Pancreatic Cancer, Cystic Neoplasms and Endocrine Tumors: Diagnosis and Management

By Hans G. Beger, John P. Neoptolemos and Michael G. Sarr

Pancreatic Cancer, Cystic Neoplasms and Endocrine Tumors: Diagnosis and Management is a modern, expertly crafted and clinically focused guide to the diagnosis, management and best-practice care of patients suffering from pancreatic cancer, cystic neoplasms and endocrine tumours.

Packed with outstanding figures and with reference to the leading society guidelines, its main focus is on the many endoscopic and radiologic diagnostic techniques, medical and surgical management of both full-blown cancer and other tumors, and the risks of each form of treatment.  Also covered in detail are issues of tumor recurrence and long-term outcome of treatment.

Brought to you by highly skilled national and international leaders in the specialty and an experienced editor team, this is an invaluable guide to practicing gastroenterologists and surgeons in the hospital and clinical environment, as well as oncologists and endocrinologists managing patients with pancreatic tumorous lesions.

• Language: English
• Publisher: Wiley
• Release date: Feb 26, 2015
• ISBN: 9781118307830

Book preview

Table of Contents

Title page

Copyright page

Contributors

Preface

Abbreviations

PART I: Ductal Adenocarcinoma of the Pancreas

CHAPTER 1: Histologic Classification and Tumor Staging of Pancreatic Cancer

Histologic Classification of Pancreatic Ductal Neoplasms

Tumor Staging

References

CHAPTER 2: What We Know about Carcinogenesis of Ductal Adenocarcinoma of the Pancreas

Pancreatic Cancer Cell

Pancreatic Cancer Stem Cells

Tumor Stroma Cells

References

CHAPTER 3: Familial Cancer of the Pancreas

Introduction

Definition

Phenotype

Pathology

Genetic Background

Genetic Counselling and Testing

Screening

Conclusion

References

CHAPTER 4: Clinical, Laboratory, and Radiologic Presentation of Pancreatic Cancer

Clinical Presentation

Laboratory Investigations

Radiologic Investigations

References

CHAPTER 5: Standards of Oncologic Pancreatic Surgery

Overview

Preoperative Considerations

Goals of Surgical Treatment

Operative Techniques

Minimally Invasive Pancreatic Resections

Postoperative Course, Complications, and Adjuvant Treatment

Conclusion

References

CHAPTER 6: Extended Resection for Pancreatic Cancer: Risks and Benefits

Introduction

History of Portal Vein Resection

Diagnosis of Cancer Invasion of the Portal Vein

Indications for Portal Vein Resection

Isolated Pancreatoduodenectomy with Portal Vein Resection

Mesenteric Approach

Catheter Bypass of the Portal Vein

Portal Vein Resection and Reconstruction

Postoperative Mortality at Nagoya University Hospital

Long-Term Survival Following Portal Vein resection

References

CHAPTER 7: Risk/Benefit of Total Pancreatectomy for Pancreatic Cancer: Are There Indications?

Historical Notes

Benefits Versus Disadvantages

New Indications

Modified Surgical Techniques

Re-Resection for Recurrent Cancer

Results of Total Pancreatectomy

Conclusion

References

CHAPTER 8: Is there a benefit from additional arterial resection of ductal cancer of the pancreas?

Introduction

Arterial Resection in Pancreatectomy Following Preoperative Chemotherapy or Chemoradiotherapy

Distal Pancreatectomy with Resection of the Celiac Axis

References

CHAPTER 9: Who benefits from ultraradical pancreatic cancer resection?

Introduction

Lymphadenectomy for Pancreatic Head Cancer

Extrapancreatic Nerve Plexus Excision

Vascular Resection

Multivisceral Resection

Randomized Controlled Trials of Standard Versus Extended Lymphadenectomy in Radical Pancreatoduodenectomy

References

CHAPTER 10: Risk and Results of Pancreatic Cancer Resection

The Appropriate Patient and the Appropriate Clinic—Probably the Most Important Presupposition of Successful Pancreatic Surgery

General and Specific Surgical Aspects of Operative and Perioperative Measures to Reduce Complications

Complications and Their Management after Pancreatic Surgical Procedures

References

CHAPTER 11: Pancreatic Cancer: The Role of Bypass Procedures

Obstructive Jaundice

Gastric Outlet Obstruction

Laparoscopic Palliation in Selected Patients

Bypass Versus Palliative REsection

Conclusion

References

CHAPTER 12: Evidence of Adjuvant Chemotherapy of Ductal Pancreatic Cancer

Introduction

Rationale for Adjuvant Chemotherapy

Randomized Controlled Trials of Adjuvant Chemotherapy

Evidence of Adjuvant Chemoradiotherapy

Randomized Controlled Trials of Adjuvant Chemoradiation

Rationale for Adjuvant Combination Therapy

Randomized Controlled Trials of Adjuvant Combination Therapy

Meta-Analyses

Conclusions

Future Directions

References

CHAPTER 13: Neoadjuvant Chemotherapy and Radiochemotherapy: Is There a Survival Advantage for Pancreatic Cancer Patients?

Introduction

Surgery First Followed by Adjuvant Therapy: Overview of Clinical Trials, Lack of Progress, and Reasons Why

Surgery after Induction therapy: pros and Cons of the Neoadjuvant Approach

Importance of Accurate Pretreatment Staging: Eligibility for Clinical Trials Must Be Standardized

Neoadjuvant Therapy for Resectable Pancreatic Cancer: Evidence in Support of a Survival Advantage

Neoadjuvant Treatment Schemas for Resectable Disease: Current Recommendations from the Medical College of Wisconsin

Neoadjuvant Therapy for Borderline Resectable Pancreatic Cancer: Consensus Has Developed in Support of this Approach

Neoadjuvant Treatment Schemas for Borderline Resectable Disease: Current Recommendations from the Medical College of Wisconsin

Pretreatment Molecular Diagnostics as a Guide to Neoadjuvant Therapy: Is the Future Now?

Conclusions

References

CHAPTER 14: Standards of Palliative Chemotherapy and Chemoradiotherapy of Local Advanced Pancreatic Cancer, Side Effects, and Survival Benefits

Introduction

Locally Advanced PC: Palliative Chemoradiotherapy

Locally Advanced PC: Palliative Chemotherapy

References

CHAPTER 15: Management of Local and Distant Recurrence after Pancreatic Cancer Resection

Introduction

Rate and Site of Recurrence after Pancreatic Resection

Management of Local Recurrence

Management of Distant Recurrence

Conclusion

References

CHAPTER 16: Survival 3, 5, and 10 years after adjuvant regional and neoadjuvant chemotherapy in resectable pancreatic cancer patients: an institutional experience

Introduction

Actual 3- and 5-Year Survival after Pancreatic Cancer Resection

Patients Who Survived More Than 5 Years postoperatively

Comment

References

CHAPTER 17: Nonductal Primary Malignancies of the Pancreas: Acinus Cell Carcinoma

Introduction

Clinical Presentation

Diagnostic Investigations

Treatment

Conclusion

References

CHAPTER 18: Nonductal Primary Malignancies of the Pancreas: Metastatic Malignancies

Overview

Burden of Disease

Diagnosis and Evaluation

Patient Selection for Metastasectomy

Operative Approach

Primary Neoplasms Metastatic to the Pancreas

Safety and Efficacy of Metastasectomy

References

PART II: Periampullary Cancers

CHAPTER 19: Histopathology of Tumors of the Ampulla of Vater

Adenoma

Invasive Carcinoma of the Ampullary Region

Neuroendocrine Neoplasm of the Ampulla of Vater

Mesenchymal Tumors of the Ampullary Region

Secondary Tumors

References

CHAPTER 20: Clinical Approach to Periampullary Cancer

Clinical Presentation: Most-Frequent and Rare Clinical Symptoms

Diagnostic Protocol, Fast Track, and Regular Diagnostic Procedures

Laboratory Investigation

Standard Radiologic Procedures for Diagnosis and Staging

References

CHAPTER 21: Adenoma of the Papilla of Vater and Endoscopic Management

Introduction

Clinical Presentations

Diagnosis by Imaging Modalities

Laboratory Measurements

Strategy for Endoscopic Management

Endoscopic Resection

Conclusion

References

CHAPTER 22: Controversies about Local or Regional Treatment of Adenoma of the Papilla of Vater: the Japanese Experience

Introduction

Standard Operative Procedures for Adenoma of the Papilla of Vater

Surgical Outcome in Our Institution

Overall Discussion

References

CHAPTER 23: Cancer of the Papilla: Surgical Management

Introduction

Treatment Principles for Adenoma of the Papilla and Ampullary Cancer

References

CHAPTER 24: Evidence of Surgical Management of Distal Common Bile Duct Cancer

Goals of Surgical Treatment

Indication for Standard Surgical Procedures and Specific Limited Surgical Techniques

Bile Duct Resection

Duodenum-Preserving Total Pancreatic Head Resection

Lymphadenectomy for DCBDC

References

CHAPTER 25: Evidence of Surgical Management of Duodenal Cancer

References

CHAPTER 26: Survival and Chance of Cure after Surgery, Adjuvant Chemotherapy, and Palliative Chemotherapy of Periampullary Cancers

Introductions

Ampullary Carcinoma

Duodenal Carcinoma

Distal Cholangiocarcinoma

Pathologic Factors

Adjuvant Therapy

References

PART III: Cystic Neoplastic Lesions of the Pancreas

CHAPTER 27: Histologic Classification and Staging of Cystic Neoplastic Lesions of the Pancreas

Serous Cystic Neoplasm

Intraductal Papillary Mucinous Neoplasm (IPMN)

Mucinous Cystic Neoplasm

Solid Pseudopapillary Neoplasm

References

CHAPTER 28: Clinical Presentation of Cystic Neoplastic Lesions of the Pancreas

Intraductal Papillary Mucinous Neoplasm

Mucinous Cystic Neoplasm

Serous Cystic Neoplasm

Solid Pseudopapillary Neoplasm

References

CHAPTER 29: Endoscopic Ultrasonography and Cystic Fluid Analysis of the Pancreas: Evidence of Diagnostic Measures

Introduction

Pancreatic Cystic Fluid Aspiration

Components of Pancreatic Cystic Fluid Analysis

EUS-FNA of Pancreatic Cystic Lesions: When to Do and What to Test

Summary

References

CHAPTER 30: Natural History of IPMN: Adenoma–Carcinoma Sequence in IPMN

Introduction

Age of Patients with Benign IPMN and with Malignant IPMN

Nonoperative Follow-Up of IPMN

Nonoperative Follow-Up of Main-Duct IPMN

Follow-Up after Surgery for IPMN

Conclusion

References

CHAPTER 31: What Are the Pathologic Criteria That Justified Observational Management in Patients with Cystic Neoplastic Lesions of the Pancreas?

