Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1100_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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

26525 Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
The incidence of PMS-VT may be influenced
by the lack of clear recommendation regarding
anticoagulation following “high-risk” surgery
procedures (i.e., major venous reconstruction,
extended hepatic resection, pancreaticoduodenectomy). In particular, some surgeons delay or
completely withhold routine venous thromboembolism prophylaxis following major hepatectomy, because it is believed that these patients
are at risk for postoperative liver insufficiency,
leading to the concern they are already anticoagulated. This belief is often supported by the
resulting laboratory derangements in measurable liver function, including elevations in the
prothombin time/international normalized ratio
(PT/INR) and partial thromboplastin time (PTT),
as well as occasional thrombocytopenia. Because of that, many surgeons carefully observe
patients with portal vein thrombosis following
hepatectomy and initiate anticoagulation therapy
only when the thrombus extended to the superior
mesenteric vein or reduced portal venous flow.
In contrast with this practice, Ejaz et
that despite
having alterations in platelets, PT/
al. showed
INR, and PTT, patients with liver insufficiency
actually often have significant increased risk for
venous thrombosis, leading to the routine use of
thromboprophylaxis in these patients [33].
Interventional Techniques
Because anticoagulation only leads to a recanalization of the PMS-VT in nearly 40 % of patients,
alternative and more aggressive treatment strategies are used by some centers. During the last
decade, several treatment modalities have been
used, including percutaneous transhepatic thrombolysis, mechanical thrombectomy, and percutaneous transhepatic balloon angioplasty and/or
stent placement without thrombolysis or thrombectomy. Advancements in interventional radiologic techniques have made it possible to administer thrombolytic agents in the proximity of the
clot. Local infusion of thrombolytic agents (urokinase 15,000–30,000 IU/h or recombinant tissue
plasminogen activator 1.8 mg/h, for 4–5 days.)
has been reported to achieve recanalization in
60
%, up to 100 %, of patients [34
–36]. The effect
of thrombolysis can be visualized with angiographies via the catheter on a regular basis or, if
clinically indicated, until the catheter is removed.
Removal is conducted under fluoroscopy. However, positioning a radiologic catheter adjacent to
clot might be technically problematic (especially
in patients with complete intra- and extrahepatic
thrombosis), and thrombolysis might be prohibitively hazardous in the early postoperative period
after major HPB procedures, due to the risk of
major bleeding [36]. Most clinicians therefore
consider pharmacologic thrombolysis as therapy
reserved for patients with severe disease with
propagation of thrombus or without improvement of symptoms. Furthermore, catheter-directed thrombolytic therapy may fail, especially in
the setting of acute thrombus superimposed on
chronic thrombus [35, 36]. To avoid the drawbacks of thrombolysis, several investigators have
successfully treated the cases of postoperative
PMS-VT by mechanical percutaneous thrombectomy [37]. Venous thrombectomy is generally considered to be less successful than arterial
thrombectomy because of difficulties in removing adherent clot from the thin, delicate vein
wall. In the acute setting, however, percutaneous
venous thrombectomy may be technically easier,
because the clot has not yet become adherent to
the vein wall [38].
By debulking the thrombus burden, mechanical percutaneous thrombectomy may reduce
the duration and the total dose of thrombolytic
agents, thereby reducing the bleeding risk for
the patient. However, thrombectomy has potential risks of embolism, intimal trauma, and
re-thrombosis [39]. Balloon angioplasty and/or
stent placement for treating postoperative PMSVT has several advantages. The procedure can
restore the patency of the portal vein-superior
mesenteric vein (if there is no thrombosis in the
intrahepatic portal vein) without the need for
prolonged thrombolysis, reducing the bleeding
risk in this group of postoperative patients [40].
When balloon angioplasty and/or stent placement
without thrombolysis or thrombectomy are used
to treat thrombotic vessels, there is a risk that the
thrombus will prolapse through the stent mesh,

266 G. Malleo et al.
causing re-occlusion or distal embolism. Balloon
angioplasty or stent placement also has several
potential limitations. First, there is a risk of suture dehiscence during balloon angioplasty if the
patient has thrombosis in the early postoperative
period and has undergone venorraphy during the
surgical treatment. The use of a balloon catheter
with a smaller diameter relative to that of the patent portal vein or superior mesenteric vein and
careful under-inflation of a balloon catheter relative to the diameter of the deployed stent may
prevent this complication. Second, the long-term
patency rate is not excellent, although these results are limited to small case series [40–42].
