Colorectal Surgery E-Book
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- Herausgeber: John Wiley & Sons
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- Sprache: Englisch
Using a case-based approach, Colorectal Surgery: Clinical Care and Management provides practical, clinical and expert guidance to illustrate the best care and clinical management of patients requiring colorectal surgery for colorectal disease.
Real-life cases illustrate the entire syllabus of GI/colorectal surgery, being specially selected to highlight topical or controversial aspects of colorectal care. Cases have a consistent approach throughout and as well as outlining the actual management of each individual case, also offer an honest appraisal of the chosen management route, its successes and areas that could have been managed differently. Pedagogic features such as learning and decision points boxes aid rapid understanding/learning, enabling the reader to improve their patient management.
In full colour and containing over 100 outstanding clinical photos and slides to support the cases, each section also covers recent developments/ landmark papers/ scoring systems and a thorough discussion of clinical management based on the major society guidelines from NICE, ASCRS and ECCO.
Reliable, well-written and perfect for consultation in the clinical setting, Colorectal Surgery: Modern Clinical Care and Management is the perfect tool for all members of the multi-disciplinary team managing patients suffering from colorectal disease, specifically GI surgeons, gastroenterologists, oncologists and general surgeons.
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Veröffentlichungsjahr: 2016
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Table of Contents
Title Page
Copyright
List of contributors
Foreword
Section A: Colorectal cancer
Incidence
Pathogenesis
Risk factors for colorectal cancer
Pathology
Clinical presentation
Investigation of colorectal cancer
Decision making: the multidisciplinary team (MDT)
Surgical treatment
Postoperative management
Other tumors
References
Case 1: A screen-detected colonic conundrum
Could we have done better?
Case 2: Serrated Pathways
Could we have done better?
Reference
Case 3: Large tubulovillous adenoma of the rectum treated by TEM
Could we have done better?
Reference
Case 4: To stent or not to stent?
Could we have done better?
Case 5: Advanced rectal cancer: Brazil or Japan?
Case 6: Marginal decisions
Could we have done better?
Case 7: Locally advanced rectal cancer invading prostate
Could we have done better?
Reference
Case 8: Low rectal cancer and synchronous polyps
Could we have done better?
Case 9: Liver or rectum first?
Could we have done better?
Case 10: Beware bad livers!
Could we have done better?
Reference
Case 11: Anastomotic recurrence?
Could we have done better?
Case 12: Challenging warts
Could we have done better?
Case 13: An unusual right iliac fossa mass
Could we have done better?
Section B: Inflammatory bowel disease
Introduction
Crohn's disease
Ulcerative colitis
References
Case 14: A problem teenager
Case 15: Recurrent Crohn's disease with intraabdominal abscess: when to operate?
Case 16: Very extensive small bowel stricturing disease
Reference
Case 17: Long-standing Crohn's colitis and enterocutaneous fistula
Could we have done better?
Case 18: Crohn's colitis
Case 19: Fistulating anal Crohn's disease: conservative management
Case 20: Tail end carnage
Could we have done better?
Case 21: Acute severe colitis
Could we have done better?
Case 22: Snare or pouch? The problem of dysplasia in ulcerative colitis
Could we have done better?
References
Case 23: Anal fistula and ulcerative colitis
Could we have done better?
Case 24: Poor pouch function
Case 25: Low rectal cancer in a patient with ulcerative colitis: late reconstruction with continent Kock ileostomy
References
Section C: Pelvic floor disorders
Introduction
External rectal prolapse
Fecal incontinence
Obstructed defecation
Slow transit constipation
Anismus
Chronic anorectal pain (see Case 32)
References
Case 26: Constrictions of prolapse surgery
Could we have done better?
Case 27: Elderly prolapse dilemma
Could we have done better?
Case 28: Chasing incontinence
Could we have done better?
Case 29: Sphincter disruption
Could we have done better?
Case 30: Stimulating complications
Could we have done better?
Case 31: Crohn's evacuation trouble
Case 32: Disabling anal pain
Could we have done better?
Section D: Proctology
Hemorrhoids
Anal fistula
Anal fissure
Pilonidal sinus
Pruritus ani
References
Case 33: Hemorrhoids and HIV
Could we have done better?
Case 34: Refractory fissure
Could we have done better?
Case 35: Hirschsprung's fistula
Case 36: Complex fistula in a young woman
Could we have done better?
Case 37: Recurrent rectovaginal fistula
Case 38: Adolescent cleft trouble
Could we have done better?
Case 39: Extreme itch
Section E: Emergency colorectal surgery
Abdominal trauma
Emergency presentations of diverticular disease
Emergency presentations of colorectal cancer
Colorectal vascular emergencies
Volvulus
Postoperative colorectal complications
References
Case 40: Occupational blast disaster
Could we have done better?
Case 41: Wash and go?
Could we have done better?
Case 42: Absolute constipation
Could we have done better?
Case 43: Multiply ischemic parts
Could we have done better?
Case 44: Seriously obscure bleeding
Could we have done better?
Case 45: Complicated twist
Could we have done better?
Case 46: Obscure postoperative obstruction
Could we have done better?
Case 47: Gynecological disaster
Could we have done better?
Case 48: Pelvic leak and salvage
Could we have done better?
Section F: Surprise cases
Case 49: Radiology 0, Pathology 1
Could we have done better?
Case 50: An appendix mass?
Could we have done better?
Case 51: A worrying-looking rectal ulcer
Could we have done better?
Case 52: Think the unthinkable
Could we have done better?
Section G: New technologies and techniques
Laparoscopic (multiport) colorectal surgery
Single port surgery
Three-dimensional (3-D) laparoscopy
Robotic-assisted surgery
NOTES
Transanal minimally invasive surgery (TAMIS)
Perfusion studies
Lymph node mapping
References
Index
End User License Agreement
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Guide
Cover
Table of Contents
Preface
Begin Reading
List of Illustrations
Section A: Colorectal cancer
Figure A.1 Paris classification.
Figure A.2 Polyp pit patterns.
Figure A.3 Haggitt system for cancer invasion in a pedunculated polyp.
Figure A.4 The Kikuchi classification for sessile malignant polyps.
Figure A.5 Histological representation of the anal canal including the anal transition zone.
Case 1: A screen-detected colonic conundrum
Figure 1.1 Polypectomy specimen with invasive mucinous adenocarcinoma extending into stalk (Haggitt level 3).
Case 2: Serrated Pathways
Figure 2.1 Endoscopic image of serrated polyp.
Figure 2.2 Endoscopic image of ileocecal lesion at colonoscopy.