References

CHAPTER 32: Indications for Operative Intervention of Cystic Neoplasms of the Pancreas

Introduction

Serous Cystic Neoplasms (SCNs)

Mucinous Cystic Neoplasms (MCNs)

Intraductal Papillary Mucinous Neoplasms (IPMNs)

Rare Primary Pancreatic Cystic Neoplasms

References

CHAPTER 33: Surgical Management of IPMN Lesions of the Pancreas

Limited Resection for Noninvasive Branch-Duct IPMN

Approach to Multifocal BD-IPMN

Total Pancreatectomy for Diffuse Main-Duct IPMN

Role of Intraoperative Frozen Section

Surveillance of IPMN (Nonresected or Resected)

Follow-Up of Resected IPMN

References

CHAPTER 34: Surgical Management of Mucinous Cystic Neoplastic Lesions of the Pancreas

Preoperative Evaluation

Indications for Operative resection

Operative Treatment

Surgery for MCN and Pregnancy

Prognosis after Resection and Follow-Up

References

CHAPTER 35: Surgical Management of Serous Cystic Neoplasms of the Pancreas

General Aspects

Surgical Management

What Kind of Pancreatic Resection?

Final Remarks

References

CHAPTER 36: Surgical Management of Solid Pseudopapillary Neoplasms of the Pancreas

Surgical Treatment Goals

Standard Surgical Procedures and Specific Surgical Techniques

References

CHAPTER 37: Limited Oncologic Resection or Major Surgery for Cystic Neoplasms of the Pancreas?

Introduction

Options for Surgical Treatment of Cystic Neoplasm of the Pancreas

References

CHAPTER 38: Enucleation of Cystic Neoplasia of the Pancreas

Introduction

Patient Selection

Contraindications to Enucleation

Preoperative Evaluation for Potential Enucleation

Operative Technique of Enucleation

Postoperative Management after Enucleation

Complications of Enucleation

Outcomes after Enucleation

Conclusions

References

CHAPTER 39: Long-Term Outcome after Observation and Surgical Treatment of Cystic Neoplasms of the Pancreas

Introduction

Serous Cystic Neoplasms

Primary Mucinous Cystic Neoplasms

Intraductal Papillary Mucinous Neoplasms

Solid Pseudopapillary Neoplasms

Summary

References

PART IV: Endocrine Neoplasms of the Pancreas

CHAPTER 40: Classification of Endocrine Tumors of the Pancreas

Introduction

Nomenclature

Classification

Conclusions

References

CHAPTER 41: Clinical Manifestation of Endocrine Tumors of the Pancreas

Clinical Manifestations of Pancreatic Neuroendocrine Neoplasms

Endocrine Function of the Pancreas

Specific PNETs

Conclusion and Summary

References

CHAPTER 42: Evidence of Hormonal, Laboratory, Biochemical, and Instrumental Diagnostics of Endocrine Tumors of the Pancreas

Introduction

Investigations of Pancreatic Incidentaloma without Symptoms

Diagnosis and Localization of Specific Tumors

Imaging of Pancreatic Endocrine Secreting Tumors

Conclusion

References

CHAPTER 43: Evidence of Medical and Radionuclide-Targeted Treatment of Endocrine Tumors of the Pancreas

Insulinomas

Gastrinomas

Glucagonomas

Adrenocorticotrophic Hormone–Secreting Tumors

Carcinoid Tumors

VIPomas, Somatostatinomas, and Others

General Comments on Medical and Radionuclide Treatment for Pancreatic Endocrine Tumors

Conclusion

Addendum

References

CHAPTER 44: Insulinoma: Evidence of Surgical Treatment

Open Procedures for Insulinomas

Laparoscopic Surgery for Insulinomas

Operative Complications of Resection of Insulinomas

Prognosis

References

CHAPTER 45: Gastrinoma: Evidence of Surgical Treatment

Introduction

Clinical Symptoms

Diagnosis and Differential Diagnosis

Gastrinoma Localization

Surgical Care

References

CHAPTER 46: Rare Endocrine Tumors of the Pancreas: Evidence of Management

Epidemiologic Evidence

General Principle of Diagnosis and Localization

Glucagonoma

Somatostatinoma

VIPoma

PPoma

GRFoma

ACTHoma

Nonfunctional PNETs

General Approaches to rPNETs

Nonoperative Management

Management of Hepatic Metastasis in rPNET

rPNETs associated Multiple Endocrine Neoplasia Type 1

References

CHAPTER 47: Long-Term Outcome after Clinical Management of Endocrine Tumors of the Pancreas

Functional Status of PENs affects Prognosis

Prognosis of Nonfunctional PENs after Resection

Prognosis of Functional PENs after Resection

References

PART V: Chronic Pancreatitis with Inflammatory Tumor of the Pancreas

CHAPTER 48: Chronic Pancreatitis with Inflammatory Mass in the Pancreatic Head

Definition

Incidence

Symptoms, Pathophysiology, and Clinical Problems

Clinical Workup and Differential Diagnosis

Treatment

Summary

References

CHAPTER 49: Chronic Tropical Pancreatitis: Clinical Syndromes, Natural Course Management Principles

Introduction

Epidemiology

Etiopathogenesis

Clinical Syndromes and Natural Course

Diagnosis

Management

Conclusion

References

CHAPTER 50: Laboratory, Endoscopic, and Radiologic Diagnostics of Chronic Pancreatitis with Inflammatory Mass in the Head

Diagnosis of Chronic Pancreatitis

Differential Diagnosis of Mass-Forming Chronic Pancreatitis and Pancreatic Cancer

References

CHAPTER 51: Autoimmune Pancreatitis: How to Recognize This Entity and Avoid Surgical Treatment

Introduction

AIP Subtypes

Prevalence of AIP

Clinical Presentation: AIP versus PC

The International Consensus Diagnostic Criteria

Diagnostic Approach

Clinical Diagnosis

Pitfalls

Conclusion

References

CHAPTER 52: What Is the Place of Interventional Endoscopic Treatment in Chronic Pancreatitis with Inflammatory Tumor of the Pancreatic Head?

Introduction

Management of Main Pancreatic Duct Strictures

Management of Pancreatic Stones

Pancreatic Pseudocyst

Chronic Pancreatitis–Related Biliary Strictures

References

CHAPTER 53: When to Change from Conservative to Surgical Management in Alcoholic Chronic and Tropical Chronic Pancreatitis

Introduction

Diagnostic Investigations and Management of CP

Conclusion

References

CHAPTER 54: Duodenum-Preserving Pancreatic Head Resection in Chronic Pancreatitis with Inflammatory Mass

Introduction

Surgical Technique of Duodenum-Preserving Pancreatic Head Resection for Chronic Pancreatitis

Outcome after Duodenum-Preserving Pancreatic Head Resection

References

CHAPTER 55: Major Resection for Chronic Pancreatitis

Introduction

Surgery for Chronic Pancreatitis

Pancreatoduodenectomy

Distal Pancreatectomy

Total Pancreatectomy

Conclusion

References

CHAPTER 56: Short-Term and Long-Term Outcome after Interventional and Surgical Treatment of Chronic Pancreatitis with Inflammatory Mass

Pain Management in Chronic Pancreatitis

Decompression of Pseudocysts

Therapeutic Concepts for Ductal Stenoses

References

Index

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List of Tables

Table 1.1  Histological classification and distribution of pancreatic ductal carcinoma in Japan, 2001–2007a

Table 1.2  WHO classification of tumors of the pancreatic ductal neoplasma

Table 1.3  TNM classification (3). Reproduced with permission of the Japan Pancreas Society.