Surgery
Surgical exploration must be undertaken when
clinical, biochemical, and radiologic signs of
bowel infarction are detected, in order to eradicate the source of septic shock. The first report of
a successful portal vein/superior mesenteric vein
thrombectomy for acute PMS-VT was provided
in 1968 by Mergenthaler and Harris [43]. However, surgeons have been historically hesitant to
embrace this approach. The surgical principles
are simple: the superior mesenteric vein can be
accessed at the inferior border of the pancreas,
whereas the portal vein is accessed and controlled dissecting the hepatoduodenal ligament.
Once the involved vessel has been isolated and
taped proximally and distally to the thrombosis
site, a venotomy is performed, and thrombotic
material is mechanically removed with forceps
and a surgical suction device [24]. Recently,
a combined surgical/interventional approach
has been described. After conventional surgical
thrombectomy, a guiding sheath is inserted into
the superior mesenteric vein or in the portal vein
via the venotomy, and radiologic interventional
mechanical thrombectomy is performed. An important advantage of the combined approach is
the possibility to remove thrombi in both directions (antegrade and retrograde) and in formerly
inaccessible areas as the intrahepatic portal vein
branches. To keep the portal vein patent after successful thrombectomy, it seems to be essential to
have sufficient blood inflow from the mesenteric
and splenic veins and downstream into the liver
parenchyma [24].
Conclusion
The ability to diagnose and, therefore, to treat
PMS-VT is of paramount importance in order to
prevent the catastrophic case of mesenteric ischemia resulting from this complication. Awareness of the potential for PMS-VT thrombosis will
allow for early detection and immediate anticoagulation. Overall, prognostic factors for recanalization are needed and have to be validated to
define the best possible therapy in the individual
patient. It must be assessed which patients should
be treated more aggressively to achieve patency
of the portal vein and which patients have good
chances for recanalization by mere anticoagulation treatment. According to the current knowledge, the treatment of PMS-VT should be determined by the individual clinical situation of
the patient, the pathophysiology involved, and
the available expertise. It is important to search
for the causes of PMS-VT after the treatment.
In many patients, coagulation disorders can be
found that impact on the additional postoperative
or postinterventional course. Specialists in hematology should therefore be involved in the care of
these patients. For extensive interventional and
surgical procedures, experienced interventional
radiologists and surgeons with hepato-pancreatic-biliary and vascular expertise are definitely
necessary.
Key Points for Diagnosis
1. Clinical symptoms of acute PMS-VT are mostly
non-specific and variable and clinical presenta-
tions range from incidental findings in an asymp-
tomatic patient to life-threatening complications.
2. Due to the absence of symptoms in many pa-
tients, PMS-VT is often found when chronic
changes including portal hypertension, sple-
nomegaly, and formation of esophageal vari-
ces with possible bleeding have occurred.

26725 Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
3. Ultrasonography with color Doppler is a valuable screening tool to visualize the thrombus
and the local venous flow, but it is user-dependent and may be limwited by the body habitus
or by the overlying bowel gas.
4. Contrast-enhanced CT of the abdomen is
highly sensitive and specific and provides a
better visualization of the extent of PMS-VT
and an accurate delineation of the portal vein
anatomy that contains thrombus.
5.
Portal venography allows for diagnosis and
also treatment of the thrombus, although it
is more
invasive and associated with risks of
bleeding in the early postoperative period.
Key Points for Treatment
1. Treatment of PMS-VT should be determined
by the individual clinical situation of the patient, the pathophysiology involved, and the
available expertise.
2. The goal of the treatment of acute PMS-VT
is the permanent recanalization of the portal
vein/superior mesenteric vein and their large
branches, with sufficient transhepatic blood
flow to prevent the development of portal venous collaterals and portal hypertension, and
is dictated by the acuity of the clinical picture
and by the associated complications.
3. Patients with documented PMS-VT need to
be treated with intravenous or subcutaneous
heparin in order to prevent propagation of the
thrombus as the risks of clot propagation or
complete superior mesenteric vein/portal vein
occlusion far outweighs the risk of bleeding.
4. Advancements in interventional radiologic
techniques have made it possible to administer thrombolytic agents in the proximity of
the clot or balloon angioplasty and/or stent
placement. However, these interventions can
pose increased risks of major bleeding in the
postoperative period, suture dehiscence, poor
long-term patency, and re-occlusion or distal
embolism and therefore are generally reserved
for patients with severe disease with propagation of thrombus or without improvement of
symptoms.
5. Surgical exploration is undertaken when
clinical, biochemical, and radiologic signs of
bowel infarction are detected.
References
1. Cohen J, Edelman RR, Chopra S. Portal vein throm-
bosis: a review. Am J Med. 1992;92:173–82.
2. Witte CL,
manifestations of pylethrombosis. A review of thirtyfour patients. Ann Surg. 1985;202:191–202.
