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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_636_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Contributors
- •Puborectalis Muscle
- •Iliococcygeus Muscle
- •Pubococcygeus Muscle
- •Mesorectum
- •Presacral Fascia
- •Retrosacral Fascia
- •Waldeyer’s Fascia
- •Denonvilliers’ Fascia
- •Lateral Ligaments
- •Anorectal Spaces
- •Perianal Space
- •Intersphincteric Space
- •Submucous Space
- •Ischioanal/Ischiorectal Space
- •Supralevator Space
- •Anal Canal Epithelium
- •Internal Anal Sphincter
- •Conjoined Longitudinal Muscle
- •External Anal Sphincter
- •Perineal Body
- •Pelvic Floor Muscles
- •Retrorectal Space
- •Rectal Blood Supply
- •Superior Rectal Artery
- •Middle Rectal Artery
- •Inferior Rectal Artery
- •Cecum
- •The Appendix
- •Ascending Colon
- •Transverse Colon
- •Descending Colon
- •Sigmoid Colon
- •Rectosigmoid Junction
- •Blood Supply
- •Superior Mesenteric Artery
- •Inferior Mesenteric Artery
- •Venous Drainage
- •Lymphatic Drainage
- •Nervous Innervation
- •Embryology
- •Non-rotation
- •Malrotation
- •Reversed Rotation
- •Omphalocele
- •Internal Hernias
- •Proximal Colon Duplication
- •Meckel’s Diverticulum
- •Hirschsprung’s Disease
- •Anorectal Malformations
- •Anal Stenosis
- •Membranous Atresia
- •Anal Agenesis
- •Anorectal Agenesis
- •Rectal Atresia or “High Atresia”
- •Persistent Cloaca
- •2: Colonic Physiology
- •Colonic Anatomy
- •Introduction
- •Colonic Wall Anatomy
- •Colonic Epithelial Cell Types
- •Colonic Flora
- •Electrolyte Regulation and Water Absorption
- •Short-Chain Fatty Acid Absorption
- •Secretory Role of the Colonic Epithelium
- •Regulation of Electrolyte and Water Absorption and Secretion
- •Colonic Innervation
- •Colonic Motility
- •Cellular Basis of Motility
- •Motility Patterns and Measurement
- •Introduction
- •Normal Continence
- •Rectal Capacity
- •Structural Considerations
- •Normal Defecation
- •Obstructed Defecation
- •Functional Anorectal Pain
- •4: Endoscopy
- •Introduction
- •The Complete Anorectal Examination
- •Patient Position
- •Prone Jackknife
- •Left Lateral
- •Digital Rectal Examination
- •Anoscopy/Proctoscopy
- •Anoscopy
- •Proctoscopy
- •Flexible Endoscopy
- •Flexible Endoscopic Insertion Techniques
- •Torque
- •Dithering/Jiggle
- •Slide-By
- •Special Considerations
- •The Patient Requiring Antibiotics
- •The Anticoagulated Patient
- •Incomplete Colonoscopy
- •Procedure
- •The Endoscopy Suite
- •Instruments
- •Sedation
- •Nitrous Oxide
- •Ketamine
- •Propofol
- •Colonoscopy Technique
- •Anal Intubation
- •Sigmoid Colon
- •Sigmoid-Descending Junction
- •Descending Colon
- •Splenic Flexure
- •Transverse Colon
- •Hepatic Flexure
- •Cecum
- •Patient Position
- •Abdominal Pressure
- •Sigmoidoscopy
- •Colonoscopy
- •Bowel Preparation
- •Ileocecal Valve Intubation
- •Terminal Ileum
- •Alternate Techniques
- •Chromocolonoscopy (Chromoendoscopy)
- •Full-Spectrum Endoscopy
- •Complications
- •Sedation Complications
- •Vasovagal/Cardiac Arrhythmia
- •Pulmonary
- •Procedural Complications
- •Splenic Injury
- •Perforation
- •Post-polypectomy Syndrome
- •Bleeding
- •Infectious Complications
- •Simulation
- •Documentation
- •Quality
- •PillCam Endoscopy
- •Introduction
- •Polypectomy Techniques
- •Endoscopic Mucosal Resection
- •Endoscopic Submucosal Dissection
- •Combined Endo-Laparoscopic Surgery (CELS)
- •Major Abdominal Surgery
- •Anorectal Surgery
- •Preoperative Testing
- •Laboratory Studies
- •Electrocardiogram
- •Chest X-ray
- •Initial Workup
- •Who Needs Additional Testing?
