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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1100_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Preface
- •Contents
- •Contributors
- •Part I
- •Esophageal Surgery
- •Tracheo-Esophageal Fistula
- •Overview
- •Etiology
- •Clinical Presentation
- •Diagnosis
- •Management
- •Conservative Management
- •Endoscopic Management
- •Operative Management
- •Postesophagectomy TEF
- •Postintubation TEF
- •Bronchoesophageal Fistula
- •Prevention of Tracheoesophageal Fistula
- •Outcomes
- •Conclusion
- •Five Key Points to Avoid Complications
- •Five Key Points to Diagnose or Manage Complications Intra or Postoperatively
- •References
- •Esophageal Strictures Refractory to Endoscopic Dilatation
- •Introduction
- •Etiology of Esophageal Strictures
- •Treatment
- •Treatment of Benign Esophageal Strictures
- •Nonsurgical Options
- •Endoscopic Dilatation
- •Steroid Injection
- •Esophageal Stenting
- •Rendez-Vous Procedure
- •Incisional Therapy
- •Surgical Options
- •Antireflux Surgery for Peptic Strictures
- •Esophagectomy
- •Malignant Esophageal Strictures
- •Endoscopic Treatment
- •Dilatation
- •Stent Placement
- •Laser Therapy
- •Brachytherapy
- •Chemotherapy and Radiation Therapy
- •Surgical Treatment
- •Conclusion
- •Key Points for Avoiding Postsurgical Esophageal Strictures
- •Key Points for Managing Esophageal Strictures
- •References
- •Esophageal Anastomotic Leak
- •Introduction
- •Risk Factors for Anastomotic Leak
- •Presentation and Identification of a Leak
- •Prevention and Management of Anastomotic Leaks
- •Future Directions
- •Conclusion
- •Key Points on Avoiding an Esophageal Anastomotic Leak
- •Key Points on Diagnosis and Managing an Esophageal Anastomotic Leak
- •References
- •Transhiatal Esophagectomy—Intraoperative Disasters
- •Introduction
- •Preoperative Risk Factors for Bleeding with a THE
- •General Considerations
- •Anesthetic Considerations
- •Conduct of the Operation
- •Bleeding Scenarios During THE
- •Tracheal Tear
- •Summary
- •Key Points: Avoiding Catastrophic Complications—Mediastinal Bleeding and Airway Injury—During Transhiatal Esophagectomy
- •Key Points: Diagnosing and Managing Catastrophic Complications—Mediastinal Bleeding and Airway Injury—During Transhiatal Esophagectomy
- •References
- •Chyle Leak After Esophageal Surgery
- •Introduction
- •Historical Review
- •Basic Science
- •Embryology
- •Anatomy
- •Physiology
- •Composition of Chyle
- •Chylothorax
- •Etiology/Cause
- •Post-esophagectomy Chylothorax
- •Diagnosis
- •Clinical Features
- •Fluid Studies
- •Imaging
- •Treatment
- •Conservative Management
- •Surgical Management
- •Summary
- •Key Points on Avoiding an Esophageal Anastomotic Leak
- •Key Points on Diagnosis and Managing an Esophageal Anastomotic Leak
- •References
- •Evaluation of the Vocal Cords
- •Treatment of Unilateral Vocal Cord Dysfunction
- •Injection Augmentation
- •Framework Surgery for Unilateral Vocal Cord Dysfunction
- •Treatment of Bilateral Vocal Paralysis
- •Key Summary Points
- •References
- •Introduction
- •Pathophysiology
- •Classification
- •Symptoms
- •Diagnosis
- •Management of Airway, Hoarseness, and Vocal Cord Dysfunction After Esophagectomy
- •Introduction
- •Vocal Fold Dysfunction
- •Symptoms of Unilateral Vocal Cord Dysfunction
- •Symptoms of Bilateral Vocal Cord Dysfunction
- •Treatment
- •Complications
- •Conclusion
- •Five Key Points on How to Avoid Complications
- •Five Key Points on Diagnosing and/or Managing the Complications Either Intraoperatively or Postoperatively
- •References
- •Intraoperative Solutions for the Gastric Conduit that Will Not Reach
- •Colon as an Alternative Conduit
- •Jejunum as an Alternative Conduit
- •Pedicled Jejunal Interposition
- •Free Jejunal Interposition
- •Summary
- •Key Points
- •References
- •Injury to the Right Gastroepiploic Artery
- •Introduction
- •Anatomy of the RGEA
- •Vascular Considerations in Esophagectomy
- •Preoperative Evaluation of the RGEA
- •Preparation and Mobilization of the Gastric Conduit
- •Techniques for Improving Tissue Oxygenation
- •Tension-Free Anastomosis
- •“Supercharging”
- •Venous Drainage
- •Conclusion
- •Five Key Points: Avoiding Injury to the Right Gastroepiploic Artery
- •References
- •Intra-Operative Solutions for Ischemic Gastric Conduit
- •Gastric Esophageal Replacement Conduit
- •Diagnosis of Gastric Conduit Ischemia
- •Summary
- •Key Points for Avoiding Gastric Conduit Necrosis
- •Key Points for Managing Gastric Conduit Necrosis Postoperatively
- •References
- •Jejunal Feeding Tube Complications
- •Introduction
- •Technique for Placement
- •Open Surgical Jejunostomy Tubes
- •Laparoscopic Jejunostomy Tubes
- •Complications
- •Bowel Necrosis
- •Bowel Obstruction
- •Tube Dysfunction
- •Infectious Complications
- •Aspiration
- •Conclusion
- •Key Points
- •References
- •Part II
- •Gastric Surgery
- •Gastroparesis
- •Etiology
- •Clinical Presentation and Evaluation
- •Management
- •Bile Reflux
- •Etiology
- •Clinical Presentation and Evaluation
- •Management
- •Conclusion
- •Key Points (Prevention)
- •Key Points (Management)
- •References
- •Dealing with Dumping Syndrome
- •Introduction
- •Diagnosis
- •Prevention
- •Management of Dumping Syndrome
- •Diet
- •Pharmacologic Therapy
- •Acarbose
- •Somatostatin Analogs
- •Studies of the Fast-Acting Somatostatin Analog Octreotide
- •Studies of Long-Acting Octreotide LAR
- •Adverse Effects of Somatostatin Analogs
- •Surgical Treatment
- •Conversion of Billroth II to Billroth I Anastomosis
- •Roux-en-Y Conversion
- •Continuous Enteral Feeding
- •Conclusion
- •Key Points
- •References
- •Introduction
- •Epidemiology
- •Etiology
- •Pathophysiology
- •Clinical History
- •Physical Findings
- •Differential Diagnosis
- •Diagnosis