Case 3: Large tubulovillous adenoma of the rectum treated by TEM
Figure 3.1 MRI image demonstrating “intussuscepting lesion.”
Figure 3.2 CT demonstrating free air between rectum and bladder.
Case 4: To stent or not to stent?
Figure 4.1 A distal sigmoid tumor visible on CT with distended large bowel loops upstream full of feculent matter.
Figure 4.2 Abdominal X-ray 2 days after stent insertion. The stent is just visible over the sacrum but there are still some dilated large bowel loops containing fecal residue.
Case 5: Advanced rectal cancer: Brazil or Japan?
Figure 5.1 (a) MRI (sagittal) of pelvis, showing tumor 6 cm from the anal verge and probable involved lymph node just inferior to aortic bifurcation (
white arrow
).
Figure 5.2 Endoscopic view of the rectum showing scarring at the site of the original cancer, with no evidence of residual tumor.
Case 6: Marginal decisions
Figure 6.1 Sagittal MRI scan showing lymph node at the circumferential resection margin.
Case 7: Locally advanced rectal cancer invading prostate
Figure 7.1 Pelvic MRI scan at presentation. Axial slices through the tumor show prostatic encroachment (a) and an enlarged pathological mesorectal lymph node (b).
Figure 7.2 Operative view of ureterosigmoid anastomosis (
left
) and loop “wet” colostomy (
right
).
Case 8: Low rectal cancer and synchronous polyps
Figure 8.1 Endoscopic image of the rectal cancer (
arrow
) with adjacent polyp and plaque-like lesion below (
arrow
).
Figure 8.2 Appearance following EMR of both polyps – note how close to the lower end of the cancer the EMR margin appears.
Case 9: Liver or rectum first?
Figure 9.1 PET-CT scan showing two liver metastases (
arrowed
).
Figure 9.2 Pelvic MRI showing significant mesorectal nodal disease (
arrow
).
Case 10: Beware bad livers!
Figure 10.1 Reconstructed CT colonography showing desending colon cancer.
Case 11: Anastomotic recurrence?
Figure 11.1 PET-CT scan showing area of increased uptake in left side of pelvis, adjacent to previous anastomosis.
Case 12: Challenging warts
Figure 12.1 Three perianal lesions.
Case 13: An unusual right iliac fossa mass
Figure 13.1 Large abdominal mass and liver metastases on CT scan.
Figure 13.2 Ten months following commencement of imatinib, FDG uptake in the liver was absent, with only a small area of avidity in the pelvis.
Case 14: A problem teenager
Figure 14.1 Growth chart showing slowing of growth before surgery and improvement after surgery.
Figure 14.2 Operative photograph showing exteriorized terminal ileum. Fat wrapping of the ileum, normal-looking cecum, and prominent mesenteric lymph nodes may be seen.
Case 15: Recurrent Crohn's disease with intraabdominal abscess: when to operate?
Figure 15.1 CT scan showing abscess within the small bowel mesentery.
Case 16: Very extensive small bowel stricturing disease
Figure 16.1 Small bowel enema showing extensive jejunal stricturing prior to first surgery age 23.
Figure 16.2 Operative sketch showing distribution of disease.
Figure 16.3 Operative photograph with sutures marking the site of strictures.
Figure 16.4 Operative photograph showing the strictures in the small bowel after it has been opened along its length.
Figure 16.5 Operative photograph showing the appearance after the Michelassi stricturoplasty.
Case 17: Long-standing Crohn's colitis and enterocutaneous fistula
Figure 17.1 CT scan of abdomen and pelvis demonstrating free air in the retroperitoneum and abdomen following iatrogenic perforation of an anastomotic stricture.
Figure 17.2 Endoscopic picture of anastomotic stricture during a dilatation.
Figure 17.3 Contrast enema demonstrating free passage of contrast through the ileorectal anastomosis following dilatation of stricture.
Figure 17.4 Inflammatory mass arising out of pelvis with enterocutaneous fistula.
Case 18: Crohn's colitis
Figure 18.1 MRE showing thickened abnormal left colon.
Figure 18.2 Contrast studies showing colonic strictures.
Case 19: Fistulating anal Crohn's disease: conservative management
Figure 19.1 MRI scan showing bilateral fluid collections and horse-shoe communication.
Figure 19.2 Appearances at EUA showing posterior ulcer lined by purulent fluid, healed left-sided scar, and external opening on right. Probing of the external opening showed fistulous communication to posterior ulcer (internal opening).
Case 20: Tail end carnage
Figure 20.1 MRI scan showing persisting proctitis and perianal disease.
Figure 20.2 Clinical appearance 6 months after defunctioning colostomy formation.
Case 21: Acute severe colitis
Figure 21.1 Appearances at flexible sigmoidoscopy at presentation.
Case 22: Snare or pouch? The problem of dysplasia in ulcerative colitis
Figure 22.1 (a) A 12 mm flat (Paris 0-IIa) lesion on a background of quiescent colitis on the transverse colon.
Figure 22.2 Surveillance for colorectal cancer in patients with UC and Crohn's colitis (BSG Guidelines, 2010).
Case 24: Poor pouch function
Figure 24.1 Pouchogram showing persistent mild narrowing in mid-section of pouch.
Case 25: Low rectal cancer in a patient with ulcerative colitis: late reconstruction with continent Kock ileostomy
Figure 25.1 Creation of the pouch starting with the opening antemesenterically of 30 cm of distal ileum, leaving the the most distal 15 cm of the ileum untouched.
Figure 25.2 The nipple is created from the most proximal part of the remaining terminal ileum using three cartridges and a bladeless stapler.
Figure 25.3 Intraoperative filling of pouch with saline to check continence of nipple valve.
Figure 25.4 One year after formation of the pouch, a pouchoscopy was performed. The nipple valve is quite low but still completely continent.
Section C: Pelvic floor disorders
Figure C.1 Endoanal ultrasound appearance of the normal sphincter. The dotted line delineates the probe itself. The internal anal sphincter (delineated by the hollow arrows) appears as a dark circle with the external sphincter (solid arrows) appearing as a lighter structure due to its lower water content.
Figure C.2 Still image from a defecating proctogram. The intussusception is shown as an infolding of the rectal wall, delineated by the white arrows. The rectocele bulges forward from the rectum into the vagina (shown in this study with a dotted line; the patient consented to having a contrast-soaked tampon inserted into the vagina). An enterocele is also shown (indicated by the dashed line), the patient having ingested oral contrast 1 hour prior to the start of the study.