- •Preoperative “Optimization”
- •Coronary Stent Management
- •AICD/Pacemaker Management
- •COPD
- •Obstructive Sleep Apnea (OSA)
- •Diabetes
- •Obesity
- •Malnutrition
- •Solid Organ Transplant Recipients
- •Substance Abuse
- •Alcohol
- •Tobacco
- •Opioids
- •Medications
- •Anticoagulation
- •Immunosuppressive Agents
- •Chemotherapy
- •Introduction
- •Preoperative Management
- •Patient Education
- •Intraoperative Pathway
- •Minimally Invasive Colorectal Surgery
- •Intraoperative Fluid Administration
- •Analgesia
- •Venous Thromboembolism (VTE) Prophylaxis
- •Postoperative Recovery
- •Analgesia
- •Intravenous Fluid Management
- •Venous Thromboembolism (VTE) Prophylaxis
- •Quality Pathway Evaluation Measures
- •Quality Improvement Measures
- •8: Postoperative Complications
- •Introduction
- •Ureteral Injury
- •Bladder Injury
- •Urethral Injury
- •IV Fluid Management
- •Wound Management
- •Bladder Management
- •Pain Management
- •Academic Medical Center
- •Wound Complications
- •Preoperative Considerations
- •Perioperative Interventions
- •Long-Term Complications
- •Genitourinary Complications
- •Fertility Complications
- •Bowel Dysfunction
- •9: Anastomotic Construction
- •Introduction
- •Surgical Staplers
- •Handsewn Anastomoses
- •Compression Anastomoses
- •Tension
- •Blood Supply
- •Prophylactic Drainage
- •Diversion
- •High-Risk Anastomoses
- •Abdominal Anastomoses
- •Small Bowel Anastomoses
- •Ileocolic Anastomoses
- •Pelvic Anastomoses
- •Stapled Colorectal Anastomoses
- •Handsewn Colorectal Anastomosis
- •Ileorectal Anastomosis
- •Neorectal Reservoirs
- •Handsewn Coloanal Anastomosis
- •Unanticipated Pelvic Anastomosis
- •Inadequate Colonic Length
- •Intraoperative Anastomotic Failure
- •10: Anastomotic Complications
- •Anastomotic Leak
- •Overview
- •Consequences
- •Prevention
- •Diagnosis
- •Treatment
- •Anastomotic Stricture
- •Anastomotic Bleeding
- •Introduction
- •Patient History
- •Levator Syndrome
- •Physical Examination
- •Abdominal Examination
- •Inguinal Examination
- •Digital Rectal Examination
- •Conclusion
- •12: Hemorrhoids
- •Anatomy
- •Etiology
- •Epidemiology
- •Clinical Presentation
- •History
- •Physical Examination
- •Treatment
- •Medical Management
- •Dietary
- •Topical Therapies
- •Oral Therapy
- •Rubber Band Ligation
- •Infrared Photocoagulation
- •Sclerotherapy
- •Excisional Hemorrhoidectomy-Closed Technique
- •Excisional Hemorrhoidectomy Open Technique (Milligan-Morgan)
- •Excisional Hemorrhoidectomy (Circumferential or Whitehead)
- •Urinary Retention
- •Postoperative Hemorrhage
- •Anal Stenosis
- •Postoperative Infection
- •Fecal Incontinence
- •Stapled Hemorrhoidopexy
- •Transanal Hemorrhoidal Dearterialization
- •Special Clinical Scenarios
- •Thrombosed External Hemorrhoid
- •Pregnancy
- •Crohn’s Disease
- •Immunocompromised Patients
- •13: Anal Fissure
- •Pathogenesis
- •Non-operative Treatment
- •Healing Rates in Acute Anal Fissure
- •Healing Rates in Chronic Anal Fissure
- •Topical
- •Nitroglycerin
- •Calcium Channel Blockers
- •Botulinum Toxin Type A
- •Operative Treatment
- •Anal Dilation
- •Anal Sphincterotomy (Technique)
- •Outcomes Between Closed and Open Anal Sphincterotomy
- •Extent of Sphincterotomy
- •Fissurectomy
- •Results of Sphincterotomy
- •Fissures Without Anal Hypertonicity
- •Crohn’s Disease
- •Conclusions
- •Pathophysiology
- •Anatomy
- •Etiology
- •Evaluation
- •Physical Examination
- •Imaging
- •Computed Tomography (CT)
- •Magnetic Resonance Imaging (MRI)
- •Endoanal Ultrasound (EAUS)
- •Transperineal Sonography (TP-US)
- •Treatment
- •Catheter Drainage
- •Postoperative Management
- •Complications
- •Immediate Postoperative Period
- •Misdiagnosis
- •Special Considerations
- •Necrotizing Anorectal Infection (Fournier’s Gangrene)
- •Diagnosis
- •Treatment
- •Outcomes
- •Anal Fistula
- •Etiology
- •Diagnosis
- •Fistulography
- •Endoanal Ultrasound
- •Magnetic Resonance Imaging
- •Treatment
- •Lay-Open Technique (Fistulotomy)
- •Setons
- •Advancement Flap
- •Technique
- •Technique
- •Fibrin Glue
- •Technique
- •Anal Fistula Plug
- •Technique
- •Novel Techniques
- •15: Complex Anorectal Fistulas
- •Introduction
- •Complex or Recurrent Cryptoglandular Fistulas
- •Surgical Treatment
- •Seton
- •Anal Flap
- •Anal Fistula Plug
- •Fibrin Glue
- •Outcomes
- •Seton
- •Advancement Flap
- •Anal Fistula Plug
- •Fibrin Glue
- •Rectourethral Fistulas
- •Surgical Treatment
- •Transanal Approach
- •Posterior Approach
- •Transperineal Approach