- •Noninvasive Imaging Studies
- •Treatment
- •Medical Treatment
- •Endoscopic/Interventional Radiology
- •Surgical Intervention
- •Summary
- •Key Points for Avoiding
- •Key Points for Diagnosing/Managing
- •References
- •Duodenal Stump Blowout
- •Introduction
- •Clinical Presentation of Blowout
- •Mechanisms Contributing to Blowout
- •Staple Line Failure
- •Distal Obstruction
- •Malnutrition
- •The Difficult Duodenum
- •Techniques for Reducing the Risk of Blowout
- •Management of the Difficult Duodenum
- •General Principles of Closure
- •Nissen Technique
- •Bancroft Technique
- •Tube Duodenostomy and Drainage
- •Management of Stump Blowout
- •Medical Management
- •Percutaneous Radiologic Techniques
- •The Decision to Operate and Surgical Approach
- •Summary of Management
- •Ramifications of Blowout
- •Conclusions
- •Key Points: Avoiding Duodenal Stump Blowout
- •Key Points: Diagnosing and Managing Stump Blowout
- •References
- •Postoperative Complications After Surgery for Gastric Cancer: Anastomotic Leakage
- •Introduction
- •Incidence
- •Prospective Factors
- •Detection
- •Differential Diagnosis
- •General Management
- •External Drainage
- •Treatment of the Leakage Site
- •Duodenal Stump Leakage
- •Summary
- •Five Key Points to Avoid Anastomotic Leakage
- •Five Key Points to Diagnose and Manage Leakage
- •References
- •Part III
- •Hepatobiliary and Pancreatic Surgery
- •Introduction
- •Definition of PHI
- •Risk Factors for PHI
- •Prevention of PHI
- •Systematic Volumetry of the “Fully Functioning” Part of the Liver
- •Portal Vein Embolization
- •Limiting the Duration of Preoperative Chemotherapy
- •Treatment of PHI
- •Conclusion
- •Key Points
- •References
- •Biliary Leaks and Thoracobiliary Fistula
- •Introduction
- •Definitions
- •Biliary Leak and Grading System
- •Controlled and Uncontrolled Biliary Leaks
- •Source
- •Risk Factors and Prevention
- •Prevention
- •Risk Factors for Bile Leaks After Extrahepatic Bilioenteric Anastomosis
- •Prevention
- •Risk Factors for Bile Leak After Liver Resection
- •Prevention of Biliary Leaks After Hepatectomy
- •Intraoperative Tests for Bile Leaks
- •Postoperative Drains
- •Diagnosis
- •Investigations
- •Ultrasonography or CT Scan
- •Fistulogram
- •MRC, ERC, and PTC
- •HIDA
- •Management
- •Medical Management
- •Endoscopic Management
- •Interventional Radiology
- •Combined Endoscopic and Interventional Radiology Approaches—Rendezvous Procedures
- •Thoracobiliary Fistula
- •Diagnosis
- •Treatment
- •Five Key Points to Avoid Complications
- •Five Key Points to Diagnosis or Manage Complications
- •References
- •Contralateral Bile Duct Injury During Hepatic Resection
- •Introduction
- •Etiology and Risk Factors
- •Anatomical Variations
- •Difficult Surgical Resection and Reoperation
- •Type of Liver Resection
- •Aggressive Dissection and Devascularization of Bile Ducts
- •Initial Investigations and Management
- •Initial Investigations
- •Stabilization and Operative Planning
- •No Evidence of Distal Obstruction with Fistula
- •Evidence of Distal Obstruction with Fistula
- •Evidence of Distal Obstruction but no Fistula
- •Definitive Management
- •Anatomy Relevant to Operative Repair of Biliary Outflow of Remnant
- •Operative Repair
- •Repair of Injury to Right Liver Outflow
- •Repair of Injury to Left Liver Outflow
- •Prevention of Contralateral Bile Duct Injury
- •Attention to Variation in Biliary
- •Intrahepatic Control of Biliary Radicals
- •Tumor Close to the Hilum
- •Outcomes
- •Five Key Points to Avoid Contralateral Bile Duct Injury
- •Five Key Points to Diagnose and Treat Contralateral Bile Duct Injury
- •References
- •Massive Intraoperative Hemorrhage During Hepato-Biliary and Pancreatic Surgery
- •Introduction
- •Hemorrhage During Liver Surgery
- •Magnitude of Problem
- •Hepatic Vascular Anatomy
- •Prevention of Major Hemorrhage During Hepatic Resection
- •Techniques Aimed at Reducing Blood Loss During Hepatic Surgery
- •Deliberate Dissection and Exposure of Retro-Hepatic Vena Cava and Major Hepatic Veins
- •Hepatic Inflow Control
- •Vascular Isolation
- •Acute Normovolemic Hemodilution (ANH)
- •Management of Intra-Operating Bleeding During Liver Resection
- •Massive Hemorrhage During Pancreatic Surgery
- •Pancreatic Anatomy
- •Bleeding During Pancreaticoduodenectomy
- •Summary
- •5 Key Points to Avoid Complications
- •References
- •Intraoperative Injury to Hepatic Arterial Structures
- •Introduction
- •Normal Anatomy of the Hepatic Arterial Vasculature
- •Variant Anatomy of the Hepatic Arterial Vasculature
- •Replaced and Accessory Right Hepatic Arteries
- •Replaced and Accessory Left Hepatic Arteries
- •Replaced Common Hepatic Artery
- •Celiac Artery Stenosis
- •Preoperative Radiographic Assessment
- •Preoperative Considerations
- •Intraoperative Considerations
- •Specific Intraoperative Considerations
- •Pancreaticoduodenectomy (PD)
- •Replaced/Accessory Right Hepatic Artery
- •Replaced Common Hepatic Artery
- •Celiac Artery Stenosis
- •Hemi-hepatectomy
- •Conclusions
- •Key Points: Preoperative Interventions
- •Key Points: Intraoperative Principles
- •References
- •Hepatic Abscess
- •Etiology
- •Diagnosis
- •Computed Tomography
- •Ultrasound
- •Magnetic Resonance Imaging
- •Treatment
- •Five Key Points on How to Avoid Complications
- •Five Separate Key Points on Diagnosing and/or Managing the Complication
- •References
- •Hepaticojejunostomy Anastomotic Strictures
- •Introduction
- •Diagnosis
- •Clinical and Biological Presentation
- •Morphological Evaluation
- •Incidence and Risk Factors According to the Clinical Context
- •Iatrogenic Bile Duct Injury
- •Liver Transplantation (LT)
- •Pancreatic Head Resection
- •Choledochal Cyst
- •Therapeutic Options
- •Conservative Management
- •Choice of the Approach
- •To Stent or Not to Stent?