3. Sobhonslidsuk A, Reddy KR. Portal
bosis: a concise review. Am J Gastroenterol.
2002;97:535–41.
4. Sarin SK, Sollano JD, Chawla
Hamid S, Hashizume M, Jafri W, Kumar A, Kudo
M, Lesmana LA, Sharma BC, Shiha G, de Silva HJ,
Members of the APASL Working Party on Portal
Hypertension. Consensus on extra-hepatic portal vein
obstruction. Liver Int. 2006;26:512–9.
5. Li MX, Zhang XF
clinical characteristics of portal vein thrombosis after
splenectomy in patients with liver cirrhosis. Hepatobiliary Pancreat Dis Int. 2013;12:512–9.
6. Thomas RM, Ahmad SA. Management of acute
operative portal venous thrombosis. J Gastrointest
Surg. 2010;14:570–7.
7. Hibi T, Nishida S, Levi DM, Selvaggi G, Tekin A,
Fan J, Ruiz P, Tzakis AG. When and why portal vein
thrombosis matters in liver transplantation. Ann Surg.
2014;259:760–6.
8. Smoot RL, Christein
portal venous reconstruction following resection during pancreaticoduodenectomy. J Gastrointest Surg.
2006;10:1371–5.
9. Yoshiya S, Shirabe
Y, Yoshizumi T, Ikegami T, Yamashita Y, Harimoto N, Nishie A, Yamanaka T, Maehara Y. Portal
vein thrombosis after hepatectomy. World J Surg.
2014;38:1491–7.
Butturini G, Inama M, Malleo
10.
GL, Piccoli M, Perandini S, Pederzoli P, Bassi C.
Perioperative and long-term results of laparoscopic
spleen-preserving distal pancreatectomy with or
without splenic vessels conservation: a retrospective
analysis. J Surg Oncol. 2012;105:387–92.
Iacono C, V
11.
Bachelli C, Valdegamberi A, Bortolasi L, Guglielmi
A. Systematic review of central pancreatectomy and
meta-analysis of central versus distal pancreatectomy. Br J Surg. 2013;100:873–85.
Girelli R, Frigerio I, Salvia
12.
Martini P, Bassi C. Feasibility and safety of radiofrequency ablation for locally advanced pancreatic
cancer. Br J Surg. 2010;97:220–5.
James AW
13.
Posselt AM, Campos GM. Portomesenteric venous
Brewer ML, Witte MH, Pond GB. Protean
vein throm-
YK, Amarapurkar D,
, Liu ZW, Lv Y. Risk factors and
post-
JD, Farnell MB. Durability of
K, Nakagawara H, Soejima
G, Manfredi R, Melotti
erlato G, Ruzzenente A, Campagnaro T,
R, Barbi E, Tinazzi
, Rabl C, Westphalen AC, Fogarty PF,

268 G. Malleo et al.
thrombosis after laparoscopic surgery. Arch Surg.
2009;144:520–6.
14. Capron JP, Lemay JL, Muir JF, Dupas JL, Lebrec D, Gineston JL. Portal vein thrombosis and
fatal pulmonary thromboembolism associated with
oral contraceptive treatment. J Clin Gastroenterol.
1981;3:295–8.
Yang YY
15.
Chiang JH, Tasy SH, Chang FY, Lee SD. Case report:
portal vein thrombosis associated with hereditary
protein C deficiency: a report of two cases. J Gastroenterol Hepatol. 1999;14:1119–23.
16.
Rhee RY, Gloviczki P
Serry RD, Sarr MG, Johnson CM, Bower TC, Hallett JW Jr, Cherry KJ Jr. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg.
1994;20(5):688–97.
17. Yoon YS, Lee KH, Han HS, Cho JY, Ahn KS.
Patency of splenic vessels after laparoscopic spleen
and splenic vessel-preserving distal pancreatectomy.
Br J Surg. 2009;96:633–40.
18.
Kobayashi S, Yokoyama
numa M, Ebata T, Igami T, Sugawara G, Takahashi
Y, Nagino M. Increased von Willebrand factor to
ADAMTS13 ratio as a predictor of thrombotic complications following a major hepatectomy. Arch Surg.
2012;147:909–17.
19. Kang CM, Chung YE, Jung MJ, Hwang HK, Choi
SH, Lee WJ. Splenic vein thrombosis and pancreatic
fistula after minimally invasive distal pancreatectomy. Br J Surg. 2014;101:114–9.
20. Ho HS, Saunders CJ, Gunther RA, Wolfe BM. Effector of hemodynamics during laparoscopy: CO2
absorption or intra-abdominal pressure? J Surg Res.
1995;59:497–503.