Table 1.4  TNM classification (5)

Table 3.1  Settings of an inherited predisposition to pancreatic cancer

Table 3.2  Candidates for PDAC screening

Table 5.1  Summary of randomized controlled trials analyzing PPPD versus classic PD for patients with periampullary or pancreatic cancera,b

Table 5.2  Critical postoperative pathway for patients undergoing PPPD and DPa

Table 5.3  Postoperative outcomes from PD from two of the largest series published in the literaturea

Table 9.1  Randomized controlled trials of standard versus extended lymphadenectomy

Table 10.1  Consensus definitions of the ISGPS for the severe complications of pancreatic fistula, delayed gastric emptying, and hemorrhage

Table 10.2  Postoperative early complications after resection for malignant pancreatic tumorsa

Table 11.1  Results of biliary bypass procedures with or without gastroenterostomy for advanced pancreatic cancer

Table 11.2  Prospective randomized controlled trials comparing endoscopic or percutaneous drainage with surgical biliary drainagea

Table 11.3  Two prospective randomized controlled trials analyzing prophylactic gastrojejunostomy in patients with unresectable periampullary cancera

Table 11.4  Prospective randomized controlled trial analyzing gastrojejunostomy versus endoscopic stent placement in patients with preoperative symptoms of GOO

Table 11.5  Results of laparoscopic biliary and gastric bypass for advanced periampullary cancer

Table 11.6  Studies that compared palliative resection (R) and bypass surgery (B)

Table 12.1  Randomized controlled trials of adjuvant systemic chemotherapy

Table 12.2  Randomized controlled trials of adjuvant chemoradiation

Table 12.3  Randomized controlled trials of combination therapy

Table 13.1  Patterns of failure after curative resection of pancreatic cancer

Table 13.2  Prospective randomized trials of adjuvant therapy for pancreatic cancer

Table 13.3  Potential advantages and disadvantages of neoadjuvant chemoradiotherapy

Table 13.4  CT-based clinical staging of pancreatic cancer at the Medical College of Wisconsin

Table 13.5  Selected neoadjuvant trials for resectable pancreatic cancer

Table 13.6  Clinical studies of hENT1 expression in pancreatic cancer

Table 14.1  Trials comparing chemoradiation versus radiotherapy alonea

Table 14.2  Trials comparing chemoradiation versus chemotherapy alonea

Table 14.3  Study included in comparison of chemoradiation, followed by chemotherapy versus best supportive carea

Table 14.4  Summary of FOLFIRINOX in the nonclinical trial setting, with 90.9% chemonaivea

Table 15.1  Rates and patterns of recurrence in randomized trials for adjuvant therapy after pancreatic cancer resection

Table 15.2  Recurrence patterns and survival periods in retrospective studies

Table 16.1  Actual survival rates and types of cancer recurrence compared among four treatment groupsa

Table 16.2  Cancer stages (UICC) in 71 patients who survived 5 years after surgery

Table 16.3  Sites of cancer recurrence and second primary cancer

Table 16.4  Noncancer deaths in 5-year survivorsa

Table 18.1  Primary pathologic diagnoses of patients with metastatic malignancies of the pancreasa

Table 18.2  Operative approach for pancreatic metastasectomya

Table 19.1  WHO classification of tumors of the ampullary region. Bosman, et al., 2010. Reproduced with permission from IARC and WHO.

Table 21.1  Outcome of endoscopic papillectomy for ampullary adenoma

Table 23.1  Indication for limited surgery: ampullectomy

Table 23.2  Indication for surgery in advanced ampullary cancer

Table 23.3  Survival and hospital mortality after oncologic duodenal pancreatectomy of ampullary cancer

Table 23.4  Cancer of the papilla of Vater, stage-related cancer disseminationa

Table 26.1  5-year survival rate of resected ampullary carcinoma

Table 26.2  5-year survival rate of resected duodenal carcinoma

Table 26.3  5-year survival rate of resected distal cholangiocarcinoma

Table 26.4  Univariate and multivariate analysis of risk factor for long-term survival in patients with periampullary carcinoma undergoing pancreatoduodenectomy

Table 27.1  WHO classification of selected pancreatic tumors

Table 27.2  Epithelial types in IPMN

Table 27.3  Immunohistochemical evaluation of SPN and its imitators

Table 30.1  Nonoperative follow-up of IPMN

Table 31.1  Series of BD-IPMN evaluating the risk of malignancy in observed and/or resected BD-IPMN without suspicious findings according the 2006 IAP guidelines

Table 34.1  Laparoscopic distal pancreatectomy (LDP) for cystic neoplasms

Table 36.1  Early morbidity and late endocrine and exocrine complications after left-side pancreatectomy and pancreatoduodenectomy

Table 37.1  Indications for surgical treatment of cystic neoplasms and endocrine tumors of the pancreasa

Table 37.2  Options for surgical treatment of cystic neoplasm of the pancreas

Table 37.3  Enucleation of cystic tumors of the pancreas: early postoperative outcome, postoperative morbidity, and hospital mortalitya

Table 37.4  Pancreatic middle segment resection: early postoperative morbidity and hospital mortalitya

Table 37.5  Duodenum-preserving total or subtotal pancreatic head resection: early postoperative morbidity, hospital mortality, and late outcome criteriaa

Table 37.6  Procedure-related indications for cystic neoplastic lesions and neuroendocrine tumors of the pancreas

Table 38.1  Factors supporting surgical treatment of a pancreatic cysta

Table 38.2  Contraindications for enucleation

Table 38.3  Preoperative evaluation

Table 40.1  Functional pancreatic neuroendocrine tumorsa

Table 40.2  Pancreatic neuroendocrine tumors associated with hereditary syndromesa

Table 40.3  Capella classification of pancreatic neuroendocrine tumors 1995a

Table 40.4  Memorial Sloan Kettering classification of pancreatic neuroendocrine tumors 2002a

Table 40.5  World Health Organization (WHO) classification of pancreatic neuroendocrine tumors (2004)a

Table 40.6  European Neuroendocrine Tumour Society 2006 grading proposal for pancreatic neuroendocrine tumorsa

Table 40.7  World Health Organization (WHO) 2010 classification and grading of pancreatic neuroendocrine tumorsa

Table 40.8  TNM classification and disease staging for endocrine tumors of the pancreas (ENETS 2006)a

Table 40.9  TNM classification and disease staging for endocrine tumors of the pancreas (UICC/AJCC/WHO 2010)a

Table 41.1  Clinical manifestations of pancreatic endocrine neoplasms

Table 42.1  Differential diagnosis of insulinoma

Table 42.2  Relative frequencies of MEN-1 tumors

Table 42.3  Common terms used in SSTR radionuclides

Table 44.1  Diagnostic criteria for insulinomasa

Table 44.2  Location of insulinomas (N = 349)a

Table 44.3  Several reports on laparoscopic management of pancreatic insulinomas

Table 46.1  Epidemiology of rPNETsa

Table 46.2  Presentation of rPNETsa

Table 46.3  Diagnostic values for plasma hormonal assaysa

Table 49.1  Comparison of the existing evidence on the most common genetic mutations among the various types of chronic pancreatitis and postulations on their association with disease causation

Table 49.2  Pathological features of TCPa

Table 49.3  Characteristic radiologic features and utility of the different imaging modalities in TCP

Table 49.4  Indications for endoscopic therapy in TCPa

Table 49.5  Surgical strategies in TCP with specific indications for each procedure

Table 50.1  Accuracy of different imaging methods for the differential diagnosis of solid pancreatic masses (diagnosis of malignancy) (33–36,38–52,64–68,70–72)

Table 51.1  Differences in clinical features of type 1 and type 2 AIP

Table 51.2  Summary of diagnostic features in the ICDC for AIP (see text for details)

Table 51.3  Features of imaging, serology, and OOI in AIP and PCa,b

Table 53.1  Diagnostic workup of a patient with CP (5,6)

Table 53.2  Postulated mechanisms for development of duodenal obstruction in CPa

Table 53.3  Classification of the causes of bleeding in CP with their clinical presentations, based on the underlying pathology

Table 54.1  Indications for duodenum-preserving pancreatic head resection

Table 54.2  Early and late postoperative results after DPPHR in chronic pancreatitisa

Table 54.3  Results of randomized controlled trials comparing DPPHR with Whipple-type pancreatic head resection, respectively, pylorus-preserving pancreatic head resection and the Frey procedure and the Itzbicki modification

Table 56.1  Overview of results of studies on lateral anastomotic techniques after Partington–Rochelle and V-shaped excision of the ventral pancreasa

Table 56.2  Overview of results of studies on pancreatic resection proceduresa

List of Illustrations

Figure 1.1  Developmental pathway of ductal adenocarcinoma, from ductal epithelium to invasive ductal carcinoma. Part A is classified as "carcinoma in situ and Part B is classified as invasive ductal carcinoma."

Figure 1.2  (a) Very small ductal adenocarcinoma (arrowheads), 3 mm in diameter. (b) Noninvasive ductal adenocarcinoma (left, arrow) and normal pancreatic duct (right). (c) Immunofluorescence shows the atypical duct (left, arrow) is positive for p53, but the normal pancreatic duct (right) is negative.

Figure 1.3  Differential variants of ductal adenocarcinoma: (a) carcinoma in situ, flat type and low papillary type; (b) papillary adenocarcinoma (pap); (c) papillotubular adenocarcinoma, well-differentiated type; (d) tubular adenocarcinoma, well-differentiated type (tub1); (e) tubular adenocarcinoma, moderately differentiated type (tub2); (f) poorly differentiated adenocarcinoma (por); (g) adenosquamous carcinoma (asc).

Figure 1.4  Mucinous carcinoma (muc): (a) cut surface of resected specimen; (b) main pancreatic duct carcinoma; (c) invasion of pancreatic parenchyma.

Figure 1.5  Anaplastic carcinoma: (a) giant cell carcinoma of osteoclastoid type; (b) pleomorphic type; (c) spindle-cell type.

Figure 3.1  Representative FPC family of the FaPaCa registry.

Figure 4.1  Typical pancreatic cancer findings on enhanced CT. Low-density mass with splenic artery invasion was seen in the pancreas body.

Figure 4.2  FDG-PET revealed peritoneal disseminations of pancreatic cancer that could not be detected by enhanced CT.