- •Periprocedural Management
- •Surgery
- •Revisionary Surgery
- •Liver Resection
- •Liver Transplantation (LT)
- •Key Points: How to Avoid HJ Stricture
- •Key Points: Diagnostic and Management
- •References
- •Defining Pancreatico-Jejunostomy Strictures (PJS) and Pancreatico-Jejunostomy Strictures (PGS) by Symptoms, Morphology and Function
- •Management of Intractable Pain Due to PJA or PGS Stenosis in Surgical Case Series
- •Endoscopic Techniques for Management of PJA Strictures
- •Technical Clinical Results for ERP
- •EUS-Guided Access and Drainage
- •EUS-Guided Rendezvous
- •Pancreatic Antegrade Needle Knife (PANK) Technique
- •EUS-Guided Pancreatogastrostomy
- •Jejunal Stenosis Mimicking PJA Stenosis
- •Conclusions
- •Key Points
- •References
- •Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
- •Introduction
- •Pathophysiology
- •Diagnosis: Clinical Manifestations and Blood Tests
- •Diagnosis: Imaging Tests
- •Treatment
- •Anticoagulation
- •Interventional Techniques
- •Surgery
- •Conclusion
- •Key Points for Diagnosis
- •Key Points for Treatment
- •References
- •Postpancreatectomy Hemorrhage: Early and Late
- •Introduction
- •Prevention of Late PPH
- •The Falciform Ligament
- •The Portal Dissection
- •GDA Ligation
- •Reinforcing the Pancreatic Transection Site (Distal Pancreatectomy)
- •Diagnosis of Late PPH
- •Symptoms/Signs
- •Imaging for Late PPH
- •Management of PPH
- •Early PPH
- •Late PPH
- •Conclusion
- •Key Points to Avoid Complications
- •Key Points to Diagnose/Manage
- •References
- •Major Disruptions of Pancreaticojejunostomy
- •Introduction
- •Conclusion
- •Key Points: How to Avoid Complications
- •Key Points: Diagnosis/Management
- •References
- •Persistent Pancreatic Fistula
- •Introduction
- •Definition of Pancreatic Fistula
- •Procedure-Specific Incidence and Risk Factors for Pancreatic Fistula
- •Pancreaticoduodenectomy
- •Distal Pancretectomy
- •Duodenum-Preserving Pancreatic Head Resection/Lateral Pancreaticojejunostomy
- •Pancreatic Pseudocyst Drainage/Pancreatic Necrosectomy
- •Other Pancreatic Resections
- •Prevention of Pancreatic Fistula
- •Complications of Pancreatic Fistula
- •Management of Pancreatic Fistula
- •Initial Management
- •Delineation of Pancreatic Duct
- •Definitive Treatment of Pancreatic Fistula
- •Operative Management of Pancreatic Fistula
- •Conclusion
- •Key Points to Avoid Complications
- •Key Points: Diagnosing and/or Managing Complications Either Intra- or Postoperatively
- •References
- •Management of Chyle Leaks Following Pancreatic Resection
- •Introduction
- •Background
- •Anatomy and Physiology of Visceral Lymphatics
- •Diagnosis of a Chyle Leak
- •Management of a Chyle Leak
- •The Contained Chyle Leak
- •Chylous Ascites
- •Management of Refractory Chyle Leaks
- •Conclusion
- •Key Points in Managing a Chyle Leak
- •References
- •Overview
- •Diagnosis
- •Prevention
- •Identifying Risk Factors
- •Role of Octreotide
- •Role of Pancreatic Stenting
- •Dissection and Management of the Pancreatic Stump
- •Minimally Invasive Versus Open Techniques
- •Drain Placement and Management
- •Management of Complications of Pancreatic Leak
- •Goal-Directed Resuscitation and Infection Control
- •Further Definition of Anatomy and Source Control
- •Optimizing Patient Clinical Status for Ongoing Conservative Management
- •Deliberate Reintervention When Clinically Indicated
- •Summary
- •Key Points on Avoiding Complications
- •Key Points on Diagnosis/Management of Complications
- •References
- •Part IV
- •Colorectal Surgery
- •Pearls for the Small Bowel and Colon That Will Not Reach
- •Introduction
- •Anatomic Constraints
- •Diagnosing the Problem
- •Specific Techniques: Making It Reach
- •Colorectal and Coloanal Anastomosis
- •Lateral-to-Medial Approach
- •Medial-to-Lateral Approach
- •Ileal-Pouch Anal Anastomosis (IPAA)
- •Stomas that Do Not Reach
- •Bailout Maneuvers—It Just Does Not Reach
- •Conclusions
- •Key Points on How to Avoid the Complication
- •Key Points on Diagnosing/Managing the Complication
- •References
- •Anastomotic Leak/Pelvic Abscess
- •Introduction
- •Prevention
- •Diagnosis and Management
- •Diagnosis
- •Management
- •Type I: Generalized Peritonitis
- •Type II: Localized Pelvic Abscess
- •Type III: Fistula
- •Long-Term Outcome
- •Need for a Permanent Stoma
- •Stenosis or Stricture
- •Local Recurrence
- •References
- •Management of Anastomotic Stricture
- •Introduction
- •Etiology of Anastomotic Stricture
- •Presentation and Diagnosis
- •Nonoperative Treatment
- •Balloon Dilation and Endoscopic Options
- •Stents
- •Operative Treatment
- •Reoperative Surgery
- •Anastomotic Revision and Diverting Stomas
- •New Technology
- •Conclusion
- •To Avoid Anastomotic Strictures in Colorectal Resections
- •Five Points on Diagnosing and Managing Anastomotic Strictures
- •References
- •Intraoperative Ureteral Injury
- •Introduction
- •Role of Preoperative Stenting
- •Incidence of Ureteric Injury and Early Identification of Injury
- •Placement of Ureteral Stents
- •Detection of Ureter Injury
- •Management of Ureter Injury
- •Proximal Third Injuries
- •Middle Third Ureteral Injuries
- •Lower Third Ureteral Injuries
- •Delayed Ureteral Transection or Ligation
- •Management Post Repair
- •Outcomes
- •Key Points to Avoiding Injury
- •Key Points to Diagnosis and Manage the Complication
- •References
- •Introduction
- •Anatomy
- •Incidence
- •Types of Prostatic Urethral Injury
- •Prevention
- •Detection
- •Management
- •Delayed Rectourethral Fistula
- •Conclusion
- •Key Points on Avoiding Complications
- •Key Points on Diagnosing/Managing Prostatic Urethral Injuries
- •References
- •Vaginal Injury During Stapled Anastomosis
- •Introduction
- •How to Avoid Vaginal Injury
- •How to Fix Vaginal Injury
- •Key Points on How to Avoid Vaginal Injury
- •Management of Rectovaginal Fistula
- •Introduction
- •General Principles
- •Local Repair
- •Mucosal Advancement Flap Repair
- •Endorectal Advancement Flap with Muscular Plication (Anterior Levatorplasty)
- •Transanal Sleeve Advancement Flap
- •Transvaginal Repair
- •Fistulotomy
