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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

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M. Hernandez et al.
Most choledochal cysts are diagnosed in childhood, yet nearly 25% can be
detected during adulthood. Choledochal cysts are more common in females compared to males with the ratios being as high as 4:1 or 3:1 [56]. Choledochal cysts are
classied according to location within the biliary tree and have been described previously by Todani etal. Patients who have a choledochal cyst often will report nonspecic and vague symptoms such as abdominal pain [57]. Biliary cystic dilation
complications due to local compression can include pancreatitis, cholangitis, secondary biliary cirrhosis, spontaneous rupture, and increase the risk of
cholangiocarcinoma.
Choledochal cysts can be categorized into ve types [54, 57]. Type I represents
about 50 to 80% of all choledochal cysts, type II 2%, type III 1 to 4%, type IV
15–30%, type V 20%. Type I choledochal cyst can be classied into three additional
phenotypes. Type Ia is a cystic dilation of the entire extrahepatic biliary tree that
does not involve the intrahepatic ducts. Often the gallbladder and cystic duct will
arise from a dilated common bile duct. Type Ib represents a focal segmental dilation
of the extrahepatic biliary tree. Type Ic represents a fusiform dilation of the entire
extrahepatic biliary tree that involves an intrahepatic duct. Type II choledochal cysts
are a saccular diverticulum on the common bile duct. Type III choledochal cysts are
also called choledochoceles, and these represent a cystic dilation of the intramural
portion of the distal common bile duct that often will bulge into the duodenum. Type
IV includes types IVa and IVb. Type IVa is the second most common choledochal
cyst and it is represented by an intrahepatic and extrahepatic dilation of the biliary
ducts. Type IVb represents multiple dilations of only the extrahepatic biliary tree.
Type V choledochal cyst, also known as Caroli’s disease, represents multiple dilations of the intrahepatic biliary ducts. This anatomic anomaly is often associated
with congenital hepatic brosis which can present with cirrhosis and is termed
Caroli’s syndrome [58].
The etiology of choledochal cysts is an ongoing debate with both congenital and
acquired proposed mechanisms. The most common is Babbitt’s theory where choledochal cysts are thought to be due to an aberrant pancreaticobiliary ductal junction
[59]. This manifests as the pancreatic duct joining the bile duct 1–2cm proximal to
the sphincter of Oddi. This length of a common channel can vary between 10 and
45mm. A long common channel allows pancreatic juice to reux into the biliary
tree which increases intraluminal pressure and can in theory result in ductal dilation
[60]. This is supported in that there is often a high amylase concentration within the
bile samples of patients with choledochal cysts [60]. Further pancreatic enzyme
reux can lead to inammation, epithelial breakdown, dysplasia, and subsequently
malignancy. Despite this proposed mechanism, the long common channel is only
observed in about 50–80% of patients with choledochal cysts. Another theory is due
to obstruction of the distal common bile duct. Sphincter of Oddi dysfunction can
predispose to the development of choledochal cysts.
Because most choledochal cysts present in childhood and about 25% will present
in adulthood, it is important to recognize a set of classic symptoms. Often there is a
triad which includes abdominal pain, palpable abdominal mass, and jaundice. This

11 Benign, Premalignant, andMalignant Duodenal Neoplasms
183
is seen altogether in about <20% of all cases. In children, 85% will have these two
features of the triad whereas in adults only 25% will present with at least two features of the triad.
Due to chronic inammation and subsequent bile stasis, stones and infections
can develop. This can manifest in ascending cholangitis and obstructive jaundice.
The symptoms of this include abdominal pain and fever. Chronic inammation
especially along the distal common bile duct can cause pancreatitis. Secondary biliary cirrhosis can be due to chronic biliary obstruction. There is an increased risk for
malignancy in patients with choledochal cysts. The incidence of developing malignancy varies between 2% and 18% [61]. In a series of 38 adult patients this was
reported to be as high as 21%. The incidence of malignancy increases with age [62].
Malignancy is often observed in the extrahepatic ducts and about 50–60% of
patients, gallbladder in about 30–50% of patients, intrahepatic biliary ductal malignancies in about 2% of patients, and about <1% of patients with liver and pancreas
malignancies [62].
Clinical investigation should be performed using imaging as well as liver function tests, serum amylase and lipase levels, INR and complete blood count to evaluate for obstructive jaundice or pancreatitis kidney function and altered coagulation
proles. Tumor biomarkers can be obtained including a CA 19–9in patients who
have suspicion for malignancy.
Diagnostic workup using imaging should be performed to assist with operative
planning and complete excision of all choledochal cysts. Abdominal ultrasound is
often a rst step. Sensitivity of ultrasound is about 70–97% [63]. Ultrasounds can
also be used for postoperative surveillance [64]. In addition to an ultrasound, contrasted MRI and MRCP can be used to delineate biliary anatomy [65]. HIDA scans
can be used and have a sensitivity of 100% for type I choledochal cyst, meanwhile
the sensitivity diminishes for the other types [66]. Computed tomography is highly
accurate and can be used to help delineate arterial and vascular anatomy assisting in
surgical planning [65]. CT scans can also be utilized to estimate cyst wall thickening which can be seen in malignancy. ERCP is extremely sensitive and diagnostic
for choledochal cysts; the sensitivity decreases in patients who have developed considerable inammation and scarring over time. ERCP is an invasive technique
which can potentially cause cholangitis and pancreatitis [67]. MRCP is still considered the gold standard for diagnosis as the sensitivity is as high as 90 to 100%
MRCP also avoids ionizing radiation and is noninvasive compared to ERCP [65].
MRCP can also be used with MRI imaging to evaluate surrounding vascular anatomy, presence of biliary sludge or stones and malignancies.
Management of choledochal cysts has changed considerably over time. Several
decades ago, initial management consisted of a cyst enterostomy. However, this was
associated with recurrence of symptoms and a high risk of malignancy within the
remaining in situ cyst wall several decades later. There was an observed malignancy
rate of nearly 30% in patients who had previously undergone a cyst enterostomy for
the management of a choledochal cyst [62]. Complete excision of the biliary cyst
was then recommended and reconstructed or diverted biliary tree was subsequently

