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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

555 Chyle Leak After Esophageal Surgery
Fig. 5.3 Adult anatomy of the thoracic duct, relationship to mediastinal structures. (Reprinted with permission from
[48])
position of the cisterna chyli is adjacent to the
vertebral column and to the right of the aorta at
the level of L2, but it can be found from T10 to
L3. The thoracic duct ascends from the cisterna
chyli in the posterior mediastinum through the
aortic hiatus. The aortic hiatus resides at the level
of T10. Moving cephalad, the duct lies along the
anterior surface of the vertebral column, posterior
to the esophagus, between the aorta and the azygos vein and anterior to the right intercostal arteries. This anatomic region is emphasized because
this is the optimal location for duct ligation in the
chest [12]. The thoracic duct typically crosses behind the aorta to the left at T5–T7 and continues
its ascent behind the aortic arch and to the left
of the esophagus until it reaches the level of the
left subclavian artery posteriorly. The change in
laterality of the duct position explains the development of a right-sided chylothorax if the duct is
injured below T5 and a left-sided chylothorax if
the duct is injured above T5. Collateral drainage
into the azygos, intercostal, and lumbar veins occurs 40–60 % of the time.
The course of the duct continues cephalad
until approximately 3 cm above the level of the
clavicle when it traverses laterally. The duct is
then positioned anterior to the vertebral artery
and vein, innominate vein, and phrenic nerve and
medial to the anterior scalene muscle. The duct
terminates by joining the venous drainage system
near the confluence of the left subclavian and
left internal jugular veins, but has also been reported to drain into the left innominate vein, left
or right internal jugular or the left vertebral vein
(Fig. 5.3 ) [13–15].
The duct is known to have unidirectional
valves of variable number and location. A valve
is always present, however, at the junction of the
thoracic duct and the venous supply to protect
against the reflux of blood into the lymphatic
system [16].
Other small lymphatic pathways exist. A small
and short right thoracic duct drains lymph from
the right head, neck, arm and chest wall via the
jugular trunk. A bronchomediastinal trunk drains
lymph from the right lung, heart, and left lung.
And an additional trunk drains lymph from the
dome of the liver, right chest wall, and right diaphragm via the right internal mammary trunk.
Variations in anatomy include lymphatic duct
doubling, left-sided course, right-sided course,
bilateral termination, or azygos vein termination.

56 E. M. Ziarnik and J. C. Nesbitt
In addition, in the neck, the duct can run posteriorly to the vertebral and subclavian veins [17].
Physiology
Chyle consists of lymph (comparable to blood
plasma) and emulsified fats (free fatty acids). It
is formed within the small intestine during digestion of fatty foods. Long-chain fatty acid molecules diffuse into the low-pressure wall of the
intestinal villi. They form micelles and are reassembled into triglycerides. The triglycerides are
coated with cholesterol and protein to form chylomicrons that then enter lacteals before flowing into the larger lymphatic vessels. The higher
pressure in intestinal veins allows only smaller
products of digestion, such as short- and medium-chain triglycerides (MCT), amino acids and
sugars, to diffuse directly into the blood stream,
the portal system. Fat is absorbed into intestinal
lymphatics and transported into venous blood
flow in less than an hour.
Lymph flow in the thoracic duct comes from
the liver, intestines, and extremities, with the
liver and intestines contributing 95 %. Many factors influence the volume of lymph flow through
the thoracic duct. Basal rate of flow is estimated
to be 0.95 ml/min or 1.38 ml/kg body weight/
hour. Flow rates can increase with oral intake and
abdominal massage up to 3.9 ml/min [18].