Case 26: Constrictions of prolapse surgery
Figure 26.1 Examination under anesthetic with a circular anal dilator (CAD) revealed a stricture 2 cm above the dentate line (
left
). A transanal circular stapler was used to excise a ring of tissue from the stricture.
Case 27: Elderly prolapse dilemma
Figure 27.1 External prolapse evident on patient bearing down.
Case 28: Chasing incontinence
Figure 28.1 Endoanal ultrasound showing intact sphincters but a thickened internal sphincter.
Figure 28.2 Defecating proctography showing a full-thickness rectal prolapse with a moderate anterior rectocele trapping some barium. The pin corresponds to the level of the pelvic floor.
Figure 28.3 Operative photograph from a laparoscopic ventral mesh rectopexy, showing the “hockey stick dissection” into the rectovaginal septum and the mesh being slid into position prior to suture fixation to the rectum and sacral promontory.
Case 29: Sphincter disruption
Figure 29.1 Endoanal ultrasound showing a defect (area between arrows) in both the external (ES) and internal anal sphincter (IS).
Figure 29.2 (a) Bony landmarks give an excellent guide to locate the foramen of S3 and S4, negating the need for fluoroscopic guidance. S3 is located halfway between the posterior superior iliac spine (PSIS) and the sacrococcygeal joint (SC). S4 is located 9 cm above the tip of the coccyx (c). (b) To ensure optimal lateral positioning, the needle should be inserted about 1 fingerbreadth (FB) from the midline. The needle is then introduced at a 60° angle.
Case 31: Crohn's evacuation trouble
Figure 31.1 Examination under anesthetic using a circular anal dilator (CAD), showing internal prolapse.
Case 32: Disabling anal pain
Figure 32.1 Pudendal nerve blockade.
Section D: Proctology
Figure D.1 Parks' classification of cryptogenic anal fistulae.
Figure D.2 Horse-shoe abscesses.
Figure D.3 Goodsall's rule, here shown in practice for an anterior fistula. Note also the clear change in pigmentation which anatomically marks the outer border of the external anal sphincter.
Figure D.4 Drainage of horse-shoe abscess. There has been wide drainage and a corrugated drain has been passed around the horseshoe cavity. Part of the clean wound (at second look) has been closed and a large Foley catheter has been inserted into the anus for irrigation and to reduce wound contamination.
Figure D.5 Fistulotomy wound. Note the distinct fistula track.
Figure D.6 Marsupialization of transsphincteric fistulotomy wound.
Figure D.7 A loose silastic seton through a transsphincteric fistula in a female.
Figure D.8 Postoperative wound following rhomboid (Limberg) flap operation.
Figure D.9 Bilateral gluteal advancement flaps for extensive sacrococcygeal disease.
Figure D.10 Topical negative pressure therapy following excision of complex pilonidal disease.
Case 33: Hemorrhoids and HIV
Figure 33.1 Appearance of the anus under anesthesia with obvious circumferential hemorrhoidal prolapse.
Case 34: Refractory fissure
Figure 34.1 Botox injection for posterior fissure. Conventionally, the Botox is injected into the IAS either side of the fissure. The use of a 1 mL insulin syringe allows more accurate dosing.
Figure 34.2 Internal sphincterotomy. The IAS should be isolated from the external sphincter laterally and from the mucosa medially, and then divided up to a chosen level under direct vision.
Case 35: Hirschsprung's fistula
Figure 35.1 MRI scan demonstrating a wide track and abscess cavity extending out towards the left hip.
Figure 35.2 Gradual recovery with wound contraction. The silastic seton has been replaced with an Ethibond seton.
Figure 35.3 Marked improvement after the first ERAF.
Figure 35.4 Repeat ERAF. A mushroom catheter is evident posteriorly and the curette has been placed in the rectal lumen. Note the use of Lonestar and Gelpey retractors for improved exposure.
Case 36: Complex fistula in a young woman
Figure 36.1 Lockhart-Mummery probe within TS fistula. Note the outer border of the external sphincter where there is a subtle pigment change. The external fistula opening clearly lies well outside this.
Figure 36.2 Initial dissection of the intersphincteric space via a posterior curvilinear inscision. The probe remains through the track to aid identification.
Figure 36.4 The anal wound has been sutured and the external opening excised with curettage of an associated cavity. A Malecot catheter has been inserted via a counter-incision into the cavity to allow for gentle irrigation.
Case 37: Recurrent rectovaginal fistula
Figure 37.1 Large rectovaginal fistula admitting tip of index finger. Note adjacent scarring.
Figure 37.2 Mobilization of left gracilis muscle.
Figure 37.3 Subcutaneous tunneling of muscle to perineum. Note also repair of fistula on anorectal side.
Figure 37.4 Suturing of vaginal flap over interposed gracilis muscle.
Case 38: Adolescent cleft trouble
Figure 38.1 Appearance at second EUA (patient prone). The track close to the anus has healed and the main secondary track is seen arising from midline sinuses.
Figure 38.2 Appearance at 6 months showing complete healing.
Case 39: Extreme itch
Figure 39.1 Perianal area showing excoriation.
Figure 39.2 Appearance following methylene blue injection, showing tattooing of the perianal skin.
Section E: Emergency colorectal surgery
Figure E.1 Seatbelt sign. This is associated with a high chance of visceral injury. This young woman sustained injuries to the jejunum and rectosigmoid.
Case 40: Occupational blast disaster
Figure 40.1 Initial CT scan showing evisceration and the projectile in the right retroperitoneum.
Figure 40.2 AbdoVac in place following laparotomy and before negative pressure application.
Case 41: Wash and go?
Figure 41.1 CT scan demonstrating pockets of free intraperitoneal gas and abscess anterior to rectum.
Figure 41.2 Laparoscopic view of fibrin over the liver.
Case 42: Absolute constipation
Figure 42.1 Plain abdominal radiograph showing gross colonic dilatation.
Figure 42.2 CT showing decompressed cecum containing a large Foley catheter.
Case 43: Multiply ischemic parts
Figure 43.1 Ischemic left hand.
Figure 43.2 Infarcted and necrotic small bowel at initial laparotomy. A linear stapled transection has been carried out prior to resection.
Case 44: Seriously obscure bleeding
Figure 44.1 Capsule endoscopy images showing discrete ileal ulceration.
Case 45: Complicated twist
Figure 45.1 CT scan showing sigmoid volvulus.
Figure 45.2 Operative image showing grossly distended sigmoid colon.
Case 46: Obscure postoperative obstruction
Figure 46.1 Sagittal CT scan image showing anastomotic leak.