- •Transabdominal Approach
- •Outcome
- •Postoperative Fistulas
- •Surgical Treatment
- •Outcome
- •16: Rectovaginal Fistula
- •Obstetric Injury
- •Cryptoglandular Disease
- •Crohn’s Disease
- •Endorectal Repairs
- •Transperineal Repairs
- •Tissue Transposition Repairs
- •Martius Flap
- •Gracilis Muscle Transposition
- •Transvaginal Repairs
- •Transabdominal Repair
- •Alternate Repairs
- •Background
- •Etiology
- •Clinical Presentation/Diagnosis
- •Treatment
- •Non-operative Management
- •Operative/Excisional Management
- •Basic Procedures
- •Complex Procedures
- •Karydakis Flap
- •Cleft Lift Procedure (See Video 17.1)
- •Rhomboid/Limberg Flap (See Video 17.2)
- •Disease Recurrence
- •Hidradenitis Suppurativa
- •Etiology/Presentation/Diagnosis
- •Treatment
- •Medical Therapy
- •Surgical/Excisional Therapy
- •Introduction
- •Irritants
- •Steroid-Inducing Itching
- •Infectious
- •Dermatologic
- •Neoplasms
- •Anorectal Conditions
- •Systemic Diseases
- •Physical Examination
- •Infectious
- •Dermatologic
- •Neoplasms
- •Biochemical Testing
- •Microbiology Testing
- •Patch Testing
- •Anoscopy: Proctoscopy
- •Biopsy
- •Evidence-Based Management
- •Primary Prutitis Ani
- •Secondary Prutitis Ani
- •Infectious
- •Dermatologic
- •Systemic Diseases
- •19: Sexually Transmitted Infections
- •Introduction
- •Perianal or Genital Lesions
- •Proctitis
- •Proctocolitis
- •Enteritis
- •Gonorrhea
- •Epidemiology
- •Clinical Presentation
- •Emerging Antibiotic Resistance
- •Chlamydia
- •Epidemiology
- •Clinical Presentation
- •Lymphogranuloma Venereum
- •Epidemiology
- •Clinical Presentation
- •Treatment
- •Syphilis
- •Epidemiology
- •Clinical Presentation
- •Testing Recommendations
- •Treatment
- •Chancroid
- •Granuloma Inguinale aka Donovanosis
- •Herpes
- •Epidemiology
- •Clinical Presentation
- •Treatment
- •Human Papillomavirus
- •Epidemiology
- •Clinical Presentation
- •Testing
- •Treatment
- •Vaccine
- •Epidemiology
- •Testing
- •Anorectal Issues
- •Molluscum Contagiosum
- •Pubic Lice: Phthirus pubis
- •Scabies
- •20: Anal Intraepithelial Neoplasia
- •Introduction
- •Symptoms
- •Epidemiology
- •Screening/Surveillance
- •Diagnosis
- •Treatment
- •Management Strategies
- •Progression
- •Prevention
- •21: Anal Cancer
- •Anal Squamous Cell Carcinoma
- •Anal Melanoma
- •Anal Adenocarcinoma
- •22: Presacral Tumors
- •General Considerations
- •Anatomic Considerations
- •Diagnosis
- •Management
- •Outcomes
- •Chromosomal Instability
- •Microsatellite Instability
- •CpG Island Methylator Phenotype (CIMP)
- •Adenomatous Polyposis Syndromes
- •Familial Adenomatous Polyposis
- •Clinical Presentation
- •Underlying Genetics
- •Diagnosis
- •CRC Risk
- •FAP Extracolonic Manifestations
- •Management
- •Screening
- •Treatment
- •Colorectal
- •Duodenal Adenomas
- •Desmoid Disease
- •Thyroid Neoplasia
- •MUTYH-Associated Polyposis
- •Clinical Presentation
- •Underlying Genetics
- •Diagnosis
- •CRC Risk
- •Extracolonic Cancer Risk
- •Management
- •Screening
- •Treatment
- •Polymerase Proofreading-Associated Polyposis
- •Hamartomatous Polyposis Syndromes
- •Juvenile Polyposis Syndrome
- •Clinical Presentation
- •Underlying Genetics
- •Diagnosis
- •Management
- •Screening
- •Treatment
- •Peutz-Jeghers Syndrome
- •Clinical Presentation
- •Underlying Genetics
- •Diagnosis
- •Management
- •Surveillance
- •Polypectomy
- •Surgery
- •PTEN Hamartoma Tumor Syndrome (PHTS)
- •Clinical Presentation
- •Underlying Genetics
- •Diagnosis
- •CRC Risk Management
- •Serrated Polyposis Syndrome (SPS)
- •Clinical Presentation
- •Underlying Genetics
- •Diagnosis
- •CRC Risk
- •Management
- •Screening
- •Treatment
- •Lynch Syndrome
- •Genotype-Phenotype Correlations
- •Muir-Torre Syndrome (MTS)
- •Turcot’s Syndrome
- •Colorectal Cancer Risk
- •Other LS-Associated Cancer Risk
- •Diagnosis
- •Individual Whose Family Meets Amsterdam Criteria but Does Not Have Any Clinical Phenotype
- •Clinical Management
- •Screening
- •Introduction
- •Recommended Screening Guidelines
- •Screening Cessation
- •Colonoscopy
- •Incomplete Colonoscopy
- •Complications
- •CT Colonography (CTC) or Virtual Colonoscopy
- •Flexible Sigmoidoscopy
- •Complications
- •Fecal Occult Blood Testing (FOBT)/Fecal Immunochemical Testing (FIT)
- •Stool DNA Testing
- •Double-Contrast Barium Enema (DCBE)
- •Surveillance
- •History
- •Adenoma
- •Hamartomas Polyps
- •Early Cancer (T1) Within Polyp
- •Chemoprevention
- •Background
- •Clinical Presentation
- •Preoperative Evaluation