- •Ligation of Intersphincteric FistulaTract
- •Biological Agents: Fibrin Glue and Fistula Plug
- •Miscellaneous
- •Tissue Transfer Procedures
- •Gracilis Muscle Interposition Flap
- •Martius Flap
- •Abdominal Procedure
- •Transperineal Omental Flap
- •Perioperative Management
- •Conclusion
- •Key Points to Avoid Complications
- •Key Points on Diagnosis and/or Managing Complications
- •References
- •Management of Presacral/Pelvic Bleeding
- •Introduction
- •Anatomy
- •Patterns of Injury
- •Management
- •Role of the Anaesthesiologist
- •Role of the Surgeon
- •Minimal-Access Surgery
- •The Postoperative Period
- •Summary
- •Key Points
- •References
- •Introduction
- •Preoperative Evaluation
- •Medical Comorbidities
- •Radiation Therapy
- •Chemotherapy
- •Imaging
- •Timing of Reconstruction
- •Classification of Defect
- •Reconstructive Surgical Tenants
- •Adjuncts to Flap Surgery
- •Negative Pressure Wound Therapy
- •Tissue Expansion
- •Biologic Tissue Matrices
- •Rectus Abdominis Muscle
- •Gracilis Muscle Flap
- •Gluteus Maximus Muscle
- •Pudendal Flap
- •Anteriolateral Thigh Flap
- •Postoperative Care
- •Ambulation
- •Drain Management
- •Complications
- •Summary
- •Key Points: Preventing Complications
- •Key Points: Managing Complications
- •References
- •Complications After TEM (Transanal Endoscopic Microsurgery) and TAMIS (Transanal Minimally Invasive Surgery)
- •Background
- •Complications of TEM and TAMIS
- •Postoperative Fever
- •Wound Dehiscence
- •Rectal Pain
- •Peritoneal Perforation
- •Pelvic Phlegmon and Abscess
- •Fistula
- •Bleeding
- •Incontinence
- •Conclusion
- •Key Points: Avoiding a Complication
- •Key Points: Managing/Diagnosing Septic Complications
- •References
- •Parastomal Hernia
- •Overview
- •Definition and Classification
- •Incidence
- •Pathophysiology
- •Risk Factors
- •Complications
- •Prevention
- •Preoperative Considerations
- •Operative Considerations
- •Diagnosis
- •History and Physical Exam
- •Imaging
- •Management
- •Nonoperative Management
- •Operative Management
- •Open Approach
- •Laparoscopic Approach
- •Postoperative Complications
- •Management of Recurrent Parastomal Hernias
- •Key Points: Diagnosing/Managing Parastomal Hernia
- •Key Points: Avoiding Parastomal Hernia Complications
- •References
- •Stoma Retraction/Ischemia/Stenosis
- •Introduction
- •Etiology/Incidence/Risk Factors
- •Prevention
- •Recognition/Assessment/Severity/Therapy
- •Conclusions
- •Five Keys Points in Diagnosing and Managing Stenosis, Retraction, and Ischemia in an Ostomy
- •Five Key Points on How to Avoid Tension and Ischemia in an Ostomy
- •References
- •Incontinence After Lateral Internal Sphincterotomy/Fistulotomy
- •Introduction
- •Lateral Internal Sphincterotomy
- •Fistulotomy
- •Management
- •Evaluation
- •Treatment
- •Injectables
- •Magnetic Bowel Sphincter
- •Sacral Nerve Stimulator
- •Artificial Bowel Sphincter
- •Diversion
- •Key Points: Strategies to Avoid the Complication of Incontinence
- •Key Points: Diagnosing and/or Managing the Complication of Incontinence Either Intraoperatively or Postoperatively
- •References
- •Anal Stenosis After Hemorrhoidectomy: Avoidance and Management
- •Introduction
- •Diagnosis
- •Classification of Stenosis
- •Treatment
- •Prevention
- •Nonoperative Intervention
- •Operative Intervention
- •Anatomic Versus Functional Stenoses
- •Preoperative Planning
- •Postoperative Care
- •Summary
- •Key Points: Managing Complications
- •References
- •Part V
- •Other Considerations
- •Delivering Bad News: Conversations with My Surgeon
- •Introduction
- •Informed Consent
- •The Family Does Not Want the Patient to be Fully Informed
- •Perioperative Death
- •When an Intraoperative Death Does Occur
- •Discussion of Unresectability or Metastatic Disease that Precludes Resection
- •Discussion of a Postoperative Complication
- •Discussion of the Unanticipated Major Postoperative Complication
- •Discussion of Operative Findings
- •The Need for Reoperation
- •Complications that Occur in your Absence from the Hospital
- •Withdrawal of Life-Sustaining Measures
- •Discussing the Pathology Report
- •Discussion of Long-term Survival Prospect
- •Management of the Difficult Family
- •References
- •Index

120 R. E. Roses and D. L. Fraker
after pancreaticoduodenectomy, Yeo and associates defined DGE as either (1) nasogastric tube
requirement for 10 or more days plus one of the
following: (a) emesis after nasogastric tube removal, (b) postoperative use of prokinetic agents
after postoperative day 10, (c) reinsertion of a nasogastric tube, or (d) failure to progress with diet;
or (2) nasogastric tube requirement fewer than
10 days plus two of (a) through (d) above [7].
The 10-day cutoff for nasogastric tube requirement has been adopted in some, but certainly not
all subsequent studies.
In practice, DGE or postoperative gastroparesis are often diagnoses of exclusion. Anastomotic leak (particularly an evolving pancreatic
fistula after pancreatoduodenectomy) may present with proximal ileus and be accompanied by
leukocytosis, tachycardia, or turbid output from a
postoperative drain. Mechanical obstruction can
likewise be difficult to differentiate from gastroparesis on clinical grounds alone. A CT scan with
enteric contrast is often an appropriate first imaging modality and can identify undrained fluid
collections, extraluminal air, or transition points
between enhanced and collapsed viscera. A dynamic upper GI contrast study may be more sensitive in identifying partial mechanical obstruction. The experienced gastrointestinal radiologist
will often identify delayed transit time as contrast
traverses the stomach and proximal bowel. The
use of barium for these studies may further enhance sensitivity but should be reserved for those
cases in which the index of suspicion for an enteric leak or high-grade mechanical obstruction
is low, as barium extravasation into the peritoneal cavity or retained barium can be problematic in these settings, respectively. Furthermore,
retained barium can limit interpretation of subsequent CT scans.