Figure 46.2 Coronal CT image showing the left colonic conduit containing contrast to the right of the midline and most of the small bowel lying in the left of the abdomen, following herniation underneath the colonic mesentery.
Case 47: Gynecological disaster
Figure 47.1 Appearance following third laparotomy. The ileostomy has been matured in the lower part of the midline wound and the “mucus fistula” is controlled with a Foley catheter. VAC has been applied to the open wound with a bridge to the previous ileostomy site.
Figure 47.2 At 3 weeks. Fascia and skin have been partly closed and a vicryl mesh used for containment. A skin bridge between ileostomy and mucus fistula facilitated stoma care.
Case 48: Pelvic leak and salvage
Figure 48.1 Sagittal CT image demonstrating a presacral fluid collection with a wisp of rectally administered contrast leaking from the staple line posteriorly.
Figure 48.2 Endoscopic image following Endosponge use. Whilst there is evidence of granulation tissue in a clean cavity, the anastomotic defect was 50% of the circumference.
Case 49: Radiology 0, Pathology 1
Figure 49.1 CT scan showing presacral and pelvic masses. The paucity of body fat makes interpretation difficult.
Figure 49.2 Laparoscopic appearances of patient showing tenting of small bowel and omentum to anterior abdominal wall from a peritoneal nodule.
Figure 49.3 Soft tissue showing nidus of actinomyces in association with suppurative inflammatory reaction and surrounded by chronic inflammation and fibrosis. (
Inset
) Periodic acid-Schiff stain highlighting the organized aggregate of delicate bacterial filaments.
Case 50: An appendix mass?
Figure 50.1 CT showing inflammatory mass involving cecum and terminal ileum.
Case 51: A worrying-looking rectal ulcer
Figure 51.1 Endoscopic appearance of the rectal ulcer.
Figure 51.2 Evacuation proctogram. The left-hand image shows the appearances at rest. In the right-hand image, there is invagination of the rectal wall with the lead point outside the anal canal on straining. The small bowel drops down significantly (enterocele), compressing the anterior rectum.
Case 52: Think the unthinkable
Figure 52.1 Sagittal MRI. The rectal mass is difficult to see but the L3 metastasis is evident.
Figure 52.2 Multiple liver metastases.
List of Tables
Section A: Colorectal cancer
Table A.1 TNM classification system for colorectal cancer
Table A.2 Five-year survival rate based on TMN staging of colon and rectal cancers
Case 10: Beware bad livers!
Table 10.1 Child–Turcotte–Pugh Score
Section B: Inflammatory bowel disease
Table B.1 Extraintestinal manifestations of Crohn's disease
Table B.2 Drugs used to treat Crohn's disease
Table B.3 Scoring system for endoscopic appearances in ulcerative colitis
Table B.4 Pouchitis scoring system. A score of over 7 with at least one point from each domain is required for a strict definition of pouchitis
Case 17: Long-standing Crohn's colitis and enterocutaneous fistula
Table 17.1 Risk factors for colonic malignancy in IBD
Section C: Pelvic floor disorders
Table C.1 Classification of anal sphincter injuries
Table C.2 Oxford Prolapse Grading System
Table C.3 Rome III criteria for functional constipation. These must have been fulfilled for the previous 3 months with symptom onset at least 6 months prior to diagnosis
Case 28: Chasing incontinence
Table C.1 Results of anorectal physiology
Case 29: Sphincter disruption
Table C.1 Anorectal physiology results
Case 30: Stimulating complications
Table 30.1 Expected responses on test stimulation
Section D: Proctology
Table D.1 Differential diagnosis of anal fistulae
Table D.2 Sphincter-preserving procedures for anal fistulae
Section E: Emergency colorectal surgery
Table E.1 Hinchey classification
Table E.2 Risk factors for anastomotic leakage after colorectal surgery
Colorectal Surgery
Clinical Care and Management
EDITED BY
Bruce George
Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Richard Guy
Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Oliver Jones
Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Jon Vogel
University of Colorado, Colorado, USA
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Library of Congress Cataloging-in-Publication Data
Names: George, Bruce, 1960- , editor. | Guy, Richard, 1964- , editor. |
Jones, Oliver, 1971- , editor. | Vogel, Jon, 1970- , editor.
Title: Colorectal surgery : clinical care and management / edited by Bruce
George, Richard Guy, Oliver Jones, Jon Vogel.
Other titles: Colorectal surgery (George)
Description: Chichester, West Sussex, UK ; Hoboken, NJ : John Wiley & Sons
Inc., 2016. | Includes bibliographical references and index.
Identifiers: LCCN 2015039644 | ISBN 9781118674789 (cloth)
Subjects: | MESH: Colonic Diseases\endash surgery. | Colonȓsurgery. | Colorectal
Surgeryȓmethods. | Rectal Diseases\endash surgery. | Rectumȓsurgery.