Composition of Chyle
Tab le 5.1 Composition of chyle. (Adapted from [47])
Component Amount (per 100
Total fat 0.4–5.0 g
Cholesterol 65–220 mg
Protein 2.2–5.9 g
Albumin 1.2 − 4.1 g
Globulin 1.1–3.6 g
Fibrogen 16–24 g
Antithrombin 25 % of plasma concentration
Prothrombin 25 % of plasma concentration
Fibrinogen 25 % of plasma concentration
Sugar 48–200 g
Electrolytes Similar to plasma
Cellular elements
L
ymphocytes 400
Erythrocytes 50–600/L
− 6800/L
ml)
related to ingested quantity and composition of
fat and can range from 14 to 210 mmol/L. Up to
60 % of ingested fat, consisting mostly of longchain triglycerides (12 or more carbon atoms in
size), is absorbed into the lymphatic channels.
Small-chain triglycerides, considered less than 6
carbon atoms in size, are absorbed directly into
the portal venous system. MCT (6–12 carbon
atoms in size) are also absorbed passively into
the portal system, though only 30–40 % of MCTs
are directly absorbed.
Protein Chyle is a transporter of extravascular
protein back to the vascular space. Total protein
concentration in chyle is generally half that of
protein concentration in the plasma, ranging from
21 to 59 g/L [18]. In large chyle leaks, significant
protein losses can occur.
The concentration of fat, protein, and lymphocytes within chyle is variable depending on the
timing, type, and amount of food ingested. During the period of fasting, ductal lymph fluid is
clear. The milky white color occurs from the absorption of chylomicrons following fat ingestion.
Chyle is considered bacteriostatic and causes a
very little pleural reaction due to its alkaline pH
(Table 5.1).
Lipids As noted, the main component of chyle
consists of emulsified fats, or free fatty acids.
The concentration of fat in chyle is directly
Electrolytes The electrolyte content of lymph
in the thoracic duct is the same as that of plasma.
Fat-soluble vitamin concentrations in chyle are
proportional to the amount ingested. Pancreatic
lipase, amylase, and deoxyribonuclease can also
flow into the lymph system and are subsequently
transported to the blood stream by way of the
thoracic duct.
Lymphocytes Lymphocytes contribute the
main cellular element of thoracic duct lymph.
Ninety percent are T-lymphocytes. Lymphocytes
are in constant to and fro circulation from lymph

575 Chyle Leak After Esophageal Surgery
Tab le 5.2 Causes of chylothorax. (Adapted from [47])
Congenital anomalies
Trauma
Birth trauma
Blunt trauma
Penetrating trauma
Surgical trauma
Cervical lymph node dissection
Thoracic
Ligation of patent ductus arteriosus
Coarctation repair
Esophagectomy
Thoracic aortic aneurysm repair
Resection of mediastinal tumor
Pulmonary resection
Sympathectomy
Abdominal
Abdominal lymph node dissection
Neoplasms
Lymphoma, breast cancer, lung cancer
Miscellaneous
Subclavian vein thrombosis
Radiation
Tuberculosis
nodes to the bloodstream. Prolonged drainage of
lymph due to a thoracic duct injury can significantly deplete lymphocytes with resultant immunosuppression.
Chylothorax
(incidence of 0.2–0.5 %), pulmonary resection
with lymphadenectomy (incidence of 0.42–
2.3 %.), and esophagectomy. The incidence of
chylothorax after esophagectomy ranges from
0.5 to 10.5 %, irrespective of the approach to resection [19–22]. A meta-analysis completed by
Rindani and colleagues evaluated 44 reports involving 5483 patients with an incidence of chylothorax of 2.8 % [23]. Patients who had a transthoracic esophagectomy (2675) and those who had
a transhiatal esophagectomy (2808) developed
chylothoraces with an incidence of 2.1 and 3.4 %,
respectively. In a report by Dugue of 850 patients
undergoing Ivor-Lewis esophagectomy, the incidence of chylothorax was 2.7 % [24]. Orringer
reported < 1 % incidence for 1085 patients who
underwent a transhiatal esophagectomy [25].