Figure 4.3  (a) CT could detect only pancreatic duct dilatation and pancreatic duct cutoff, but it could not detect the pancreas mass itself. (b) On EUS imaging, the 10-mm low-echoic mass could be detected clearly.

Figure 4.4   Pancreatic head cancer. (a) ERCP: main pancreatic duct (MPD) stenosis is obvious in the pancreatic head, and the branch duct within the stenotic area is depicted clearly. (b) MRCP: MPD stenosis is seen in the pancreatic head with dilated upstream MPD.

Figure 4.5  EUS-FNA for pancreatic cancer. (a) Low-density 30-mm mass lesion is seen on enhanced CT. (b) EUS-FNA for mass lesion (arrow, FNA needle). (c) Cytology shows atypical cells consistent with adenocarcinoma.

Figure 5.1  (a) A replaced RHA (black arrow) coursing posterior to the SMV and attaching to the SMA. The pancreas has been divided (white arrow). (b) Reconstruction of an excised RHA with the GDA stump. The GDA is dissected inferiorly and divided as low as possible, and is swung up to be anastomosed to the excised RHA. (RHA, right hepatic artery; SMV, superior mesenteric vein; SMA, superior mesenteric artery; GDA, gastroduodenal artery; CBD, common bile duct; CHA, common hepatic artery; PV, portal vein.) [a: From Hiatt, et al., 1994 (10). Reproduced with permission from Lippincott Williams & Wilkins–Journals. b: From Allendorf & Bellemare, 2009 (12). Reproduced with permission from Springer Science + Business Media.]

Figure 5.2  A generous Kocher maneuver is performed to separate the second portion of the duodenum off its retroperitoneal attachments, which allows the surgeon to appreciate the tumor's location in relation to the SMA and the PV–SMV axis. (SMA, superior mesenteric artery; PV, portal vein; SMV, superior mesenteric vein.) [From Cameron & Sandone, 2007 (20), p. 243. Reproduced with permission from PMPH-USA.]

Figure 5.3  Transection of the pancreatic parenchyma with electrocautery with a Penrose drain passed under posteriorly to protect the PV–SMV confluence. The duodenum has been previously divided distally to the pylorus by a GIA stapler as shown. (PV, portal vein; SMV, superior mesenteric vein.) [From Cameron & Sandone, 2007 (20), p. 291. Reproduced with permission from PMPH-USA.]

Figure 5.4  The uncinate process of the pancreas is divided between two hemostatic clamps just lateral to the superior mesenteric artery. An energy device (i.e., harmonic scalpel) could be an alternative to prevent hemorrhage from the posterior pancreatoduodenal artery that traverses within the uncinate parenchyma. [From Cameron & Sandone, 2007 (20), p. 292. Reproduced with permission from PMPH-USA. Reproduced with permission from PMPH-USA.]

Figure 5.5  Anatomy of pylorus-preserving pancreatoduodenectomy. (Left) Anatomy prior to pylorus-preserving pancreatoduodenectomy, with superimposed lines indicating points of transection at the duodenum, distal common bile duct, pancreas, and jejunum. (Right) Anatomy after reconstruction showing end-to-side pancreaticojejunostomy, hepaticojejunostomy, and duodenojejunostomy. [Both from Cameron & Sandone, 2007 (20), p. 302. Reproduced with permission from PMPH-USA.]

Figure 5.6  Surgical anatomy of a classic Whipple after reconstruction, noting an end-to-side Hofmeister-type gastrojejunostomy. [From Cameron & Sandone, 2007 (20), p. 302.]

Figure 5.7  Operative steps of distal pancreatectomy en bloc splenectomy. (a) The transverse colon is displaced inferiorly to provide countertraction for the division of the inferior peritoneal attachments of the body–tail of the pancreas. (b) Transection of the pancreatic parenchyma with electrocautery over a Penrose drain placed to protect the PV–SMV axis. (c) Pancreatic duct ligation with 5-0 polydioxanone figure-eight sutures, with the parenchyma oversewn with 3-0 polyglycolic acid, interlocking horizontal mattress sutures. (d) The postresection bed, with the splenic vein ligated just distal to the insertion of the IMV. (PV, portal vein; SMV, superior mesenteric vein; IMV, inferior mesenteric vein.) [(a), (b), (c), and (d) from Cameron & Sandone, 2007 (20), p. 302. Reproduced with permission from PMPH-USA.]

Figure 5.8  Nomenclature for lymph node stations according to the Japan Pancreas Society: first-, second-, and third-order lymph node echelons are shown. [Adapted from Japan Pancreas Society, 1996, with permission (47), p. 11.]

Figure 6.1  Radiological classification of portal vein invasion by portography and computed tomography. [From Nakao et al., 2012 (14). Reproduced with permission from Lippincott Williams & Wilkins Journals.]

Figure 6.2  Correlations between radiological type and pathological grade of portal vein invasion. [From Nakao et al. 1999 (12). Reproduced with permission from Springer Science + Business Media.]

Figure 6.3  Completion of the mesenteric approach portion of pancreatoduodenectomy (Panc, pancreas; SMA, superior mesenteric artery; SMV, superior mesenteric vein).

Figure 6.4  Ligation of the inferior pancreatoduodenal artery after division of the pancreas along the line of the superior mesenteric artery (IPDA, inferior pancreatoduodenal artery; JA1, first division of the jejunal artery; MCA, middle colic artery; PLsma, nerve plexus around the superior mesenteric artery; SMA, superior mesenteric artery; SMV, superior mesenteric vein).

Figure 6.5  Procedures for bypassing the portal vein using an antithrombogenic catheter (8) (FV, femoral vein; GSV, greater saphenous vein; IMV, inferior mesenteric vein; IVC, inferior vena cava; PV, portal vein; SMV, superior mesenteric vein; SV, splenic vein; UV, umbilical vein). [From Norton & Eiseman, 1975 (8). Reproduced with permission from Elsevier.]

Figure 6.6  Preservation of the left gastric vein during portal vein reconstruction without splenic vein reconstruction (CA, celiac artery; CHA, common hepatic artery; GDA, gastroduodenal artery; IVC, inferior vena cava; LGV, left gastric vein; Panc, pancreas; PV, portal vein; SMA, superior mesenteric artery; SMV, superior mesenteric vein; SA, splenic artery; SV, splenic vein).

Figure 6.7  Extent of portal vein resection in various procedures (CA, celiac artery; DP, distal pancreatectomy; PD, pancreatoduodenectomy; PPPD, pylorus-preserving pancreatoduodenectomy; PPTP; pylorus-preserving total pancreatectomy; PV, portal vein; SMV, superior mesenteric vein; TP, total pancreatectomy). [Data from Nakao et al., 2012 (14).]

Figure 6.8  Cumulative survival rates according to radiological type of portal vein invasion.

Figure 8.1  Schematic cross-sectional view showing the resection area of a distal pancreatectomy with en bloc resection of the celiac axis. Dotted line indicates dissection plane (adr, adrenal gland; Ao, aorta; CA, celiac axis; CHA, common hepatic artery; crus, crus of the diaphragm; Du, duodenum; g, celiac ganglion; IVC, inferior vena cava; pl, celiac plexus; PV, portal vein; SA, splenic artery; SV, splenic vein). [From Hirano et al., 2007 (5). Reproduced with permission from Lippincott Williams & Wilkins Journals.]

Figure 8.2  Postresectional overview during distal pancreatectomy with en bloc resection of the celiac axis (Ao, aorta; CA, celiac axis; CHA, common hepatic artery; crus, crus of diaphragm; GDA, gastroduodenal artery; graft, interposed iliac vein graft; IVC, inferior vena cava; RV, renal vein; SMA, superior mesenteric artery; SMV, superior mesenteric vein). [From Hirano et al., 2007 (5). Reproduced with permission from Lippincott Williams & Wilkins Journals.]

Figure 9.1  Extensive lymphadenectomy and dissection of the retroperitoneal tissues for pancreatic cancer (Aor, aorta; CA, celiac axis; CHA, common hepatic artery; IVC, inferior vena cava; LRV, left renal vein; PV, portal vein; SMA, superior mesenteric artery; SMV, superior mesenteric vein).

Figure 9.2  Classification of lymph node metastasis in pancreatic head cancer. Group 1 nodes are shown in red, group 2 nodes in blue, and group 3 nodes in yellow. [From Japan Pancreas Society, 2011 (2). Reproduced with permission of Japan Pancreas Society.]

Figure 9.3  Lymphadenectomy around the superior mesenteric artery and vein, and nerve plexus excision around the superior mesenteric artery, via the mesenteric approach (IPDA, inferior pancreatoduodenal artery; J1A, first branch of the jejunal artery; J2A, second branch of the jejunal artery; MCA, middle colic artery; SMA, superior mesenteric artery; SMV, superior mesenteric vein).

Figure 9.4  Survival rates of patients according to the extent of lymph node involvement (MST, median survival time; UR, ultraradical).

Figure 9.5  Survival rates of patients with or without metastasis to station 16 lymph nodes (LN, lymph node; MST, median survival time).

Figure 9.6  Schematic representation of the extrapancreatic nerve plexus (SMA, superior mesenteric artery). [From Japan Pancreas Society, 2011 (2). Reproduced with permission of Japan Pancreas Society.]

Figure 10.1  Risk assessment and postoperative complications with regard to the surgical approach after making the diagnosis of pancreatic carcinoma. Besides preoperative aspects of resectability of the tumor and operability of the patient (see Chapters 5, 6, 8, and 9), different operative procedures and techniques are discussed against the backdrop of postoperative complications. Pancreatic surgery is complex, and an adequate complication management is essential to provide reliable diagnostics and successful therapy for postoperative problems.