- •Tumor Localization
- •Total Colon Evaluation
- •Carcinoembryonic Antigen (CEA)
- •Radiographic Evaluation
- •Lymph Node Evaluation
- •Lynch Syndrome Phenotype
- •26: The Surgical Management of Colon Cancer
- •Preoperative Preparation
- •Physiologic Assessment
- •Tumor Localization
- •Surgical Technique
- •Extent of Resection
- •Mesocolic Resection
- •Right Colectomy
- •Open Approach
- •Lateral-to-Medial Approach
- •Posterior (Inferior-to-Superior) Approach
- •Superior to Inferior Approach
- •Medial-to-Lateral Approach
- •Anastomosis
- •Laparoscopic Approach
- •Medial-to-Lateral Approach
- •Posterior (Inferior-to-Superior) Approach
- •Left Colectomy
- •Open
- •Anastomotic Assessment
- •Hand-Assisted Medial-to-Lateral Approach
- •Subtotal Colectomy
- •Open Approach
- •Laparoscopic Approach
- •Total Abdominal Colectomy with Ileorectal Anastomosis
- •Special Circumstances
- •Laparoscopy
- •Obstructing Colon Cancers
- •Perforated Colon Cancers
- •Management of Primary Colon Cancer in the Setting of Distant Metastasis
- •Outcomes for Colon Cancer
- •Short-Term Outcomes
- •Long-Term Outcomes
- •Introduction
- •Total Colon Evaluation
- •Locoregional Imaging
- •Computed Tomography
- •Endorectal Ultrasound
- •T Staging
- •N Staging
- •Magnetic Resonance
- •Whole-Body Imaging
- •Computed Tomography
- •Positron Emission Tomography (PET)
- •28: Rectal Cancer: Neoadjuvant Therapy
- •Introduction
- •Historical Context
- •Postoperative Radiotherapy
- •Preoperative Radiotherapy
- •Radiosensitizing Agents
- •Preoperative Versus Postoperative Radiation
- •Short- Versus Long-Course Preoperative Radiotherapy
- •Choosing Optimal Treatment Regimens
- •The European Approach
- •Selected Adjuvant Systemic Chemotherapy
- •Selective Nonoperative Management
- •Techniques
- •Results
- •Lymphovascular Invasion
- •Tumor Budding
- •Introduction
- •Neoadjuvant Chemoradiotherapy
- •31: Proctectomy
- •Pathological Assessment
- •Preoperative Preparation
- •Operative Approaches
- •Open Low Anterior Resection (LAR)
- •Laparoscopic Low Anterior Resection
- •Robotic Low Anterior Resection
- •Abdominoperineal Resection (APR)
- •Extralevator or “Cylindrical” APR
- •Special Considerations
- •Distal Margin
- •Coloanal Anastomosis
- •Fecal Diversion
- •Extended Resection
- •Intraoperative Radiation Therapy
- •Flap Closure Following Abdominoperineal Resection
- •Functional Outcomes
- •Oncologic Outcomes
- •Multidisciplinary Rectal Cancer Care
- •32: Rectal Cancer Decision-Making
- •Assessment
- •Early Rectal Neoplasms
- •Local Excision
- •Endoscopically Excised Malignant Polyps
- •Surgical Considerations
- •Intraoperative Decisions
- •Midrectal Cancers
- •Low Rectal Cancers
- •Low Hartmann Resection Versus APR
- •Special Situations
- •Obstructing Rectal Cancer
- •Perforated Rectal Cancer
- •Synchronous Hepatic Metastases
- •33: Colorectal Cancer: Postoperative Adjuvant Therapy
- •Colon Cancer
- •Stage III Colon Cancer
- •Stage II Colon Cancer
- •Rectal Cancer
- •Patients Who Did Not Undergo Neoadjuvant Therapy
- •Patients Who Underwent Neoadjuvant Radiotherapy/Chemoradiotherapy
- •Patients Undergoing Local Excision
- •34: Colorectal Cancer: Surveillance After Curative-Intent Therapy
- •Introduction
- •Physical Examination
- •Laboratory Testing
- •Abdominal Imaging
- •Chest Imaging
- •Colonoscopy
- •Stage 1 Disease
- •Cost
- •Introduction
- •Determining Resectability
- •Multimodal Therapy Including Intraoperative Radiation
- •General Considerations
- •Recurrent Colon Cancer
- •Recurrent Rectal Cancer
- •Recurrences that Extend Anteriorly
- •Resection that Includes Sacrectomy
- •Stage I: Anterior Component
- •Stage II: Posterior Component
- •Stage III: Spinal Reconstructive Component
- •Soft Tissue Reconstruction
- •Recurrent Colon Cancer
- •Recurrent Rectal Cancer
- •Sacropelvic Resections
- •Palliative Approach
- •Introduction
- •Diagnostic Strategies
- •Computed Tomography
- •Positron Emission Tomography (PET)
- •Magnetic Resonance Imaging
- •Contrast-Enhanced Ultrasound
- •Biopsy
- •Multidisciplinary Evaluation
- •Surgical Emergency
- •Self-Expanding Intraluminal Metal Stents
- •Liver-First Strategy
- •Colon-First Strategy
- •Margin Status
- •Other Liver Metastasis Strategies: Hepatic Intra-arterial Chemotherapy/Chemoembolization
- •Pulmonary Metastasis
- •Peritoneal Metastasis
- •Ovarian Metastases
- •Bone
- •Brain
- •Pancreas
- •Adrenal
- •Retroperitoneal Lymph Nodes
- •37: Appendiceal Neoplasms