Classification: LCC RD543.C57 | NLM WI 650 | DDC 617.5/547--dc23 LC record available at http://lccn.loc.gov/2015039644
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Cover image: © Eraxion/Getty
List of contributors
Mohamed Abdelrahman
Research Fellow, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Shazad Ashraf
Consultant Colorectal Surgeon, University Hospital, Birmingham, UK
Sujata Biswas
Gastroenterology Registrar, Translational Gastroenterology Unit, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Emma Bracey
Surgical Fellow, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Nicolas Buchs
Colorectal Surgeon, University Hospitals of Geneva, Geneva, Switzerland
Marcus Chow
Medical Officer, Tan Tock Seng Hospital, Singapore
Christopher Cunningham
Consultant Colorectal Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
James East
Consultant Gastroenterologist, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Charles Evans
Consultant Colorectal Surgeon, University Hospitals of Coventry and Warwickshire, Coventry, UK
Myles Fleming
Colorectal Surgical Fellow, Auckland Hospital, Auckland, New Zealand
Luana Franceschilli
Colorectal Surgeon, University of Rome Tor Vergata, Rome, Italy
Bruce George
Consultant Colorectal Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Kim Gorissen
Consultant Colorectal and Emergency Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Martijn Gosselink
Colorectal Surgeon, Erasmus Medical Centre, Rotterdam, The Netherlands
Richard Guy
Consultant Colorectal Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Roel Hompes
Consultant Colorectal Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Gareth Horgan
Consultant Gastroenterologist, Naas General Hospital, Dublin, Ireland
Oliver Jones
Consultant Colorectal Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Heman Joshi
Specialist Surgical Registrar, St Helens and Knowsley NHS Trust, Merseyside, UK
Rebecca Kraus
Colorectal Surgeon, University Hospital, Basel, Switzerland
Simon Leedham
Consultant Gastroenterologist, Translational Gastroenterology Unit, Oxford University Hospitals NHS Foundation Trust, Oxford, UK; Wellcome Trust Centre for Human Genetics, Oxford University, Oxford, UK
Ian Lindsey
Consultant Colorectal Surgeon, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Richard Lovegrove
Colorectal Fellow, Mount Sinai Hospital, University of Toronto, Toronto, Canada
Marc Marti-Gallostra
Colorectal Surgeon, University Hospital Vall d'Hebron, Barcelona, Spain
Ami Mishra
Consultant Colorectal Surgeon, West Suffolk Hospital, Bury St. Edmunds, Suffolk, UK
Neil Mortensen
Professor of Colorectal Surgery, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Alistair Myers
Colorectal Surgeon, Hillingdon Hospital NHS Foundation Trust, London, UK
Par Myrelid
Colorectal Surgeon, University Hospital of Linkoping, Linkoping, Sweden
Jonathan Randall
Consultant Surgeon, University Hospitals, Bristol, UK
Frederic Ris
Consultant Colorectal Surgeon, University Hospitals of Geneva, Geneva, Switzerland
Astor Rodrigues
Consultant Paediatric Gastroenterologist, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Silvia Silvans
Colorectal Surgeon, Hospital del Mar, Barcelona, Spain
Richard Tilson
Colorectal Foundation Doctor, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Christian Toso
Visceral Surgeon and Associate Professor, University Hospitals of Geneva, Geneva, Switzerland
Koen van Dongen
Colorectal Surgeon, Maashospital Pantein, Beugen, The Netherlands
Jon Vogel
Colorectal Surgeon and Associate Professor of Surgery, University of Colorado, Colorado, US
Lai Mun Wang
Consultant Histopathologist, Department of Cellular Pathology, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Sara Q. Warraich
Colorectal Foundation Doctor, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Kate Williamson
Gastroenterologist, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Massarat Zutshi
Colorectal Surgeon, Cleveland Clinic, Cleveland, US
Foreword
Mastering the art and science of surgery is becoming increasingly difficult. The explosion of knowledge and technology is a threat to even a relatively new specialty like colorectal surgery. Our medical students have little exposure to the subject and need instant tutorials, our trainees struggle with the increasing complexity of operative surgery, and consultant staff are beginning to subspecialize. Everyone is finding it difficult to keep up. If you agree then this accessible, readable, and very enjoyable book will help.
Although not in quite the same league as the Case Records of the Massachusetts General Hospital, we have a weekly academic meeting in Oxford at which one of the residents or consultant staff presents a “case of the week.” The diagnosis, management, and outcome of each are poked, prodded, and recorded so that we can address our ignorance, learn from our mistakes, and look at controversies from every point of view.
This book distils some of these cases into 52 clinical vignettes arranged into groups of colorectal cancer, inflammatory bowel disease, proctology, and emergency surgery. For each group, there is a background chapter, and then the cases are presented with a discussion point, a series of learning points, and an important paragraph, “Could we have done better?” A particularly nice touch is the Letter from America in which one of our former residents looks at how US guidelines and practice might have differed from ours.
The Editors have done a great job choosing and putting together a terrific range of cases, some of which I remember only too well. And on reflection, yes, we could have done better.
Neil Mortensen, Oxford
Section AColorectal cancer
Bruce George
Oxford University Hospitals NHS Foundation Trust, Oxford, UK
Incidence
Colorectal cancer (CRC) is the second most common cause of cancer-related mortality in the Western world. Approximately 6% of the population will develop CRC during their lifetime.
Pathogenesis
Colorectal cancer develops through a stepwise accumulation of genetic and epigenetic alterations. There are three major molecular mechanisms involved in colorectal carcinogenesis:
chromosomal instability
microsatellite instability
CpG island methylation.
Chromosomal instability
In the late 1980s, Vogelstein et al. described a series of genetic alterations resulting in change from normal colonocytes through adenoma to carcinoma. Key genes in this process include adenomatous polyposis coli (APC), k-ras and p53, all of which code for proteins critically involved in regulation of cell turnover. APC is a tumor suppressor gene on chromosome 5q21 (long arm of chromosome 5). The APC protein controls degradation of beta-catenin which is involved in the control of epithelial cell turnover. Mutation of the APC gene results in accumulation of beta-catenin which, in turn, alters expression of several genes affecting cell proliferation, differentiation, and apoptosis. Germline mutation in the APC gene results in familial adenomatous polyposis (FAP).
Microsatellite instability
Microsatellites are short repeat nucleotide sequences found throughout the genome and are prone to errors during replication. Mutations in mismatch repair genes result in an increased risk of CRC. Tumors associated with defects in DNA mismatch repair are characterized by increased microsatellite instability. Germline mutations in mismatch repair genes result in hereditary nonpolyposis colorectal cancer (HNPCC).
CpG island methylation
More recently, epigenetic influences such as DNA methylation have been found to be involved in tumorigenesis. Normally, only about 3–4% of all cytosines in DNA are methylated and methylation only occurs at cytosines at the 5' end of guanine (CpGs). Clusters of CpGs tend to occur in the promoter region of many genes. Increased methylation of CpGs at the promoter end of tumor suppressor genes may result in reduced activation of the genes, resulting in increased tumor risk. Environmental factors may exert their influence on carcinogenesis through epigenetic mechanisms.
Awareness of the molecular changes in individual tumors is likely to become increasingly important in individualizing treatment. Sporadic tumors, for example, with features of high microsatellite instability, tend to respond poorly to 5-fluorouracil (5FU) chemotherapy.
Risk factors for colorectal cancer
Increasing age, a family history of CRC and long-term ulcerative colitis (UC) or Crohn's colitis are major risk factors for the development of CRC. Rare situations in which the risk is slightly increased include acromegaly, renal transplantation, and a history of abdominal irradiation.
Family history
Twin studies suggest that about 20% of CRC have an inherited predisposition. The mechanism of inherited risk is well characterized in patients with FAP (about 1% of all CRC) and HNPCC (about 3–5% of all CRC), but not in the remainder of those with a positive family history.
Familial adenomatous polyposis is an autosomal dominant condition resulting from mutation in the APC gene. The disease is characterized by the development of multiple polyps, usually over 100, in adolescence and, unless treated, inevitable progression to colon cancer. Extracolonic features include gastroduodenal polyps – with a lifetime risk of duodenal cancer of 12% – and desmoid tumors. The precise site of the mutation in the APC gene correlates with the clinical phenotype, for example the risk of developing desmoid tumors.