Gastric emptying scintigraphy provides perhaps the most nuanced assessment of gastric
emptying; however, the role of this study in evaluating the postoperative patient remains poorly
defined and standardized definitions of normal
scintigraphic findings after gastric resection remain elusive. In general, there is delay in the
emptying of solids and accelerated emptying of
liquids after partial gastrectomy [8]. After Roux-
en-y reconstruction, there is often retention of
solids in both gastric remnant and the Roux limb
[9]. Scintigraphy does allow assessment of regional emptying of the fundic and antral regions
and can be helpful in explaining dyspeptic symptoms, particularly when global gastric emptying
values are normal [10]. For example, nausea,
early satiety, and abdominal distention have been
associated with proximal gastric retention; in
contrast, vomiting is more often associated with
delayed distal GE.
Management
In the early postoperative period, gastroparesis
often necessitates prolonged NG tube decompression. Early dysmotility often improves with
time, and a deliberate management approach is
justified. Correction of hyperglycemia, electrolyte abnormalities, and the reduction of narcotic
use are recommended. While waiting for recovery, nutritional support is requisite, in the form
of either enteral feeding (if the patient has a jejunostomy feeding tube) or parenteral nutrition.
Depending on the severity of symptoms and the
scope of the initial operation, placement of a jejunostomy feeding tube or a decompressive gastrostomy tube may expedite recovery.
The use of promotility agents is sometimes
helpful and fairly safe although convincing evidence of efficacy in the postoperative setting is
lacking. Macrolide antibiotics (e.g., erythromycin) agonize the motilin receptor. In patients with
diabetes mellitus and delayed gastric emptying, intravenous administration of erythromycin
200 mg before a test meal has been shown to normalize gastric emptying of liquids and solids [11].
The clinical efficacy of oral erythromycin, however, has not been consistently demonstrated. In a
randomized placebo controlled trial, intravenous
erythromycin after pancreaticoduodenectomy
did not significantly reduce delayed gastric emptying as defined by the authors; though, fewer patients required reinsertion of a nasogastric tube or
retained liquids by scintigraphy in the treatment
group [7]. Even in those patients who do appear
to respond favorably, a tolerance phenomenon is

12112 Bile Reflux and Gastroparesis
frequently observed and drug interactions with
agents that are metabolized by CYP3A4 further
limit utility.
Metoclopramide is a dopamine-2 (D2) antagonist with apparent efficacy in a subset of
patients with gastroparesis. Sedative effects can
limit utility and extrapyramidal side effects,
though not as frequent as with older antipsychotic drugs (e.g., haloperidol and chlorpromazine),
can be irreversible. A majority of cases of tardive
dyskinesia occur with longer-term use, and limiting metoclopramide use to less than 3 months is
prudent.
Pyloroplasty when applicable has also been
proposed, and botulinum toxin injections may
transiently improve gastric emptying in a subset of patients. In the majority of postsurgical
patients who have undergone either gastric or
pancreatic resection, these approaches are not
relevant. Historically, completion or subtotal
gastrectomy was offered to patients with refractory gastroparesis. A number of reports from
single institutions support the efficacy of such
an approach [12, 13]. Importantly, these should
represent options of last resort considered only
after exhausting all more conservative measures.
In most cases, enteral access with a jejunostomy
feeding tube with or without a decompressive
gastrostomy and dietary modification affords
prompter improvement in the quality of life
than does near-total gastrectomy. Placement of
a percutaneous endoscopic gastrostomy (PEG)
tube with jejunostomy tube extension represents
a useful alternative to traditional enteral access
procedures in selected patients requiring gastric
decompression and distal enteral access for nutrition support.
More recent experiences with gastric electrical stimulation (GES) suggest an alternative therapeutic option. Initial studies in dogs demonstrated increased peristaltic pressure waves and the
gastric emptying rate with electrical stimulation
[14]. A series of small trials using implantable
electronic devices in patients with diabetic gastroparesis followed. Recently, patients with refractory postsurgical gastroparesis were reported
to achieve symptomatic improvement with GES
[15, 16]. Interestingly, the stimulation impulses
used (5 mA, duration 330 ms) are too weak to
excite gastric smooth muscles (hence the term
“gastric pacemaker” is a misnomer). Moreover,
objective measurements of gastric emptying have
not consistently demonstrated effect [17].
Bile Reflux
Etiology
Pancreaticobiliary reflux into the stomach is obligate after resection or ablation of the pylorus (e.g.,
pyloroplasty or Billroth I) or loop reconstruction
to a gastric remnant (e.g., gastrojejunostomy or
Billroth II). Only a subset of patients, however,
develop bile reflux gastritis or esophagitis as a
result. Billroth II reconstruction to a small gastric pouch may anticipate particularly severe bile
esophagitis and should be avoided (Fig. 12.1).
Resection of greater than 60 % of the distal stomach should be reconstructed with a Roux-en-Y
gastrojejunostomy to prevent this complication.
The syndrome of bile reflux has also been recognized after cholecystectomy. In this setting, it
has been attributed to loss of gallbladder reservoir function and continuous passage of biliary
Fig. 12.1 Enlarged hyperemic folds in gastric remnant,
after Billroth II reconstruction. (Image courtesy of Gregory Ginsberg, MD)

122 R. E. Roses and D. L. Fraker
Fig. 12.2 Erosive alkaline reflux esophagitis. (Image
courtesy of Gregory Ginsberg, MD)
secretions, more of which reflux into the stomach than would otherwise be the case (Fig. 12.2).
Delayed gastric emptying or gastric stasis may
be contributory in many cases as well, and the
denervating procedures of the past era of peptic
ulcer disease surgery (i.e., truncal vagotomy)
yielded an experience that informs the current
understanding of this clinical syndrome. In the
presence of gastric stasis, exposure of gastric
mucosa to duodenal fluids is increased. A higher
gastric pH may allow bacterial overgrowth and
subsequent conversion of bile salts to unconjugated bile acids, which are particularly noxious
to the gastric mucosa. Pathological changes in
the gastric mucosa develop over time and include
foveolar hyperplasia, glandular cystic degeneration, edema of the lamina propria, and vasocongestion of the mucosal capillaries [18].