21. Schmandra TC, Kim ZG, Gutt
flation gas and intraabdominal pressure on portal
venous flow during pneumoperitoneum in the rat.
Surg Endosc. 2001;15:405–8.
22. Gutt CN, Schmedt CG, Schmandra T, Heupel O,
Schemmer P, Büchler MW. Insufflation profile
and body position influence portal venous blood
flow during pneumoperitoneum. Surg Endosc.
2003;17:1951–7.
23.
Sheen CL, Lamparelli H, Milne
JK. Clinical features, diagnosis and outcome of acute
portal vein thrombosis. Q J Med. 2000;93:531–4.
24. Loss M, Lang SA, Uller W, Wohlgemuth WA, Schlitt
HJ. Combined surgical and interventional therapy
of acute portal vein thrombosis without cirrhosis:
a new effective hybrid approach for recanalization of the portal venous system. J Am Coll Surg.
2014;218:e79–86.
25. Tessler FN, Gehring BJ, Gomes AS, Perrella
Ragavendra RR, Busuttil RW, Grant EG. Diagnosis
of portal vein thrombosis: value of color Doppler
imaging. Am J Roentgenol. 1991;157:293–6.
26.
Bach AM, Hann LE, Brown KT
Herman SK, Fong Y, Blumgart LH. Portal vein
evaluation with US: comparison to angiography
, Chan CC, Wang SS, Chiu CF, Hsu HC,
, Mendonca CT, Petterson TM,
Y, Matsushita T, Kai-
CN. Effect of insuf-
A, Green I, Ramage
RR,
, Getrajdman GI,
combined with CT arterial portography. Radiology.
1996;201:149–54.
27.
Turnes J, Garcia-Pagan JC, Gonzalez M,
Calleja JL, Ripoll C, Abraldes JG, Bañares R, Villanueva C, Albillos A, Ayuso JR, Gilabert R, Bosch J.
Portal hypertension-related complications after acute
portal vein thrombosis: impact of early anticoagulation. Clin Gastroenterol Hepatol. 2008;6:1412–7.
DeLeve LD, Valla DC,
28.
orders of the liver. Hepatology. 2009;49:1729–64.
Kearon C, Akl EA, Comerota AJ,
29.
nameaux H, Goldhaber SZ, Nelson ME, Wells PS,
Gould MK, Dentali F, Crowther M, Kahn SR, American College of Chest Physicians. Antithrombotic
therapy for VTE disease: antithrombotic therapy and
prevention of thrombosis, 9th ed: American College
of Chest Physicians evidence-based clinical practice
guidelines. Chest. 2012;141(Suppl):e419S–94S.
30. Plessier A, Darwish-Murad S, Hernandez-Guerra M,
Consigny Y, Fabris F, Trebicka J, Heller J, Morard I,
Lasser L, Langlet P, Denninger MH, Vidaud D, Condat B, Hadengue A, Primignani M, Garcia-Pagan JC,
Janssen HL, Valla D. European network for vascular disorders of the liver (EN-Vie). Acute portal vein
thrombosis unrelated to cirrhosis: a prospective multicenter follow-up study. Hepatology. 2010;51:210–8.
Plessier A, Murad SD, Hernandez-Guerra
31.
signy Y, Fabris F, Heller J, Morard I, Langlet P,
Bahr M, Eapen E, Miranda H, Deninger M, Vidaud
D, Condat B, Hadengue A, Elias E, Primignani M,
Garcia-Pagan JC, Janssen HL, Valla D. A prospective
multicentric follow-up study on 105 patients with
acute portal vein thrombosis (PVT): results from the
European network for vascular disorders of the liver
(EN-VIE). Hepatology. 2007;46(Suppl. 1):310A.
32. Condat B, Pessione F, Helene
aire S, Valla D. Recent portal or mesenteric venous
thrombosis: increased recognition and frequent
recanalization on anticoagulant therapy. Hepatology.
2000;32:466–70.
33. Ejaz A, Spolverato G, Kim Y, Lucas DL, Lau B,
Weiss M, Johnston FM, Kheng M, Hirose K, Wolfgang CL, Haut E, Pawlik TM. Defining incidence and
risk factors of venous thromboembolism after hepatectomy. J Gastrointest Surg. 2014;18:1116–24.
34. Hollingshead M, Burke CT, Mauro MA, W
Dixon RG, Jaques PF. Transcatheter thrombolytic
therapy for acute mesenteric and portal vein thrombosis. J Vasc Interv Radiol. 2005;16:651–61.
35.
Woo DH, Laberge
Kerlan RK Jr. Management of portal venous complications after liver transplantation. Tech Vasc Interv
Radiol. 2007;10:233–9.