Hereditary nonpolyposis colorectal cancer is an autosomal dominant condition caused by a germline mutation in DNA mismatch repair genes. Loss of mismatch repair genes results in replication errors, increased mutations, and an increased risk of malignancy. The hallmark of HNPCC is microsatellite instability. Individuals with HNPCC tend to develop tumors at a younger age than those with sporadic tumors and are also at increased risk of other tumors, especially endometrial, gastric, ovarian, and urinary tract.
It is impractical to genetically test all family members of patients with CRC for HNPCC, and various criteria have been developed to identify patients and families likely to have HNPCC, the most common being the Amsterdam Criteria (Box A.1).
Box A.1 Amsterdam criteria for the diagnosis of HNPCC
Amsterdam I
At least three relatives with CRC, one of which should be a first-degree relative of the other twoAt least two successive generations affectedAt least one CRC diagnosed before the age of 50 yearsFAP excludedTumors verified histologicallyAmsterdam II
At least three relatives with an HNPCC-associated cancer, one of which should be a first-degree relative of the other twoAt least two successive generations affectedAt least one CRC diagnosed before age 50 yearsFAP excludedTumors verified histologically
Diet and lifestyle
A high-fiber diet has been postulated for many years to be associated with a reduced risk of CRC, although results from several meta-analyses show conflicting results. The EPIC study suggests that a high-fiber diet is associated with a 40% risk reduction. On the other hand, red meat, smoking, alcohol, and obesity have been associated with an increased risk. Increased physical exercise has been shown to be independently associated with a reduced risk.
Long-term aspirin therapy has been shown in several studies with over 20-year follow-up to be associated with a reduced risk, although a recent consensus group felt that further research was needed before aspirin could be recommended as chemoprevention for high-risk groups [1].
Pathology
Most CRCs are thought to arise from adenomatous polyps. A variety of polyps is found in the colon and rectum, varying in their premalignant potential (Box A.2).
Box A.2 Types of polyp in the colon and rectum
The site, size, number, and shape of polyps are important in assessing risk. The majority of polyps are sessile or pedunculated, although the Paris classification is useful, particularly when assessing small flat lesions (Figure A.1).
Figure A.1 Paris classification.
Source: Participants in the Paris Workshop. 2003. Reproduced with permission of Elsevier.
When viewed colonoscopically using adjuncts such as chromoendoscopy (“dye spray”) and high-definition imaging, different “pit patterns” may be observed on the surface of polyps, which may help to identify the type of polyp (Figure A.2).
Figure A.2 Polyp pit patterns.
Source: Williams [2]. Reproduced with permission of Wiley.
Broadly speaking, pit patterns 1 and 2 tend to be associated with normal or nonneoplastic lesions, types 3 and 4 with adenomas, and type 5 with invasive malignancy.
Adenomatous polyps show cellular dysplasia and are potentially premalignant. Architecturally, they may be classified as tubular, tubulovillous or villous. Thus, larger villous lesions with high-grade dysplasia have a higher risk of malignant transformation.
Serrated lesions are being increasingly recognized, particularly since the advent of screening programs, although their natural history remains unclear. There are three types of serrated lesions.
Hyperplastic polyp
. These tend to be small sessile lesions mainly in the rectum and have no malignant potential.
Sessile serrated adenoma (SSA)
. These tend to occur in the right colon, may be large in size but can be difficult to identify colonoscopically. They are associated with a risk of synchronous advanced neoplasms.
Traditional serrated adenoma (TSA)
. These are more likely to be situated in the left colon and are easier to identify colonoscopically.
It is thought that SSAs and TSAs may progress to invasive malignancy by a distinct molecular pathway, involving BRAF mutation and epigenetic silencing of mismatch repair genes. The importance of thorough colonoscopic clearance and surveillance is being realized. Multiple hyperplastic polyposis syndromes are being increasingly recognized and have a 50% lifetime risk of CRC (see Case 2).
Appearance and distribution
Macroscopically, CRC may be polypoid, ulcerated or annular. The distribution of tumors is approximately as follows: 40% rectum or rectosigmoid junction, 25% sigmoid, 25% cecum or ascending colon, and the remainder (10%) in the transverse or descending colon.
Pathological features
Microscopically, tumors are adenocarcinomas with varying degrees of differentiation. Histological features associated with a poor prognosis include mucinous, signet ring, and neuroendocrine differentiation. Immunohistochemically, colorectal carcinomas tend to be CK20 positive and CK7 negative.
Colorectal cancer staging
The most common pathological staging systems in use are the Dukes and TNM (Tumor, Node, Metastases) systems (Table A.1). Dukes' original stages are as follows.
A – tumor confined to the bowel wall without lymph node involvement
B – tumor beyond the wall with no lymph node involvement
C – any tumor with lymph node involvement
Later modifications included C1 (apical node not involved), C2 (apical node involved), and Dukes' D to indicate distant metastases.
Table A.1 TNM classification system for colorectal cancer
T stage
N stage
M stage
T1
Tumor confined to the submucosa
N0
No lymph nodes contain tumor cells
M0
No metastases seen in distant organs
T2
Tumor has grown into (but not through) the muscularis propria
N1
Tumor cells seen in up to 3 regional lymph nodes
*
M1
Metastases seen in distant organs
T3
Tumor has grown into (but not through) the serosa
N2
Tumor cells seen in 4 or more regional lymph nodes
**
T4
Tumor has penetrated the serosa and peritoneal surface
T4a
Extension into adjacent structures or organs
T4b
Bowel perforation
* A tumor nodule in the pericolic or perirectal adipose tissue without evidence of residual lymph node is regarded as a lymph node metastasis if it is >3 mm in diameter. If it is <3 mm in diameter, it is regarded as discontinuous tumor extension.
** If there are tumor cells in nonregional lymph nodes (i.e. in a region of the bowel with a different pattern of lymphatic drainage to that of the tumor), that is regarded as distant metastasis (pM1).
Source: American Joint Committee on Cancer [5].
The prognosis following CRC resection is largely dependent upon the pretreatment radiological staging [3, 4]. This can only be determined for TNM stages, in various permutations and combinations (Table A.2), as Dukes' staging relies on the histopathological examination of a resected specimen.
Table A.2 Five-year survival rate based on TMN staging of colon and rectal cancers
TMN
Colon 5-year survival rate
Rectal 5-year survival rate
T1, T2 N0
97.1%
94.4%
T3 N0
87.5%
78.7%
T4 N0
71.5%
61.4%
T1, T2 N1
87.1%
85.1%
T1, T2 N2
75.0%
63.9%
T3 N1
68.7%
63.3%
T3 N2
47.3%
43.7%
T4 N1
50.5%
47.1%
T4 N2
27.1%
29.5%
Clinical presentation
Colorectal malignancy may be detected in asymptomatic individuals, either through screening or incidentally during investigation of other problems. More commonly, tumors present due to symptoms related to the primary tumor or due to metastatic spread.