Clinical Presentation and Evaluation
The occasional patient complains of profound reflux pain in the early postoperative period. More
often, symptoms evolve a year or more after the
index operation. A symptom complex of nausea,
pain, and bilious emesis is characteristic but, by
no means, specific to bile reflux. As with gastroparesis, other more common etiologies must be
excluded. Cross-sectional imaging or dynamic
upper gastrointestinal contrast studies are useful
for excluding mechanical obstruction. The former can rule out fluid collections as well, more
relevant in the early postoperative period. Upper
endoscopy may identify marginal ulceration or
mucosal irritation. Scintigraphy (bile reflux scan
or HIDA scan) may be useful, particularly in determining a role for remedial surgery. An abnormal study is not that informative. A normal study,
however, anticipates a poor response to surgical
management.
Management
A variety of pharmacologic agents have been
utilized in the treatment of bile reflux; none are
consistently effective. Sucralfate may buffer the
stomach or gastric remnant and provide symptomatic relief and is often a good first choice.
Cholestyramine has been advocated but is probably of little utility [19]. Promotility agents (e.g.,
metaclopromide) may have a role, particularly if
a contribution of gastroparesis is suspected. Persistent symptoms over months despite pharmacologic intervention in the face of an abnormal bile
reflux scan point to a role for remedial surgery.
In the patient with severe symptoms, objective
signs of bile reflux (e.g., endoscopic evidence of
gastritis, scintigraphy confirming duodenal reflux into the stomach) surgery can be considered.
A variety of operative approaches can be utilized
for the remediation of bile reflex. The most commonly chosen and most familiar is Roux-en Y
gastrojejunostomy; however, Braun entero-enterostomy and the Henley procedure (antiperistaltic jejunal interposition) are reasonable alternatives (Fig. 12.3). If Roux-en Y reconstruction is
selected, a limb in excess of 40 cm (some have
advocated > 60 cm) should be constructed to
maximize isolation of the stomach from duodenal secretions. Longer limbs (> 80 cm) should be
avoided to decrease the risk of malabsorption and
Roux stasis. Assuming careful patient selection, a
high rate of success can be expected.
The major disadvantage of Roux-en Y reconstruction is an incidence of “Roux stasis
syndrome,” generally attributed to small bowel
denervation and diminished prograde peristalsis

12312 Bile Reflux and Gastroparesis
Fig. 12.3 Isoperistaltic jejunal loop interposition. (Henley procedure)
in the Roux limb. Bacterial overgrowth, diarrhea,
jejunal ulceration, and impaired protein digestion
may result. Abdominal pain and vomiting are
typical symptoms and there is often overlap with
gastroparesis, as this syndrome is observed with
greater frequency in patients with larger gastric
remnants. These concerns may necessitate completion antrectomy or even subtotal gastrectomy,
and truncal vagotomy at the time of remediation
in the appropriate clinical setting.
While bilious emesis is mitigated by Roux-en
Y reconstruction, a number of larger published
experiences suggested recurrent symptoms in approximately 30 % of patients long term [20]. This
substantial rate of long-term morbidity justifies
consideration of other remedial approaches. Perhaps the simplest of these is creation of a Braun
enteroenterostomy. This is most applicable in
the setting of prior Billroth II construction and
is achieved by side-to-side anastomosis of the af-

124 R. E. Roses and D. L. Fraker
Fig. 12.4 “Uncut Roux” reconstruction
ferent limb to the jejunum at least 40 cm distal
to the gastrojejunostomy. Diminution of duodenal fluid into the stomach or gastric remnant
can be achieved with the application of a staple
line across the afferent limb just proximal to the
gastrojejunostomy. Use of a thoracoabdominal
(TA) stapler facilitates the creation of a partition
without transection, and may, therefore, preserve
prograde peristalsis through the small bowel.
Importantly, this partition is temporary in most
cases (recanalization is a likelihood over time).
For this reason, this so-called uncut Roux may
not be the best option in a younger patient for
whom effective long-term remediation is necessary (Fig. 12.4).
Interposition of an isoperistaltic segment of
small bowel between the gastric remnant and duodenum was advocated by Henley in the 1950s
for the management of dumping syndrome. The
Henley procedure has been used with reported
success for the treatment of Bile reflux. In the
setting of prior Billroth II reconstruction, the afferent limb just proximal to the gastrojejunostomy is divided. The jejunum is divided 20–45 cm
distal to the anastomosis at a point that allows for
convenient anastomosis to the proximal duodenum. Jejuno-duodenstomy and downstream jejunojejunostomy are performed to restore continuity. This configuration has been associated with
effective amelioration of biliopancreatic reflux
on scintigraphic examination [21] and may result
in less of the long-term morbidity associated with
Roux reconstruction.
Conclusion
Gastroparesis and bile reflux after foregut surgery remain distinct clinical challenges. Both
diagnoses require exclusion of other correctable
surgical complications, particularly mechanical
obstruction or undrained infection. Scintigraphic
studies can be used to confirm either diagnosis.
Even when the diagnosis has been secured, a trial
of conservative management is almost always in
order during which time attention to nutritional
status, correction of metabolic disturbances, and
reduction of narcotic exposure are critical. Pharmacologic therapies are associated with only
modest benefit, but may be helpful in selected
cases and are relatively safe. In the setting of
persistent severe refractory symptoms, remedial surgery should be considered. In the case of
gastroparesis, distal enteral feeding access with
gastric decompression may be an appropriate
intermediate step before subtotal gastrectomy. A
role for gastric electrical stimulation is evolving.
A variety of remedial operations for bile reflux
have been used with moderate success including
conversion to Roux-en Y reconstruction, Braun
enteroenterostomy, and Henley jejunal interposition.
Key Points (Prevention)
1. Although definitive data are lacking, antecolic
reconstruction after pylorus-preserving pancreaticoduodenectomy may be associated

12512 Bile Reflux and Gastroparesis
with a lower rate of delayed gastric emptying
compared to retrocolic reconstruction.
2. Gastric and intestinal denervation may contribute to the incidence of gastroparesis after
gastric resection favoring Billroth II over
Roux-en Y in appropriate circumstances.
3. Correction of hyperglycemia and electrolyte
abnormalities and the reduction of narcotic
use are self-recommending after abdominal
surgery and may decrease the incidence of
postoperative gastrointestinal dysmotility.
4.
Loop reconstruction to a small gastric pouch
may anticipate particularly
severe bile esoph-
agitis and should be avoided.
Key Points (Management)
1. Initial priorities in the management of postoperative gastroparesis include decompression
and treatment of postsurgical infection.
2. Bile reflux is most often a late complication
and must be distinguished from mechanical
obstruction.
3. Nutritional repletion is critical in the initial
management of gastroparesis or bile reflux.
When appropriate, surgical or percutaneous
enteral access should be obtained early.
4. Remedial surgery for gastroparesis or bile reflux should be reserved for refractory cases
after exclusion of reversible etiologies, nutritional repletion, and confirmatory scintigraphic studies.