36. Smalberg JH, Spaander
van Buuren HR, van den Berg B, Janssen HL, Leebeek FW. Risks and benefits of transcatheter thrombolytic therapy in patients with splanchnic venous
thrombosis. Thromb Haemost. 2008;100:1084–8.
37. Klempnauer J, Grothues F, Bektas H, Pichlmayr
R.
Results of portal thrombectomy and splanch-
Garcia-Tsao G. Vascular dis-
Denninger M, Hill-
JM, Gordon RL, Wilson MW,
MV, Jie KS, Pattynama PM,
Aracil C,
Prandoni P, Bou-
M, Con-
eeks SM,

26925 Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
nic thrombolysis for the surgical management of
acute mesentericoportal thrombosis. Br J Surg.
1997;84:129–32.
Valla DC, Condat B. Portal vein thrombosis in adults:
38.
pathophysiology, pathogenesis and management.
Hepatol. 2000;32:865–71.
39.
Biederer J, Schoene A, Reuter
Hülsbeck S. Suspected pulmonary artery disruption
after transvenous pulmonary embolectomy using a
hydrodynamic thrombectomy device: clinical case
and experimental study on porcine lung explants. J
Endovasc Ther. 2003;10:99–110.
40.
Cao G, Ko GY, Sung KB, Y
JH. Treatment of postoperative main portal vein and
superior mesenteric vein thrombosis with balloon
angioplasty and/or stent placement. Acta Radiol.
2013;54:526–32.
M, Heller M, Müller-
oon HK, Gwon DI, Kim
41. Cherukuri R, Haskal ZJ, Naji A, Shaked A. Percutaneous thrombolysis and stent placement for the
treatment of portal vein thrombosis after liver transplantation: long-term follow-up. Transplantation.
J
1998;65:1124–6.
Schellhammer F, am Esch JS,
42.
Knoefel WT, Fürst G. Surgical access to jejunal
veins for local thrombolysis and stent placement in
portal vein thrombosis. Cardiovasc Intervent Radiol.
2008;31:S185–7.
43.
Mergenthaler FW
vein thrombosis complicating pancreatoduodenectomy: successful treatment by thrombectomy. Ann
Surg. 1968;167:106–11.
, Harris MN. Superior mesenteric
Hammerschlag S,

Postpancreatectomy Hemorrhage: Early and Late
Albert Amini, Kathleen K. Christians and
Douglas B. Evans
26
Introduction
The mortality rate after pancreaticoduodenectomy (PD) has decreased markedly over the last
several decades. However, the morbidity rate has
not decreased to the same extent; complications
continue to occur in 30–40 % of patients who undergo pancreatectomy (PD or distal pancreatectomy) [1, 2]. Postpancreatectomy hemorrhage
(PPH) is one of the major causes of morbidity
and can result in mortality after PD or distal pancreatectomy [3, 4]. In particular, late PPH is associated with a high mortality rate because the
diagnosis may not be apparent, the patient may
no longer be an inpatient and the hemorrhage
may present as abrupt, massive bleeding [5, 6].
PPH occurs between 1 and 8 % of all pancreatic resections and accounts for 11–38 % of
overall mortality [3, 7–9]. This wide variation is
caused by different definitions used by authors in
the reporting of results. The International Study
Group of Pancreatic Surgery has clinically graded PPH based on onset, location, and severity
D. B. Evans () · K. K. Christians
Department of Surgery, Medical College of Wisconsin,
9200 W. Wisconsin Avenue, Milwaukee, WI 53226, USA
e-mail: devans@mcw.edu
A. Amini
Department of Surgical Oncology, Medical College of
Wisconsin, Milwaukee, WI, USA
K. K. Christians
Department of Surgery, Froedtert Hospital,
Milwaukee, WI, USA
[10]. Generally, PPH can be divided into early
and late postoperative bleeding. Early PPH is
that which occurs within 24 h of surgery. It often
is caused by technical failure to achieve appropriate hemostasis during the index operation or
an underlying perioperative coagulopathy. Late
PPH occurs more than 24 h after the operation,
and usually after 7–10 postoperative days. Late
PPH typically results from complications of the
operation and becomes clinically apparent several days or even weeks after surgery. For example,
late PPH may occur following the diagnosis of
an intra-abdominal abscess, erosion of a peripancreatic vessel secondary to a pancreatic fistula or
an intra-abdominal drain, ulceration at the site of
an anastomosis, or in association with an arterial
pseudoaneurysm. Late PPH or delayed bleeding
is one of the most feared postoperative complications because it is often not accurately diagnosed
and therefore not treated effectively. Late PPH
under these circumstances is associated with a
high mortality rate because of the already poor
condition of the patient [11].