184
M. Hernandez et al.
needed. Biliary diversion can be performed using a hepaticoduodenostomy or
hepaticojejunostomy.
Complete excision of the cyst followed by Roux-en-Y hepaticojejunostomy is
the standard of choice for the treatment of most choledochal cysts. This procedure
can be performed via the open, laparoscopic, or robotic approach. Long-term surveillance and outcomes are dependent on complete cyst excision and appropriate
surveillance.
Duodenal Lymphoma
Duodenal follicular lymphomas are often found incidentally [68]. Often upper
endoscopic surveillance is performed for another reason and patients who have low
stage follicular lymphomas often do not have overt clinical symptoms [68]. If the
patient presents with symptoms it is often vague with abdominal pain. The mean
age at diagnosis is 65years [68]. There is no difference between male and female.
Most commonly the second portion of the duodenum is involved.
At the time of endoscopy, a duodenal follicular lymphoma can be found as either
a solitary or multiple nodular masses [69]. These can present as a polypoid lesion,
and they are usually between 1 and 5mm in size. As the masses grow, they can
become ulcerated which can make endoscopic sampling easier. Multifocal disease
is not uncommon with lesions located elsewhere in the jejunum or ileum [70]. On
histologic evaluation, most follicular lymphomas of the duodenum are low grade
[71]. On microscopy, these appear as well-circumscribed germinal centers with no
visible macrophages and without mantle cell zones. Sheets of lymphoid cells that
contain irregular nuclei are often present, and the lymphoma will involve the mucosa
and submucosa [70]. The immunophenotype is similar to other low-grade follicular
lymphomas and these will express CD20, CD10, BCL–6, BCL–2 and lack expression for CD5, CD23, CD43, BCL–1, and T-cell markers [72]. Often these lymphomas will have a low Ki-67 rate [72].
The classic genetic aberration often found is a translocation (14; 18)(q. 32; q. 21)
for the genes of the immunoglobulin heavy chain and B-cell leukemia lymphoma
[72]. Duodenal follicular lymphoma has a pathogenesis that is often related to
repeat inammation and antigen stimulation and shares some similarities with
mucosa-associated lymphoid tissue (MALT) lymphomas [73]. Differential diagnosis includes MALT lymphoma, chronic lymphocytic leukemia, mantle cell lymphoma, and gastrointestinal involvement by systemic follicular lymphoma [74].
Duodenal follicular lymphomas often have a good prognosis with median survival exceeding 12years [75]. The only treatment for this is chemotherapy. Patients
who have limited stage follicular lymphomas within the duodenum can also be
treated with radiation therapy [76, 77]. This is associated with a good overall outcome as relapse impacts subsequent outcomes. Even though treatment with radiotherapy to the duodenal lymphoma is quite successful most patients will not undergo
treatment initially [78]. There is an option to watch and wait which has also been

11 Benign, Premalignant, andMalignant Duodenal Neoplasms
185
demonstrated to be effective as well. Other approaches for early stage disease consist of rituximab with chemotherapy, rituximab alone, combined modality therapies,
or a variety of other systemic therapies [78].
Conclusion
Duodenal lesions span the spectrum of benign, premalignant, and malignant etiologies. Their presentation is often as obstruction, bleeding, or pain and their treatment
is primarily endoscopic or surgical resection when appropriate.
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M. Hernandez et al.