References
1. Tani M, et al. Improvement of delayed gastric empty-
ing in pylorus-preserving pancreaticoduodenectomy:
results of a prospective, randomized, controlled trial.
Ann Surg. 2006;243(3):316–20.
2.
Qu H, et al. Clinical
emptying in patients after pancreaticoduodenectomy:
a systematic review and meta-analysis. Eur J Surg
Oncol. 2013;39(3):213–23.
3. Tran KT, et al. Pylorus preserving pancreaticoduo-
denectomy versus standard Whipple procedure: a
prospective, randomized, multicenter analysis of 170
patients with pancreatic and periampullary tumors.
Ann Surg. 2004;240(5):738–45.
risk factors of delayed gastric
4. Fraser AG, Brunt PW
of highly selective vagotomy with truncal vagotomy
and pyloroplasty–one surgeon’s results after 5
Br J Surg. 1983;70(8):485–8.
5. Stoddard CJ, V
tive vagotomy or truncal vagotomy and pyloroplasty
for chronic duodenal ulceration: a randomized, prospective clinical study. Br J Surg. 1978;65(11):793–6.
6. Traverso LW
ing: the state of the highest level of evidence. J Hepatobiliary Pancreat Surg. 2008;15(3):262–9.
7. Yeo CJ, et al. Erythromycin accelerates
tying after pancreaticoduodenectomy. A prospective,
randomized, placebo-controlled trial. Ann Surg.
1993;218(3):229–37. Discussion 237–8.
8. Fich A, et al. Stasis syndromes following gastric surgery: clinical
patients. J Clin Gastroenterol. 1990;12(5):505–12.
9. Miedema BW, et al. Human gastric
sit and motility after Roux gastrojejunostomy. Gastroenterology. 1992;103(4):1133–43.
10.
Troncon LE, et al. Abnormal intragastric distribution
of food during gastric emptying in functional dyspepsia patients. Gut. 1994;35(3):327–32.
11. Janssens J, et al. Improvement of gastric emptying in
diabetic gastroparesis by erythromycin. Preliminary
studies. N Engl J Med. 1990;322(15):1028–31.
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Speicher JE, et al. Results of completion
mies in 44 patients with postsurgical gastric atony. J
Gastrointest Surg. 2009;13(5):874–80.
13. Forstner-Barthell AW, et al. Near-total completion
gastrectomy for severe postvagotomy gastric stasis:
analysis of early and long-term results in 62 patients.
J Gastrointest Surg. 1999;3(1):15–21. Discussion
21–3.
14. Familoni BO, et al. Efficacy of electrical stimulation
at frequencies higher than basal rate in canine stomach. Dig Dis Sci. 1997;42(5):892–7.
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McCallum R, et al. Clinical response to gastric
electrical
cal gastroparesis. Clin Gastroenterol Hepatol.
2005;3(1):49–54.
16. Oubre B, et al. Pilot study on gastric electrical stimulation on surgery-associated gastroparesis: long-term
outcome. South Med J. 2005;98(7):693–7.
17. Abrahamsson H. Treatment options for patients with
severe gastroparesis. Gut. 2007;56(6):877–83.
18. Dixon MF, et al. Reflux gastritis: distinct histopathological entity? J Clin Pathol. 1986;39(5):524–30.
19. Meshkinpour H, et al. Effect of cholestyramine on
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gastrecto-

Dealing with Dumping Syndrome
Kyung Ho Pak and Sung Hoon Noh
13
Introduction
Although gastric surgery for ulcer disease has
decreased, gastric cancer surgery and bariatric
surgery are still frequently performed worldwide. Accordingly, the number of patients suffering from dumping syndrome has increased.
In particular, in Korea and Japan, early gastric
cancer (EGC) comprises up to 60–70 % of gastric
cancer; therefore, the life expectancy of patients
with gastric cancer is quite high. Surgeons, therefore, must better understand dumping syndrome
and be familiar with its management. Previously,
there was a greater focus on finding a radical
cure rather than on improving quality of life to
increase the survival rate for gastric cancer; in
contrast, concerns regarding the development
of postgastrectomy syndromes such as dumping
syndrome or reflux disease are now increasing.
Dumping syndrome is one of the most common complications after gastric surgery. Approximately 25–50 % of patients develop some
manifestation of dumping syndrome. Among
S. H. Noh ()
Department of Surgery, Yonsei University Health
System, Yonsei University College of Medicine, Seoul,
Republic of Korea
e-mail: sunghoonn@yuhs.ac
K. H. Pak
Department of Surgery, Dongtan Sacred Heart Hospital,
Hallym University College of Medicine, Hwasung,
Kyunggi-do, Republic of Korea
e-mail: sweetpkh@hallym.or.kr
them, 5–10 % have clinically significant symptoms, and 1–2 % are debilitated by them. [1]
Mallory et al.[2] reported that the incidence of
dumping syndrome after gastric bypass was as
high as 75 % in the early postoperative period,
and most symptoms disappeared 15–18 months
after surgery. However, many patients exhibit
symptoms throughout life. Dumping syndrome
has also been reported after Nissen fundoplication in children and adults [3–5], and in pediatric and adult patients receiving gastrostomy
feeding with a persistent vegetative state [6, 7].
In recent years, bariatric surgery has become the
principal cause of postoperative dumping syndrome [8].
The symptoms of early and late dumping syndrome are believed to have distinct underlying
pathophysiologies (Fig. 13.1). Early dumping,
typically starting 20–30 min after a meal, usually causes both vasomotor and gastrointestinal
complaints such as sweating, palpitation, weakness and faintness, abdominal bloating, cramping, and profound diarrhea. These symptoms, in
severe cases, can occur during meals, but usually
happen after meals. Although these symptoms
can occur after any type of gastrointestinal surgery, Billroth-II reconstruction after gastrectomy is the leading cause of dumping syndrome.
The probability of occurrence increases when
a greater amount of stomach is resected. Early
dumping appears to be caused by the excessive
secretion of gastrointestinal hormones after the
rapid flow of a hypertonic diet into the small intestine, which shifts intravascular fluid into the
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_13,
© Springer Science+Business Media New York 2015
127

128 K. H. Pak and S. H. Noh
Fig. 13.1 Pathophysiology of dumping syndrome
small intestine [9]. It causes the abrupt expansion
of the small bowel, which causes increased frequency and amplitude of bowel contractility. Up
to 25 % of the blood circulation can be utilized in
this process.