Figure 11.1  Kaplan–Meier curve of the survival and food intake of patients after stent placement or gastrojejunostomy (GJJ, gastrojejunostomy; GOOSS, gastric outlet obstruction scoring system). [Adapted from Jeurnink et al., 2010 (39) with permission from Elsevier.]

Figure 11.2  Kaplan–Meier survival curves of patients undergoing R1 resection and bypass for locally advanced or metastatic disease. [Adapted from Kuhlmann et al., 2006 (70) with permission from Elsevier.]

Figure 11.3  Morbidity (a), surgical morbidity (b), and mortality (c) in the resection group versus the double-bypass group (random-effects model), in studies by Schniewind (73), Köninger (75), Bockhorn (77), and Tachezy (69). [(a), (b) and (c) adapted from Gillen et al., 2012 (82) with permission from Elsevier.]

Figure 13.1  Contrast-enhanced, multidetector axial CT images of a resectable pancreatic cancer: (a) arterial phase and (b) venous phase. On the arterial phase the superior mesenteric artery (SMA, thin arrow) is seen, and the superior mesenteric vein (SMV, wide arrow) is more difficult to appreciate as distinct from the tumor (T). On the venous phase (b), the opposite is now apparent. Importantly, this is a resectable tumor because there is no evidence of tumor extension to the SMA and no evidence of distortion or narrowing of the SMV. Note that the interface between the tumor and the SMV (green arrows) appears to also have a normal tissue plane.

Figure 13.2  Axial (a) and coronal (b) contrast-enhanced multidetector CT images of a borderline resectable pancreatic cancer (T) obtained in the arterial phase. The tumor abuts the SMA (thin arrow) for slightly less than 180°. The SMA (wide arrow) is more difficult to appreciate on the arterial phase of contrast enhancement.

Figure 13.3  Axial (a) and sagittal (b) contrast-enhanced, multidetector CT images of a locally advanced pancreatic cancer obtained in the arterial phase. The tumor encases the celiac artery (thin arrow) proximal and distal to the origins of the hepatic and splenic arteries; note the atrophic pancreas with a dilated main pancreatic duct distal to the tumor. The sagittal view (b) illustrates the origin of the celiac artery with a view of the left gastric artery (wide arrow).

Figure 13.4  Sequencing of therapy for (a) resectable and (b) borderline resectable pancreatic cancer (PreTx, pretreatment).

Figure 14.1  GERCOR LAP 07 phase 3 trial: chemoradiation therapy flow diagram (IV, intravenously; PO, orally).

Figure 16.1  The annual numbers of pancreatic cancer resections and 3- and 5-year survivors.

Figure 16.2  Liver perfusion chemotherapy via both the hepatic artery and portal vein.

Figure 16.3  The schedules of preoperative chemoradiation using a full dose of gemcitabine and conformal 3D-radiation (d, days; w, weeks; RT, radiation therapy).

Figure 16.4  The observed and expected survival rates and the relative survival rate in 5-year survivors (Kaplan–Meyer method).

Figure 16.5  The cumulative rate of death and cause of death at 5 years after surgery (Kaplan–Meyer method).

Figure 17.1  Pancreatic tissue with normal acinar lobules at the top surrounded by dense fibrotic tissue that contains scattered irregularly shaped large tumor cells in the lower half of the picture. Hematoxylin and eosin (H&E) morphology, original magnification ×100. [Courtesy of D. Aust, Institute for Pathology, University Hospital Carl Gustav Carus Dresden.]

Figure 17.2  Acinar cell carcinoma: solid sheets of eosinophilic tumor cells with dark round nuclei. Preoperative H&E morphology, original magnification ×25. [Courtesy of D. Aust, Institute for Pathology, University Hospital Carl Gustav Carus Dresden.]

Figure 18.1  (a) CT coronal view of well-marginated and hypervascular, but irregular, metastatic renal cell carcinoma in the uncinate process. (b) CT coronal view of well-marginated, round, and hypervascular metastatic renal cell carcinoma in the head of the pancreas.

Figure 18.2  Pancreatic head and uncinate process. Metastasis of renal cell carcinoma is well circumscribed within the pancreatic parenchyma.

Figure 18.3  CT coronal view of pancreatic head and uncinate process with pancreatic ductal dilatation and a duct cutoff (arrow). An isodense mass obstructing the pancreatic duct is suspected. Subsequent EUS identified a mass, and an FNA biopsy confirmed metastatic melanoma (corresponding specimen shown in Fig. 18.4).

Figure 18.4  Bivalved pancreatoduodenectomy specimen with a focus of metastatic melanoma (black arrow) and tumor thrombus in pancreatic duct (white arrow).

Figure 19.1  Intestinal-type adenoma composed of glandular epithelial cells with elongated and compact nuclei located in the upper portion of neoplastic epithelium identical to a high-grade intraepithelial neoplasm.

Figure 19.2  Pancreatobiliary-type adenoma with characteristic cuboid cells arranged in short papillary pattern and with oval nuclei located in the lower portion of neoplastic epithelium suggesting a low-grade intraepithelial neoplasm.

Figure 19.3  Pancreatobiliary-type adenocarcinoma consisting of cuboid cells with slightly clear cytoplasm and round nuclei and arranged in a glandular pattern.

Figure 19.4  Mucinous adenocarcinoma composed of well-differentiated mucinous gland and abundant mucin in glandular lumen.

Figure 19.5  Carcinoid composed of uniform epithelioid cells with round nuclei and arranged in nests and sheets within fibrovascular stroma. Mitosis and necrosis are absent.

Figure 20.1  Diagnostic approach to periampullary cancer.

Figure 20.2  Periampullary tumor detected by a contrast-enhanced CT.

Figure 20.3  MRCP: obstruction dilatation of biliary duct imaged by three-dimensional biliary reconstruction of magnetic resonance.

Figure 20.4  A tumor of the duodenal papilla visualized by endoscopy.

Figure 21.1  Ultrasonography of ampullary tumor. (a) Ultrasonography shows dilated bile duct and ampullary tumor (arrow). (b) Contrast-enhanced ultrasonography using Sonazoid shows enhanced tumor (dynamic image). (c) Microflow imaging (MFI).

Figure 21.2  Computed tomography of ampullary tumors. (a) Multiplanar reconstruction (MPR) shows dilated bile duct and ampullary tumor (arrowheads). (b) MPR shows dilated bile duct and pancreatic duct (arrowhead).

Figure 21.3  Magnetic resonance cholangiopancreatography (MRCP) of ampullary tumor. MRCP shows dilated bile duct and pancreatic duct.

Figure 21.4  Endoscopic ultrasonography (EUS) of ampullary tumor. EUS shows pancreatobiliary system and ampullary tumors (MP, muscularis propria; BD, bile duct; PD, pancreatic duct).

Figure 21.5  EUS of ampullary tumor showing tumor spread in the pancreatic duct. (a) Longitudinal image; (b) cross-section. EUS shows dilated bile duct (BD) and pancreatic duct (PD) including spreading tumor (*).

Figure 21.6  Standard esophagogastroscopy (EGD) of ampullary tumor. EGD shows large and whitish papilla, suggesting tumor.

Figure 21.7  Intraductal ultrasonography (IDUS) of ampullary tumor. IDUS shows dilated bile duct (BD) and pancreatic duct (PD) including spreading tumor (*).

Figure 21.8  En bloc endoscopic papillectomy: (a) large ampullary tumor; (b) snaring the tumor; (c) grasping the tumor; (d) cutting the tumor; (e) cutting the surgace; (f) placing biliary stent and pancreatic duct stent.

Figure 21.9  Endoscopic piecemeal papillectomy: (a) large ampullary tumor showing lateral spread; (b) submucosal injection; (c) piecemeal resection of the oral-side tumor; (d) piecemeal resection of main lesion; (e) complete resection; (f) all specimens.

Figure 21.10  Argon plasma coagulation (APC) for residual tumor: (a) residual tumor in the bile duct; (b) ablation using APC; (c) no residual tumor 6 months after the APC.

Figure 22.1  Steps of transduodenal ampullectomy (TDA). (a,b) The tumor is resected circumferentially with the mucosa and duodenal muscle layers surrounding the tumor. (c) The orifices of the bile and pancreatic ducts are sewn to the edge of the duodenal mucosa with absorbable sutures. [(a), (b), and (c) from Takasaki et al., 2005 (9). Reproduced with permission from the author.]

Figure 22.2  Steps of segmental pancreas-sparing duodenectomy (PSD). (a) The second part of the duodenum is detached completely from the head of the pancreas except for the junction with the bile and pancreatic ducts. (b) The bile and pancreatic ducts are transected outside of the duodenum, and the duodenum is transected proximal and distal to the ampulla. (c) Pancreatobiliary enteric continuity is reconstructed using a jejunal interposition to which the bile and pancreatic ducts are anastomosed. [(a), (b), and (c) from Takasaki et al., 2005 (9). Reproduced with permission from the author.]

Figure 24.1  An extensive Kocher maneuver is performed by elevating the duodenum and head of the pancreas out of the retroperitoneum (IVC, inferior vena cava; LRV, left renal vein; AA, abdominal aorta).

Figure 24.2  The omentum is elevated and the lesser sac is then accessed by opening the gastrocolic ligament along the gastroepiploic vein until Henle's trunk.

Figure 24.3  Lymphadenectomy of hepatoduodenal ligament is carried out along the proper hepatic artery from the liver toward the duodenum (PHA, proper hepatic artery).