Merigliano reported 1787 esophagectomies with
an incidence of chylothorax of 1.1 % [26]. Of the
1787 patients evaluated, 1237 patients underwent
a transthoracic approach and 464 patients had a
transhiatal approach with chylothorax incidence
of 1 and 1.3 %, respectively. Minimally invasive esophagectomy (MIE) has reported rates of
chylothorax similar to those of open approaches.
Shen reported 344 MIEs with a chylothorax incidence of 2.9 % [27]. A postoperative chyle leak
is also more likely to occur in direct relationship
with the aggressiveness of a mediastinal lymph
node dissection [28].
Etiology/Cause
Chylothorax occurs when lymphatic fluid accumulates within the pleural space. Though a chylothorax can occur spontaneously, it is usually
related to an injury to the thoracic duct or one
of its branches. Other causes include occlusion
of the lymphatic system from venous thrombosis,
neoplastic infiltration, or radiation. The causes
are listed in Table 5.2.
Post-esophagectomy Chylothorax
Thoracic operations most commonly associated with chylothorax include aortic procedures
Diagnosis
Clinical Features
Clinical features related to chylothorax often
present in a delayed fashion because postoperative patients frequently have a limited dietary intake. As oral or enteral intake occurs, lipids are
absorbed through the intestinal tract and into the
lymphatic system that travels through the region
of the resected esophagus. If thoracic duct channels have been disrupted and are not ligated,
the pleural cavity will gradually fill with chyle.
Clinical complaints are related to compression
of the lung by the chylous effusion and include
dyspnea, cough, and fatigue. If pleural drainage

58 E. M. Ziarnik and J. C. Nesbitt
tubes are present, a milky effluent will occur.
The quantity of accumulated or drained fluid depends upon the degree of thoracic duct injury and
amount of enteral intake. High-volume drainage
(> 1–2 L/day) can occur with losses of fluid, electrolytes, and lymphocyte reserves.
Fluid Studies
After thoracentesis or catheter drainage of the
suspected effusion, the diagnosis of chylothorax
is supported by nonclotting, milky-colored fluid.
Chyle can resemble pus, but it is odorless, and no
bacteria are seen on Gram stain. Clear fluid does
not rule out chylothorax, particularly in patients
on limited diets. The rate of daily fluid accumulation, alone, is a key piece of data. A higher-thanusual volume of serous drainage (700–1200 ml/
day) is characteristic of a thoracic duct injury and
chylothorax. In such circumstances, a complete
blood count of the fluid with differential that
shows lymphocytes > 90 % is diagnostic.
Biochemical and microscopic examination of
the pleural fluid is important. Diagnostic findings include triglyceride level > 110 mg/dL and/
or a concentration greater than plasma triglyceride level. Pleural fluid triglyceride concentrations, however, can be less than 110 mg/dl in
15 % of patients with a chylothorax. Therefore,
lipoprotein analysis can be performed as another
diagnostic tool. A microscopic examination that
shows chylomicrons is also diagnostic of a chylothorax and can be used as a confirmatory test if
the triglyceride levels are equivocal. On microscopy, fat globules will clear with alkali or ether
and will stain with Sudan III.
Imaging
Chest radiography and computed tomography
will often show a unilateral pleural effusion in
an undrained chest cavity. Other findings can
include bilateral effusions, a widened mediastinum, and a pericardial effusion. Though uncommonly performed and usually unnecessary, lymphangiography can show the site of injury [29].
This procedure involves injection of 10 mL of
ethiodized oil into the lymphatic vessels in the
dorsum of the foot. Coupled with lymphangiography, post-procedure computed tomography of
the chest can be highly accurate in localizing a
chyle leak [30].
Treatment
The best treatment of chylothorax is prevention.