PPH may originate from arterial or venous
vessels, suture lines, areas of resection (pancreatic stump, retroperitoneum), gastric/duodenal
ulcer or diffuse gastritis, eroded and ruptured
pseudoaneurysms, or hemobilia from previously
placed endobiliary stents [10] (Table 26.1). Vascular structures that may be the source of PPH
include the stump of the gastroduodenal artery
(GDA; most common and well known cause
of late PPH), splenic artery, branches of the superior mesenteric artery (SMA) (e.g., inferior
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_26,
© Springer Science+Business Media New York 2015
271

272 A. Amini et al.
Table 26.1 Location, onset, diagnosis, and management of postpancreatectomy hemorrhage (PPH)
Location Onset Diagnosis/management
Vessel
Gastroduodenal artery stump Usually late Angiography and embolization/stent
Hepatic artery Late Angiography and embolization
Inferior pancreaticoduodenal artery Early Reoperation following PD
Inferior pancreaticoduodenal artery Late Angiography and embolization/stent as this usually
Splenic vein stump Early Reoperation following distal pancreatectomy
Splenic artery stump Late Angiography and embolization following distal
Intrapancreatic arteries (smaller
un-named)
Anastomoses
Hepaticojejunostomy Early Reoperation
Pancreaticojejunostomy Early Reoperation
Gastrojejunostomy Early or Late Endoscopy or reoperation
Early refers to the first 24–48
pancreatodudenectomy
PD
h after surgery; late most commonly refers to after the first postoperative week
Early or late Early—reoperation
presents as a pseudoaneurysm
pancreatectomy
Late—angiography and embolization
pancreaticoduodenal artery especially in the setting of a clinically significant pancreatic anastomotic leak), the splenic vein stump, or, rarely, an
intrapancreatic artery. In addition, PPH can be
grouped into intraluminal and extraluminal; intraluminal PPH manifests itself as hematemesis,
bleeding from the nasogastric tube, or melena,
and extraluminal PPH is characterized by bleeding from intra-abdominal drains, an abdominal
wound, or intra-abdominal hemorrhage. True extraluminal bleeding has an extraluminal source.
False extraluminal bleeding is a manifestation of
primary intraluminal bleeding that becomes extraluminal owing to coexisting anastomotic disruption [12–14].
Early PPH (within 24 h after surgery) is most
commonly the result of technical failure to properly secure the inferior pancreaticoduodenal arteries (IPDAs). One can also see bleeding at any
of the three anastomotic suture lines (following
PD) and rarely a GDA stump hemorrhage due to
failure to properly secure this vessel. If the SMA
dissection is performed sharply with direct identification and ligation of the IPDAs at their origin
from the SMA, this complication can largely be
avoided. Intra-abdominal hemorrhage from poorly secured IPDAs would present as early postoperative intra-abdominal hemorrhage and would
require immediate reoperation. Bleeding from
the post-PD reconstruction (pancreatic, biliary,
or gastric anastomosis) is very uncommon, and
the anastomosis of greatest risk is the pancreaticojejunostomy if an invagination anastomosis is
performed. With this type of anastomosis, the cut
surface of the pancreas is open to the inside of
the jejunum and small vessels which are partially
cauterized may retract at the time of pancreatic
transection only to bleed when the patient is in
the recovery room or during the first postoperative night. Hemorrhage from the biliary anastomosis should not occur, and bleeding from the
gastrojejunostomy is also very uncommon in the
absence of a technical error. Marginal ulceration
at the gastrojejunostomy, if it were to occur, presents months or years after the date of surgery.
Yekebas et al. presented an analysis of 1669 consecutive pancreatic resections and in their experience, early PPH was due to 3 causes: (1) technical failures in terms of inadequate hemostasis
in the operative field always associated with extraluminal PPH (IPDAs being the most common
involved vessels); (2) suture line of gastroenteric
or one of the enteroenteric anastomoses leading
uniformly to intraluminal PPH on the first or second postoperative day; and (3) resection cavity
or transection surface of the pancreas resulting
in PPH originating from the pancreatico-enteric
anastomosis [15].
Late PPH may occur from a gastrointestinal
source but more commonly originates from an

27326 Postpancreatectomy Hemorrhage: Early and Late
intra-abdominal site often associated with intraabdominal infection or abscess formation due to
leakage of an anastomosis (most commonly the
pancreaticojejunostomy). Intra-abdominal infection is thought to be the major cause of late PPH
due to erosion into ligated vessels, most notably
the GDA. Bleeding from a disrupted anastomotic
suture line can also be caused by intra-abdominal
infection and can mimic bleeding from major
vessels [7, 8, 16]. Finally, some patients may
present with bleeding from the wound after a
wound infection but significant hemorrhage from
this etiology is uncommon.