Symptoms of colorectal cancer
The classic symptoms of colorectal malignancy depend on the site of the tumor. Rectal tumors tend to present with overt rectal bleeding, passage of mucus or tenesmus. Sigmoid and descending colon lesions tend to present with darker blood mixed with stool or an alteration in bowel pattern. Cancers in the right colon are more likely to be “silent” and to present with anemia, weight loss or anorexia.
In clinical practice, many patients present with symptoms which may fit for CRC but could also be attributed to a variety of benign disorders. Identification of significant (“red flag”) symptoms (Box A.3) has been attempted in order to expedite appropriate investigations, and to exclude those who probably do not warrant urgent referral. In the UK, these have been used to facilitate rapid assessment, although the efficacy is questioned and there may still be a tendency for overreferral.
Box A.3 “Red flag” symptoms suggesting CRC
The majority of patients presenting with significant symptoms require luminal investigation, either by colonoscopy or CT colonography (“virtual colonoscopy”). A recent UK multicenter trial compared colonoscopy to CT colonography in patients referred with bowel symptoms [6]. Detection rates for cancers and large polyps were similar (11%), although significantly more patients required additional investigation after CT colonography than after colonoscopy.
Emergency presentation
About 25% of patients with CRC present as an emergency, most commonly with colonic obstruction. Tumor perforation, major bleeding or anemia may also prompt emergency admission.
Symptoms due to metastatic disease
Approximately 25% of patients with CRC have metastatic disease at the time of presentation, often with nonspecific symptoms such as weight loss, anorexia, lethargy or anemia. Less commonly, patients present with focal symptoms due to metastases in the liver (such as capsular pain), lung or brain.
Incidental detection following other investigations
Potentially important colorectal lesions may be detected on radiological imaging during investigations for unrelated pathology. Focal colonic uptake on PET scans, for example, is quite often an indicator of significant pathology. In a recent study [7], CRC was diagnosed in 12 of 28 patients undergoing colonoscopy for PET scan abnormalities.
Screening (see Cases 1, 2 and 8)
Colorectal cancer may be “the most screenable but least screened” of the major cancers. Screening methods include stool tests for occult blood, flexible sigmoidoscopy, colonoscopy or CT colonography.
Guaiac fecal occult blood testing (FOBT) is the most widely used screening method. Blood in the stool is detected by peroxidase activity of the heme part of the hemoglobin molecule, which is not specific to human blood. A positive test usually triggers further assessment by colonoscopy, and this forms the basis of the UK's NHS Bowel Cancer Screening Programme (BCSP) for individuals aged 60–75 years. A Cochrane review of major screening trials worldwide concluded that screening by FOBT decreases mortality from colorectal cancer by about 16%, although there may not be a difference in all-cause mortality between screened and unscreened groups [8].
Newer occult blood tests which are specific to human hemoglobin, such as detection of globin, may yield better results than guaiac-based FOBT.
Colonoscopy as a primary screening modality is attractive in being both diagnostic and potentially therapeutic and is generally considered to be the gold standard investigation for colorectal neoplasia. Whilst not perfect, with a measurable “miss rate” for adenomas, and the requirement for oral bowel preparation carrying some risk, application to large populations has been proven in the NHS BCSP, and endoscopist expertise continues to improve.
Flexible sigmoidoscopy (FS) as a screening tool has been subject to a major UK-based trial [9], involving 55–64 year olds. Polyps detected at flexible sigmoidoscopy were removed and high-risk patients underwent colonoscopy. At median follow-up of 11 years, screening was associated with a 31% reduction in mortality from colorectal cancer and a 23% reduction in CRC incidence. FS has now been incorporated into the NHS BCSP for those aged 55 years and over. The American College of Gastroenterology recommends screening by colonoscopy from the age of 50 years at 10-yearly intervals [10].
Radiological imaging of the colon by CT colonography (virtual colonoscopy) may be used as a screening investigation, and is incorporated into the NHS BCSP for less fit patients and for those in whom colonoscopy was incomplete. There are few procedural risks but exposure to ionizing radiation is of slight concern (see Case 14). A head-to-head comparison of colonoscopy and CT colonography [11] showed broadly similar detection rates, with CT colonography slightly outperforming colonoscopy for larger lesions.
Investigation of colorectal cancer
Ideally, all patients with CRC should be assessed by full colonoscopy with biopsy of the primary tumor. Synchronous tumors may be detected in around 4% of cases. Convincing CT colonography may negate the requirement for colonoscopic biopsy, particularly for proximal colonic tumors. All rectal cancers should have histological confirmation.
Staging should be undertaken with CT scanning of the abdomen and chest in order to exclude metastatic disease. Rectal tumors usually require MRI for local staging, allowing assessment of T stage, N stage, vascular invasion, and the mesorectal margin. Endoanal ultrasound may be useful for assessing the T stage of small or early tumors. Liver MRI or PET-CT may be indicated for further clarification of disease stage.
Measurement of serum carcinoembryonic antigen (CEA) at the time of diagnosis is controversial and not universal, but may be useful for assessing response to treatment and during follow-up, particularly in the presence of liver metastases [12].
Decision making: the multidisciplinary team (MDT)
There is some evidence that outcomes may be improved by formal discussion in multidisciplinary meetings at which surgeons, radiologists, oncologists, and pathologists, amongst others, review individual cases. Burton et al. [13] showed that this process was associated with a lower R1 resection rate and Morris et al. [14] demonstrated better surgical and oncological outcomes.
Colonic cancer
Most patients without metastatic disease proceed to surgical resection. A small proportion of locally advanced colonic tumors may benefit from preoperative neoadjuvant chemotherapy, although good evidence and indications are lacking.
Malignant colonic obstruction (see Cases 4 and 10)
Surgical options for the management of malignant colonic obstruction have traditionally included defunctioning stoma, Hartmann's procedure or resection with on-table colonic lavage and primary anastomosis. Self-expanding metallic stents, usually inserted under endoscopic and radiological guidance, may rapidly relieve obstruction. In the elderly, unfit patient or those with advanced or metastatic disease, stenting is an attractive palliative option but stenting as a “bridge to surgery” with curative intent is more controversial. The aim is to relieve obstruction, allow correction of physiological abnormalities and then proceed to semi-elective surgery, potentially after bowel preparation. Such surgery is more likely to be undertaken laparoscopically and to be restorative. A recent metaanalysis of randomized trials describes technical and clinical success rates for stenting of 71% and 69%, respectively [15]. Potential complications include stent migration, blockage, and, more seriously, perforation, a clinical perforation rate of 7% and a silent perforation rate of 14% being reported in the metaanalysis. Stenting may cause tumor fracturing [16] and perhaps hematological and lymphatic dissemination.