Attention to the anatomy of the thoracic duct
and its variability is required to avoid injury to
the structure and its tributaries. Because of the
proximity of the thoracic duct to the esophagus
and aorta, intrathoracic aortic and esophageal
procedures carry a particular risk for duct injury. The judicious use of tying and clipping of
the lymphatic, periaortic, and periesophageal
tissues during dissection minimizes the risk of
chylothorax occurrence. The duct and lymphatic
channels are not often visualized at the time of
surgery because flow through the duct system is
minimal as a result of a patient’s nil per os (NPO)
status prior to surgery. If the duct must be visualized during an operation, for inspection or repair,
30 cc’s of fluid that is rich in fat (milk or olive
oil) can be given orally or through a nasogastric
tube 1 h prior to anticipated exposure of the duct.
Another method to prevent postoperative chyle
leakage is ligation of the thoracic duct at the level
of the aortic hiatus. Guo and colleagues reported
a group of 135 minimally invasive esophagectomies for cancer [31]. Of the 65 patients who had
prophylactic thoracic duct ligation, one patient
developed a chylothorax, whereas 7 chylothoraces occurred in 65 patients who did not have ligation of their ducts. No complications occurred
from duct ligation.
Patients who have received preoperative
therapy (radiation or chemoradiotherapy) and
who develop a chylothorax after resection of a
malignancy, such as esophageal cancer, are less
likely to respond to conservative measures. The
lymphatic collaterals seldom heal spontaneously
because radiation therapy to the periesophageal
tissues damages the adjacent lymphatic network
and reduces their healing capacity.

595 Chyle Leak After Esophageal Surgery
Management is determined by the amount of
chyle drainage. The objectives of treatment are to
drain and minimize chyle production, which, in
turn, allows time for the establishment of rerouting of chyle flow within lymphatic collaterals and
fusion of the pleural surfaces (pleurosymphysis),
which obstructs the free flow of chyle into the
pleural space. Patients who respond promptly
to conservative measures within 48 h are likely
to seal their leak. If high-output drainage occurs
over 1–2 L/d, patients can quickly become nutritionally and immunologically depleted. Morbidity and mortality are known to increase if such
quantities of drainage continue beyond 5–7
days,
and these patients are unlikely to respond to conservative
therapy. If the patient is able to tolerate a second operation, surgical exploration with
duct ligation is indicated [20, 21, 28].
Conservative Management
Conservative management is considered firstline therapy for most cases of postsurgical chylothorax and includes drainage of the pleural space
to establish complete re-expansion of the lung,
nutritional support, and medication to reduce the
flow of chyle.
Drainage of the pleural space is effectively
achieved with tube thoracostomy. Additionally,
it assists with lung re-expansion and daily measurement of chyle flow. Thoracentesis can be effective, but often needs to be repeated to achieve
adequate drainage and full lung expansion.
Nutritional support is a key component to
management. If patients have less than 500 cc/d
of chyle flow, usually they can continue oral intake. But the diet is modified to minimize the
consumption of long-chain triglycerides that increase chyle flow. A high-protein, low-fat diet
with oral or nasogastric tube feeding of MCT
can be used. Restriction of long-chain triglycerides avoids the breakdown of the compound into
monoglycerides and free fatty acids that are carried as chylomicrons into the lacteals and then
into the thoracic duct. MCTs are commercially
available in liquid or capsule form for use as a
nutritional supplement three to four times per
day. Common adverse effects are nausea, occasional vomiting, abdominal pain, and diarrhea.
To achieve the most optimal outcome with
conservative management, complete fasting and
total parenteral nutrition (TPN) must be used
[30]. Complete bowel rest is the best method to
minimize chyle production. Even water taken by
mouth can increase the flow of chyle by 20
[18]. Fasting
with success rates as high as 80
has been shown to be associated
% [32, 33
%
] compared with use of a modified enteral diet where
successes have been reported to be as low as
23 % [21, 34–36].
Somatostatin and its analog octreotide have
also been shown to decrease the flow of chyle
in cases of postoperative chylothorax [37–39].