The core difference between the etiology of
early and late PPH is the association of late PPH
with pancreatic fistula and intra-abdominal infection. This finding is consistent throughout the
surgical literature which notes an elevated risk
of late PPH in patients with pancreatic fistula
as well as a near 100 % prevalence of pancreatic
fistula in patients who exhibit late arterial bleeding [16, 17]. Surgical reports are consistent in
describing a sequence of events at the beginning
of which pancreatic fistula causes erosions, pseudoaneurysms, and other vascular irregularities,
which eventually result in clinically significant
hemorrhage. Clearly, the majority of postoperative pancreatic fistulas do not result in late PPH
and the cause of PPH within the population of
patients who have a pancreatic leak is likely multifactorial. Extended lymphadenectomy or the
need for concomitant adjacent organ resection
(resulting in a large retroperitoneal space), soft
texture of the pancreatic remnant in the setting
of a complete anastomotic disruption, or insufficient drainage of pancreatic fistula (failure to obtain source control) may be the cofactors increasing the risk of fistula-induced vascular injury and
PPH [16–18].
Possible pathophysiologic explanations for
pancreatic anastomotic leak-associated late PPH
include enzymatic digestion of the blood vessel
wall by trypsin, elastase, and other pancreatic
exocrine enzymes, intra-abdominal infection/abscess with direct involvement of the vessel wall,
and/or vascular injury at the time of operation that
leads to pseudoaneurysm formation [3]. Most re-
ports and anecdotal clinical observations favor
the theory of local sepsis resulting from pancreatic fistula as the main cause of late PPH. Local
sepsis may erode the vascular wall and adjacent
bowel. This mechanism of injury may result in
acute arterial bleeding with or without arterial
pseudoaneurysm formation, which typically occurs days to weeks after the operation [19]. There
is minimal data regarding the impact of newer
energy devices, especially when using them for
ligating the IPDAs arising from the SMA; however, anecdotal experiences with such situations
have generated reason for caution. Many of us
have managed PPH in patients where the use of
such energy devices close to arterial structures
has been implicated in the etiology of late PPH.
Skeletonization of the hepatic artery and SMA
which is performed with PD, and similar dissection of the celiac artery and splenic artery stump
associated with distal pancreatectomy make these
vessels vulnerable to pseudoaneurysm formation
due to local sepsis arising from the pancreatic
fistula, anastomotic leakage, or intra-abdominal
abscess [20]. In a series reported by Lee et al., of
27 patients with PPH, 26 had an antecedent pancreatic fistula, as shown by drain amylase level
and computed tomography (CT) findings. This
report confirms the association between late PPH
and pancreatic fistula. The onset of the infectious
complication ranged from 7 to 13 days but the
hemorrhage developed after postoperative day
28 in 9 patients. The high frequency of late-onset
(after 4 weeks from the date of operation) hemorrhage in this study led the authors to conclude
that PPH can occur more than 4 weeks postoperatively, particularly in patients with pancreatic
fistula and/or a complicated initial postoperative
course [21].
Prevention of Late PPH
The Falciform Ligament
When opening the abdomen, we carefully preserve the falciform ligament (obliterated umbilical vein) for later use as coverage of the GDA

274 A. Amini et al.
Fig. 26.1 Intraoperative photograph of preserved falci-
form ligament pedicle flap. Debakey forceps are retracting the liver. White arrows point to the falciform flap
stump, vascular anastomoses, or other peripancreatic vessels [22]. A pedicled falciform ligament is easily and rapidly obtained during a midline abdominal incision. After incising the linea
alba, the preperitoneal fat is dissected laterally (to
the left) when incising the peritoneum. The falciform ligament is mobilized by dividing it near
the umbilicus and incising its anterior peritoneal
reflections along the posterior rectus sheath. An
additional length is obtained by continuing the
anterior incision cephalad to the anterior surface
of the liver. The pedicled falciform ligament is
completed by taking down the attachments of
the liver until just the obliterated umbilical vein
remains attached. Note that the pedicled falciform ligament (Fig. 26.1) normally reaches the
space between the pancreaticojejunostomy and
the major vessels exposed during resection. After
completion of the pancreatectomy, the pedicled
falciform ligament is spread widely anterior to
the common/proper hepatic artery with special
attention to coverage of the GDA stump. A robust flap usually also covers the superior mesenteric vein (SMV), portal vein (PV), and splenic
vein confluence effectively separating the vessels
from the afferent jejunal limb (Fig. 26.2). When a
distal pancreatectomy is performed, the pedicled
falciform ligament can be fixed with 4-0 prolene
sutures to the remnant pancreas thereby reinforcing the pancreatic closure. This procedure
enables the complete separation of these vessels
Fig. 26.2 Intraoperative photograph of completed pan-
creaticoduodenectomy. The falciform ligament pedicle
flap ( white arrows) completely covers the common he-
patic artery and GDA stump from any possible PJ leak.