Effects on local or distant recurrence have not been fully evaluated, although a Dutch study did not identify a major increased risk of recurrence [17], despite a high perforation rate. A study from Oxford, however, did identify a higher rate of local recurrence in patients treated by stenting before surgery compared to resection alone [18].
The randomized CReST trial (www.crest.bham.ac.uk) is evaluating short- and long-term outcomes from stenting as a bridge to surgery and may shed more light on these important questions.
Rectal cancer
The challenge of rectal cancer management in the absence of advanced metastatic disease is to achieve curative treatment with minimal morbidity. Total mesorectal excision, popularized by Heald [19], and preoperative radiotherapy [20, 21] have been associated with dramatic improvements in oncological outcome. Furthermore, improvements in preoperative imaging have permitted a more tailored approach to patient management.
Anterior resection remains the default treatment for rectal cancer. The MDT must identify:
patients with early tumors amenable to local resection
patients with tumors at risk of local recurrence who may require preoperative radiotherapy or chemoradiotherapy
cases of complete clinical response after chemoradiotherapy
patients who require abdominoperineal excision of the rectum (APER) or are “on the cusp” of ultra-low anterior resection or APER
patients with potentially curative synchronous liver and rectal tumors
patients with locally advanced or recurrent disease (see case 11).
Local excision
Local excision may be reasonably considered for early rectal tumors. Whilst the avoidance of major abdominal and pelvic surgery may be attractive and less morbid, the reduced radicality of the resection, and the lack of lymph node retrieval, may have consequences which must be discussed with the patient.
The risk of lymph node involvement in T1 tumors may be difficult to estimate but depends on tumor size, extent of penetration into the submucosa, and degree of differentiation.
Invasive tumor within a pedunculated polyp is assessed by the Haggitt system [22] (Figure A.3) (see Case 1). Invasion in a sessile polyp is assessed by the Kikuchi et al. [23] system (Figure A.4). This simply describes invasion into the upper third (sm1), the middle third (sm2) or the lower third (sm3) of the submucosa.
Figure A.3 Haggitt system for cancer invasion in a pedunculated polyp.
Source: Haggitt et al. [22]. Reproduced with permission of Elsevier.
Figure A.4 The Kikuchi classification for sessile malignant polyps.
Source: Kikuchi et al. [23]. Reproduced with permission of Springer publications.
Disruption of a locally excised specimen or piecemeal removal of a sessile polyp by endoscopic mucosal resection (EMR) may prevent accurate Kikuchi assessment. An alternative approach focuses on the depth and width of invasion beyond the muscularis mucosa.
Current opinion is that tumors suitable for local excision with curative intent should:
be less than 3 cm diameter
not be poorly differentiated
have early T1 invasion only (sm1 or 2)
have no evidence of nodal involvement on MRI.
Tumors which do not meet these criteria have a greater risk of tumor in lymph nodes and should generally be treated by conventional resection. A recent trial comparing local excision by transanal endoscopic microsurgery (TEM) with laparoscopic anterior resection for T1/T2 rectal tumors showed less morbidity following TEM. There were two local recurrences after TEM (2/28, 7%) compared to none after anterior resection, although this difference was not statistically significant [24].
Local excision may be employed as a compromise for patients who are medically unfit for major resection.
Preoperative radiotherapy (see Cases 5–7)
Preoperative radiotherapy (RT) may be delivered in short or long courses. Short-course RT is typically 5 × 5 Gy over 5 days followed by surgery the next week. Long-course RT is usually 45–50 Gy given over about 5 weeks with 5FU given during weeks 1 and 5. Surgery is undertaken about 6–8 weeks after completion of chemoradiotherapy. There is increasing evidence that a longer interval to surgery, perhaps out to 12 weeks, may be associated with more tumor shrinkage [25].
Several large trials have shown a significant reduction in local recurrence following surgery after short-course RT compared to surgery alone [20, 21, 26–28]. Only one of these trials – the Swedish rectal cancer trial – showed an improvement in overall survival.
Long-course chemoradiotherapy (CRT) has the advantage over short-course RT (with early surgery) of achieving tumor shrinkage (“downstaging”). This may permit surgical resection with negative margins – which might not have been achieved without CRT – with a significantly reduced risk of local recurrence. Downstaging by CRT may also increase the chance of sphincter-preserving surgery.
Complete clinical response
Around 10–15% of patients will achieve a complete pathological response to long-course CRT, with the result that no viable tumor cells are found in the surgical resection specimen. Such patients have a better prognosis [29]. The idea of avoiding major resectional surgery in patients with a complete clinical response has been popularized by Habr-Gama et al. from Brazil [30] although other groups have not been able to obtain such good results [31]. It is recommended that a “watch and wait” approach after an apparently complete clinical response should only be considered within a rigorous follow-up regime or, ideally, a clinical trial (see Case 5).
Need for APER
Patients with very low rectal tumors are at the highest risk of positive margins, and either a poor functional outcome following restorative surgery or the need for a permanent stoma. The vast majority of such patients will receive preoperative chemoradiotherapy.
A decision regarding feasibility of sphincter preservation versus APER requires detailed clinical assessment, review of MR scans, and discussion with the patient. If a decision is made to undertake an APER, the plane of dissection, position of threatened margins, and the method of perineal reconstruction should be planned in advance.
Metastatic disease
In patients with metastatic disease, the dominant treatment is usually chemotherapy. Surgery may only be indicated to alleviate symptoms from the primary tumor not controllable by conservative means. For patients with potentially curative synchronous liver and colonic tumors, 60–70% undergo resection of the primary as initial treatment. This may be associated with significant postoperative morbidity preventing subsequent chemotherapy or liver surgery. Furthermore, R1/R2 rates are higher when the surgeon is aware of metastatic disease [32]. Over the last decade, there has been a move towards a “liver first” approach [33] or, in selected cases, simultaneous liver resections if both are relatively straightforward (see Case 9). A similar approach has been adopted for metastatic rectal disease [34]. Clearly, the liver first approach is not appropriate if the primary tumor is causing obstructive symptoms due to the risk of complete obstruction occurring during chemotherapy or liver surgery.