- •Introduction
- •Epidemiology
- •Epithelial Neoplasms
- •Neuroendocrine Appendiceal Lesions/Carcinoid Tumors
- •Goblet Cell Carcinoids
- •Clinical Features
- •Diagnostic Procedures
- •Medical Management
- •Appendectomy
- •Right Hemicolectomy

Ascending
colon
Descending
1 Anatomy andEmbryology oftheColon, Rectum, andAnus
Return to the abdomen
180°
70 days 77 days
180°
Fig. 1.15 Return of the intestinal loop to the abdomen
Fig. 1.16 Later fetal
development
Later fetal period
23
colon
Sigmoid colon
Cecum and
appendix

24
omentum and transverse
Plane of median section
J. C. Carmichael and S. Mills
Omental bursa
Plane of horizontal section
Horizontal section
Descending colon
Jejunum
Median section
Upper recess
omental bursa
Epiploic foramen
Pancreas
Duodenum
Pyloric stomach
Lesser
omentum
Greater
omentum
Ascending colon
Liver
Transverse colon
and mesocolon
Fig. 1.17 Development of the mesentery and omental fusion
(Fig.1.18). This condition can remain asymptomatic (a nding noted at laparoscopy or
laparotomy) or result in volvulus affecting the
entirety of the small intestine. The twist generally occurs at the duodenojejunal junction as
well as the midtransverse colon.
Omental bursa
Fused layers of greater
mesocolon
Fused layers of
greater omentum
Malrotation
• There is normal initial rotation, but the cecum
fails to complete the normal 270° rotation
around the mesentery. This results in the
cecum being located in the mid-upper
abdomen with lateral bands (Ladd’s bands)

Jejunoileal
g
Cecum
Stomach
Small intestine
1 Anatomy andEmbryology oftheColon, Rectum, andAnus
Fig. 1.18 Intestinal
non-rotation
Nonrotation
Duodenum
loops
25
Stomach
Ascending
colon
Transverse
colon
Descendin
colon
xating it to the right abdominal wall
(Fig.1.19). These bands can result in extrinsic
compression of the duodenum.
Reversed Rotation
• Clockwise (rather than counterclockwise) rotation of the midgut results in the transverse
colon being posterior to the superior mesenteric
artery, while the duodenum lies anterior to it.
Omphalocele
• An omphalocele is, basically, the retention of
the midgut within the umbilical sac and its
failure to return to the peritoneal cavity.
Internal Hernias
• Internal hernias, as well as congenital obstructive bands, can cause congenital bowel obstructions. These are considered failures of the
Intestinal Malrotation
Duodenum
Ladd’s bands
Cecum
Fig. 1.19 Intestinal malrotation

26
process of xation (the third stage of rotation).
This can be the result of an incomplete fusion
of the mesothelium or when structures are
abnormally rotated. Retroperitoneal hernias
can occur in various positions, most notably
paraduodenal, paracecal, and intersigmoid.
Other Congenital Malformations
oftheColon andSmall Intestine
Proximal Colon Duplication
• There are three general types of colonic duplication: mesenteric cysts, diverticula, and long
colon duplication. Mesenteric cysts are lined
with intestinal epithelium and variable amounts
of smooth muscle. They are found within the
colonic mesentery or posterior to the rectum
(within the mesorectum). They generally present as a mass or with intestinal obstruction as
they enlarge.
• Diverticula can be found on the mesenteric or
antimesenteric sides of the colon and are outpouchings of the bowel wall. They often contain heterotopic gastric or pancreatic tissue.
• Long colonic duplications of the colon are the
rarest form of duplication. They usually run
the entire length of the colon and rectum, and
there is an association with other genitourinary abnormalities.
Meckel’s Diverticulum
• A Meckel’s diverticulum is the remnant of the
vitelline or omphalomesenteric duct
(Fig. 1.13). It arises from the antimesenteric
aspect of the terminal ileum, most commonly
within 50cm of the ileocecal valve.
• They can be associated with a brous band
connecting the diverticulum to the umbilicus
(leading to obstruction), or it may contain
ectopic gastric mucosa or pancreatic tissue
(leading to bleeding or perforation) (Fig.1.20).
• An indirect hernia containing a Meckel’s
diverticulum is termed a Littre’s hernia.
• Meckel’s diverticulum is generally asymptomatic and, per autopsy series, is found in up
to 3% of the population.
• Surgical complications are more common in
children than adults and include hemorrhage,
J. C. Carmichael and S. Mills
Fig. 1.20 Perforated Meckel’s diverticulum with stula
to the ileum
obstruction, diverticulitis, perforation, and
umbilical discharge.