Figure 24.4  Lymphadenectomy was performed from the left gastric artery to the common hepatic artery (LGA, left gastric artery; SA, splenic artery; SV, splenic vein).

Figure 24.5  The right gastric artery can often be spared in PPPD (CHA, common hepatic artery; PHA, proper hepatic artery).

Figure 24.6  The uncinate process of the pancreas is separated from the portal vein, superior mesenteric vein, and superior mesenteric artery (1, superior mesenteric artery; 2, superior mesenteric vein; 3, surgeon's maneuver).

Figure 24.7  (a) Binding pancreaticojejunostomy (BPJ): the remnant of the pancreas and the covering jejunum are looped around and ligated together; a bundle of vessels is spared for an intact blood supply to the jejunum end. (b,c) Binding pancreaticogastrostomy (BPG): after the pancreas remnant is pulled into the gastric lumen, the first purse-string suture is tied (inner binding); then the second purse-string suture is tied (outer binding). [(a), (b), and (c) from Peng et al., 2011 (25). Reproduced with permission from Springer Science + Business Media.]

Figure 24.8  Total pancreatic head resection with additional segment resection of the peripapillary duodenum. [From Beger et al., 2008 (38). Reproduced with permission from Springer Science + Business Media.]

Figure 27.1  Serous cystadenoma, with the characteristic central scar accompanied by multiple small cysts.

Figure 27.2  Serous cystadenoma: the cysts are lined by cuboidal cells with round nuclei and clear cytoplasm.

Figure 27.3  (a) IPMN involving the main pancreatic duct as well as branch ducts. (b) IPMN limited to a branch duct.

Figure 27.4  (a) IPMN with low-grade dysplasia; the nuclei are regular and are arranged at the base of the cell. (b) Moderate dysplasia features disorganized nuclei with variability in size and shape. (c) High-grade dysplasia has complex architecture and marked nuclear pleomorphism.

Figure 27.5  Epithelial types in IPMN: (a) gastric foveolar; (b) intestinal; (c) pancreatobiliary; (d) oncocytic.

Figure 27.6  (a) Ductal adenocarcinoma of the pancreas arising from IPMN. (b) The intestinal type of IMPN can give rise to colloid carcinoma.

Figure 27.7  Mucinous cystic neoplasm, showing multiple locules and occasional solid areas.

Figure 27.8  The diagnostic features of MCN; mucinous epithelium above ovarian-like stroma.

Figure 27.9  Solid pseudopapillary neoplasm in the head of the pancreas. Note the well-circumscribed borders and the variegated cut surface, with areas of hemorrhage.

Figure 27.10  The solid part of SPN. Cuboidal cells with regular nuclei; many cells have eosinophilic globules in the cytoplasm. Note the delicate blood vessels.

Figure 27.11  Viable cells are retained around blood vessels, producing the pseudopapillary appearance.

Figure 28.1  Markedly dilated orifice of the duodenal papilla caused by profuse mucin secretion in a patient with main-duct IPMN.

Figure 28.2  (a) Computed tomography shows a mucinous cystic neoplasm (MCN) in the tail of the pancreas with a cyst-in-cyst appearance (encircled by arrowheads). (b) Endoscopic balloon catheter pancreatogram shows a communication with the MCN (arrow).

Figure 28.3  (a) Magnetic resonance pancreatogram shows a microcystic serous cystic neoplasm (SCN; encircled by arrowheads) with upstream dilatation of the main pancreatic duct. (b) Endoscopic retrograde cholangiopancreatography shows a stricture of the main pancreatic duct (arrow) with upstream dilatation caused by the SCN.

Figure 28.4  Magnetic resonance cholangiopancreatography shows a serous cystic neoplasm (arrowheads) mimicking branch-duct intraductal papillary mucinous neoplasm.

Figure 28.5  Computed tomography shows a large spherical mass, 8.5 cm in diameter, in the pancreatic head. After laparoscopic resection, this tumor proved to be a solid pseudopapillary neoplasm.

Figure 29.1  Endoscopic ultrasonography findings before (a) and after (b) fine-needle aspiration of a pancreatic cystic lesion. Note that the lesion has completely collapsed.

Figure 29.2  Appearance of pancreatic cystic fluid aspirated from (a) a mucinous pancreatic cystic lesion (note the mucoid fluid) and (b) a serous cystic neoplasm (the fluid is thin, clear, and bloody).

Figure 31.1  MRI of a small BD-IPMN without worrisome features in a 55-year-old female being observed.

Figure 31.2  CT scan of a BD-IPMN with mural nodule (arrow) as a worrisome finding indicating surgical therapy.

Figure 31.3  Small BD-IPMN with low-grade dysplasia in the pancreatic body (circle) with concurrent ductal adenocarcinoma of the pancreatic head (arrow).

Figure 34.1  Large, typical multicystic MCN: (a) contrast-enhanced CT with an enhancing nodule and focal calcification; note the larger (>2 cm) size of each cystic lesion; (b) operative specimen with thick wall and mural nodules.

Figure 34.2  Operative specimen and contrast-enhanced CT of a small, eccentric oligocystic MCN with focal calcification.

Figure 34.3  Operative specimen and endoscopic ultrasonogram of a unilocular MCN with a mural nodule.

Figure 35.1  Giant serous cystic neoplasm (approximately 12 cm) of the body–tail of the pancreas. This lesion was found in an 80-year-old woman who complained of abdominal pain and fullness. She underwent distal pancreatectomy with splenectomy; the postoperative course was uneventful.

Figure 35.2  Solid-looking serous cystic neoplasm of the pancreatic head (arrow). This lesion was incidentally found in a 75-year-old man, has a hypervascular pattern, and was thought to be a neuroendocrine neoplasm. Because of the deep location of the lesion, the patient underwent pancreaticoduodenectomy. The asterisk (*) indicates the accessory spleen.

Figure 35.3  Von Hippel–Lindau associated serous cystic neoplasm of the whole pancreatic gland. The patient, who was 30 years old, underwent total pancreatectomy because of symptoms.

Figure 35.4  Multifocal serous cystic neoplasm (not associated with Von Hippel–Lindau syndrome) in a 41-year-old woman. This patient is asymptomatic and currently under radiologic periodic surveillance.

Figure 36.1  Frequency of malignant SPNs and type of malignancy at surgery.

Figure 36.2  Estimated overall survival rate after resection of SPN.

Figure 37.1  Pancreatic middle segment resection.For recontstruction an excluded jejunal loop is used; end-to-side pancreaticojejunostomosis with mucosa-to-mucosa duct anastomosis.

Figure 37.2  Duodenum-preserving total pancreatic head resection, preserving the duodenum and the common bile duct. Two anastomoses are required.

Figure 37.3  Duodenum-preserving subtotal pancreatic head resection. (a) Pancreatic tissue between common bile duct and duodenum preserved. (b) Resection of the uncinate process. Two additional anastomoses are required.

Figure 37.4  Duodenum-preserving total pancreatic head resection with segmental resection of the peripapillary duodenum and segmental resection of the intrapancreatic common bile duct. Four anastomoses are required.

Figure 38.1  (a) Computed tomography (CT) of a cystic pancreatic neuroendocrine tumor with a hypervascular rim. [From Kiely et al., 2003 (14). Reproduced with permission from Springer Science + Business Media.] (b) Operative picture of the same lesion being enucleated. [From Pitt et al., 2009 (8). Reproduced with permission from Springer Science + Business Media.]

Figure 38.2  (a) Computed tomography (CT) of a mucinous cystic neoplasm (MCN) that was enucleated. [From the personal collection of Dr. Henry A. Pitt, MD.] (b) Operative picture of an MCN being enucleated. [From Pitt et al., 2009 (8). Reproduced with permission from Springer Science + Business Media.]

Figure 38.3  (a) Magnetic resonance cholangiopancreatography (MRCP) of a side-branch IPMN of the uncinate process that was enucleated. (b) Operative picture of the IPMN being enucleated. The arrow shows a side-branch duct that was ligated. [a and b: From Turrini et al., 2011 (9). Reproduced with permission from John Wiley & Sons.]

Figure 41.1  Skin manifestations in glucagonoma, before (a) and after (b) surgery. [a and b: From Lee et al., 1985 (6). Reproduced with permission from Annals Academy of Medicine Singapore.]

Figure 41.2  (a) Glossitis and perioral rash in glucagonoma at head of pancreas. (b) Glucagonoma seen on CT of the pancreas. [a and b: From Lee et al., 1985 (6). Reproduced with permission from Annals Academy of Medicine Singapore.]

Figure 42.1  Comparison of traditional and SSTR radionuclide imaging. Data pooled from 41 studies. Median, range, and calculated sensitivity [S] are given for each modality (¹¹C, carbon-11; ¹⁸F, fluorine-18; ⁶⁸Ga, gallium-68; ⁶⁴Cu, copper-64; SRS, somatostatin receptor scintigraphy; FDG, fluorodeoxyglucose; CT, computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography). [From Modlin et al., 2008 (8). Reproduced with permission from Elsevier.]

Figure 42.2  Comparison of combined imaging with conventional and SSTR radionuclides. (a) Patient has multiple hepatic metastases from NET primary in the pancreatic tail. This is well visualized on the gallium-68 DOTA-TATE PET/CT (coronal section) with multiple sites of increased uptake in both lobes of the liver. (b) Corresponding contrast-enhanced CT abdominal scan performed at the same sitting shows hypervascular hepatic metastases on the arterial phase of the CT. (c) Corresponding unfused functional PET image of the same slice, showing the somatostatin-receptor-rich hepatic metastases. (d) On the fused PET/CT image, in which the functional image is superimposed on the anatomic image, there is better delineation and characterization of the hepatic metastases.

