnostic Laparoscopy
- •Radical Antegrade Modular Pancreatosplenectomy (RAMPS)
- •Splenic Vein Stump Length
- •Ligamentum Teres/Falciform Pedicle Flap
- •References
- •History
- •Early Exploration
- •Trends Over Time
- •Morbidity
- •Safety
- •Oncologic Safety
- •Preoperative Planning
- •Clinical Considerations
- •Anatomical Considerations
- •Surgical Technique
- •Conclusion
- •References
- •Introduction
- •Indications
- •Preoperative Testing
- •Operative Approach
- •Peritoneal Access
- •Specimen Extraction
- •Closure
- •Clinical Outcomes
- •Conclusions
- •References
- •Introduction
- •Preoperative Preparation
- •Key Shared Operative Steps
- •Trocar Placement
- •Splenic Flexure Mobilization
- •Pancreas Mobilization
- •Identify Pancreatic Pathology
- •Pancreatic Transection
- •Splenic Vein Dissection
- •Splenic Artery Dissection
- •Conclusion
- •References
- •Introduction
- •Historical Evolution
- •Perioperative Outcomes
- •Oncologic Outcomes
- •Neoadjuvant Therapy
- •Preoperative Adjuncts
- •Preoperative Coiling
- •Aortic Stenting
- •Robotic DP-CAR Surgical Technique
- •Positioning
- •Port Placement
- •Surgical Steps
- •Perioperative Care
- •Conclusion
- •References
- •Introduction
- •Preoperative Considerations
- •Laparoscopic Enucleation
- •Patient Positioning
- •Procedure
- •Robotic Enucleation
- •Patient Positioning
- •Procedure
- •Open Enucleation
- •Postoperative Management
- •Postoperative Outcomes
- •References
- •Introduction
- •Indications
- •Preoperative Assessment
- •Serologic Testing
- •Surgical Management
- •Patient Preparation
- •Diagnostic Laparoscopy
- •Surgical Steps
- •Step 1: Gastric Mobilization
- •Step 2: Pancreatic Resection
- •Step 3: Reconstruction
- •Jejunojejunostomy
- •Pancreaticojejunostomy
- •Discussion
- •References
- •Introduction
- •Biliary Obstruction
- •Endoscopic Interventions
- •Plastic Versus Metal Stents
- •Covered Versus Uncovered Metal Stents
- •Stent Obstruction
- •Surgical Options
- •Endoscopic Versus Surgical Intervention
- •Duodenal Obstruction
- •Duodenal Stents
- •Venting Percutaneous Gastrostomy Tubes (PEG)
- •Surgical Gastrojejunostomy (Duodenal Bypass)
- •Endoscopic Versus Surgical Intervention
- •Abdominal Pain
- •Celiac Plexus Neurolysis
- •Surgical Celiac Plexus Block
- •Summary
- •References

46
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49

Chapter 4
Acute Pancreatitis: Surgical Therapies
OsaidAlser, KanakDas, andEdwinOnkendi
Introduction
According the 2012 Revised Atlanta Classication of Acute Pancreatitis (RACAP),
acute pancreatitis is classied 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 classied 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 dened 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 dened as acute pancreatitis associ-
ated with persistent organ failure (>48h).
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 dened 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 difcult 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 4weeks or more) sequelae of
APFC from interstitial pancreatitis that has developed encapsulation in the form
of a well-dened 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)
(Table4.1) [4–6].
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 7weeks
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 conuent 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 sufcient [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 conrmed 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 difcult especially early in the
course (the rst 2weeks 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 classication is
summarized in Table4.1 below.

4 Acute Pancreatitis: Surgical Therapies
a b
c
55
d
Fig. 4.4 (a–d) Evolution of pancreatic necrosis. Contrast-enhanced CT 2weeks after onset of
pancreatitis pain showing non-enhancement of the pancreatic body and tail due to conuent necrosis (a). This transforms into an acute necrotic collection 3weeks after onset of pancreatitis pain
(b). Patient was discharged asymptomatic. She returned 10weeks after onset of pancreatitis pain,
with abdominal pain, nausea, and emesis, and CT showed that the ANC had evolved into a predominantly intraabdominal, 17cm 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
(≥4weeks after onset of pain)
Pancreatic pseudocyst
Homogenous uid density
A well-dened 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-dened wall completely encapsulates the necrosis, separating it
from the surrounding tissues and structures
Can be sterile or infected
Acute peripancreatic collection
(<4weeks 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 Classication 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
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