Atresia oftheColon
• Colonic atresia, representing only 5% of all
gastrointestinal atresias, is a rare cause of congenital obstruction. They are likely the result
of vascular compromise during development.
They vary in severity from a membranous diaphragm blocking the lumen to a brous cordlike remnant, on to a complete absence of a
segment.
Hirschsprung’s Disease
• This nonlethal anomaly, which is more common in males, results from the absence of ganglion cells within the myenteric plexus of the
colon.
• It is caused by interruption of the normal migration of the neuroenteric cells from the neural
crest before they reach the rectum. This results in
dilation and hypertonicity of the proximal colon.
• The extent of the aganglionosis is variable,
though the internal sphincter is always
involved. Its severity is dependent upon the
length of the involved segment.

1 Anatomy andEmbryology oftheColon, Rectum, andAnus
27
Anorectal Malformations
• Abnormalities in the normal development of
the anorectum can be attributed to “developmental arrest” at various stages of normal
development. Skeletal and urinary anomalies are associated in up to 70%, while
digestive tract anomalies (e.g., tracheoesophageal stula or esophageal stenosis)
and cardiac and abdominal wall abnormalities are also noted in patients with anorectal
anomalies.
Anal Stenosis
• Twenty-ve to twenty-nine percent of infants
are born with anal stenosis, but only about
25% of these are symptomatic. The majority
of these children undergo spontaneous dilation by 6months of age.
Membranous Atresia
• This very rare condition is characterized by
the presence of a thin membrane of the skin
between the blind end of the anal canal and the
surface. It is also termed the covered anus. It is
more common in males.
Anal Agenesis
• The rectum develops below the puborectalis
where it either ends in an ectopic opening
(stula) in the perineum, vulva, or urethra or
it ends blindly (less commonly). The sphincter is present at its normal site.
Anorectal Agenesis
• Anorectal agenesis is the most common type
of “imperforate anus.” More common in
males, the rectum ends well caudal to the surface, and the anus is represented by a dimple
with the anal sphincter usually being normal
inlocation. In most cases, there is a stula to
the urethra or vagina. High stulae (to the
vagina or urethra) with anorectal agenesis
develop as early as the sixth or seventh week
of gestation, while the low stulae (perineal)
or anal ectopia develop later, in the eighth or
ninth week of development.
Rectal Atresia or “High Atresia”
• In rectal atresia, the rectum and the anal canal
are separated from one another by an atretic
portion. It is embryologically the distal-most
type of colon atresia but is still considered an
anorectal disorder clinically.
Persistent Cloaca
This rare condition, which only occurs in female
infants, is the result of total failure of descent of
the urorectal septum. It occurs at a very early
stage of development.

Colonic Physiology
Joshua I. S. Bleier and Kirsten Bass Wilkins
2
Key Concepts
• Colonic innervation is supplied by both extrinsic and intrinsic pathways. The extrinsic pathways are derived from the autonomic nervous
system including parasympathetic and sympathetic routes. Parasympathetic input is excitatory, while sympathetic input is inhibitory to
colonic motor function. The intrinsic colonic
nervous system consists of the myenteric plexus.
• Short-chain fatty acids are produced by the
colon as a result of the fermentation of complex carbohydrates by colonic ora. The
SCFA, butyrate, is the primary energy source
of the colon.
• The colon absorbs sodium and water and
secretes bicarbonate and potassium. Aldosterone
mediates the process of active sodium absorption in the colon.
• Colonic contractile events are divided into (1)
segmental contractions and (2) propagated
contractions (including low-amplitude and
J. I. S. Bleier (*)
Clinical Surgery, University of Pennsylvania Health
System, Perelman School of Medicine,
Philadelphia, PA, USA
Department of Surgery, Hospital of the University of
Pennsylvania/Pennsylvania Hospital,
Philadelphia, PA, USA
e-mail: Joshua.bleier@uphs.upenn.edu
K. B. Wilkins
Department of Surgery, RWJ Barnabas Health,
Edison, NY, USA
high-amplitude propagating contractions,
LAPC and HAPC, respectively). The main
function of HAPC is to propagate colonic contents toward the anus.
• The interstitial cells of Cajal (ICC) are the primary pacemaker cells governing the function
of the enteric nervous system.
Colonic Anatomy
Introduction
• The colon is highly efcient at absorbing
sodium chloride, water, and short-chain fatty
acids.
• The colonic epithelium is a typical electrolytetransporting layer that is capable of moving
large quantities of water and salt from the
lumen toward the blood.
• It is presented with between 1 and 2 liters of
electrolyte-rich uid per day, and nearly
90% of this uid is absorbed resulting in the
excretion of feces with a sodium concentration of approximately 30 mmol/liter and a
potassium concentration of approximately
75mmol/liter. Fecal and plasma osmolality
are similar.
• The colonic epithelium secretes bicarbonate, potassium chloride, and mucus. Colonic
epithelial cells are polarized and equipped
with numerous ion channels, carriers, and
pumps that are localized on both the luminal
© ASCRS (American Society of Colon and Rectal Surgeons) 2019
S. R. Steele et al. (eds.), The ASCRS Manual of Colon and Rectal Surgery,
https://doi.org/10.1007/978-3-030-01165-9_2
29

30
subserosasubmucosamuscularismucosa
Fig. 2.1 Normal
colonic mucosa. H&E,
250x. The layers of the
normal colonic wall are
indicated by the
brackets. (Courtesy of
Julieta E.Barroeta, MD)
J. I. S. Bleier and K. B. Wilkins
and basolateral membranes. Many transport
proteins have been identied and their functions elucidated.