HJ hepaticojejunostomy, PJ pancreaticojejunostomy,
SMV superior mesenteric vein, SV splenic vein
from the pancreas in the event that a pancreatic
fistula and associated abscess were to develop.
The Portal Dissection
The portal dissection is initiated by removing the
lymph node that lies directly anterior to the common hepatic artery (CHA) proximal to the right
gastric artery and GDA. This facilitates exposure
of the CHA proximal and distal to the GDA. The
right gastric artery is ligated and divided followed by the GDA. Dissection of the hepatic artery should be performed with gentle, sharp dissection, especially in patients who have received
prior chemotherapy or chemoradiation and in
those with extensive peritumoral inflammation
from a previous laparotomy or stent-related pancreatitis. Blunt dissection at the GDA origin can
result in intimal dissection of the hepatic artery.
Division of the GDA allows mobilization of the
hepatic artery and exposure of the anterior surface of the PV directly posterior to the inferior
border of the CHA. The PV should always be

27526 Postpancreatectomy Hemorrhage: Early and Late
exposed in this way before dividing the common
hepatic duct. Care during this critical step in the
performance of PD can minimize trauma to the
hepatic artery and allow for a secure closure of
the GDA stump [22].
GDA Ligation
Occasionally, ligation of the GDA is complicated
by close proximity of the pancreatic tumor. If the
tumor extends to within a few millimeters of the
GDA, our technique is to obtain proximal and
distal control of the hepatic artery and then divide
the GDA flush at its origin. The resulting arteriotomy can be closed primarily with interrupted
6-0 prolene sutures. If 2
available,
we often use a small vascular pledget,
as the hepatic artery can be quite fragile in this location; if the arteriotomy is flush with the CHA, a
pledget cannot be used. When the tumor extends
to the GDA origin, we divide the GDA prior to
any form of ligation of the distal GDA on the
specimen side. The GDA on the specimen side
is suture ligated with 4-0 Prolene after it is divided; control of back-bleeding from this vessel
is easily accomplished with simple hand pressure
if a complete Kocher maneuver was performed
earlier in the operation. This maneuver decreases
trauma and handling of the GDA and decreases
chances of intimal dissection of the hepatic artery
[22]. When adequate length of GDA allows for
a simple ligation, we usually use a 0-silk tie on
the hepatic artery side with a 4-0 Prolene suture
on the specimen side (so as to avoid unnecessary
mobilization which is often needed to place a tie
distally on the specimen side).
mms of GDA origin is
Fig. 26.3 Intraoperative photograph of a completed dis-
tal pancreatectomy. Arrowheads point to the cut margin
of the pancreas closed with pledgeted sutures. CHA common hepatic artery, SMA superior mesenteric artery, SMV
superior mesenteric vein
or with pledgeted sutures. The limitation to using
the stapler is in proximal neck/body tumors
where there is limited room (due to the proximity
of the intrapancreatic bile duct) for achieving an
adequate margin. In addition, as one moves to the
patient’s right of the pancreatic neck (and enters
the region of the pancreatic head), the pancreas
becomes too thick for a staple line. In this scenario, after confirming a negative margin, we identify the pancreatic duct and close it directly with
a horizontal mattress suture. We then close the
remaining pancreas with additional horizontal
mattress sutures with a pledget on both the posterior and anterior surfaces (Fig. 26.3). The first
such pledgeted suture is placed at the site of the
pancreatic duct so that the duct closure is covered
by the location of the pledget. Both a stapled closure and a suture closure with pledgets are done
to minimize the risk of pancreatic fistula, which
can increase the risk of PPH.
Reinforcing the Pancreatic Transection Site (Distal Pancreatectomy)
When performing a distal or subtotal pancreatectomy, the remnant pancreas can lead to a potential pancreatic fistula and subsequent PPH from
a splenic artery pseudoaneurysm. We routinely
divide the pancreas and perform the pancreatic
closure either with Gore-Tex reinforced staples
Diagnosis of Late PPH
Symptoms/Signs
The occurrence of a sentinel bleed is a key sign
and symptom of late PPH [8, 16]. Sentinel bleeding refers to isolated bleeding, usually from the
gastrointestinal tract or an abdominal drain/drain
Соседние файлы в папке Библиотека им академика М.И. Перельмана