Chapter 12
Endoscopic Duodenal Resection
CatherineVozzo andAshleyFaulx
Introduction
Endoscopic duodenal resection of lesions and polyps is a complex topic. This is due
to the variety of pathology encountered in the duodenum, their proximity to the
ampulla, and the unique anatomical considerations within the duodenum including
its robust blood supply, thin muscle layer, and scope positioning. In addition, the
management of lesions will vary depending on the presence or absence of polyposis
syndromes [1]. Careful consideration and thought must be given to each case prior
to scheduling a patient for endoscopic resection.
Pre-procedural Considerations
Pre-procedural discussion will include thorough discussion of risks, benets, and
alternatives to the procedure. The patient’s comorbidities, surgical history, and medications should be reviewed prior to the procedure. Anticoagulant and antiplatelet
agents should be held according to society guidelines based on risk of bleeding [2].
The sedation plan should be discussed with the patient and anesthesiologist (if
applicable).
C. Vozzo · A. Faulx (*)
Division of Gastroenterology, University Hospitals of Cleveland, Case Western Reserve
University School of Medicine, Cleveland, OH, USA
e-mail: catherine.vozzo@uhhospitals.org; Ashley.faulx@uhhospitals.org
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_12
189© The Author(s), under exclusive license to Springer Nature

190
C. Vozzo and A. Faulx
Indications
Careful endoscopic evaluation should take place prior to resection of any lesion.
The lesions may appear mucosal or subepithelial. The lesion’s proximity to the
ampulla should be noted because endoscopic resection technique is vastly different
if the lesion is considered ampullary or non-ampullary. Finally, the patient’s medical history should be evaluated for genetic polyposis syndromes as the management
of a sporadic duodenal polyp will differ from a patient with familial adenomatous
polyposis or MUTYH-associated polyposis. As discussed in Chap. 11, some duodenal lesions may harbor malignant potential, whereas others are benign. Lesions
should be considered for resection if they are pre-malignant or if they are symptomatic, such as bleeding or obstruction [1]. Lesions with malignant potential include
gastrointestinal stromal tumors, carcinoids, solitary Peutz-Jeghers polyps, leiomyomas, and adenomas. Benign lesions include lipomas, gastric metaplasia, inammatory polyps, and Brunner’s glands or hamartomas (Fig.12.1) [1, 3].
Table 12.1 outlines a suggested broad approach for various polyps encountered
in the duodenum. However, the remainder of this chapter will primarily focus on
resection of ampullary and non-ampullary adenomas.
Endoscopic Assessment ofNon-ampullary Adenomas
Detection and characterization of duodenal polyps can be challenging because the
duodenum is a xed structure in the retroperitoneum. Distal attachment of a cap to
the endoscope may improve stability, allow for better visualization of the papilla,
and identify polyps in between folds [4]. It may be necessary to utilize a
Fig. 12.1 Previously
bleeding duodenal polyp in
second portion of the
duodenum, marked with
clip and tattoo, pathology
ultimately positive for
Brunner’s gland
hamartoma

12 Endoscopic Duodenal Resection
Table 12.1 Approach by polyp type
Polyp type Resection approach
Non-ampullary
adenomas
Ampullary adenomas Endoscopic retrograde cholangiopancreatography and endoscopic
Brunner’s gland
hamartoma
Gastric heterotopia No intervention required. Consider H pylori testing
Inammatory broid
polyp
Lipoma Cold snare polypectomy only if symptomatic
Carcinoid If no evidence of invasion of the muscularis layer and 1cm or less in
Gastrointestinal
stromal tumors
Solitary PeutzJeghers polyp
Table modied from Culver and Mcintyre [3]
<6mm in size: Cold snare polypectomy
>6mm in size: Endoscopic mucosal resection (EMR) technique
ultrasound to assess extension with endoscopic papillectomy
Cold snare polypectomy or EMR only if symptomatic
Cold snare polypectomy or EMR only if symptomatic
size can be removed via EMR
Endoscopic ultrasound-guided FNB for diagnostic purposes, but in most
cases endoscopic resection is not considered (refer to GI surgeon)
Cold snare polypectomy
191
Table 12.2 Paris
classication (Major variants
of type 0 neoplasia)
0-Ip Protruded, pedunculated
0-Is Protruded, sessile
0-IIa Slightly elevated
0-IIb Flat
0-IIc Supercial, shallow, depression
0-III Excavated (ulcer)
Table adapted from Ref. [6]
side- viewing endoscope to clearly outline the location of the polyp in relation to the
papilla and should be photo documented prior to intervention [5]. The polyp’s macroscopic appearance is typically milk white or reddish mucosa. Once the polyp is
identied, tumor size should be estimated with an open biopsy forceps or snare.
Inspection using high-denition white light endoscopy and denition should be provided according to the Paris classication (Table12.2) [7]. Endoscopic example of
a non-ampullary duodenal adenoma is seen in Fig.12.2.
Histologic assessment varies depending on the region of the world in which you
are practicing. When magnifying endoscopy with narrow-band imaging is available,
biopsy of the lesion may not be necessary. This technique, not available in the
United States, may distinguish neoplastic from non-neoplastic lesions in addition to
low- and high-grade dysplasia [8, 9]. Features concerning for advanced histology
include the size of the adenoma larger than 1cm, the degree of involved mucosal
circumference, and relation to the ampulla. Features concerning for submucosal
invasion are Paris IIc, surface ulceration, and non-lifting after submucosal injection
(Fig.12.3). The role of EUS in small duodenal adenomas is minimal but may impact
the management of polyps <2cm, or in cases where metastases are noted [5].
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