These agents act by inhibiting gastrointestinal
and endocrine function, which, in turn, decreases
foregut secretions [40]. Dosing of octreotide is
100–500 μg subcutaneously three times per day
[41]. When used in conjunction with a strict dietary regimen, somatostatin typically reduces
chyle drainage within 48 h. Daily monitoring of
output is important to ensure continued dissipation, and resolution can be seen within a 2-week
period. Side effects are typically minor and include flushing, nausea, diarrhea, abdominal distension, and hyperglycemia.
Percutaneous catheterization and embolization of the thoracic duct has shown success in
limited series. For patients who are refractory to
previously mentioned management techniques,
who are debilitated, and who are poor operative
candidates, embolization should be considered.
The procedure involves pedal lymphangiography and transabdominal accession of the cisterna
chyli. The technique has low associated morbidity, but can be constrained by variations and size
of the lymphatic channels. Success has been reported to range from 45 to 70 % [42, 43].
If patients with high-output drainage (> 1 L/d)
do not promptly improve within 48 h from the
initiation of conservative management, surgical
intervention should be considered [28]. Shah and
colleagues reported significant failure of conservative management if patients continued to have
chest tube output over 11 cc/kg/d after beginning
the treatment [44]. Dugue and colleagues used

60 E. M. Ziarnik and J. C. Nesbitt
an output of chyle based upon body-weight ratio
as an indicator of conservative treatment success
and suggested that an output of less than 10 cc/
kg/d at day 5 of conservative treatment is justification to continue conservative management
[24]. Merigliano and colleagues recommended
early duct ligation to avoid complications related
to nutritional and immunologic depletion caused
by delayed surgical intervention [26]. As a general guideline, if drainage remains unabated more
than 500 cc/d for 5–7 days following the initiation of treatment, surgical intervention should be
considered.
Most cases of chylothorax that resolve with
conservative management will do so within 2
weeks of the implementation of treatment. During this time of bowel rest and TPN, thoracostomy tube output must be closely monitored to
ensure progressive dissipation of the drainage.
Ideally, drainage should be less than 100
fore allowing oral intake.
Particular attention is
cc/d be-
given to the quantity and quality of drainage as
oral intake is re-instituted. If drainage character
and volume do not increase with oral intake, the
pleural drainage tubes can be removed.
If drainage subsides but does not completely
resolve, chemical pleurodesis can be performed
to enhance the process. Though a number of
chemical agents have been used, the most common sclerosants include talc and doxycycline.
Success of this procedure is challenged by highoutput chylous leaks and should only be performed in patients with complete evacuation of
fluid, with full lung expansion, and with less than
300–500
cc/d of drainage.
Surgical Management
The timing of surgical intervention is influenced
by the rate of chyle drainage, the response to conservative therapy, and the risk for further surgery.
A key consideration is the condition of the patient
since the risk of a thoracotomy to correct a chyle
leak can be associated with a mortality rate over
20 % [24, 45].
The objectives of surgical intervention are to
evacuate all fluid from the pleural cavity, to fully
re-expand the lung, and to control of the lymph
leak. These can be achieved with pleuroperitoneal shunting, direct ligation of the thoracic duct at
the level of the leak, mass ligation of the thoracic
duct below the level of the leak, pleurectomy, and
pleurodesis.
Pleuroperitoneal shunts have been successfully used for management of patients with refractory chylothoraces and are options for management of difficult patients who have exhausted
other treatments or who are too ill to underdo
more major surgery. The shunts can usually be
placed easily and with little risk. They, however,
require regular pumping by the patient or family
members to be effective for long term [46].
The most definitive management of a postesophagectomy chylothorax involves exploration
of the chest cavity by thoracotomy or thoracoscopy. Patients with a unilateral chylothorax can be
managed with an ipsilateral thoracic procedure
because the duct and the site of leakage usually
can be accessed from the side of the effusion. For
patients with bilateral chylothoraces, however,
the entire thoracic duct region must be visualized
and is optimally exposed where it resides in the
lower aspect of the right pleural cavity.