Colonic Wall Anatomy
• The luminal surface of the colon is lined by
the epithelium. Deep to this is the submucosal
layer, rich in vascular and lymphatic supply.
This is surrounded by the continuous inner
circular muscle layer and the outer longitudinal muscle layer which has three condensations known as taenia coli. The serosa, or
outer layer of the colon, is surrounded by the
visceral peritoneum.
Colonic Epithelial Cell Types
• Three main cell types are present in the
colonic epithelium including columnar epithelial cells, goblet cells, and enterochromafn cells. Columnar epithelial and goblet cells
comprise nearly 95% of the cells in the
colonic epithelium.
• Crypt epithelium is highly proliferative and
relatively undifferentiated and secretes chloride. The surface epithelium in contrast has
low proliferative activity, is well- differentiated,
and is highly absorptive.
• Epithelial cells become increasingly differentiated the farther they are from the crypt base.
The base of the crypts forms the source of continually regenerating epithelial cells (Figs.2.1
and 2.2). Ion absorption and secretion occur at
both the surface and crypt levels.
• The cells responsible for the enteric nervous
system, the enteric ganglia, are located in the
submucosa (Meissner’s plexus). An additional
layer of ganglia is located between the inner
circular and outer longitudinal muscle layers
known as Auerbach’s plexus.
• The interstitial cells of Cajal (ICC), c-kitpositive cells that primarily serve as the pacemaker cell of the enteric nervous system, link
the colonic submucosa electrochemically with
the myenteric plexi. These are the cells of origin of GI stromal tumors (GISTs) which arise
from the colonic wall rather than the mucosa.
Colonic Flora
Feces contain as many as 1011–1012 bacteria/
gram of stool (over 400 species) contributing to
approximately 50% of fecal mass. The majority
are anaerobes that feed on residual proteins and
undigested carbohydrates. They contribute to
the metabolic support of the colonocyte and
gut- associated lymphoid tissue (GALT), which

2 Colonic Physiology
Fig. 2.2 Normal
colonic mucosa. H&E,
1000x. Epithelial cells
types are clearly visible
including goblet cells
and columnar epithelial
cells. The crypts are the
source of the continually
regenerating mucosal
cells. (Courtesy of
Julieta E.Barroeta, MD)
31
contributes signicantly to both innate and
adaptive immunity.
• Bacteroides species are the predominant bacterial type throughout the colon and are responsible for almost 2/3 of the bacteria within the
proximal colon. The other predominant species are facultative aerobes – Escherichia,
Klebsiella, Proteus, Lactobacillus, and
Enterococci.
• The colonic mucosa receives its nutrition from
undigested dietary ber which is metabolized
by colonic bacteria through the process of fer-
mentation and produces gas and short-chain
fatty acids including butyrate – the main
energy source for colonocytes.
• Cellulose is a partially fermented starch,
which leaves behind bulk, whereas fruit pectins are completely metabolized.
• Several dietary complex carbohydrates,
including lignin and psyllium, are not metabolized at all but remain as hydrophilic molecules in stool. These lead to water retention
and stool bulking.
• Protein fermentation (putrefaction) results in
the formation of potentially toxic metabolites
including phenols, indoles, and amines. Toxic
end products of bacterial metabolism may
promote carcinogenesis.
• Increased stool bulk is felt to provide enhanced
colonic transit resulting in decreased time of
exposure of the colonic lumen to these toxins,
as well as a decreased need for higher intracolonic pressures necessary for segmental motility, a process that may retard the development
of diverticular disease. These aspects are the
reason for many of the recommendations for
dietary supplementation with indigestible ber.
Electrolyte Regulation and Water Absorption
• A majority of sodium chloride absorption
occurs in the proximal colon and is driven primarily through electroneutral absorption by
tightly-coupled luminal Na+/H+ and Cl-/
HCO3- exchange. Three types of Na+/H+
exchangers (NHE) have been identied in
colonic epithelium. Similarly, several Clexchange mechanisms have been identied.
The luminal Cl-/HCO3- exchange is represented by the anion exchanger type 1 (AE1). A
separate Cl-/OH- exchange is represented by a
protein called DRA (downregulated in colonic
adenomas).
• Epithelial cells in the distal colon participate
in electrogenic absorption of sodium. The

32
Proximal Colon Distal Colon
Cl
Cl
J. I. S. Bleier and K. B. Wilkins
epithelial sodium channel (ENaC) mediates
this absorption and is located on the luminal
surface. Potassium is secreted on the luminal
side and is driven by the electrogenic uptake
of sodium.
• Chloride is absorbed through luminal cystic
brosis transmembrane conductance regulator
(CFTR) and other chloride channels. It is
excreted on the basolateral side via multiple
mechanisms including KCL cotransporter
(KCC1), Cl- channels, and CL-/HCO3- anion
CFTR
-
Cl
+
Na
-
Cl
CFTR
-
CFTR
-
+
Na
-
Cl
CFTR
-
Cl
CFTR
-
Cl
CFTR
-
Cl
+
Na
-
Cl
Luminal
Secretion
Absorption
Luminal
Secretion
Absorption
exchangers. The net result is tight regulation
of electrolyte secretion in excreted stool
(Fig.2.3).