Late dumping, often occurring 2–3 h postprandially, involves mainly vasomotor complaints
characterized by perspiration, palpitation, mental
confusion, and sometimes syncope. Rapid delivery of a meal to the small intestine leads to an initial higher concentration of carbohydrates in the
proximal small bowel, followed by rapid absorption of glucose into the blood. This is countered
by the excessive release of insulin, the so-called
“hyperinsulinemic response,” responsible for
the subsequent reactive hypoglycemia [10]. The
majority of patients exhibit early dumping, approximately 25 % of them exhibit late dumping,
and only a minority of patients have symptoms
of both [11].
Diagnosis
Dumping syndrome is diagnosed based on a
group of symptoms in patients who have undergone gastric surgery, or by the dumping provocation test. In 1970, Sigstad [12] proposed a scoring system based on the occurrence of different
symptoms of dumping syndrome, to calculate a
diagnostic index (Table 13.1). A diagnostic index
> 7 is suggestive of dumping syndrome. This
system is simple to use, but its disadvantage is
that it is difficult to distinguish other postprandial symptoms from dumping. The score index
is helpful in clinical practice to assess response
to therapy.
A provocative test for assessing dumping
syndrome can be used to confirm clinical suspicions. This test is a modification of the oral
glucose tolerance test (OGTT) and involves the
ingestion of 50 or 75 g glucose in solution after
an overnight fast. Immediately before and up to

Table 13.1 Sigstad score. Weighting factors allocated to the symptoms and signs of dumping syndrome
Sigstad score
Preshock, shock 5
Almost fainting, syncope, loss of consciousness 4
Desire to lie or sit down 3
Breathlessness, dyspnea 3
Weakness,
Sleepiness, drowsiness, yawning, apathy
Palpitation 3
Restlessness 2
Dizziness 2
Headache 1
Feeling of warmth, sweating, pallor, clammy skin 1
Nausea 1
Fullness in the abdomen, meteorism 1
Borborygmus 1
Eructation −
V
omiting −
exhaustion 3
, falling asleep 3
1
4
12913 Dealing with Dumping Syndrome
180 min after ingestion of this solution, the blood
glucose concentration, hematocrit, pulse rate,
and blood pressure are measured at 30 min intervals. The provocative test is considered positive
if late (120–180 min) hypoglycemia occurs, or if
an early (30 min) increase in hematocrit of more
than 3 % occurs. The best predictor of dumping
syndrome seems to be a rise in pulse rate of more
than 10 bpm (beat per min) after 30 min [13].
Assessments of the speed of gastric emptying
might show that this process occurs rapidly in
patients with dumping syndrome—especially for
liquid nutrients—but this test does not seem to
have good diagnostic sensitivity or specificity,
probably because rapid emptying occurs early
after meal ingestion, a phase that is not analyzed
closely or separately in most protocols that test
gastric emptying [10, 13, 14].
Prevention
Prevention, rather than treatment, is recommended for dumping syndrome. The introduction of
proton pump inhibitors and Helicobacter pylori
eradication decrease the need for elective surgery in peptic ulcer disease. In addition, highly
selective gastric vagotomy, which causes minimal disturbance of the gastric emptying mechanism, results in a lower incidence of dumping
syndrome [15]. If more extensive surgery is necessary, a Roux-en-Y gastrojejunostomy (RYGJ)
is preferable because of its decreased rate of
dumping, when compared with pyloroplasty or
loop gastrojejunostomy [16–18].
The choice of reconstructional method after
distal gastrectomy is still controversial. The use
of the Billroth I procedure after distal gastrectomy is preferred in Japan, whereas Billroth II
is more common in Korea because it facilitates
wider dissection and less anastomotic tension.
There are some advantages in Billroth I compared to Billroth II, as follows: a more natural route for food passage, potentially less operative time due to one anastomosis, no risk of
duodenal stump leakage, and less incidence of
postoperative weight loss, anemia, and dumping syndrome. The disadvantage of Billroth I,
however, is that the dissection area can be limited in order to facilitate a tension-free anastomosis. Therefore, the Billroth I procedure is
commonly used for benign disease or distally
located EGC in Korea. However, Kim et al.
[19] compared results from 122 gastric carcinoma patients undergoing Billroth I and Billroth II gastrectomy. They evaluated postgastrectomy syndrome with a survey of abdominal
symptoms, and dumping syndrome was measured using the Sigstad dumping score. According to their results, the occurrence of abdominal

130 K. H. Pak and S. H. Noh
symptoms and dumping syndrome was lower in
the Billroth I group than in the Billroth II group.
Furthermore, pylorus-preserving gastrectomy
(PPG) is a kind of reduced-gastric operation
that preserves the distal portion (1.5 cm) of the
gastric antrum and reduces postoperative complications such as dumping syndrome and reflux esophagitis [20]. However, a limitation of
this operation is that complete lymph node (LN)
dissection of the suprapyloric LN is undesirable
for the preservation of the pyloric branch of the
vagus nerve. Nowadays, some reports state that
this procedure may be applicable in EGC confined to the mucosa and located at the gastric
mid-body [21].
According to a recent Japanese large-scale investigation into dumping syndrome after gastrectomy for gastric cancer, [22] many more patients
suffer from early dumping syndrome (67.6 %)
than from late dumping syndrome (38.4 %) after
gastrectomy. This study revealed that patients
suffering from at least one symptom of early
dumping syndrome were significantly more likely to also experience symptoms of late dumping
syndrome. The study also demonstrated that two
clinical factors, the surgical procedures used and
the amount of weight loss, were significantly associated with the occurrence of both early and
late dumping syndromes. Consistent with previous reports, [23, 24] patients who underwent
PPG showed the lowest incidence of dumping
syndrome. In addition, patients who underwent
PG (proximal gastrectomy with jejunal interposition) showed the second highest incidence of
early dumping syndrome. Patients who underwent RYGJ showed a lower incidence of dumping syndrome symptoms relative to Billroth I patients. Taken together, RYGJ or Billroth I is less
associated with dumping syndrome after distal
gastrectomy than Billroth II.
Management of Dumping Syndrome
The first step in treating dumping syndrome is the
introduction of dietary modification. If this approach is insufficient, medical therapy and, in some
cases, surgery might be considered (Fig. 13.2).
Fig.13 .2 Proposed treatment algorithm for dumping syn-
drome
Diet
The resolution of dumping symptoms is achieved
in most cases by dietary modification, in particular by the reduction of carbohydrate intake, and
lifestyle adjustment.
Dietary measures include advising patients
to consume smaller amounts at one time by dividing the recommended daily energy intake between six meals. Dietary prohibitions are very
important. Fluid intake during meals should be
restricted. Drinking liquids should be avoided for
at least one half-hour after a meal. Complex carbohydrates (e.g., unsweetened cereals, pasta, potatoes, fresh fruit, and vegetables) are preferred.
All rapidly absorbable carbohydrates (e.g., all
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