The thoracic duct and adjacent accessory lymphatic channels are typically located in the supradiaphragmatic position within the recess between
the spine, aorta, and esophageal bed. The duct
is indiscreet and blends with the soft tissues in
this region. To facilitate intraoperative identification of the lymphatic pathways, fat in the form
of cream or olive oil is administered by a nasogastric tube. The material is absorbed through the
bowel wall into the lacteals within an hour after
administration. The lymphatic channels become
engorged with chyle, and the site of injury can be
visualized by the leakage of milky fluid.
Closure of a chyle leak is performed either
by direct occlusion or by mass ligation of the
thoracic duct and adjacent lymphatic pathways
below the level of the area of injury or leakage.
Direct closure is performed using clips or pledgetted suture ligatures applied to the injured site.
Mass ligation involves passing a ligature completely around all tissues located between the
aorta, spine, esophageal bed, and pericardium

615 Chyle Leak After Esophageal Surgery
Fig. 5.4 Mass ligation of the thoracic duct through a
right thoracotomy incision. A right angle clamp is placed
around the lymphatic tissues at the level of the diaphragm.
(Fig. 5.4 ). The hemiazygous or azygous vein can
be included within the ligature that is positioned
near the level of the aortic hiatus to ensure occlusion of the duct well below the site of injury.
Double ligation is prudent to ensure complete
isolation and occlusion. Some surgeons advocate
ligation of the duct above the site of injury, but
this is typically unnecessary. The same technique
of supradiaphragmatic direct or mass ligation is
also used if thoracic duct injury is noted or suspected at the time of the initial esophageal operation. Immediate and complete cessation of leakage should happen and is an assurance of a satisfactory result that occurs in over 95 % of patients.
Following closure of the leak, fibrin glue can
be applied to the region to enhance its sealing.
A mechanical pleurodesis is also performed to
enhance pleurosymphysis. Pleural tubes are positioned to monitor subsequent lymph drainage and
to optimize complete lung expansion. The results
with ligation of the thoracic duct are excellent
with 90–100 % resolution of the leak. In unusual
All tissues between the aorta, spine, esophageal bed, and
azygous vein are incorporated. The azygous vein can also
be included with the ligation
cases where lymph drainage continues following
ligation, aberrant pathways may be present. In
such circumstances, lymphangiography is helpful to better define the lymphatic anatomy and to
enhance the surgical outcome.
Summary
The keys to successful management of a postesophagectomy chyle leak are early recognition
and prompt intervention to correct the problem
(Fig. 5.5 algorithm). Conservative management
can result in the resolution of the leak if the quantity of drainage declines promptly within the first
48 h of treatment and continues to drop to less
than 100 cc/d by the end of day 7–10 of treatment. Surgeons should have a low threshold for
recognizing when conservative management
fails and when surgical intervention is indicated.
When correction of a chyle leak occurs without
delay, overall recovery is enhanced and further
morbidity is avoided.

62 E. M. Ziarnik and J. C. Nesbitt
Fig. 5.5 Treatment algorithm for chylothorax
Key Points on Avoiding an Esophageal Anastomotic Leak
1. Chylothorax is an important but infrequent
cause of pleural effusion.
2. The most common causes of chylothorax are
iatrogenic and neoplastic.
3. Diagnosis is made by the analysis of the pleu-
ral fluid.
4. Prompt treatment is indicated to avoid pleural
and nutritional complications.
Key Points on Diagnosis and Managing an Esophageal Anastomotic Leak
1. If the injury is identified intraoperatively, the
thoracic duct should be ligated proximal to the
injury.
2. If injury is identified postoperatively, initial
conservative treatment consists of manage-
ment of the pleural effusion, nothing per os
(NPO) status, and TPN.
3. If conservative management fails, operative
intervention is indicated and requires proximal
ligation of the thoracic duct by thoracotomy.
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