Figure 43.1  (a) CT abdominal scan showing prior right hemihepatectomy and hepatic metastases in the left lobe. (b) Gallium-68 DOTA-TATE PET/CT showing high uptake of highly specific radiotracer in the hepatic metastases. There is also urinary excretion of tracer seen in the right kidney. (c) SPECT/CT abdominal scan performed 24 hours after lutetium-177 DOTA-TATE infusion, showing highly specific uptake of the therapeutic tracer in the hepatic metastases, similar to the uptake seen on the pretreatment gallium-68 DOTA-TATE PET/CT.

Figure 44.1  A 25-year-old female with recurrent hypoglycemia. (a) No obvious lesions are seen on CT. (b) A nodule of 10 mm with smooth contour is shown on MRI.

Figure 44.2  A standard array of five ports for laparoscopic pancreatic surgery.

Figure 44.3  Distal pancreatectomy with splenectomy: (a) separating the splenic artery from the superior border of the pancreas and transecting it; (b) transecting the pancreas with an endoscopic linear cutter; (c) transecting the splenic vein; (d) the resected distal pancreas and the spleen.

Figure 44.4  Spleen-preserving distal pancreatectomy: (a) dissecting the splenic vessels from the posterior side of the pancreas; (b) dividing and ligating the small branches of splenic vessels when dissecting the distal pancreas from its posterior attachments after transecting the pancreas; (c) the resected distal pancreas.

Figure 44.5  Central pancreatectomy: (a) transecting the proximal pancreas with an endoscopic linear cutter and the distal pancreas with harmonic scalpel; (b) laparoscopic pancreatojejunostomy with a stent; (c) the resected central segment of the pancreas.

Figure 46.1  An algorithm for establishing the diagnosis of PNET (VIP, vasoactive intestinal polypeptide; PP, pancreatic polypeptide; GHRH, growth-hormone-releasing hormone; SRS, somatostatin receptor scintigraphy; U/S, ultrasonography; EUS, endoscopic ultrasonography; FNA, fine-needle aspiration; CT, computed tomography; MRI, magnetic resonance imaging; IHC, immunohistochemistry). [Adapted from Oberg & Eriksson, 2005 (1).]

Figure 46.2  An algorithm of localization of rPNETs (SRS, somatostatin receptor scintigraphy; EUS, endoscopic ultrasonography; CT, computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography). [Adapted from Oberg & Eriksson, 2005 (1).]

Figure 48.1  Inflammatory pancreatic head mass. Computed tomography showing a large inflammatory pancreatic head mass in a patient with chronic pancreatitis, with typical diffuse pancreatic calcifications. The impacted dislocated main pancreatic duct stent was removed during surgery.

Figure 48.2  Irregularities of the main pancreatic duct. Magnetic resonance cholangiopancreatography disclosing marked pancreatic duct irregularities and narrowing of the common bile duct in a patient with inflammatory pancreatic head mass.

Figure 48.3  Walled-off necrosis. Magnetic resonance imaging depicting an inflammatory pancreatic head mass with walled-off necrosis that developed after an episode of acute pancreatitis in a patient with chronic pancreatitis.

Figure 49.1  Axial CT image of a patient with an inflammatory head mass secondary to chronic pancreatitis suspicious for a malignant transformation.

Figure 49.2  Axial CT image of a patient with an inflammatory head mass secondary to chronic pancreatitis with multiple calculi and indistinct planes with the surrounding vasculature.

Figure 50.1  Computed tomography (CT) of solid pancreatic masses: (a) inflammatory mass of the pancreatic head (arrow), showing an irregular isoattenuating pattern with a calcification; (b) adenocarcinoma of the pancreatic head (arrow), presenting the typical contrast hypoenhancement.

Figure 50.2  Endoscopic ultrasonography of solid pancreatic masses: (a) inflammatory mass of the pancreatic head (arrow), showing an irregular heteroechogenic pattern, predominantly hypoechoic, without infiltration of surrounding vessels; (b) adenocarcinoma of the pancreatic head (arrow), with irregular borders and infiltration of surrounding vessels (portal vein and confluence).

Figure 50.3  Quantitative EUS elastographic evaluation of solid pancreatic masses: (a) inflammatory mass of the pancreatic head (right, B-mode; left, elastographic evaluation), showing a heterogeneous green predominant pattern and a strain ratio of 6.03 (normal <1.93); (b) adenocarcinoma of the pancreatic head (right, B-mode; left, elastographic evaluation), showing a heterogeneous blue predominant pattern and a strain ratio of 33.87.

Figure 51.1  Histologic features of type 1 and type 2 autoimmune pancreatitis. Type 1 AIP (lymphoplasmacytic pancreatitis—LPSP): (a) periductal lymphoplasmacytic infiltrate with storiform fibrosis (arrow) and (b) obliterative phlebitis with storiform fibrosis (arrow). (c) Staining for IgG4 reveals abundant positive inflammatory cells (>10/HPF). Type 2 AIP (idiopathic duct-centric pancreatitis): (d) periductal inflammation with fibrosis and pathognomic granulocyte epithelial lesion (arrow). Staining for IgG4 is negative (or scant positivity, ≤10/HPF).

Figure 51.2  Features of AIP on CT. (a) Typical feature: diffuse enlargement of the pancreas, which shows delayed enhancement (brighter on the venous phase than the arterial phase of contrast). Only arterial phase image is shown here to illustrate periaortic fibrosis (retroperitoneal fibrosis, arrow) and renal lesions (arrowhead). (b) Supportive feature: focal enlargement of pancreatic tail with delayed enhancement (venous phase is shown here). No atypical features are present. (c) Atypical features: focal enlargement in the pancreatic tail with low density mass (arrowhead), upstream duct dilatation, and abrupt duct cutoff (arrow).

Figure 51.3  The diagnostic approach to diagnosing both type 1 and type 2 AIP and differentiating AIP from pancreatic cancer (PC). While Type 2 AIP can be diagnosed based only on histology currently, Type 1 AIP can be diagnosed noninvasively in about 70% cases. As shown, presence of typical imaging with any collateral evidence or presence of strong collateral evidence with supportive imaging is sufficient for diagnosis of Type 1 AIP. With moderate collateral evidence and supportive imaging, positive steroid response is required. See text for details. Asterisk (*) indicates in presence of atypical imaging features, negative workup for pancreatic cancer including FNA required. Dagger (†): The subgroup with mild collateral evidence without typical imaging can be diagnosed based on one of two strategies: EUS biopsy or a combination of ERP and steroid trial. (ERP, endoscopic retrograde pancreatography; FNA, fine-needle aspiration; IgG4, immunoglobulin G4.)

Figure 53.1  Surgical treatment algorithm for intractable pain depending on the size of the main pancreatic duct with or without an inflammatory head mass (MPD, main pancreatic duct; PJ, pancreaticojejunostomy).

Figure 53.2  Surgical treatment algorithm for biliary obstruction depending on the size of the main pancreatic duct and head pathology (MPD, main pancreatic duct).

Figure 53.3  Algorithm for surgical decision making in duodenal obstruction in CP (GJ, gastrojejunostomy; TV, truncal vagotomy).

Figure 54.1  Contrast-enhanced CT of a patient with chronic pancreatitis and an inflammatory mass in the head of the pancreas.

Figure 54.2  Endoscopic retrograde cholangiopancreatograhy of a patient with an advanced stage of chronic pancreatitis causing the following: stenosis of the intrapancreatic segment of the common bile duct; stenosis of the prepapillary pancreatic main duct with poststenotic dilatations; and a segmental and extended stenosis of the duodenum. The patient suffered recurrent jaundice and an increasing gastric outlet syndrome.

Figure 54.3  Duodenum-preserving subtotal pancreatic head resection. Most important, the following are preserved: dorsal capsule of pancreatic head; posterior branch of gastroduodenal artery; anterior and posterior branches of inferior pancreaticoduodenal artery.

Figure 54.4  Modification of duodenum-preserving pancreatic head resection because of severe stenosis of the prepapillary common bile duct. An internal anastomosis between the common bile duct and the jejunal loop has been created.

Figure 54.5  Combination of duodenum-preserving subtotal pancreatic head resection with duct drainage is shown. In case of multiple stenoses and dilatations and pancreatic main duct stones, an additional jejunal loop is used for an additional side-to-side anastomosis between pancreatic main duct of the neck, body, and tail of the pancreas and the excluded jejunal loop. [From Beger & Bittner, 1987 (23). Reproduced with permission from Springer Science + Business Media.]

Figure 54.6  The Bern modification of duodenum-preserving pancreatic head resection; the inflammatory tissue of the pancreatic head is cored out. Transection of the pancreatic neck is avoided. The pancreatic main duct is anastomosed with an excluded jejunal loop.

Figure 55.1  Chronic pancreatitis with inflammatory mass involving the head of the gland; note multiple calcifications.

Figure 55.2  Chronic pancreatitis limited to body and tail; note moderately dilated pancreatic duct. The proximal head parenchyma was normal, and the pancreatic duct was not dilated.

Figure 55.3  Chronic pancreatitis with diffusely enlarged pancreas with no ductal dilatation.

Title page

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Library of Congress Cataloging-in-Publication Data

Pancreatic cancer, cystic neoplasms and endocrine tumors : diagnosis and management / edited by Hans G. Beger, Akimasa Nakao, John P. Neoptolemos, Shu You Peng, Michael G. Sarr.

        p. ; cm.

    Includes index.