• Changes in intracellular sodium concentration
during sodium chloride absorption downregulates ENaC activity.
• Blood pressure and potassium levels also regulate sodium absorption via angiotensin II.
• Aldosterone targets the renal and colonic epithelium and increases activity of NHE3.
Early- and late-phase aldosterone actions have
ENaC
ENaC
ENaC
CFTR
-
Cl
ENaC
CFTR
-
Cl
CFTR
-
Cl
CFTR
-
Cl
CFTR
-
Cl
CFTR
-
Cl
Na
Cl
Na
Cl
+
Na
+
Na
+
Na
-
Cl
+
Na
-
Cl
+
-
+
-
Luminal
Secretion
Absorption
Luminal
Secretion
Absorption
+
Na
-
Cl
Luminal
+
Na
OH
-
-
Cl
-
Cl
NHE
2/3
DRA
AE1
H
NHERF
+
HCO
Basolateral
+
2K
+
3Na
+
K
-
3
KCC1
AE
1/2
+
K
-
Cl
-
Cl
Impact on Na
+
Na
-
Cl
+
H
-
Cl
α,β,γ
ENac
CFTR
NHES
+
Absorption Impact on HCO
NHERF
+
Na
CFTR
HCO
HCO
-
3
-
Cl
CFTR
HCO
Cl
Cl
-
3
Fig. 2.3 Schematic of ion-transport channels in proximal and distal colonocytes. (Courtesy of Robin Noel)
-
Secretion
3
-
3
-
-

2 Colonic Physiology
33
been identied. In the rst 1–6h, aldosteroneinduced proteins including serum and
glucocorticoid- inducible kinase (Sgk), corticosteroid hormone-induced factor (CHIF),
and K-Ras (KRAS) increase the posttranslational activation of existing ion channels and
other proteins involved in ion transport such
as ENaC.In the late phase (>6h), aldosterone
acts via the upregulation of nuclear transcription of these receptors. In addition, electroneutral absorption is known to be regulated in
response to some G protein-linked receptors,
tyrosine kinase-coupled receptors, and protein
kinases. For example, activation of protein
kinase C and Ca2+/calmodulin-dependent
kinase and increases in cAMP inhibit NHE3.
• ENaC, NHE3, and CFTR are coexpressed in
colonic epithelial cells, and thus CFTR plays a
role in both the electrogenic and electroneutral absorption of electrolytes. CFTR inhibits
both electroneutral NaCl absorption and electrogenic Na+ absorption. In the crypts, CFTR
is a cAMP-mediated chloride channel that is
essential for chloride secretion. In patients
with cystic brosis, mutations in CFTR result
in both impaired chloride secretion and
enhanced sodium absorption.
• Along with the kidneys, the colon assists with
potassium homeostasis through the absorption
and secretion of potassium. Active potassium
absorption is restricted to the distal colon and
is mediated by H+-K+-ATPase.
• Water is passively absorbed and can be transported by various pathways including through
paracellular shunts and through transcellular
ux potentially through aquaporin channels
located on luminal and basolateral membrane
surfaces.
Short-Chain Fatty Acid Absorption
• Short-chain fatty acids (SCFA) are produced
during fermentation of dietary bers by luminal bacteria and are absorbed by nonionic diffusion and paracellular absorption in the
proximal colon. Butyrate plays a major role in
the stimulation of sodium chloride absorption
and inhibition of chloride secretion. Chloride
absorption is also upregulated by increased
HCO3- production and stimulation of the
luminal Cl-/HCO3- exchanger. This HCO3luminal secretion is paramount in regulating
luminal intestinal pH. It has been proposed
that antibiotic-associated diarrhea is secondary to decreased butyrate production resulting
in net secretion of uid.
• Butyrate stimulates cell proliferation in the
crypts and reduces the number and size of
aberrant crypt foci– the earliest precursors of
colonic neoplasms. In colon cancer cell lines,
butyrate induces apoptosis and cell cycle
arrest. It also has an anti-inammatory role
via inhibition of nuclear factor kB (NF-kB).
Butyrate stimulates the production of MUC2
mucin part of the colonic defense barrier. And
it may decrease visceral sensitivity.
• Commercially available butyrate for oral
administration is limited by its short half-life,
poor palatability, and side effects such as nausea and anorexia. Rectal formulations are
most commonly utilized at this time. Prebiotics
and probiotics which produce butyrate are
alternative methods of delivery. Prebiotics are
nutrients (typically carbohydrates) that support the growth of probiotics bacteria.
Probiotics are live bacteria that when consumed in sufcient quantities confer positive
health benets.
Secretory Role of the Colonic Epithelium
Electrolyte secretion helps transport mucus from
the crypts and is activated by an increase in intracellular cAMP that parallels electrolyte
secretion.
• Chloride secretion occurs predominantly in
the crypt cells and is activated by cAMPdependent stimulation of CFTR chloride
channels.
• Additional Cl- channels have been identied
in the colonic mucosa that belongs to a family
of ClC Cl- channels. Lubiprostone accelerates
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