    ISBN 978-0-470-67318-8 (cloth)

    I. Beger, H. G. (Hans G.), editor. II. Nakao, Akimasa, editor. III. Neoptolemos, John, editor. IV. Peng, Shu You, editor. V. Sarr, Michael G., 1950-, editor.

    [DNLM: 1.  Pancreatic Neoplasms—diagnosis. 2.  Neoplasms, Cystic, Mucinous, and Serous—diagnosis. 3.  Neoplasms, Cystic, Mucinous, and Serous—therapy. 4.  Neuroendocrine Tumors—diagnosis. 5.  Neuroendocrine Tumors—therapy. 6.  Pancreatic Neoplasms—therapy.  WI 810]

    RC280.P25

    616.99′437—dc23

                                                                                                                                                            2014048459

A catalogue record for this book is available from the British Library.

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Cover images courtesy of the author

Cover design by Sarah Dickinson

Contributors

Hana Algül MD, MPH

Associate Professor

II. Medizinische Klinik

Klinikum rechts der Isar

Technische Universität München

Munich, Germany

Peter J. Allen MD, FACS

Attending Surgeon

Department of Surgery

Memorial Sloan Kettering Cancer Center

New York, New York, USA

Åke Andrén-Sandberg MD, PhD

Professor of Surgery

Department of Surgery

Karolinska Institutet

Karolinska University Hospital

Stockholm, Sweden

M.K. Angele Dr med

Oberarzt

Pankreaszentrum

Klinikum der Universität München

Campus Großhadern

Ludwig-Maximilians-Universität München

Munich, Germany

Volker Assfalg MD

Consultant Surgeon

Department of Surgery

Klinikum rechts der Isar

Technische Universität München

Munich, Germany

Savio G. Barreto MBBS, MS, PhD

Consultant Surgical Oncologist

Gastrointestinal and Hepato-Pancreato-Biliary Surgical Oncology

GI Disease Management Group

Tata Memorial Centre

Mumbai, India

Detlef K. Bartsch Dr med

Chairman, Department of Visceral-, Thoracic- and Vascular Surgery

National Case Collection of Familial Pancreatic Cancer of the Deutsche Krebshilfe (FaPaCa)

Department of Surgery

Philipps-Universität Marburg

Marburg, Germany

Claudio Bassi MD, FRCS, FACS

Professor

The Pancreas Institute

Unit of Surgery B

G.B. Rossi Hospital

University of Verona Hospital Trust

Verona, Italy

Hans G. Beger MD, FACS

Emeritus Professor of Surgery

Universitätsklinikum Ulm

Universität Ulm

Ulm, Germany

William R. Brugge MD

Professor of Medicine, Harvard Medical School

Gastrointestinal Unit

Massachusetts General Hospital

Boston, Massachusetts, USA

C.J. Bruns Dr med

Direktorin, Universitätsklinik für Allgemein-, Viszeral- und Gefäßchirurgie Magdeburg

Frau Professor, Medizinische Fakultät

Universitätsklinikum Magdeburg

Otto-von-Guericke-Universität Magdeburg

Magdeburg, Germany

O.R.C. Busch MD, PhD

Professor of Surgery

Department of Surgery

Academic Medical Center

Amsterdam, The Netherlands

Xiujun Cai MD, ELSA, FACS

Professor

Department of General Surgery

Sir Run Run Shaw Hospital College of Medicine

Zhejiang University

Hangzhou, China

Suresh T. Chari MD

Professor of Medicine, Department of Medicine

Consultant, Division of Gastroenterology and Hepatology

Mayo Clinic College of Medicine

Rochester, Minnesota, USA

Lirong Chen MD, PhD

Director, Professor

Department of Pathology

Second Affiliated Hospital

Zhejiang University School of Medicine

Hangzhou, China

John D. Christein MD

Associate Professor

Department of Surgery

University of Alabama at Birmingham

Birmingham, Alabama, USA

Kathleen K. Christians MD

Professor of Surgery

Pancreatic Cancer Program

Department of Surgery

Division of Surgical Oncology

Medical College of Wisconsin

Milwaukee, Wisconsin, USA

Trevor Cox BSc, MSc, PhD

Director of Statistics and Bioinformatics Unit

The Liverpool Cancer Research UK Trials Unit

Department of Molecular and Clinical Cancer Medicine Centre

University of Liverpool

Royal Liverpool University Hospital

Liverpool, UK

Marius Distler MD

General Surgeon

Department of Visceral, Thoracic, and Vascular Surgery

Universitätsklinikum Carl Gustav Carus

Technische Universität Dresden

Dresden, Germany

J. Enrique Domínguez-Muñoz MD, PhD

Professor and Director

Department of Gastroenterology and Hepatology

University Hospital of Santiago de Compostela

Santiago de Compostela, Spain

Douglas B. Evans MD

Ausman Foundation Professor of Surgery

Pancreatic Cancer Program

Chair, Department of Surgery

Medical College of Wisconsin

Milwaukee, Wisconsin, USA

Michael B. Farnell MD

Professor of Surgery

Department of Surgery

Mayo Clinic

Rochester, Minnesota, USA

Volker Fendrich Dr med

Vice Chairman, Department of Visceral-, Thoracic- and Vascular Surgery

National Case Collection of Familial Pancreatic Cancer of the Deutsche Krebshilfe (FaPaCa)

Department of Surgery

Philipps-Universität Marburg

Marburg, Germany

Carlos Fernández-del Castillo MD

Director, Pancreas and Biliary Surgery Program

Professor of Surgery, Department of Surgery

Massachusetts General Hospital

Harvard Medical School

Boston, Massachusetts, USA

Zhi Ven Fong MD

Resident in Surgery

Department of Surgery

Massachusetts General Hospital

Boston, Massachusetts, USA

Helmut Friess MD

Director

Department of Surgery

Klinikum rechts der Isar

Technische Universität München

Munich, Germany

Ben George MD

Assistant Professor of Medicine

Pancreatic Cancer Program

Department of Medicine

Division of Surgical Hematology and Oncology

Medical College of Wisconsin

Milwaukee, Wisconsin, USA

Paula Ghaneh MB, ChB, MD, FRCS

Professor of Surgery

Deputy Director

The Liverpool Cancer Research UK Trials Unit

Department of Molecular and Clinical Cancer Medicine Centre

University of Liverpool

Royal Liverpool University Hospital

Liverpool, UK

Hidemi Goto MD, PhD

Professor

Department of Gastroenterology and Hepatology

Nagoya University Graduate School of Medicine

Nagoya, Japan

D.J. Gouma MD, PhD

Emeritus Professor of Surgery

Department of Surgery

Academic Medical Center

Amsterdam, The Netherlands

Rondell Graham MBBS

Fellow in Molecular Genetic Pathology

Department of Pathology

Mayo Clinic

Rochester, Minnesota, USA

Robert Grützmann MD, PhD

Professor, Consultant Pancreas Surgery

Department of Visceral, Thoracic and Vascular Surgery

Universitätsklinikum Carl Gustav Carus

Technische Universität Dresden

Dresden, Germany

Christopher Halloran BSc, MB, ChB, MD, FRCS

Clinical Senior Lecturer in Surgery

The Liverpool Cancer Research UK Trials Unit

Department of Molecular and Clinical Cancer Medicine Centre

University of Liverpool

Royal Liverpool University Hospital

Liverpool, UK

Kenji Hashimoto MD

Resident

Department of Hepatobiliary and Pancreatic Oncology

National Cancer Center Hospital

Tokyo, Japan

Susumu Hijioka MD, PhD

Chief Physician

Department of Gastroenterology

Aichi Cancer Center Hospital

Nagoya, Japan

Satoshi Hirano MD, PhD

Professor and Chairman

Department of Gastroenterological Surgery II

Hokkaido University Graduate School of Medicine

Sapporo, Japan

Yoshiki Hirooka PhD

Associate Professor

Department of Endoscopy

Nagoya University Hospital

Nagoya, Japan

De Fei Hong MD

Professor and Chairman

Department of Surgery

Zhejiang Provincial People's Hospital

Hangzhou, China

Norbert Hüser MD

Associate Professor

Department of Surgery

Klinikum rechts der Isar

Technische Universität München

Munich, Germany

Julio Iglesias-Garcia MD, PhD

Consultant

Department of Gastroenterology and Hepatology

University Hospital of Santiago de Compostela

Santiago de Compostela, Spain

Masafumi Ikeda MD

Chief

Department of Hepatobiliary and Pancreatic Oncology

National Cancer Center Hospital East

Chiba, Japan

Osamu Ishikawa MD

Emeritus Director of Hospital

Department of Surgery

Osaka Medical Center for Cancer and Cardiovascular Diseases

Osaka, Japan

Yuri Ito PhD

Biostatistician

Department of Epidemiology

Osaka Medical Center for Cancer and Cardiovascular Diseases

Osaka, Japan

Takao Itoi MD, PhD, FASGE

Associate Professor

Department of Gastroenterology and Hepatology

Tokyo Medical University

Tokyo, Japan

K.-W. Jauch Dr med

Ärztlicher Direktor

Chirurgische Klinik und Poliklinik

Campus Großhadern

Ludwig-Maximilians-Universität München

Munich, Germany

Tobias Keck MD, MBA, FACS

Professor and Chairman

Department of Surgery

University of Schleswig-Holstein, Campus Lübeck

Lübeck, Germany

Song Cheol Kim MD, PhD

Professor

Department of Surgery

Ulsan University College of Medicine and Asan Medical Center 388-1

Seoul, Korea

A. Kleespies Dr med

Oberarzt, Koordinator

Pankreaszentrum

Klinikum der Universität München

Campus